Medical Surgical Nursing Pinoy

MEDICAL-SURGICAL NURSING

By: Anthony T. Villegas R.N.

Overview of structures and functions:

NERVOUS SYSTEM

The functional unit of the nervous system is the nerve cells

or neurons

The nervous system is composed of the ff:

Central Nervous System

Brain

Spinal Cord – serves as a connecting link between the brain

& the periphery.

Peripheral Nervous System

Cranial Nerves –12 pairs; carry impulses to & from the brain.

Spinal Nerves – 31 pairs; carry impulses to & from spinal

cord.

Autonomic Nervous System

subdivision of the PNS that automatically controls body

function such as breathing & heart beat.

Special senses of vision and hearing are also covered in this section

Sympathetic nervous system – generally accelerate some

body functions in response to stress.

Parasympathetic nervous system – controls normal body

functioning.

CELLS

A. NEURONS

Primary component of nervous system

Composed of cell body (gray matter), axon, and dendrites

Basic cells for nerve impulse and conduction.

Axon

Elongated process or fiber extending from the cell body

Transmits impulses (messages) away from the cell body to

dendrites or directly to the cell bodies of other neurons

Neurons usually has only one axon

Dendrites

Short, blanching fibers that receives impulses and conducts

them toward the nerve cell body.

Neurons may have many dendrites.

Synapse

Junction between neurons where an impulse is transmitted

Neurotransmitter

Chemical agent (ex. Acetylcholine, norepinephrine) involved

in the transmission of impulse across synapse.

Myelin Sheath

A wrapping of myelin (whitish, fatty material) that protects

and insulates nerve fibers and enhances the speed of

impulse conduction.

o Both axons and dendrites may or may not have a

myelin sheath (myelinated/unmyelinated)

o Most axons leaving the CNS are heavily myelinated

by schwann cells

Functional Classification

1. Afferent (sensory) neurons

Transmit impulses from peripheral receptors to the CNS

2. Efferent (motor) neurons

Conduct impulses from CNS to muscle and glands

3. Internuncial neurons (interneurons)

Connecting links between afferent and efferent neurons

Properties

1. Excitability – ability of neuron to be affected by changes in

external environment.

2. Conductility – ability of neuron to transmit a wave of

excitetation from one cell to another.

3. Permanent Cell – once destroyed not capable of

regeneration.

TYPES OF CELLS BASED ON REGENERATIVE CAPACITY

1. Labile

Capable of regeneration.

Epidermal cells, GIT cells, GUT cells, cells of lungs.

2. Stable

Capable of regeneration with limited time, survival

period.

Kidney cells, Liver cells, Salivary cells, pancreas.

3. Permanent

Not capable of regeneration.

Myocardial cells, Neurons, Bone cells, Osteocytes,

Retinal Cells.

B. NEUROGLIA

Support and protection of neurons.

TYPES

1. Astrocytes

maintains blood brain barrier semi-permiable.

majority of brain tumors (90%) arises from called

astrocytoma.

integrity of blood brain barrier.

2. Oligodendria

produces myelin sheath in CNS.

act as insulator and facilitates rapid nerve impulse

transmission.

3. Microglia

stationary cells that carry on phagocytosis (engulfing of

bacteria or cellular debris, eating), pinocytosis (cell

drinking).

4. Epindymal

secretes a glue called chemo attractants that

concentrate the bacteria.

MACROPHAGE ORGAN

Microglia

Monocytes

Kupffers

Histiocytes

Alveolar Macrophage

Brain

Blood

Kidney

Skin

Lung

Central Nervous System

Composition Of Brain

80% brain mass

10% blood

10% CSF

Brain Mass

Parts Of The Brain

1. Cerebrum

largest part of the brain

outermost area (cerebral cortex) is gray matter

deeper area is composed of white matter

function of cerebrum: integration, sensory, motor

composed of two hemisphere the Right Cerebral

Hemisphere and Left Cerebral Hemisphere enclosed in

the Corpus Callosum.

Each hemisphere divided into four lobes; many of the

functional areas of the cerebrum have been located in

these lobes:

Lobes of Cerebrum

1. Frontal Lobe

controls personality, behavior

higher cortical thinking, intellectual functioning

precentral gyrus: controls motor function

Broca’s Area: specialized motor speech area - when

damaged results to garbled speech.

2. Temporal Lobe

hearing, taste, smell

short term memory

Wernicke’s area: sensory speech area

(understanding/formulation of language)

3. Pareital Lobe

for appreciation

integrates sensory information

discrimination of sensory impulses to pain, touch,

pressure, heat, cold, numbness.

Postcentral gyrus: registered general sensation (ex.

Touch, pressure)

4. Occipital Lobe

for vision

Insula (Island of Reil)

visceral function activities of internal organ like gastric

motility.

Limbic System (Rhinencephalon)

1

1

controls smell - if damaged results to anosmia (absence

of smell).

controls libido

controls long term memory

Corpus Callosum

large fiber tract that connects the two cerebral

hemisphere

Basal Ganglia

island of gray matter within white matter of cerebrum

regulate & integrate motor activity originating in the

cerebral cortex

part of extrapyramidal system

area of gray matter located deep within each cerebral

hemisphere.

release dopamine (controls gross voluntary movement).

2. Diencephalon/interbrain

Connecting part of the brain, between the cerebrum &

the brain stem

Contains several small structures: the thalamus &

hypothalamus are most important

Thalamus

acts as relay station for discrimination of sensory signals

(ex. Pain, temperature, touch)

controls primitive emotional responses (ex. Rage, fear)

Hypothalamus

found immediately beneath the thalamus

plays a major role in regulation/controls of vital function:

blood pressure, thirst, appetite, sleep & wakefulness,

temperature (thermoregulatory center)

acts as controls center for pituitary gland and affects

both divisions of the autonomic nervous system.

controls some emotional responses like fear, anxiety

and excitement.

androgenic hormones promotes secondary sex

characteristics.

early sign for males are testicular and penile

enlargement

late sign is deepening of voice.

early sign for females telarch and late sign is menarch.

3. Mesencephalon/Midbrain

acts as relay station for sight and hearing.

size of pupil is 2 – 3 mm.

equal size of pupil is isocoria.

unequal size of pupil is anisocoria.

hearing acuity is 30 – 40 dB.

positive PERRLA

4. Brain Stem

located at lowest part of brain.

contains midbrain, pons, medulla oblongata.

extends from the cerebral hemispheres to the foramen

magnum at the base of the skull.

contains nuclei of the cranial nerves and the long

ascending and descending tracts connecting the

cerebrum and the spinal cord.

contains vital center of respiratory, vasomotor, and

cardiac functions.

Pons

pneumotaxic center controls the rate, rhythm and depth

of respiration.

Medulla Oblongata

controls respiration, heart rate, swallowing, vomiting,

hiccup, vasomotor center (dilation and constriction of

bronchioles).

5. Cerebellum

smallest part of the brain, lesser brain.

coordinates muscle tone and movements and maintains

position in space (equilibrium)

controls balance, equilibrium, posture and gait.

Spinal Cord

serves as a connecting link between the brain and

periphery

extends from foramen magnum to second lumbar

vertebra

H-shaped gray matter in the center (cell bodies)

surrounded by white matter (nerve tract and fibers)

Gray Matter

1. Anterior Horns

Contains cell bodies giving rise to efferent (motor)

fibers

2. Posterior Horns

Contains cell bodies connecting with afferent

(sensory) fibers from dorsal root ganglion

3. Lateral Horns

In thoracic region, contain cells giving rise to

autonomic fibers of sympathetic nervous system

White Matter

1. Ascending Tracts (sensory pathways)

a. Posterior Column

Carry impulses concerned with touch,

pressure, vibration, & position sense

b. Spinocerebellar

Carry impulses concerned with muscle

tension & position sense to cerebellum

c. Lateral Spinothalamic

Carry impulses resulting in pain &

temperature sensations

d. Anterior Spinothlamic

Carry impulses concerned with crude

touch & pressure

2. Descending Tracts (motor pathways)

a. Corticospinal (pyramidal, upper motor neurons)

Conduct motor impulses from motor

cortex to anterior horn cells (cross in

the medulla)

b. Extrapyramidal

Help to maintain muscle tone & to

control body movement, especially

gross automatic movements such as

walking

Reflex Arc

Reflex consists of an involuntary response to a stimulus

occurring over a neural pathway called a reflex arc.

Not relayed to & from brain: take place at cord levels

Components

a. Sensory Receptors

Receives/reacts to stimulus

b. Afferent Pathways

Transmits impulses to spinal cord

c. Interneurons

Synapses with a motor neuron (anterior horn cell)

d. Efferent Pathways

Transmits impulses from motor neuron to effector

e. Effectors

Muscle or organ that responds to stimulus

Supporting Structures

1. Skull

Rigid; numerous bones fused together

Protects & support the brain

2. Spinal Column

Consists of 7 cervical, 12 thoracic, & 5 lumbar vertebrae

as well as sacrum & coccyx

Supports the head & protect the spinal cord

3. Meninges

Membranes between the skull & brain & the vertebral

column & spinal cord

3 fold membrane that covers brain and spinal cord.

For support and protection; for nourishment; blood

supply

Area between arachnoid & pia mater is called

subarachnoid space: CSF aspiration is done

Subdural space between the dura and arachnoid

Layers:

Dura Mater

outermost layer, tough, leathery

Arachnoid Mater

middle layer, weblike

2

2

Pia Mater

innermost layer, delicate, clings to surface of brain

4. Ventricles

Four fluid-filled cavities connecting with one

another & spinal canal

Produce & circulate cerebrospinal fluid

5. Cerebrospinal Fluid (CSF)

Surrounds brain & spinal cord

Offer protection by functioning as a shock absorber

Allows fluid shifts from the cranial cavity to the spinal

cavity

Carries nutrient to & waste product away from nerve

cells

Component of CSF: CHON, WBC, Glucose

6. Vascular Supply

Two internal carotid arteries anteriorly

Two vertebral arteries leading to basilar artery

posteriorly

These arteries communicate at the base of the brain

through the circle of willis

Anterior, middle, & posterior cerebral arteries are the

main arteries for distributing blood to each hemisphere

of the brain

Brain stem & cerebellum are supplied by branches of

the vertebral & basilar arteries

Venous blood drains into dural sinuses & then into

jugular veins

7. Blood-Brain-Barrier (BBB)

Protective barrier preventing harmful agents from

entering the capillaries of the CNS; protect brain &

spinal cord

Substance That Can Pass Blood-Brain Barrier

1. Amonia

Cerebral toxin

Hepatic Encephalopathy (Liver Cirrhosis)

Ascites

Esophageal Varices

Early Signs of Hepatic Encephalopathy

Asterexis (flapping hand tremors).

Late Signs of Hepatic Encephalopathy

Headache

Dizziness

Confusion

Fetor hepaticus (amonia like breath)

decrease LOC

2. Carbon Monoxide and Lead Poisoning

Can lead to Parkinson’s Disease.

Epilepsy

Treated with calcium EDTA.

3. Type 1 DM (IDDM)

Causes diabetic ketoacidosis.

And increases breakdown of fats.

And free fatty acids

Resulting to cholesterol and positive to ketones (CNS

depressant).

Resulting to acetone breath odor/fruity odor.

And kusshmauls respiration a rapid shallow respiration.

Which may lead to diabetic coma.

4. Hepatitis

Signs of jaundice (icteric sclerae).

Caused by bilirubin (yellow pigment)

5. Bilirubin

Increase bilirubin in brain (kernicterus).

Causing irreversible brain damage.

Peripheral Nervous System

Spinal Nerves

31 pairs: carry impulses to & from spinal cord

Each segment of the spinal cord contains a pair of spinal

nerves (one of each side of the body)

Each nerve is attached to the spinal by two roots:

1. Dorsal (posterior) roots

contains afferent (sensory) nerve whose cell

body is in the dorsal roots ganglion

2. Ventral (anterior) roots

Contains efferent (motor) nerve whose nerve

fibers originate in the anterior horn cell of the

spinal cord (lower motor neuron)

Cranial Nerves

12 pairs: carry impulses to & from the brain.

May have sensory, motor, or mixed functions.

Name & Number Function

Olfactory : CN I Sensory: carries impulses for

sense of smell.

Optic : CN II Sensory: carries impulses for vision.

Oculomotor : CN III Motor: muscles for papillary

constriction, elevation of upper eyelid;

4 out of 6 extraocular

movement.

Trochlear : CN IV Motor: muscles for downward,

inward, movement of the eye

Trigeminal : CN V Mixed: impulses from face, surface

of eyes (corneal reflex); muscle

Controlling mastication.

Abducens : CN VI Motor: muscles for lateral deviation

of eye

Facial : CN VII Mixed: impulses for taste from

anterior tongue; muscles for facial

Movement.

Acoustic : CN VIII Sensory: impulses for

hearing (cochlear division) & balance (vestibular

Division).

Glossopharyngeal : CN IX Mixed: impulses for

sensation to posterior tongue & pharynx; muscle

For movement of pharynx

(elevation) & swallowing.

Vagus : CN X Mixed: impulses for sensation to

lower pharynx & larynx; muscle for

Movement of soft palate,

pharynx, & larynx.

Spinal Accessory : CN XI Motor: movement of

sternomastoid muscles & upper part of trapezius

Muscles.

Hypoglossal : CN XII Motor: movement of tongue.

Autonomic Nervous System

Part of the peripheral nervous system

Include those peripheral nerves (both cranial & spinal) that

regulates smooth muscles, cardiac muscles, & glands.

Component:

1. Sympathetic Nervous System

Generally accelerates some body function in

response to stress.

2. Parasympathetic Nervous System

Controls normal body functioning

Sympathetic Nervous System

(Adrenergic) Effect

Parasympathetic Nervous System

(Cholinergic) Effect, Vagal,

Sympatholytic

- Involved in fight or aggression

response.

- Release of Norepinephrine

(cathecolamines) from adrenal

glands and causes

vasoconstriction.

- Increase all bodily activity

except GIT

EFFECTS OF SNS

- Dilation of pupils (mydriasis) in

order to be aware.

- Dry mouth (thickened saliva).

- Increase BP and Heart Rate.

- Bronchodilation, Increase RR

- Constipation.

- Urinary Retention.

- Increase blood supply to brain,

heart and skeletal muscles.

- SNS

I. Adrenergic Agents

- Involved in flight or withdrawal

response.

- Release of Acetylcholine.

- Decreases all bodily activities

except GIT.

EFFECTS OF PNS

- Constriction of pupils (miosis).

- Increase salivation.

- Decrease BP and Heart Rate.

- Bronchoconstriction, Decrease

RR.

- Diarrhea

- Urinary frequency.

I. Cholinergic Agents

- Mestinon, Neostignin.

SE:

3

3

- Give Epinephrine.

SE:

- SNS effect

Contraindication:

- Contraindicated to patients

suffering from COPD

(Broncholitis, Bronchoectasis,

Emphysema, Asthma).

II. Beta-adrenergic Blocking

Agents

- Also called Beta-blockers.

- all ending with “lol”

- Propranolol, Atenelol,

Metoprolol.

Effect of Beta-blockers

B – broncho spasm

E – elicits a decrease in

myocardial contraction.

T – treats hypertension.

A – AV conduction slows down.

- Should be given to patients

with Angina, Myocardial

Infarction, Hypertension

ANTI- HYPERTENSIVE AGENTS

1. Beta-blockers – “lol”

2. Ace Inhibitors – Angiotensin

“pril” (Captopril, Enalapril)

3. Calcium Antagonist –

Nifedipine (Calcibloc)

- In chronic cases of arrhythmia

give Lidocane, Xylocane.

- PNS effect

II. Anti-cholinergic Agents

- To counter cholinergic agents.

- Atrophine Sulfate

SE:

- SNS effect

Effectors Sympathetic (Adrenergic) Effect

Parasympathetic (Cholinergic) Effect

Eye dilate pupil (mydriasis) constrict

pupil (miosis)

Gland of Head

Lacrimal no effect

stimulate secretions

Salivary scanty thick, viscous secretions

copious thin, watery secretions

Dry mouth

Heart increase rate & force of contraction

decrease rate

Blood Vessel constrict smooth muscles of the skin, no effect

Abdominal blood vessels, and

Cutaneous blood vessels

Dilates smooth muscles of bronchioles,

Blood vessels of the heart & skeletal muscles

Lungs bronchodilation

bronchoconstriction

GI Tract decrease motility

increase motility

Constrict sphincters relaxed

sphincters

Possibly inhibits secretions

stimulate secretions

Inhibits activity of gallbladder & ducts stimulate

activity of gallbladder & ducts

Inhibits glycogenolysis in liver

Adrenal Gland stimulates secretion of epinephrine & no effect

Norepinephrine

Urinary Tract relaxes detrusor muscles

contract detrusor muscles

Contract trigone sphincter (prevent voiding)

relaxes trigone sphincter (allows voiding)

NEURO TRANSMITTER Decrease Increase

Acethylcholine Myesthenia Gravis Bi-polar Disorder

Dopamine Parkinson’s Disease Schizophrenia

Physical Examination

Comprehensive Neuro Exam

Neuro Check

1. Level of Consciousness (LOC)

a. Orientation to time, place, person

b. Speech: clear, garbled, rambling

c. Ability to follow command

d. If does not respond to verbal stimuli, apply a painful

stimulus (ex. Pressure on the nailbeds, squeeze

trapezius muscle); note response to pain

Appropriate: withdrawal, moaning

Inappropriate: non-purposeful

e. Abnormal posturing (may occur spontaneously or in

response to stimulus)

Decorticate Posturing: extension of leg, internal

rotation & abduction of arms with flexion of elbows,

wrist, & finger: (damage to corticospinal tract;

cerebral hemisphere)

Decerebrate Posturing: back arched, rigid extension

of all four extremities with hyperpronation of arms &

plantar flexion of feet: (damage to upper brain stem,

midbrain, or pons)

2. Glasgow Coma Scale

Objective measurement of LOC sometimes called as the

quick neuro check

Objective evaluation of LOC, motor / verbal response

A standardized system for assessing the degree of

neurologic impairment in critically ill client

Components

1. Eye opening

2. Verbal response

3. Motor response

GCS Grading / Scoring

1. Conscious 15 – 14

2. Lethargy 13 – 11

3. Stupor 10 – 8

4. Coma 7

5. Deep Coma 3

3. Pupillary Reaction & Eye Movement

a. Observe size, shape, & equality of pupil (note size in

millimeter)

b. Reaction to light: pupillary constriction

c. Corneal reflex: blink reflex in response to light stroking

of cornea

d. Oculocephalic reflex (doll’s eyes): present in

unconscious client with intact brainstem

4. Motor Function

a. Movement of extremities (paralysis)

b. Muscle strength

5. Vital Signs: respiratory patterns (may help localize possible

lesion)

a. Cheyne-Stokes Respiration: regular rhythmic alternating

between hyperventilation & apnea; may be caused by

structural cerebral dysfunction or by metabolic

problems such as diabetic coma

b. Central Neurogenic Hyperventilation: sustained, rapid,

regular respiration (rate of 25/min) with normal O2

level; usually due to brainstem dysfunction

c. Apneustic Breathing: prolonged inspiratory phase,

followed by a 2-to-3 sec pause; usually indicates

dysfunction respiratory center in pons

d. Cluster Breathing: cluster of irregular breathing,

irregularly followed by periods of apnea; usually caused

by a lesion in upper medulla & lower pons

e. Ataxic Breathing: breathing pattern completely

irregular; indicates damage to respiratory center of the

medulla

Neurologic Exam

1. Mental status and speech (Cerebral Function)

a. General appearance & behavior

4

4

b. LOC

c. Intellectual Function: memory (recent & remote),

attention span, cognitive skills

d. Emotional status

e. Thought content

f. Language / speech

2. Cranial nerve assessment

3. Cerebellar Function: posture, gait, balance, coordination

a. Romberg’s Test: 2 nurses, positive for ataxia

b. Finger to Nose Test: positive result mean dimetria

(inability of body to stop movement at desired point)

4. Sensory Function: light touch, superficial pain, temperature,

vibration & position sense

5. Motor Function: muscle size, tone, strength; abnormal or

involuntary movements

6. Reflexes

a. Deep tendon reflex: grade from 0 (no response); to 4

(hyperactive); 2 (normal)

b. Superficial

c. Pathologic: babinski reflex (dorsiflexion of the great toe

with fanning of toes): indicates damage to corticospinal

tracts

Level Of Consciouness (LOC)

1. Conscious: awake

2. Lethargy: lethargic (drowsy, sleepy, obtunded)

3. Stupor

Stuporous: (awakened by vigorous stimulation)

Generalized body weakness

Decrease body reflex

4. Coma

Comatose

light coma: positive to all forms of painful stimulus

deep coma: negative to all forms of painful stimulus

Different Painful Stimulation

1. Deep sternal stimulation / deep sternal pressure

2. Orbital pressure

3. Pressure on great toes

4. Corneal or blinking reflex

Conscious Client: use a wisp of cotton

Unconscious Client: place 1 drop of saline solution

Test of Memory

1. Short term memory

Ask most recent activity

Positive result mean anterograde amnesia and damage

to temporal lobe

2. Long term memory

Ask for birthday and validate on profile sheet

Positive result mean retrograde amnesia and damage to

limbic system

Consider educational background

Level of Orientation

1. Time: first asked

2. Person: second asked

3. Place: third asked

Cranial Nerves

Cranial Nerves Function

1. Olfactory S

2. Optic S

3. Oculomotor M

4. Trochlear M

(smallest)

5. Trigeminal B (largest)

6. Abducens M

7. Facial B

8. Acoustic S

9. Glossophareng

eal

B

10. Vagus B (longest)

11. Spinal

Accessory

M

12. Hypoglossal M

CRANIAL NERVE I: OLFACTORY

Sensory function for smell

Material Used

Don’t use alcohol, ammonia, perfume because it is irritating

and highly diffusible.

Use coffee granules, vinegar, bar of soap, cigarette

Procedure

Test each nostril by occluding each nostril

Abnormal Findings

1. Hyposnia: decrease sensitivity to smell

2. Dysosmia: distorted sense of smell

3. Anosmia: absence of smell

Either of the 3 may indicate head injury damaging the cribriform

plate of ethmoid bone where olfactory cells are located may indicate

inflammatory conditions (sinusitis)

CRANIAL NERVE II: OPTIC

Sensory function for vision or sight

Functions

1. Test visual acuity or central vision or distance

Use Snellen’s Chart

Snellen’s Alphabet chart: for literate client

Snellen’s E chart: for illiterate client

Snellen’s Animal chart: for pediatric client

Normal visual acuity 20/20

Numerator: is constant, it is the distance of person from

the chart (6-7 m, 20 feet)

Denominator: changes, indicates distance by which the

person normally can see letter in the chart.

20/200 indicates blindness

20/20 visual acuity if client is able to read letters above

the red line.

2. Test of visual field or peripheral vision

a. Superiorly

b. Bitemporaly

c. Nasally

d. Inferiorly

CRANIAL NERVE III, IV, VI: OCULOMOTOR, TROCHLEAR, ABDUCENS

Controls or innervates the movement of extrinsic ocular

muscle (EOM)

6 muscles:

Superior Rectus Superior Oblique

Lateral Rectus Medial

Rectus

Inferior Oblique Inferior

Rectus

Trochlear: controls superior oblique

Abducens: controls lateral rectus

Oculomotor: controls the 4 remaining EOM

Oculomotor

Controls the size and response of pupil

Normal pupil size is 2 – 3 mm

Equal size of pupil: Isocoria

Unequal size of pupil: Anisocoria

Normal response: positive PERRLA

CRANIAL NERVE V: TRIGEMINAL

Largest cranial nerve

Consists of ophthalmic, maxillary, mandibular

Sensory: controls sensation of face, mucous membrane,

teeth, soft palate and corneal reflex

Motor: controls the muscle of mastication or chewing

Damage to CN V leads to Trigeminal Neuralgia / Tic

Douloureux

Medication: Carbamezapine (Tegretol)

CRANIAL NERVE VII: FACIAL

Sensory: controls taste, anterior 2/3 of tongue

Pinch of sugar and cotton applicator placed on tip of tongue

Motor: controls muscle of facial expression

5

5

Instruct client to smile, frown and if results are negative

there is facial paralysis or Bell’s Palsy and the primary cause

is forcep delivery.

CRANIAL NERVE VIII: ACOUSTIC, VESTIBULOCOCHLEAR

Controls balance particularly kinesthesia or position sense,

refers to movement and orientation of the body in space.

CRANIAL NERVE IX, X: GLOSOPHARENGEAL, VAGUS

Glosopharenageal: controls taste, posterior 1/3 of tongue

Vagus: controls gag reflex

Uvula should be midline and if not indicative of damage to

cerebral hemisphere

Effects of vagal stimulation is PNS

CRANIAL NERVE XI: SPINAL ACCESSORY

Innervates with sternocleidomastoid (neck) and trapezius

(shoulder)

CRANIAL NERVE XII: HYPOGLOSSAL

Controls the movement of tongue

Let client protrude tongue and it should be midline and if

unable to do indicative of damage to cerebral hemisphere

and/or has short frenulum.

Pathognomonic Signs:

1. PTB – low grade afternoon fever

2. PNEUMONIA – rusty sputum.

3. ASTHMA – wheezing on expiration.

4. EMPHYSEMA – barrel chest.

5. KAWASAKI SYNDROME – strawberry tongue

6. PERNICIOUS ANEMIA – red beefy tongue

7. DOWN SYNDROME – protruding tongue

8. CHOLERA – rice watery stool.

9. MALARIA – step ladder like fever with chills.

10. TYPHOID – rose spots in abdomen.

11. DIPTHERIA – pseudo membrane.

12. MEASLES – koplick’s spots

13. SLE – butterfly rashes.

14. LIVER CIRRHOSIS – spider like varices

15. LEPROSY – lioning face

16. BOLIMIA – chipmunk face.

17. APPENDICITIS – rebound tenderness

18. DENGUE – petichae or positive herman’s sign.

19. MENINGITIS – kernig’s sign (leg pain), brudzinski sign (neck

pain).

20. TETANY – hypocalcemia (+) trousseu’s sign or carpopedal

spasm/ (+) chvostek sign (facial spasm).

21. TETANUS – risus sardonicus

22. PANCREATITIS – cullen’s sign (echymosis of umbilicus) / (+)

grey turners spots.

23. PYLORIC STENOSIS – olive like mass.

24. PDA – machine like murmur

25. ADDISON’S DISEASE – bronze like skin pigmentation.

26. CUSHING’S SYNDROME – moon face appearance and buffalo

hump.

27. HYPERTHYROIDSM/GRAVES DISEASE – exopthalmus.

DEMYELINATING DISORDERS

Alzheimer’s disease

Atrophy of brain tissue due to deficiency of

acetylcholine.

S/sx

4 A’s of Alzheimer

a. Amnesia – loss of memory.

b. Agnosia – unable to recognized inanimate/familiar

objects.

c. Apraxia – unable to determine purpose/ function of

objects.

d. Aphasia – no speech (nodding).

*Expressive aphasia

“motor speech center” unable to speak

Broca’s Aphasia

*Receptive aphasia

inability to understand spoken words.

Common to Alzheimer’s

Wernike’s Aphasia

General Knowing Gnostic Area or General

Interpretative Area.

DOC

Aricept (taken at bedtime)

Cognex

Management

1. Palliative & supportive

Multiple Sclerosis (MS)

Chronic intermittently progressive disorder of CNS

characterized by scattered white patches of

demyelination in brain and spinal cord.

Characterized by remission and exacerbation.

S/sx are varied & multiple, reflecting the location of

demyelination within the CNS.

Cause unknown: maybe a slow growing virus or

possibly autoimmune disorders.

Incident: Affects women more than men ages 20-40

are prone & more frequent in cool or temperate

climate.

Ig G - only antibody that pass placental circulation causing

passive immunity, short term protection

Ig A - present in all bodily secretions (tears, saliva,

colostrums).

Ig M - acute in inflammation.

Ig E - for allergic reaction

Ig D - for chronic inflammation.

* Give palliative or supportive care.

S/sx

1. Visual disturbances

blurring of vision (primary)

diplopia (double vision)

scotomas (blind spots)

2. Impaired sensation

touch, pain, pressure, temperature, or position sense

paresthesia such as tingling sensation, numbness

3. Mood swings or euphoria (sense of elation)

4. Impaired motor function

weakness

spasticity

paralysis

5. Impaired cerebral function

scanning speech

ataxic gait

nystagmus

dysarthria

intentional tremor

6. Bladder

Urinary retention or incontinence

7. Constipation

8. Sexual impotence in male / decrease sexual capacity

TRIAD SIGNS OF MS

Ataxia

(unsteady gait,

positive romberg’s test)

Intentional tremors

Nystagmus

Dx

1. CSF Analysis: increase in IgG and Protein.

2. MRI: reveals site and extent of demyelination.

3. CT Scan: increase density of white matter.

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6

CHARCOTS TRIAD

4. Visual Evoked Response (VER) determine by EEG: maybe

delayed

5. Positive Lhermittes Sign: a continuous and increase

contraction of spinal column.

Nursing Intervention

1. Assess the client for specific deficit related to location of

demyelination

2. Promote optimum mobility

a. Muscles stretching & strengthening exercises

b. Walking exercises to improve gait: use wide-base gait

c. Assistive devices: canes, walker, rails, wheelchair as

necessary

3. Administer medications as ordered

a. ACTH (adreno chorticotropic hormone), Corticosteroids

(prednisone) for acute exacerbations: to reduce edema

at site of demyelination to prevent paralysis.

b. Baclofen (Lioresal), Dantrolene (Dantrium), Diazepam

(Valium) - muscle relaxants: for spacity

c. Beta Interferons - Immunosuppresants: alter immune

response.

4. Encourage independence in self-care activities

5. Prevent complications of immobility

6. Institute bowel program

7. Maintain side rails to prevent injury related to falls.

8. Institute stress management techniques.

a. Deep breathing exercises

b. Yoga

9. Increase fluid intake and increase fiber to prevent

constipation.

10. Maintain urinary elimination

1. Urinary Retention

a. perform intermittent catheterization as ordered: to

prevent retention.

b. Bethanecol Chloride (Urecholine) as ordered

Nursing Management

only given subcutaneous.

monitor side effects bronchospasm and wheezing.

monitor breath sounds 1 hour after subcutaneous

administration.

2. Urinary Incontinence

a. Establish voiding schedule

b. Anti spasmodic agent Prophantheline Bromide (Pro-

banthine) if ordered

3. Force fluid to 3000 ml/day.

4. Promote use of acid ash diet like cranberry juice, plums,

prunes, pineapple, vitamin C and orange: to acidify

urine and prevent bacterial multiplication.

11. Prevent injury related to sensory problems.

a. Test bath water with thermometer.

b. Avoid heating pads, hot water bottles.

c. Inspect body parts frequently for injury.

d. Make frequent position changes.

12. Prepare client for plasma exchange if indicated: to remove

antibodies

13. Provide psychologic support to client/significant others.

a. Encourage positive attitude & assist client in setting

realistic goals.

b. Provide compassion in helping client adapt to changes

in body image & self-concept.

c. Do not encourage false hope during remission.

d. Refer to MS societies & community agencies.

14. Provide client teaching & discharge planning concerning:

a. General measures to ensure optimum health.

Balance between activity & rest

Regular exercise such as walking, swimming,

biking in mild case.

Use energy conservation techniques

Well-balance diet

Fresh air & sunshine

Avoiding fatigue, overheating or chilling, stress,

infection.

b. Use of medication & side effects.

c. Alternative methods for sexual counseling if indicated.

COMMON CAUSE OF UTI

Female

- short urethra (3-5 cm, 1-1 ½ inches)

- poor perineal hygiene

- vaginal environment is moist

Nursing Management

- avoid bubble bath (can alter Ph of vagina).

- avoid use of tissue papers

- avoid using talcum powder and perfume.

Male

- urethra (20 cm, 8 inches)

- do not urinate after intercourse

INTRACRANIAL PRESSURE ICP

Monroe Kelly Hypothesis

Skull is a closed container

Any alteration or increase in one of the intracranial components

Increase intracranial pressure

(normal ICP is 0 – 15 mmHg)

Cervical 1 – also known as atlas.

Cervical 2 – also known as axis.

Foramen Magnum

Medulla Oblongata

Brain Herniation

Increase intra cranial pressure


1. alternate hot and cold compress to prevent hematoma

CSF cushions brain (shock absorber)

Obstruction of flow of CSF will lead to enlargement of skull

posteriorly called hydrocephalus.

Early closure of posterior fontanels causes posterior

enlargement of skull in hydrocephalus.

DISORDERS

Increase Intracranial Pressure (IICP)

Increase in intracranial bulk brought due to an increase in

any of the 3 major intracranial components: Brain Tissue,

CSF, Blood.

Untreated increase ICP can lead to displacement of brain

tissue (herniation).

Present life threatening situation because of pressure on

vital structures in the brain stem, nerve tracts & cranial

nerve.

Increase ICP may be caused:

head trauma/injury

localized abscess

cerebral edema

hemorrhage

inflammatory condition (stroke)

hydrocephalus

tumor (rarely)

S/sx

(Early signs)

1. Decrease LOC

2. Irritability / agitation

3. Progresses from restlessness to confusion & disorientation

to lethargy & coma

(Late signs)

1. Changes in Vital Signs (may be a late signs)

a. Systolic blood pressure increases while diastolic

pressure remains the same (widening pulse

pressure)

b. Pulse rate decrease

c. Abnormal respiratory patterns (cheyne-stokes

respiration)

d. temperature increase directly proportional to blood

pressure.

2. Pupillary Changes

a. Ipsilateral (same side) dilatation of pupil with

sluggish reaction to light from compression of

cranial nerve III

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7

b. unilateral dilation of pupils called uncal

herniation

c. bilateral dilation of pupils called tentorial

herniation

d. Pupil eventually becomes fixed & dilated

3. Motor Abnormalities

a. Contralateral (opposite side) hemiparesis from

compression of corticospinal tract

b. abnormal posturing

c. decorticate posturing (damage to cortex and

spinal cord).

d. decerebrate posturing (damage to upper brain

stem that includes pons, cerebellum and

midbrain).

4. Headache

5. Projective Vomiting

6. Papilledema (edema of optic disc)

7. Possible seizure activity


1. Maintain patent airway and adequate ventilation by:

a. Prevention of hypoxia (decrease O2) and

hypercarbia (increase CO2) important:

Hypoxia may cause brain swelling which

increase ICP

Early signs of hypoxia:

Restlessness

Tachycardia

Agitation

Late signs of hypoxia:

Extreme restlessness

Bradycardia

Dyspnea

Cyanosis

Hypercarbia may cause cerebral vasodilation

which increase ICP

Hypercabia

Increase CO2 (most powerful respiratory

stimulant) retention.

In chronic respiratory distress syndrome

decrease O2 stimulates respiration.

b. Before and after suctioning hyperventilate the client

with resuscitator bag connected to 100% O2 & limit

suctioning to 10 – 15 seconds only.

c. Assist with mechanical hyperventilation as

indicated: produces hypocarbia (decease CO2)

causing cerebral constriction & decrease ICP.

2. Monitor V/S, input and output & neuro check frequently to

detect increase in ICP

3. Maintain fluid balance: fluid restriction to 1200-1500 ml/day

may be ordered

4. Position the client with head of bed elevated to 30-45o angle

with neck in neutral position unless contraindicated to

improve venous drainage from brain.

5. Prevent further increase ICP by:

a. Provide comfortable and quite environment.

b. Avoid use of restraints.

c. Maintain side rails.

d. Instruct client to avoid forms of valsalva maneuver like:

Straining stool: administer stool softener & mild

laxatives as ordered (Dulcolax, Duphalac)

Excessive vomiting: administer anti-emetics as

ordered (Plasil - Phil only, Phenergan)

Excessive coughing: administer anti-tussive

(dextromethorphan)

Avoid stooping/bending

Avoid lifting heavy objects

e. Avoid clustering of nursing care activity together.

6. Prevent complications of immobility.

7. Administer medications as ordered:

a. Hyperosmotic agent / Osmotic Diuretic [Mannitol

(Osmitrol)]: to reduce cerebral edema

Nursing Management

Monitor V/S especially BP: SE hypotension.

Monitor strictly input and output every hour: (output

should increase): notify physician if output is less 30

cc/hr.

Administered via side drip

Regulate fast drip to prevent crystal formation.

b. Loop Diuretics [Furosemide, (Lasix)]: to reduce cerebral

edema

drug of choice for CHF (pulmonary edema)

loop of henle in kidneys.

Nursing Management

Monitor V/S especially BP: SE hypotension.

Monitor strictly input and output every hour: (output

should increase): notify physician if output is less 30

cc/hr.

Administered IV push or oral.

Given early morning

Immediate effect of 10-15 minutes.

Maximum effect of 6 hours.

c. Corticosteroids [Dexamethasone (Decadron)]: anti-

inflammatory effect reduces cerebral edema

d. Analgesics for headache as needed:

Small dose of Codein SO4

Strong opiates may be contraindicated since they

potentiate respiratory depression, alter LOC, &

cause papillary changes.

e. Anti-convulsants [Phenytoin (Dilantin)]: to prevent

seizures.

8. Assist with ICP monitoring when indicated:

a. ICP monitoring records the pressure exerted within the

cranial cavity by the brain, cerebral blood, & CSF

b. Types of monitoring devices:

Intraventricular Catheter: inserted in lateral

ventricle to give direct measurement of ICP; also

allows for drainage of CSF if needed.

Subarachnoid screw (bolt): inserted through the

skull & dura matter into subarachnoid space.

Epidural Sensor: least invasive method; placed in

space between skull & dura matter for indirect

measurement of ICP.

c. Monitor ICP pressure readings frequently & prevent

complications:

Normal ICP reading is 0-15 mmHg; a sustained

increase above 15 mmHg is considered abnormal.

Use strict aseptic technique when handling any part

of the monitoring system.

Check insertion site for signs of infection; monitor

temperature.

Assess system for CSF leakage, loose connections,

air bubbles in he line, & occluded tubing.

9. Provide intensive nursing care for clients treated with

barbiturates therapy or administration of paralyzing agents.

a. Intravenous administration of barbiturates may be

ordered: to induce coma artificially in the client who has

not responded to conventional treatment.

b. Paralytic agents such as [vercuronium bromide

(Norcuron)]: may be administered to paralyzed the

client

c. Reduces metabolic demand that may protect the brain

from further injury.

d. Constant monitoring of the client’s ICP, arterial blood

gas, serum barbiturates level, & ECG is necessary.

e. EEG monitoring as necessary

f. Provide appropriate nursing care for the client on a

ventilator

10. Observe for hyperthermia secondary to hypothalamus

damage.

*CONGESTIVE HEART FAILURE

Signs and Symptoms

- dyspnea

- orthopnea

- paroxysmal nocturnal dyspnea

- productive cough

- frothy salivation

- cyanosis

- rales/crackles

- bronchial wheezing

- pulsus alternans

- anorexia and general body malaise

- PMI (point of maximum impulse/apical pulse rate) is

displaced laterally

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8

- S3 (ventricular gallop)

- Predisposing Factors/Mitral Valve

o RHD

o Aging

Treatment

Morphine Sulfate

Aminophelline

Digoxin

Diuretics

Oxygen

Gases, blood monitor

RIGHT CONGESTIVE HEART FAILURE (venous congestion)

Signs and Symptoms

- jugular vein distention (neck)

- ascites

- pitting edema

- weight gain

- hepatosplenomegaly

- jaundice

- pruritus

- esophageal varices

- anorexia and general body malaise

Signs and Symptoms of Lasix in terms of electrolyte

imbalances

1. Hypokalemia

- decrease potassium level

- normal value is 3.4 – 5.5 meq/L

Sign and Symptoms

- weakness and fatigue

- constipation

- positive U wave on ECG tracing

Nursing Management

- administer potassium supplements as ordered (Kalium Durule,

Oral Potassium Chloride)

- increase intake of foods rich in potassium

FRUITS VEGETABL

ES

Apple

Banana

Cantalop

e

Oranges

Asparagus

Brocolli

Carrots

Spinach

2. Hypocalcemia/Tetany

- decrease calcium level

- normal value is 8.5 – 11 mg/100 ml

Signs and Symptoms

- tingling sensation

- paresthesia

- numbness

- (+) Trousseus sign/Carpopedal spasm

- (+) Chvostek’s sign

Complications

- arrythmia

- seizures

Nursing Management

- Calcium Glutamate per IV slowly as ordered

* Calcium Glutamate toxicity – results to seizure

Magnesium Sulfate

Magnesium Sulfate toxicity

S/S

BP

Urine output DECREASE

Respiratory rate

Patellar relfex absent

3. Hyponatremia

- decrease sodium level

- normal value is 135 – 145 meq/L

Signs and Symptoms

- hypotension

- dehydration signs (initial sign in adult is thirst, in infant

tachycardia)

- agitation

- dry mucous membrane

- poor skin turgor

- weakness and fatigue

Nursing Management

- force fluids

- administer isotonic fluid solution as ordered

4. Hyperglycemia

- normal FBS is 80 – 100 mg/dl

Signs and Symptoms

- polyuria

- polydypsia

- polyphagia

Nursing Management

- monitor FBS

5. Hyperuricemia

- increase uric acid (purine metabolism)

- foods high in uric acid (sardines, organ meats and anchovies)

*Increase in tophi deposit leads to gouty arthritis.

Signs and Symptoms

- joint pain (great toes)

- swelling

Nursing Management

- force fluids

- administer medications as ordered

a. Allopurinol (Zylopril)

- drug of choice for gout.

- mechanism of action: inhibits synthesis of uric acid.

b. Colchesine

- acute gout

- mechanism of action: promotes excretion of uric acid.

* Kidney stones

Signs and Symptoms

- renal cholic

- cool moist skin

Nursing Management

- force fluids

- administer medications as ordered

a. Narcotic Analgesic

- Morphine Sulfate

- antidote: Naloxone (Narcan) toxicity leads to tremors.

b. Allopurinol (Zylopril)

Side Effects

- respiratory depression (check for RR)

Parkinson’s Disease/ Parkinsonism

Chronic progressive disorder of CNS characterized by

degeneration of dopamine producing cells in the substantia

nigra of the midbrain and basal ganglia.

Progressive disorder with degeneration of the nerve cell in

the basal ganglia resulting in generalized decline in

muscular function

Disorder of the extrapyramidal system

Usually occurs in the older population

Cause Unknown: predominantly idiopathic, but sometimes

disorder is postencephalitic, toxic, arteriosclerotic,

traumatic, or drug induced (reserpine, methyldopa

(aldomet) haloperidol (haldol), phenothiazines).

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9

Multiple loss causes suicide

Pathophysiology

Disorder causes degeneration of dopamine producing

neurons in the substantia nigra in the midbrain

Dopamine: influences purposeful movement

Depletion of dopamine results in degeneration of the basal

ganglia

Predisposing Factors

1. Poisoning (lead and carbon monoxide)

2. Arteriosclerosis

3. Hypoxia

4. Encephalitis

5. Increase dosage of the following drugs:

a. Reserpine (Serpasil)

b. Methyldopa (Aldomet) Antihypertensive

c. Haloperidol (Haldol) _______

d. Phenothiazine ___________________ Antipsychotic

Side Effects Reserpine: Major depression lead to suicide

Aloneness

Loss of spouse Loss

of Job

Nursing Intervention for Suicide

direct approach towards the client

close surveillance is a nursing priority

time to commit suicide is on weekends early morning

S/sx

1. Tremor: mainly of the upper limbs “pill rolling tremors” of

extremities especially the hands; resting tremor: most

common initial symptoms

2. Bradykinesia: slowness of movement

3. Rigidity: cogwheel type

4. Stooped posture: shuffling, propulsive gait

5. Fatigue

6. Mask like facial expression with decrease blinking of the

eyes.

7. Difficulty rising from sitting position.

8. Quite, monotone speech

9. Emotional lability: state of depression

10. Increase salivation: drooling type

11. Cramped, small handwriting

12. Autonomic Symptoms

a. excessive sweating

b. increase lacrimation

c. seborrhea

d. constipation

e. decrease sexual capacity



Anti-Parkinson Drug

a. Levodopa (L-dopa) short acting

MOA: Increase level of dopamine in the brain;

relieves tremors; rigidity; bradykinesia

SE: GIT irritation (should be taken with meal);

anorexia; N/V; postural hypotension; mental

changes: confusion, agitation, hallucination; cardiac

arrhythmias; dyskinesias.

CI: narrow-angled glaucoma; client taking MAOI

inhibitor; reserpine; guanethidine; methyldopa;

antipsychotic; acute psychoses

Avoid multi-vitamins preparation containing vitamin

B6 & food rich in vitamin B6 (Pyridoxine): reverses

the therapeutic effects of Levodopa

Urine and stool may be darkened

Be aware of any worsening of symptoms with

prolonged high-dose therapy: “on-off” syndrome.

b. Carbidopa-levodopa (Sinemet)

Prevents breakdown of dopamine in the periphery &

causes fewer side effects.

c. Amantadine Hydrochloride (Symmetrel)

Used in mild cases or in combination with L-dopa to

reduce rigidity, tremors, & bradykinesia

Anti-Cholinergic Drug

a. Benztropine Mesylate (Cogentin)

b. Procyclidine (Kemadrine)

c. Trihexyphenidyl (Artane)

MOA: inhinit the action of acetylcholine; used in mild

cases or in combination with L-dopa; relived tremors

& rigidity

SE: dry mouth; blurred vision; constipation; urinary

retention; confusion; hallucination; tachycardia

Anti-Histamines Drug

a. Diphenhydramine (benadryl)

MOA: decrease tremors & anxiety

SE: Adult: drowsiness Children: CNS excitement

(hyperactivity) because blood brain barrier is not yet

fully developed.

b. Bromocriptine (Parlodel)

MOA: stimulate release of dopamine in the

substantia nigra

Often employed when L-dopa loses effectiveness

MAOI Inhibitor

a. Eldepryl (Selegilene)

MOA: inhibit dopamine breakdown & slow

progression of disease

Anti-Depressant Drug

a. Tricyclic

MOA: given to treat depression commonly seen in

Parkinson’s disease

2. Provide safe environment

Side rails on bed

Rails & handlebars in the toilet, bathtub, & hallways

No scattered rugs

Hard-back or spring-loaded chair to make getting up

easier

3. Provide measures to increase mobility

Physical Therapy: active & passive ROM exercise;

stretching exercise; warm baths

Assistive devices

If client “freezes” suggest thinking of something to walk

over

4. Encourage independence in self-care activities:

alter clothing for ease in dressing

use assistive device

do not rush the client

5. Improve communication abilities:

Instruct the client to practice reading a loud

Listen to own voice & enunciate each syllable clearly

6. Refer for speech therapy when indicated.

7. Maintain adequate nutrition.

Cut food into bite-size pieces

Provide small frequent feeding

Allow sufficient time for meals, use warming tray

8. Avoid constipation & maintain adequate bowel elimination

9. Provide significant support to client/ significant others:

Depression is common due to changes in body image &

self-concept


a. Nature of the disease

b. Use prescribed medications & side effects

c. Importance of daily exercise as tolerated: balanced

activity & rest

walking

swimming

gardening

d. Activities/ methods to limit postural deformities:

Firm mattress with small pillow

Keep head & neck as erected as possible

Use broad-based gait

Raise feet while walking

e. Promotion of active participation in self-care activities.

* Increase Vitamin B when taking INH (Isoniazid), Isonicotinic Acid

Hydrazide

* Dopamine Agonist relieves tremor rigidity

MAGIC 2’s IN DRUG MONITORING

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10

DRUG NORMAL RANGE TOXICITY

LEVEL

INDICATION

Digoxin/Lanoxin

(increase force of

cardiac output)

.5 – 1.5 meq/L 2 CHF

Lithium/Lithane

(decrease level of

Ach/NE/Serotonin)

.6 – 1.2 meq/L 2 Bipolar

Aminophelline

(dilates bronchial tree)

10 – 19 mg/100 ml 20 COPD

Dilantin/Phenytoin 10 – 19 mg/100 ml 20 Seizures

Acetaminophen/

Tylenol

10 – 30 mg/100 ml 200 Osteo

Arthritis

1. Digitalis Toxicity

Signs and Symptoms

- nausea and vomiting

- diarrhea

- confusion

- photophobia

- changes in color perception (yellowish spots)

Antidote: Digibind

2. Lithium Toxicity

Signs and Symptoms

- anorexia

- nausea and vomiting

- diarrhea

- dehydration causing fine tremors

- hypothyroidism

Nursing Management

- force fluids

- increase sodium intake to 4 – 10 g% daily

3. Aminophelline Toxicity

Signs and Symptoms

- tachycardia

- palpitations

- CNS excitement (tremors, irritability, agitation and restlessness)

Nursing Management

- only mixed with plain NSS or 0.9 NaCl to prevent development of

crystals of precipitate.

- administered sandwich method

- avoid taking alcohol because it can lead to severe CNS depression

- avoid caffeine

4. Dilantin Toxicity

Signs and Symptoms

- gingival hyperplasia (swollen gums)

- hairy tongue

- ataxia

- nystagmus

Nursing Management

- provide oral care

- massage gums

5. Acetaminophen Toxicity

Signs and Symptoms

- hepatotoxicity (monitor for liver enzymes)

- SGPT/ALT (Serum Glutamic Pyruvate Transaminace)

- SGOT/AST (Serum Glutamic Oxalo-Acetil Transaminace)

- nephrotoxicity monitor BUN (10 – 20) and Creatinine (.8 – 1)

- hypoglycemia

Tremors, tachycardia

Irritability

Restlessness

Extreme fatigue

Diaphoresis, depression

Antidote: Acetylceisteine (mucomyst) prepare suction apparatus

as bedside.

MYASTHENIA GRAVIS (MG)

neuromuscular disorder characterized by a disturbance in

the transmission of impulses from nerve to muscle cells at

the neuromuscular junction leading to descending muscle

weakness.

Incidence rate:

highest between 15 & 35 years old for women, over 40

for men.

Affects women more than men

Cause:

Unknown/ idiopathic

Thought to be autoimmune disorder whereby antibodies

destroy acetylcholine receptor sites on the postsynaptic

membrane of the neuromuscular junction.

Voluntary muscles are affected, especially those muscles

innervated by the cranial nerve.

Pathophysiology

Autoimmune = Release of Cholinesterase Enzymes =

Cholinesterase destroy Acetylcholine (ACH) = Decrease of

Acetylcholine (ACH)

Acetylcholine: activate muscle contraction

Autoimmune: it involves release of cholinesterase an

enzyme that destroys Ach

Cholinesterase: an enzyme that destroys ACH

S/sx

1. Initial sign is ptosis a clinical parameter to determine ptosis

is palpebral fissure: cracked or cleft in the lining or

membrane of the eyelids

2. Diplopia

3. Dysphagia

4. Mask like facial expression

5. Hoarseness of voice, weakness of voice

6. Respiratory muscle weakness that may lead to respiratory

arrest

7. Extreme muscle weakness especially during exertion and

morning; increase activity & reduced with rest.

Dx

1. Tensilon Test (Edrophonium Hydrochloride): IV injection of

tensilon provides temporary relief of S/sx for about 5-10

minutes and a maximum of 15 minutes.

If there is no effect there is no damage to occipital lobe

and midbrain and is negative for M.G.

2. Electromyography (EMG): amplitudes of evoked potentials

decrease rapidly.

3. Presence of anti-acetlycholine receptors antibodies in the

serum.

Medical Management

1. Drug Therapy

a. Anti-cholinesterase Drugs: [Ambenonium (Mytelase),

Neostigmine (Prostigmin), Pyridostigmine (Mestinon)]

MOA: block the action of cholinesterase & increase

the level of acetylcholine at the neuromuscular

junction.

SE: excessive salivation & sweating, abdominal

cramps, N/V, diarrhea, fasciculations (muscle

twitching).

b. Corticosteroids: Prednisone

MOA: suppress autoimmune response

Used if other drugs are not effective

2. Surgery (Thymectomy)

a. Surgical removal of thymus gland: thought to be involve

in the production of acetylcholine receptor antibodies.

b. May cause remission in some clients especially if

performed early in the disease.

3. Plasma Exchange (Plasmapheresis)

a. Removes circulating acetylcholine receptor antibodies.

b. Use in clients who do not respond to other types of

therapy.

Nursing Interventions

1. Administer anti-cholinesterase drugs as ordered:

a. Give medication exactly on time.

b. Give with milk & crackers to decrease GI upset

c. Monitor effectiveness of drugs: assess muscle strength

& vital capacity before & after medication.

d. Avoid use of the ff drugs:

Morphine SO4 & Strong Sedatives: respiratory

depressant effects

Quinine, Curare, Procainamide, Neomycin,

Streptomycine, Kanamycine & other

aminoglycosides: skeletal muscle blocking effect

e. Observe for side effects

2. Promote optimal nutrition:

a. Mealtime should coincide with the peak effect of the

drugs: give medication 30 minutes before meals.

b. Check gag reflex & swallowing ability before feeding.

c. Provide mechanical soft diet.

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11

d. If the client has difficulty in chewing & swallowing, do

not leave alone at mealtime; keep emergency airway &

suctioning equipment nearby.

3. Monitor respiratory status frequently: Rate, Depth, Vital

Capacity; ability to deep breathe & cough

4. Assess muscle strength frequently; plan activity to take

advantage of energy peaks & provide frequent rest periods.

5. Observe for signs of myasthenic or cholinergic crisis.

MYASTHENIC CRISIS CHOLINERGIC CRISIS

Abrupt onset of severe, generalized

muscle weakness with inability to

swallow, speak, or maintain respirations.

Symptoms will improve temporarily with

tensilon test.

Causes:

under medication

physical or emotional stress

infection

Signs and Symptoms

the client is unable to see, swallow,

speak, breathe

Treatment

administer cholinergic agents as ordered

Symptoms similar to myasthenic crisis &

in addition the side effect of anti-

cholinesterase drugs (excessive

salivation & sweating, abdominal carmp,

N/V, diarrhea, fasciculation)

Symptoms worsen with tensilon test:

keep Atropine Sulfate & emergency

equipment on hand.

Cause:

over medication with the

drugs (anti-cholinesterase)

Signs and Symptoms

PNS

Treatment

administer anti-cholinergic agents

(Atrophine Sulfate)

Nursing Care in Crisis:

a. Maintain tracheostomy set or endotracheal tube with

mechanical ventilation as indicated.

b. Monitor ABG & Vital Capacity

c. Administer medication as ordered:

Myasthenic Crisis: increase doses of anti-

cholinesterase drug as ordered.

Cholinergic Crisis: discontinue anti-

cholinesterase drugs as ordered until the client

recovers.

d. Established method of communication

e. Provide support & reassurance.

6. Provide nursing care for the client with thymectomy.


a. Nature of the disease

b. Use of prescribe medications their side effects & sign of

toxicity

c. Importance of checking with physician before taking any

new medication including OTC drugs

d. Importance of planning activities to take advantage of

energy peaks & of scheduling frequent rest period

e. Need o avoid fatigue, stress, people with upper

respiratory infection

f. Use of eye patch for diplopia (alternate eyes)

g. Need to wear medic-alert bracelet

h. Myasthenia Gravis foundation & other community

agencies

Guillain-Barre Syndrome

a disorder of the CNS characterized by bilateral,

symmetrical, peripheral polyneuritis characterized by

ascending muscle paralysis.

Can occur at any age; affects women and men equally

Progression of disease is highly individual; 90% of clients

stop progression in 4 weeks; recovery is usually from 3-6

months; may have residual deficits.

Causes:

1. Unknown / idiopathic

2. May be autoimmune process


1. Immunization

2. Antecedent viral infections such as LRT infections

S/sx

1. Mild Sensory Changes: in some clients severe

misinterpretation of sensory stimuli resulting to extreme

discomfort

2. Clumsiness (initial sign)

3. Progressive motor weakness in more than one limb

(classically is ascending & symmetrical)

4. Dysphagia: cranial nerve involvement

5. Ascending muscle weakness leading to paralysis

6. Ventilatory insufficiency if paralysis ascends to respiratory

muscles

7. Absence or decreased deep tendon reflex

8. Alternate hypotension to hypertension

9. Arrythmia (most feared complication)

10. Autonomic disfunction: symptoms that includes

a. increase salivation

b. increase sweating

c. constipation

Dx

1. CSF analysis: reveals increased in IgG and protein

2. EMG: slowed nerve conduction

Medical Management

1. Mechanical Ventilation: if respiratory problems present

2. Plasmapheresis: to reduce circulating antibodies

3. Continuous ECG monitoring to detect alteration in heart rate

& rhythm

4. Propranolol: to prevent tachycardia

5. Atropine SO4: may be given to prevent episodes of

bradycardia during endotracheal suctioning & physical

therapy


1. Maintain patent airway & adequate ventilation:

a. Monitor rate & depth of respiration; serial vital capacity

b. Observe for ventilatory insufficiency

c. Maintain mechanical ventilation as needed

d. Keep airway free of secretions & prevent pneumonia

2. Check individual muscle groups every 2 hrs in acute phase

to check progression of muscle weakness

3. Assess cranial nerve function:

a. Check gag reflex

b. Swallowing ability

c. Ability to handle secretion

d. Voice

4. Monitor strictly the following:

a. Vital signs

b. Input and output

c. Neuro check

d. ECG: due to arrhythmia

e. Observe signs of autonomic dysfunction: acute period of

hypertension fluctuating with hypotension

f. Tachycardia

g. Arrhythmias

5. Maintain side rails to prevent injury related to fall

6. Prevent complications of immobility: turning the client every

2 hrs

7. Assist in passive ROM exercise

8. Promote comfort (especially in clients with sensory

changes):

a. Foot cradle

b. Sheepskin

c. Guided imagery

d. Relaxation techniques

9. Promote optimum nutrition:

a. Check gag reflex before feeding

b. Start with pureed food

c. Assess need for NGT feeding: if unable to swallow; to

prevent aspiration


a. Corticosteroids: suppress immune response

b. Anti Cholinergic Agents:

Atrophine Sulfate

c. Anti Arrythmic Agents:

Lidocaine (Xylocaine)

Bretylium: blocks release of norepinephrine; to

prevent increase of BP

11. Assist in plasmapheresis (filtering of blood to remove

autoimmune anti-bodies)

12. Prevent complications:

a. Arrythmia

b. Paralysis of respiratory muscles / respiratory arrest

13. Provide psychologic support & encouragement to client /

significant others

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14. Refer for rehabilitation to regain strength & treat any

residual deficits.

INFLAMMATORY CONDITIONS OF THE BRAIN

Meningitis

Inflammation of the meninges of the brain & spinal cord.

Cause by bacteria, viruses, & other M.O.

Etiology / Most Common M.O.

1. Meningococcus: most dangerous

2. Pneumococcus

3. Streptococcus: cause of adult meningitis

4. Hemophilus Influenzae: cause of pediatric meningitis

Mode of transmission

1. Airborne transmission (droplet nuclei)

2. Via blood, CSF, lymph

3. By direct extension from adjacent cranial structures (nasal,

sinuses, mastoid bone, ear, skull fracture)

4. By oral or nasopharyngeal route

Signs and Symptoms

2. Headache, photophobia, general body malaise, irritability,

3. Projectile vomiting: due to increase ICP

4. Fever & chills

5. Anorexia & weight loss

6. Possible seizure activity & decrease LOC

7. Abnormal posturing: (decorticate and decerebrate)

8. Signs of Meningeal Irritation:

a. Nuchal rigidity or stiff neck: initial sign

b. Opisthotonos (arching of back): head & heels bent

backward & body arched forward

c. PS: Kernig’s sign (leg pain): contraction or pain in the

hamstring muscles when attempting to extend the leg

when the hip is flexed

d. PS: Brudzinski sign (neck pain): flexion at the hip & knee

in response to forward flexion of the neck

Dx

1. Lumbar Puncture:

Measurement & analysis of CSF shows increased

pressure, elevated WBC & CHON, decrease glucose &

culture positive for specific M.O.

A hollow spinal needle is inserted in the subarachnoid

space between the L3-L4 or L4-L5.

Nursing Management Before Lumbar Puncture

1. Secure informed consent and explain procedure.

2. Empty bladder and bowel to promote comfort.

3. Encourage to arch back to clearly visualize L3-L4.

Nursing Management Post Lumbar Puncture

1. Place flat on bed 12 – 24 o

2. Force fluids

3. Check punctured site for any discoloration, drainage and

leakage to tissues.

4. Assess for movement and sensation of extremities.

CSF analysis reveals

1. Increase CHON and WBC

2. Decrease glucose

3. Increase CSF opening pressure (normal pressure is 50 –

100 mmHg)

4. (+) cultured microorganism (confirms meningitis)

CBC reveals

1. Increase WBC

Nursing Management

1. Administer large doses of antibiotic IV as ordered:

a. Broad spectrum antibiotics (Penicillin, Tetracycline)

b. Mild analgesics: for headaches

c. Antipyretics: for fever

2. Enforced strict respiratory isolation 24 hours after initiation

of anti biotic therapy (for some type of meningitis)

3. Provide nursing care for increase ICP, seizure &

hyperthermia if they occur

4. Provide nursing care for delirious or unconscious client as

needed

5. Enforce complete bed rest

6. Keep room quiet & dark: if the client has headache &

photophobia

7. Monitor strictly V/S, I & O & neuro check

8. Maintain fluid & electrolyte balance

9. Prevent complication of immobility


a. Importance of good diet: high CHON, high calories with

small frequent feedings.

b. Rehabilitation program for residual deficit

mental retardation

delayed psychomotor development

c. Prevent complications

most feared is hydrocephalus

hearing loss/nerve deafness is second

complication

consult audiologist

Cerebrovascular Accident (CVA) (Stroke/Brain

Attack/Apoplexy/Cerebral Thrombosis)

Destruction (infarction) of brain cells caused by a reduction

in cerebral blood flow and oxygen

A partial or complete disruption in the brains blood supply.

2 largest & most common cerebral artery affected by stroke:

a. Mid Cerebral Artery

b. Internal Cerebral Artery

Incidence Rate:

a. Affects men more than women; Men are 2-3 times high

risk; Incidence increase with age

Causes:

a. Thrombosis (attached)

b. Embolism (detached): most dangerous because it can

go to the lungs & cause pulmonary embolism or the

brain & cause cerebral embolism.

c. Hemorrhage

d. Compartment Syndrome: compression of nerves &

arteries

S/sx Pulmonary Embolism

1. Sudden sharp chest pain

2. Unexplained dyspnea

3. SOB

4. Tachycardia

5. Palpitations

6. Diaphoresis

7. Mild restlessness

S/sx of Cerebral Embolism

1. Headache

2. disorientation

3. Confusion

4. Decrease LOC

S/sx Compartment syndrome

1. Fat embolism is the most feared complications w/in

24 hrs after a femur fracture.

Yellow bone marrow are produced from the

medullary cavity of the long bones and produces

fat cells.

If there is bone fracture there is hemorrhage

and there would be escape of the fat cells in the

circulation.

Risk Factors

Disease:

1. Hypertension

2. Diabetes Mellitus

3. Atherosclerosis / Arteriosclerosis

4. Myocardial Infarction

5. Mitral valve replacement

6. Valvular Disease / replacement

7. Chronic atrial Fibrillation

8. Post Cardiac Surgery

Lifestyle:

1. Smoking

2. Sedentary lifestyle

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3. Obesity (increase 20% ideal body weight)

4. Hyperlipidemia more on genetics/genes that binds to

cholesterol

5. Type A personality

a. Deadline driven

b. Can do multiple tasks

c. Usually fells guilty when not doing anything

6. Related to diet: increase intake of saturated fats like whole

milk

7. Related stress physical and emotional

8. Prolong use of oral contraceptives: promotes lypolysis

(breakdown of lipids) leading to atherosclerosis that will lead

to hypertension & eventually CVA.

Pathophysiology

1. Interruption of cerebral blood flow for 5 min or more causes

death of neurons in affected area with irreversible loss of

function.

2. Modifying Factors:

a. Cerebral Edema:

Develops around affected area causing further

impairment

b. Vasospasm:

Constriction of cerebral blood vessel may occur,

causing further decrease in blood flow

c. Collateral Circulation:

May help to maintain cerebral blood flow when there

is compromise of main blood supply

Stages of Development

1. Transient Ischemic Attack (TIA)

a. Initial / warning signs of impending CVA / stroke

b. Brief period of neurologic deficit:

Visual loss / Visual disturbance

Hemiparesis

Slurred Speech / Speech disturbance

Vertigo

Aphasia

Headache: initial sign

Dizziness

Tinnitus

Possible Increase ICP

c. May last less than 30 sec, but no more than 24 hrs with

complete resolution of symptoms

2. Stroke in Evolution

Progressive development of stroke symptoms over a

period of hours to days

3. Complete Stroke

Neurologic deficit remains unchanged for 2-3-days

period

S/sx

1. Headache

2. Generalized Signs:

Vomiting

Seizure

Confusion

Disorientation

Decrease LOC

Nuchal Rigidity

Fever

Hypertension

Slow Bounding Pulse

Cheyne-Strokes Respiration

(+) Kernig’s & Brudzinski sign: may lead to hemorrhagic

stroke

3. Focal Signs (related to site of infarction):

Hemiplegia

Homonymous hemianopsia: loss of half of visual field

Sensory loss

Aphasia

Dysarthia: inability to articulate words

Alexia: difficulty reading

Agraphia: difficulty writing

Dx

1. CT & Brain Scan: reveals brain lesions

2. EEG: abnormal changes

3. Cerebral Arteriography: invasive procedure due to injection

of dye (iodine based); Uses dye for visualization

May show occlusion or malformation of blood vessels

Reveals the site and extent of malocclusion

Nursing Management Post Cerebral Arteriography

Allergy Test (shellfish)

Force fluids to release dye because it is nephro toxic

Check for peripheral pulse: distal (femoral)

Check for hematoma formation

Nursing Intervention: Acute Stage

1. Maintain patent airway and adequate ventilation by:

a. Assist in mechanical ventilation

b. Administer O2 inhalation

2. Monitor strictly V/S, I & O, neuro check & observe signs of

increase ICP, shock, hyperthermia, & seizure

3. Provide CBR as ordered

4. Maintain fluid & electrolyte balance & ensure adequate

nutrition:

a. IV therapy for the first few days

b. NGT for feeding the client who is unable to swallow

c. Fluid restriction as ordered: to decrease cerebral edema

& might also increase ICP

5. Maintain proper positioning & body alignment:

a. Elevate head 30-45 degree to decrease ICP

b. Turn & reposition every 2 hrs (20 min only on the

affected side)

c. Passive ROM exercise every 4 hrs: prevent contractures;

promote body alignment

6. Promote optimum skin integrity: turn client & apply lotion

every 2 hrs

7. Prevent complications of immobility by:

a. Turn client to side

b. Provide egg crate mattresses or water bed

c. Provide sand bag or food board.

8. Maintain adequate elimination:

a. Offer bed pan or urinal every 2 hrs; catheterized only if

necessary

b. Administer stool softener & suppositories as ordered: to

prevent constipation & fecal impaction

9. Provide quiet, restful environment

10. Provide alternative means of communication to the client:

a. Non verbal cues

b. Magic slate: not paper & pen tiring for client

c. If positive to hemianopsia: approach client on

unaffected side


a. Hyperosmotic agent: to decrease cerebral edema

Osmotic Diuretics (Mannitol)

Loop Diuretics Furosemide (Lasix)

Corticosteroids (Dexamethazone)

b. Anti-convulsants: to prevent or treat seizures

c. Thrombolytic / Fibrinolytic Agents: given to dissolve clot

(hemorrhage must be ruled out)

Tissue Plasminogen Activating Factor (tPA,

Alteplase): SE: allergic Reaction

Streptokinase, Urokinase: SE: chest pain

d. Anticoagulants: for stroke in evolution or embolic stroke

(hemorrhage must be ruled out)

Heparin: short acting

Check for Partial Thromboplastin Time (PTT): if

prolonged there is a risk for bleeding

Antidote: Protamine SO4

Warfarin (Comadin): long acting / long term therapy

Give simultaneously with Heparin cause

Warfarin (Coumadin) will take effect after 3 days

Check for Prothrombin Time (PT): if prolonged

there is a risk for bleeding

Antidote: Vitamin K (Aqua Mephyton)

Anti Platelet: to inhibit platelet aggregation in

treating TIA’s

PASA (Aspirin)

Contraindicated for dengue, ulcer and unknown

cause of headache because it may potentiate

bleeding

e. Antihypertensive: if indicated for elevated BP

f. Mild Analgesics: for pain

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12. Provide client health teachings and discharge planning

concerning

a. Avoid modifiable risk factors (diet, exercise,

smoking)

b. Prevent complication (subarachnoid hemorrhage is

the most feared complication)

c. Dietary modification (decrease salt, saturated fats

and caffeine)

d. Importance of follow up care

Nursing Intervention: Rehabiltation

1. Hemiplegia: results from injury to cell in the cerebral motor

cortex or to corticospinal tract (causes contralateral

hemiplegia since tracts crosses medulla)

a. Turn every 2 hrs (20 min only on affected side)

b. Use proper positioning & repositioning to prevent

deformities (foot drop, external rotation of hips, flexion

of fingers, wrist drop, abduction of shoulder & arms)

c. Support paralyzed arm on pillow or use sling while out of

bed to prevent subluxation of shoulders

d. Elevate extremities to prevent dependent edema

e. Provide active & passive ROM exercises every 4 hrs

2. Susceptibility to hazard

a. Keep side rails up at all times

b. Institute safety measures

c. Inspect body parts frequently for signs of injury

3. Dysphagia: difficulty of swallowing

a. Check for gag reflex before feeding client

b. Maintain a calm, unhurried approach

c. Place client in upright position

d. Place food in unaffected side of the mouth

e. Offer soft foods

f. Give mouth care before & after meals

4. Homonymous Hemianopsia: loss of right or left half of each

visual field

a. Approach the client on unaffected side

b. Place personal belongings, food etc., on unaffected side

c. Gradually teach the client to compensate by scanning

(ex. Turning the head to see things on affected side)

5. Emotional Lability: mood swings, frustrations

a. Create a quiet, restful environment with a reduction in

excessive sensory stimuli

b. Maintain a calm, non-threatening manner

c. Explain to family that client’s behavior is not purposeful

6. Aphasia: most common in right hemiplegics; may be

receptive / expressive

a. Receptive Aphasia

Give simple, slow directions

Give one command at a time; gradually shift topics

Use non-verbal techniques of communication (ex.

Pantomime, demonstration)

b. Expressive Aphasia

Listen & watch very carefully when the client

attempts to speak

Anticipate client’s needs to decrease frustrations &

feeling of helplessness

Allow sufficient time for client to answer

7. Sensory / Perceptual Deficit: more common in left

hemiplegics; characterized by impulsiveness unawareness

of disabilities, visual neglect (neglect of affected side &

visual space on affected side)

a. Assist with self-care

b. Provide safety measures

c. Initially arrange objects in environment on unaffected

side

d. Gradually teach client to take care of the affected & turn

frequently & look at affected side

8. Apraxia: loss of ability to perform purposeful, skilled acts

a. Guide client through intended movement (ex. Take

object such as wash cloth & guide client through

movement of washing)

b. Keep repeating the movement

9. Generalizations about the clients with left hemiplegia vs.

right hemiplegia & nursing care

a. Left Hemiplegia

Perceptual, sensory deficits: quick & impulsive

behavior

Use safety measures, verbal cues, simplicity in all

area of care

b. Right Hemiplegia

Speech-language deficits: slow & cautious behavior

Use pantomime & demonstration

CONVULSIVE DISORDER/CONVULSION

disorder of CNS characterized by paroxysmal seizure with or

without loss of consciousness abnormal motor activity

alternation in sensation and perception and changes in

behavior.

Seizure: first convulsive attack

Epilepsy: second or series of attacks

Febrile seizure: normal in children age below 5 years


1. Head injury due to birth trauma

2. Genetics

3. Presence of brain tumor

4. Toxicity from the ff:

a. Lead

b. Carbon monoxide

5. Nutritional and Metabolic deficiencies

6. Physical and emotional stress

7. Sudden withdrawal to anti-convulsant drug: is predisposing

factor for status epilepticus: DOC: Diazepam (Valium) &

Glucose

S/sx

Dependent on stages of development or types of seizure

1. Generalized Seizure

Initial onset in both hemisphere, usually involves loss of

consciousness & bilateral motor activity.

a. Major Motor Seizure (Grand mal Seizure): tonic-clonic

seizure

Signs or aura with auditory, olfactory, visual, tactile,

sensory experience

Epileptic cry: is characterized by fall and loss of

consciousness for 3-5 minutes

Tonic Phase:

Limbs contract or stiffens

Pupils dilated & eye roll up to one side

Glottis closes: causing noise on exhalation

May be incontinent

Occurs at same time as loss of consciousness

last 20-40 sec

Tonic contractions: direct symmetrical extension of

extremities

Clonic Phase:

repetitive movement

increase mucus production

slowly tapers

Clonic contractions: contraction of extremities

Postictal sleep: unresponsive sleep

Seizure ends with postictal period of confusion,

drowsiness

b. Absence Seizure (Petit mal Seizure):

Usually non-organic brain damage present

Must be differentiated from daydreaming

Sudden onset with twitching & rolling of eyes that last

20-40 sec

Common among pediatric clients characterized by:

Blank stare

Decrease blinking of eyes

Twitching of mouth

Loss of consciousness (5 – 10 seconds)

2. Partial or Localized Seizure

Begins in focal area of brain & symptoms are related to

a dysfunction of that area

May progress into a generalized seizure

a. Jacksonian Seizure (focal seizure)

characterized by tingling and jerky movement of

index finger and thumb that spreads to the shoulder

and other side of the body.

b. Psychomotor Seizure (focal motor seizure)

May follow trauma, hypoxia, drug use

Purposeful but inappropriate repetitive motor acts

Aura is present: daydreaming like

Automatism: stereotype repetitive and non

propulsive behavior

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Clouding of consciousness: not in contact with

environment

Mild hallucinatory sensory experience

3. Status Epilepticus

Usually refers to generalized grand mal seizure

Seizure is prolong (or there are repeated seizures

without regaining consciousness) & unresponsive to

treatment

Can result in decrease in O2 supply & possible cardiac

arrest

A continuous uninterrupted seizure activity

If left untreated can lead to hyperpyrexia and lead to

coma and eventually death.

DOC: Diazepam (Valium) & Glucose

C. Diagnostic Procedures

1. CT Scan – reveals brain lesions

2. EEG – reveals hyper activity of electrical brain waves

D. Nursing Management

1. Maintain patent airway and promote safety before seizure activity

a. clear the site of blunt or sharp objects

b. loosen clothing of client

c. maintain side rails

d. avoid use of restrains

e. turn clients head to side to prevent aspiration

f. place mouth piece of tongue guard to prevent biting or

tongue

2. Avoid precipitating stimulus such as bright/glaring lights and

noise


a. Anti convulsants (Dilantin, Phenytoin)

b. Diazepam, Valium

c. Carbamazepine (Tegnetol) – trigeminal neuralgia

d. Phenobarbital, Luminal

4. Institute seizure and safety precaution post seizure attack

a. administer O2 inhalation

b. provide suction apparatus

5. Document and monitor the following

a. onset and duration

b. types of seizures

c. duration of post ictal sleep may lead to status epilepticus

d. assist in surgical procedure cortical resection

Overview Anatomy & Physiology of the Eye

External Structure of Eye

a. Eyelids (Palpebrae) & Eyelashes: protect the eye from

foreign particles

b. Conjunctiva:

Palpebral Conjunctiva: pink; lines inner surface of

eyelids

Bulbar Conjunctiva: white with small blood vessels,

covers anterior sclera

c. Lacrimal Apparatus (lacrimal gland & its ducts & passage):

produces tears to lubricate the eye & moisten the cornea;

tears drain into the nasolacrimal duct, which empties into

nasal cavity

d. The movement of the eye is controlled by 6 extraocular

muscles (EOM)

Internal Structure of Eye

A. 3 layers of the eyeball

1. Outer Layer

a. Sclera: tough, white connective tissue (“white of the

eye”); located anteriorly & posteriorly

b. Cornea: transparent tissue through which light

enters the eye; located anteriorly

2. Middle Layer

a. Choroid: highly vascular layer, nourishes retina;

located posteriorly

b. Ciliary Body: anterior to choroid, secrets aqueous

humor; muscle change shape of lens

c. Iris: pigmented membrane behind cornea, gives

color to eye; located anteriorly

d. Pupil: is circular opening in the middle of the iris

that constrict or dilates to regulate amount of light

entering the eye

3. Inner Layer

a. Light-sensitive layer composed of rods & cones

(visual cell)

Cones: specialized for fine discrimination &

color vision; (daylight / colored vision)

Rods: more sensitive to light than cones, aid

in peripheral vision; (night twilight vision)

b. Optic Disk: area in retina for entrance of optic nerve,

has no photoreceptors

B. Lens: transparent body that focuses image on retina

C. Fluid of the eye

1. Aqueous Humor: clear, watery fluid in anterior &

posterior chambers in anterior part of eye; serves as

refracting medium & provides nutrients to lens &

cornea; contribute to maintenance of intraocular

pressure

2. Vitreous Humor: clear, gelatinous material that fills

posterior cavity of eye; maintains transparency & form

of eye

Visual Pathways

a. Retina (rods & cones) translates light waves into neural

impulses that travel over the optic nerves

b. Optic nerves for each eye meet at the optic chiasm

Fibers from median halves of the retinas cross here

& travel to the opposite side of the brain

Fibers from lateral halves of retinas remain

uncrossed

c. Optic nerves continue from optic chiasm as optic tracts &

travels to the cerebrum (occipital lobe) where visual

impulses are perceived & interpreted

Canal of schlemm: site of aqueous humor drainage

Meibomian gland: secrets a lubricating fluid inside the eyelid

Maculla lutea: yellow spot center of retina

Fovea centralis: area with highest visual acuity or acute vision

2 muscles of iris:

Circular smooth muscle fiber: Constricts the pupil

Radial smooth muscle fiber: Dilates the pupil

Physiology of vision

4 Physiological processes for vision to occur:

1. Refraction of light rays: bending of light rays

2. Accommodation of lens

3. Constriction & dilation of pupils

4. Convergence of eyes

Unit of measurements of refraction: diopters

Normal eye refraction: emmetropia

Normal IOP: 12-21 mmHg

Error of Refraction

1. Myopia: nearsightedness: Treatment: biconcave lens

2. Hyperopia: farsightedness: Treatment: biconvex lens

3. Astigmatisim: distorted vision: Treatment: cylindrical

4. Presbyopia: “old sight” inelasticity of lens due to aging:

Treatment: bifocal lens or double vista

Accommodation of lenses: based on thelmholtz theory of

accommodation

Near Vision: Ciliary muscle contracts: Lens bulges

Far Vision: ciliary muscle dilates / relaxes: lens is flat

Convergence of the eye:

Error:

1. Exotropia:1 eye normal

2. Esophoria: corrected by

corrective eye surgery

3. Strabismus: squint eye

4. Amblyopia: prolong squinting

Common Visual Disorder

Glaucoma

Characterized by increase intraocular pressure resulting in

progressive loss of vision

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May cause blindness if not recognized & treated

Early detection is very important

preventable but not curable

Regular eye exam including tonometry for person over age

40 is recommended


1. Common among 40 years old and above

2. Hereditary

3. Hypertension

4. Obesity

5. History of previous eye surgery, trauma, inflammation

Types of Glaucoma:

1. Chronic (open-angle) Glaucoma:

Most common form

Due to obstruction of the outflow of aqueous humor, in

trabecular meshwork or canal of schlemm

2. Acute (close-angle) Glaucoma:

Due to forward displacement of the iris against the

cornea, obstructing the outflow of the aqueous humor

Occurs suddenly & is an emergency situation

If untreated it will result to blindness

3. Chronic (close-angle) Glaucoma:

similar to acute (close-angle) glaucoma, with the

potential for an acute attack

S/sx

1. Chronic (open-angle) Glaucoma: symptoms develops slowly

Impaired peripheral vision (PS: tunnel vision)

Halos around light

Mild discomfort in the eye

Loss of central vision if unarrested

2. Acute (close-angle) Glaucoma

Severe eye pain

Blurred cloudy vision

Halos around light

N/V

Steamy cornea

Moderate pupillary dilation

3. Chronic (close-angle) Glaucoma

Transient blurred vision

Slight eye pain

Halos around lights

Dx

1. Visual Acuity: reduced

2. Tonometry: reading of 24-32 mmHg suggest glaucoma; may

be 50 mmHg of more in acute (close-angle) glaucoma

3. Ophthalmoscopic exam: reveals narrowing of small vessels

of optic disk, cupping of optic disk

4. Perimetry: reveals defects in visual field

5. Gonioscopy: examine angle of anterior chamber

Medical Management

1. Chronic (open-angle) Glaucoma

a. Drug Therapy: one or a combination of the following

Miotics eye drops (Pilocarpine): to increase outflow

of aqueous humor

Epinephrine eye drops: to decrease aqueous humor

production & increase outflow

Carbonic Anhydrase Inhibitor: Acetazolamide

(Diamox): to decrease aqueous humor production

Timolol Maleate (Timoptic): topical beta-adrenergic

blocker: to decrease intraocular pressure (IOP)

b. Surgery (if no improvement with drug)

Filtering procedure (Trabeculectomy / Trephining):

to create artificial openings for the outflow of

aqueous humor

Laser Trabeculoplasty: non-invasive procedure

performed with argon laser that can be done on an

out-client basis; procedure similar result as

trabeculectomy

2. Acute (close-angle) Glaucoma

a. Drug Therapy: before surgery

Miotics eye drops (Pilocarpine): to cause pupil to

contract & draw iris away from cornea

Osmotic Agent (Glycerin oral, Mannitol IV): to

decrease intraocular pressure (IOP)

Narcotic Analgesic: for pain

b. Surgery

Peripheral Iridectomy: portion of the iris is excised

to facilitate outflow of aqueous humor

Argon Laser Beam Surgery: non-invasive procedure

using laser produces same effect as iridectomy;

done in out-client basis

Iridectomy: usually performed on second eye later

since a large number of client have an acute acute

attack in the other eye

3. Chronic (close-angle) Glaucoma

a. Drug Therapy:

miotics (pilocarpine)

b. Surgery:

bilateral peripheral iridectomy: to prevent acute

attacks


1. Administer medication as ordered

2. Provide quite, dark environment

3. Maintain accurate I & O with the use of osmotic agent

4. Prepare client for surgery if indicated

5. Provide post-op care

6. Provide client teaching & discharge planning

a. Self-administration of eye drops

b. Need to avoid stooping, heavy lifting or pushing,

emotional upsets, excessive fluid intake, constrictive

clothing around the neck

c. Need to avoid the use antihistamines or

sympathomimetic drugs (found in cold preparation) in

close-angle glaucoma since they may cause mydriasis

d. Importance of follow-up care

e. Need to wear medic-alert tag

Cataract

Decrease opacity of ocular lens

Incidence increases with age

Predisposing Factor

1. Aging 65 years and above

2. May caused by changes associated with aging (“senile”

cataract)

3. Related to congenital

4. May develop secondary to trauma, radiation, infection,

certain drugs (corticosteroids)


6. Prolonged exposure to UV rays

S/sx

1. Loss of central vision

2. Blurring or hazy vision

3. Progressive decrease of vision

4. Glare in bright lights

5. Milky white appearance at center of pupils

6. Decrease perception to colors

Diagnostic Procedure

1. Ophthalmoscopic exam: confirms presence of cataract


1. Prepare client for cataract surgery:

a. Performed when client can no longer remain

independent because of reduced vision

b. Surgery performed on one eye at a time; usually in a

same day surgery unit

c. Local anesthesia & intravenous sedation usually used

d. Types of cataract surgery:

Extracapsular Extraction: lens capsule is excised &

the lens is expressed; posterior capsule is left in

place (may be used to support new artificial lens

implant); partial removal of lens

Phacoemulsification: type of extracapsular

extraction; a hollow needle capable of ultrasonic

vibration is inserted into lens, vibrations emulsify

the lens, which is aspirated

Intracapsular Extraction: lens is totally removed

within its capsules, may be delivered from eye by

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cryoextraction (lens is frozen with metal probe &

removed); total removal of lens & surrounding

capsules

e. Peripheral Iridectomy: may be performed at the time of

surgery; small hole cut in iris to prevent development of

secondary glaucoma

f. Intraocular Lens Implant: often performed at the time of

surgery

2. Nursing Intervention Pre-op

a. Assess vision in the unaffected eye since the affected

eye will be patched post-op

b. Provide pre-op teaching regarding measures to prevent

intraocular pressure (IOP) post-op

c. Administer medication as ordered:

Topical Mydriatics (Mydriacyl) & Cyclopegics

(Cyclogyl): to dilate the pupil

Topical antibiotics: to prevent infection

Acetazolamide (Diamox) & osmotic agent (Oral

Glycerin or Mannitol IV): to decrease intraocular

pressure to provide soft eyeball for surgery

3. Nursing Intervention Post-op

a. Reorient the client to surroundings

b. Provide safety measures:

Elevate side rails

Provide call bells

Assist with ambulation when fully recovered from

anesthesia

c. Prevent intraocular pressure & stress on the suture line:

Elevate head of the bed 30-40 degree

Have the client lie on back or unaffected side

Avoid having the client cough, sneeze, bend over, or

move head too rapidly

Treat nausea with anti-emetics as ordered: to

prevent vomiting

Give stool softener as ordered: to prevent straining

Observe for & report signs of intraocular pressure

(IOP):

Severe eye pain

Restlessness

Increased pulse

4. Protect eye from injury:

a. Dressing usually removed the day after the surgery

b. Eyeglasses or eye shield used during the day

c. Always use eye shield during the night

5. Administer medication as ordered:

a. Topical mydriatics & cycloplegic: to decrease spasm of

ciliary body & relieve pain

b. Topical antibiotics & corticosteroids

c. Mild analgesic as needed


a. Technique of eyedrop administration

b. Use of eye shield at night

c. No bending, stooping, or lifting

d. Report signs & symptoms of complication immediately

to physician:

Severe eye pain

Decrease vision

Excessive drainage

Swelling of eyelid

e. Cataract glasses / contact lenses

If a lens implant has not been performed the client

will need glasses or contact lenses

Temporary glasses are worn for 1-4 weeks then

permanent glasses fitted

Cataract glasses magnify object by 1/3 & distortion

peripheral vision

Have the client practice manual coordination

with assistance until new spatial relationship

becomes familiar

Have client practice walking, using stairs,

reaching for articles

Contact lenses cause less distortion of vision;

prescribe at one month

Retinal Detachment

Separation of epithelial surface of retina

Detachment or the sensory retina from the pigment

epithelium of the retina


1. Trauma

2. Aging process

3. Severe diabetic retinopathy

4. Post-cataract extraction

5. Severe myopia (near sightedness)

Pathophysiology

Tear in the retina allows vitreous humor to seep behind the

sensory retina & separate it from the pigment epithelium

S/sx

1. Curtain veil like vision coming across field of vision

2. Flashes of light

3. Visual field loss

4. Floaters

5. Gradual decrease of central vision

Dx

1. Ophthalmoscopic exam: confirms diagnosis

Medical Management

1. Bed rest with eye patched & detached areas dependent to

prevent further detachment

2. Surgery: necessary to repair detachment

a. Photocoagulation: light beam (argon laser) through

dilated pupil creates an inflammatory reaction &

scarring to heal the area

b. Cryosurgery or diathermy: application of extreme cold

or heat to external globe; inflammatory reaction causes

scarring & healing of area

c. Scleral buckling: shortening of sclera to force pigment

epithelium close to retina

Nursing Intervention Pre-op

1. Maintain bed rest as ordered with head of bed flat &

detached area in a dependent position

2. Use bilateral eye patches as ordered; elevate side rails to

prevent injury

3. Identify yourself when entering the room

4. Orient the client frequently to time of date & surroundings;

explain procedures

5. Provide diversional activities to provide sensory stimulation

Nursing Intervention Post-op

1. Check orders for positioning & activity level:

a. May be on bed rest for 1-2 days

b. May need to position client so that detached area is in

dependent position


a. Topical mydriatics

b. Analgesic as needed


a. Techniques of eyedrop administration

b. Use eye shield at night

c. No bending from waist; no heavy work or lifting for 6

weeks

d. Restriction of reading for 3 weeks or more

e. May watch TV

f. Need to check to physician regarding combing &

shampooing hair & shaving

g. Need to report complications such as recurrence of

detachment

Overview of Anatomy & Physiology Of Ear (Hearing)

External Ear

1. Auricle (Pinna): outer projection of ear composed of

cartilage & covered by skin; collects sound waves

2. External Auditory Canal: lined with skin; glands secretes

cerumen (wax), providing protection; transmits sound

waves to tympanic membrane

3. Tympanic Membrane (Eardrum): at end of external canal;

vibrates in response to sound & transmits vibrations to

middle ear

Middle Ear

1. Ossicles

a. 3 small bones: malleus (Hammer) attached to

tympanic membrane, incus (anvil), stapes (stirrup)

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b. Ossicles are set in motion by sound waves from

tympanic membrane

c. Sound waves are conducted by vibration to the

footplate of the stapes in the oval widow (an opening

between the middle ear & the inner ear)

2. Eustachian Tube: connects nasopharynx & middle ear;

bring air into middle ear, thus equalizing pressure on both

sides of eardrum

Inner Ear

1. Cochlea

Controls hearing

Contains Organ of Corti (the true organ of hearing):

the receptor end-organ for hearing

Transmit sound waves from the oval window &

initiates nerve impulses carried by cranial nerve VIII

(acoustic branch) to the brain (temporal lobe of

cerebrum)

2. Vestibular Apparatus

Organ of balance

Composed of three semicircular canals & the utricle

3. Endolymph & Perilymph

For static equilibrium

4. Mastoid air cells Air filled spaces in temporal bone in skull

Disorder of the Ear

Otosclerosis

Formation of new spongy bone in the labyrinth of the

ear causing fixation of the stapes in the oval window

This prevent transmission of auditory vibration to the

inner ear

Predisposing Factor

1. Found more often in women

Cause


2. There is familial tendency

3. Ear trauma & surgery

S/sx

1. Progressive hearing loss

2. Tinnitus

Dx

1. Audiometry: reveals conductive hearing loss

2. Weber’s & Rinne’s Test: show bone conduction is

greater than air conduction

Medical Management

1. Stapedectomy: procedure of choice

Removal of diseased portion of stapes &

replacement with prosthesis to conduct vibrations

from the middle ear to inner ear

Usually performed under local anesthesia

Used to treat otoscrlerosis


1. Provide general pre-op nursing care, including an

explanation of post-op expectation

2. Explain to the client that hearing may improve during

surgery & then decrease due to edema & packing

Nursing Intervention Post-op

1. Position the client according to the surgeon’s orders

(possibly with operative ear uppermost to prevent

displacement of the graft)

2. Have the client deep breathe every 2 hours while in bed,

but no coughing

3. Elevate side rails; assist the client with ambulation &

move slowly: may have some vertigo


Analgesic

Antibiotics

Anti-emetics

Anti-motion sickness drug: Meclesine Hcl

(Bonamine)

5. Check for dressing frequently for excessive drainage or

bleeding

6. Assess facial nerve function: Ask the client to do the ff:

Wrinkle forehead

Close eyelids

Puff out checks for any asymmetry

7. Question the client about the ff: report existence to

physicians

Pain

Headaches

Vertigo

Unusual sensations in the ear


concerning:

a. Warning against blowing nose or coughing; sneeze

with mouth open

b. Need to keep ear dry in the shower; no shampooing

until allowed

c. No flying for 6 mos. Especially if upper respiratory

tract infection is present

d. Placement of cotton balls in auditory meatus after

packing is removed; change twice daily

Meniere’s Disease

Disease of the inner ear resulting from dilatation of the

endolymphatic system & increase volume of endolymph

Characterized by recurrent & usually progressive triad of

symptoms: vertigo, tinnitus, hearing loss

Predisposing Factor

1. Incidence highest between ages 30 & 60

Cause


3. Theories include the ff:

a. Allergy

b. Toxicity

c. Localized ischemia

d. Hemorrhage

e. Viral infection

f. Edema

S/sx

1. Sudden attacks of vertigo lasting hours or days; attacks

occurs several times a year

2. N/V

3. Tinnitus

4. Progressive hearing loss

5. Nystagmus

Dx

1. Audiometry: reveals sensorineural hearing loss

2. Vestibular Test: reveals decrease function

Medical Management

1. Acute:

Atropine (decreases autonomic nervous system

activity)

Diazepam (Valium)

Fentanyl & Droperidol (Innovar)

2. Chronic:

a. Drug Therapy:

Vasodilators (nicotinic Acid)

Diuretics

Mild sedative or tranquilizers: Diazepam

(Valium)

Antihistamines: Diphenhydramine (Benadryl)

Meclizine (antivert)

b. Diet:

Low sodium diet

Restricted fluid intake

Restrict caffeine & nicotine

3. Surgery:

a. Surgical destruction of labyrinth causing loss of

vestibular & cochlear function (if disease is

unilateral)

b. Intracranial division of vestibular portion of cranial

nerve VIII

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c. Endolymphatic sac decompression or shunt to

equalize pressure in endolymphatic space


1. Maintain bed rest in a quiet, darkened room in position

of choice; elevate side rails as needed

2. Only move the client for essential care (bath may not be

essential)

3. Provide emesis basin for vomiting

4. Monitor IV Therapy; maintain accurate I&O

5. Assist in ambulation when the attack is over


7. Prepare client for surgery as indicated (pot-op care

includes using above measures)

8. Provide client care & discharge planning concerning:

a. Use of medication & side effects

b. Low sodium diet & decrease fluid intake

c. Importance of eliminating smoking

Overview of Anatomy & Physiology of Endocrine System

Endocrine System

Is composed of an interrelated complex of glands (Pituitary

G, Adrenal G, Thyroid G, Parathyroid G, Islets of langerhans

of the pancreas, Ovaries & Testes) that secretes a variety of

hormones directly into the bloodstream.

Its major function, together with the nervous system: is to

regulate body function

Hormones Regulation

1. Hormones: chemical substance that acts s messenger to

specific cells & organs (target organs), stimulating &

inhibiting various processes

Two Major Categories

a. Local: hormones with specific effect in the area of

secretion (ex. Secretin, cholecystokinin, panceozymin

[CCK-PZ])

b. General: hormones transported in the blood to distant

sites where they exert their effects (ex. Cortisol)

2. Negative Feedback Mechanisms: major means of regulating

hormone levels

a. Decreased concentration of a circulating hormones

triggers production of a stimulating hormones from

pituitary gland; this hormones in turn stimulates its

target organ to produce hormones

b. Increased concentration of a hormones inhibits

production of the stimulating hormone, resulting in

decreased secretion of the target organ hormone

3. Some hormones are controlled by changing blood levels of

specific substances (ex. Calcium, glucose)

4. Certain hormones (ex. Cortisol or female reproductive

hormones) follow rhythmic patterns of secretion

5. Autonomic & CNS control (pituitary-hypothalamic axis):

hypothalamus controls release of the hormones of the

anterior pituitary gland through releasing & inhibiting

factors that stimulate or inhibits hormone secretions

Hormone Function

Endocrine G Hormone Functions

Pituitary G

Anterior lobe : TSH : stimulate

thyroid G to release thyroid hormones

: ACTH : stimulate adrenal

cortex to produce &

release

adrenocoticoids

: FSH, LH : stimulate growth,

maturation, & function of primary

& secondary sex

organ

: GH, Somatotropin : stimulate growth of

body tissues & bones

: Prolactin or LTH : stimulate

development of mammary gland &

Lactation

Posterior lobe : ADH : regulates H2O

metabolism; release during stress

Or in response to an

increase in plasma

osmolality

To stimulate

reabsorption of H2O &

decrease urine

Output

: Oxytocin : stimulate uterine

contractions during delivery & the

Release of milk in

lactation

Intermediate lobe : MSH : affects skin

pigmentation

Adrenal G

Adrenal Cortex : Mineralocorticoid : regulate fluid &

electrolyte balance; stimulate

(ex. Aldosterone) reabsoption

of sodium, chloride, & H2O; stimulate

potassium excretion

: Glucocorticoids : increase

blood glucose level by increasing rate of

(ex. Cortisol, glyconeogenesis;

increase CHON catabolism; increase

corticosterone) mobilization of fatty

acid; promote sodium & H2O

retention; anti-inflammatory effect; aid body in

coping

with stress

: Sex Hormones : influence

development of secondary sex

(androgens, estrogens characeristics

progesterones)

Adrenal Medulla : Epinephrine, : function in acute

stress; increase HR, BP; dilates

Norepinephrine bronchioles;

convert glycogen to glucose when

Needed by the

muscles for energy

Thyroid G : T3, T4 : regulate metabolic

rate; CHO, fats, & CHON

Metabolism; aid in

regulating physical & mental

Growth &

development

: Thyrocalcitonin : lowers

serum calcium & phosphate levels

Parathyroid G : PTH : regulates serum

calcium & phosphate levels

Pancreas (islets of

Langerhans)

Beta Cells : Insulin : allows glucose to

diffuse across cell membrane;

Converts glucose to

glycogen

Alpha Cells : Glucagon : increase blood

glucose by causing glyconeogenisis

& glycogenolysis in

the liver; secreted in

response to

low blood sugar

Ovaries : Estrogen, Progesterone :

development of secondary sex characteristics in the

Female, maturation

of sex organ, sexual functioning

Maintenance of

pregnancy

Testes : Testosterone : development of

secondary sex characteristics in the

Male maturation of

the sex organs, sexual functioning

Pituitary Gland (Hypophysis)

Located in sella turcica at the base of brain

“Master Gland” or master clock

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Controls all metabolic function of body

3 Lobes of Pituitary Gland

1. Anterior Lobe PG (Adenohypophysis)

a. Secretes tropic hormones (hormones that stimulate

target glands to produce their hormones):

adrenocorticotropic H (ACTH), thyroid-stimulating H

(TSH), follicle-stimulating H (FSH), luteinizing H (LH)

ACTH: promotes development of adrenal cortex

LH: secretes estrogen

FSH: secretes progesterone

b. Also secretes hormones that have direct effects on

tissues: somatotropic or growth H, prolactin

Somatotropic / GH: promotes elongation of long

bones

Hyposecretion of GH: among children results to

dwarfism

Hypersecretion of GH: among children results to

gigantism

Hypersecretion of GH: among adults results to

acromegaly (square face)

DOC: Ocreotide (Sandostatin)

Prolactin: promotes development of mammary

gland; with help of oxytocin it initiates milk let

down reflex

c. Regulated by hypothalamic releasing & inhibiting factors

& by negative feedback system

2. Posterior Lobe PG (Neurohypophysis)

Does not produce hormones

Store & release anti-diuretic hormones (ADH) & oxytocin

produced by hypothalamus

Secretes hormones oxytocin (promotes uterine

contractions preventing bleeding or hemorrhage)

Administer oxytocin immediately after delivery to

prevent uterine atony.

Initiates milk let down reflex with help of hormone

prolactin

3. Intermediate Lobe PG

Secretes melanocytes stimulating H (MSH)

MSH: for skin pigmentation

Hyposecretion of MSH: results to albinism

Hypersecretion of MSH: results to vitiligo

2 feared complications of albinism:

1. Lead to blindness due to severe

photophobia

2. Prone to skin cancer

Adrenal Glands

Two small glands, one above each kidney; Located at

top of each kidney

2 Sections of Adrenal Glands

1. Adrenal Cortex (outer portion): produces mineralocorticoids,

glucocorticoids, sex hormones

3 Zones/Layers

Zona Fasciculata: secretes glucocortocoids

(cortisol): controls glucose metabolism: Sugar

Zona Reticularis: secretes traces of glucocorticoids

& androgenic hormones: promotes secondary sex

characteristics: Sex

Zona Glumerulosa: secretes mineralocorticoids

(aldosterone): promotes sodium and water

reabsorption and excretion of potassium: Salt

2. Adrenal Medulla (inner portion): produces epinephrine,

norepinephrine (secretes catecholamines a power

hormone): vasoconstrictor

2 Types of Catecholamines:

Epinephrine (vasoconstrictor)

Norepinephrine (vasoconstrictor)

o Pheochromocytoma (adrenal medulla): Increase

secretion of norepinephrine: Leading to

hypertension which is resistant to

pharmacological agents leading to CVA: Use

beta-blockers

Thyroid Gland

Located in anterior portion of the neck

Consist of 2 lobes connected by a narrow isthmus

Produces thyroxine (T4), triiodothyronine (T3),

thyrocalcitonin

3 Hormones Secreted:

T3: 3 molecules of iodine (more potent)

T4: 4 molecule of iodine

T3 and T4 are metabolic hormone: increase brain

activity; promotes cerebration (thinking); increase

V/S

Thyrocalcitonin: antagonizes the effects of

parathormone to promote calcium reabsorption.

Parathyroid Gland

4 small glands located in pairs behind the thyroid gland

Produce parathormone (PTH)

Promotes calcium reabsorption

Pancreas

Located behind the stomach

Has both endocrine & exocrine function (mixed gland)

Consist of Acinar Cells (exocrine gland): which secretes

pancreatic juices: that aids in digestion

Islets of langerhans (alpha & beta cells) involved in

endocrine function:

Alpha Cell: produce glucagons: (function:

hyperglycemia)

Beta Cell: produce insulin: (function: hypoglycemia)

Delta Cells: produce somatostatin: (function:

antagonizes the effects of growth hormones)

Gonads

Ovaries: located in pelvic cavity; produce estrogen &

progesterone

Testes: located in scrotum; produces testosterone

Pineal Gland

Secretes melatonin

Inhibits LH secretion

It controls & regulates circadian rhythm (body clock)

Diabetes Incipidus (DI)

DI: dalas-ihi

Decrease of anti-diuretic hormone (ADH)

Hyposecretion of ADH

Hypofunction of the posterior pituitary gland (PPG) resulting

in deficiency of ADH

Characterized by excessive thirst & urination

Anti-diuretic Hormone: Pitressin (Vasopressin)

Function: prevents urination thereby conserving water

Note: Alcohol inhibits release of ADH

Predisposing Factor

1. Related to pituitary surgery

2. Trauma

3. Inflammation

4. Presence of tumor

S/sx

1. Severe polyuria with low specific gravity

2. Polydipsia (excessive thirst)

3. Fatigue

4. Muscle weakness

5. Irritability

6. Weight loss

7. Hypotension

8. Signs of dehydration

a. Adult: thirst; Children: tachycardia

b. Agitation

c. Poor Skin turgor

d. Dry mucous membrane

9. Tachycardia, eventually shock if fluids is not replaced

10. If left untreated results to hypovolemic shock (late sign

anuria)

Dx

1. Urine Specific Gravity (NV: 1.015 – 1.030): less than 1.004

2. Serum Na: increase resulting to hypernatremia

3. H2O deprivation test: reveals inability to concentrate urine

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1. Maintain F&E balance / Force fluids 2000-3000 ml/day

a. Keep accurate I&O

b. Weigh daily

c. Administer IV/oral fluids as ordered to replace fluid loss

2. Monitor strictly V/S & observe for signs of dehydration &

hypovolemia

3. Administer hormone replacement as ordered:

a. Vasopressin (Pitressin) & Vasopressin Tannate (Pitressin

Tannate Oil): administered by IM injection

Warm to body temperature before giving

Shake tannate suspension to ensure uniform

dispersion

b. Lypressin (Diapid): nasal spray

4. Prevent complications: hypovolemic shock is the most

feared complication


a. Lifelong hormone replacement: Lypressin (Diapid) as

needed to control polyuria & polydipsia

b. Need to wear medic-alert bracelet

Syndrome of Inappropriate Anti-diuretic Hormone Secretion (SIADH)

Hypersecretion of anti-diuretic hormone (ADH) from the PPG

even when the client has abnormal serum osmolality


1. Head injury

2. Related to presence of bronchogenic cancer

Initial sign of lung cancer is non productive cough

Non invasive procedure is chest x-ray

3. Related to hyperplasia of pituitary gland (increase size of

organ brought about by increase of number of cells)

S/sx

1. Person with SIADH cannot excrete a dilute urine

2. Fluid retention & Na deficiency

a. Hypertension

b. Edema

c. Weight gain

3. Water intoxication: may lead to cerebral edema: lead to

increase ICP; may lead to seizure activity

Dx

1. Urine specific gravity: is increase

2. Serum Sodium: is decreased

Medical Management

1. Treat underlying cause if possible

2. Diuretics & fluid restriction


1. Restrict fluid: to promote fluid loss & gradual increase in

serum Na


a. Loop diuretics (Lasix)

b. Osmotic diuretics (Mannitol)

3. Monitor strictly V/S, I&O & neuro check

4. Weigh patient daily and assess for pitting edema

5. Monitor serum electrolytes & blood chemistries carefully

6. Provide meticulous skin care

7. Prevent complications

HYPOTHYROIDISM

- all are decrease except weight and menstruation

- memory impairment

Signs and Symptoms

- there is loss of appetite but there is weight gain

- menorrhagia

- cold intolerance

- constipation

HYPERTHYROIDISM

- all are increase except weight and menstruation

Signs and Symptoms

- increase appetite but there is weight loss

- amenorrhea

- exophthalmos

Thyroid Disorder

Simple Goiter

Enlargement of thyroid gland due to iodine deficiency

Enlargement of the thyroid gland not caused by

inflammation of neoplasm

Low level of thyroid hormones stimulate increased secretion

of TSH by pituitary; under TSH stimulation the thyroid

increases in size to compensate & produce more thyroid

hormone


1. Endemic: caused by nutritional iodine deficiency, most

common in the “goiter belt” area, areas where soil & H2O

are deficient in iodine; occurs most frequently during

adolescence & pregnancy

Goiter belt area:

a. Midwest, northwest & great lakes region

b. Places far from sea

c. Mountainous regions

2. Sporadic: caused by

Increase intake of goitrogenic foods (contains agent that

decrease the thyroxine production: pro-goitrin an anti-

thyroid agent that has no iodine). Ex. cabbage, turnips,

radish, strawberry, carrots, sweet potato, rutabagas,

peaches, peas, spinach, broccoli, all nuts

Soil erosion washes away iodine

Goitrogenic drugs:

a. Anti-Thyroid Agent: Propylthiouracil (PTU)

b. Large doses of iodine

c. Phenylbutazone

d. Para-amino salicylic acid

e. Lithium Carbonate

f. PASA (Aspirin)

g. Cobalt

3. Genetic defects that prevents synthesis of thyroid hormones

S/sx

1. Enlarged thyroid gland

2. Dysphagia

3. Respiratory distress

4. Mild restlessness

Dx

1. Serum T4: reveals normal or below normal

2. Thyroid Scan: reveals enlarged thyroid gland.

3. Serum Thyroid Stimulating Hormone (TSH): is increased

(confirmatory diagnostic test)

4. RAIU (Radio Active Iodine Uptake): normal or increased

Medical Management

1. Drug Therapy:

Hormone replacement with levothyroxine (Synthroid)

(T4), dessicated thyroid, or liothyronine (Cytomel) (T3)

Small dose of iodine (Lugol’s or potassium iodide

solution): for goiter resulting from iodine deficiency

2. Avoidance of goitrogenic food or drugs in sporadic goiter

3. Surgery:

Subtotal thyroidectomy: (if goiter is large) to relieve

pressure symptoms & for cosmetic reasons


1. Administer Replacement therapy as ordered:

a. Lugol’s Solution / SSKI (Saturated Solution of Potassium

Iodine)

Color purple or violet and administered via straw to

prevent staining of teeth.

4 Medications to be taken via straw: Lugol’s, Iron,

Tetracycline, Nitrofurantoin (DOC: for

pyelonephritis)

b. Thyroid Hormones:

Levothyroxine (Synthroid)

Liothyronine (Cytomel)

Thyroid Extracts

Nursing Intervention when giving Thyroid Hormones:

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1. Instruct client to take in the morning to prevent

insomnia

2. Monitor vital signs especially heart rate because drug

causes tachycardia and palpitations

3. Monitor side effects:

Insomnia

Tachycardia and palpitations

Hypertension

Heat intolerance

2. Increase dietary intake of foods rich in iodine:

Seaweeds

Seafood’s like oyster, crabs, clams and lobster but

not shrimps because it contains lesser amount of

iodine.

Iodized salt: best taken raw because it is easily

destroyed by heat

3. Assist in surgical procedure of subtotal thyroidectomy


Used of iodized salt in preventing & treating endemic

goiter

Thyroid hormone replacement

Hypothyroidism (Myxedema)

Slowing of metabolic processes caused by hypofunction of

the thyroid gland with decreased thyroid hormone secretion

Hyposecretion of thyroid hormone

Decrease in all V/S except wt & menses

Adults: myxedema non pitting edema

Children: cretinism the only endocrine disorder that can lead

to mental retardation

In severe or untreated cases myxedema coma may occur:

Characterized by intensification of S/sx of

hypothyroidism & neurologic impairment leading to

coma

Mortality rate high; prompt recognition & treatment

essential

Precipitating factors: failure to take prescribed

medications; infection; trauma; exposure to cold; use of

sedatives, narcotics or anesthetics


1. Primary hypothyroidism: atrophy of the gland possibly

caused by an autoimmune process

2. Secondary hypothyroidism: caused by decreased

stimulation from pituitary TSH

3. Iatrogenic: surgical removal of the gland or over

treatment of hyperthyroidism with drugs or radioactive

iodine; disease caused by medical intervention such as

surgery

4. Related to atrophy of thyroid gland due to trauma,

presence of tumor, inflammation

5. Iodine deficiency

6. Autoimmune (Hashimotos Disease)

7. Occurs more often to women ages 30 & 60

S/sx

1. Loss of appetite: but there is wt gain

2. Anorexia

3. Weight gain: which promotes lipolysis leading to

atherosclerosis and MI

4. Constipation

5. Cold intolerance

6. Dry scaly skin

7. Spares hair

8. Brittleness of nails

9. Decrease in all V/S: except wt gain & menses

a. Hypotension

b. Bradycardia

c. Bradypnea

d. Hypothermia

10. Weakness and fatigue

11. Slowed mental processes

12. Dull look

13. Slow clumsy movement

14. Lethargy

15. Generalized interstitial non-pitting edema (Myxedema)

16. Hoarseness of voice

17. Decrease libido

18. Memory impairment

19. Psychosis

20. Menorrhagia

Dx

1. Serum T3 and T4: is decreased

2. Serum Cholesterol: is increased

3. RAIU (Radio Active Iodine Uptake): is decreased

Medical Management

1. Drug Therapy:

Levothyroxine (Synthroid)

Thyroglobulin (Proloid)

Dessicated thyroid

Liothyronine (Cytomel)

2. Myxedema coma is a medical emergency:

IV thyroid hormones

Correction of hypothermina

Maintenance of vital function

Treatment of precipitating cause


1. Monitor strictly V/S & I&O, daily weights; observe for

edema & signs of cardiovascular complication & to

determine presence of myxedema coma

2. Administer thyroid hormone replacement therapy as

ordered & monitor effects:

a. Observe signs of thyrotoxicosis:

Tachycardia & palpitation

N/V

Diarrhea

Sweating

Tremors

Agitation

Dyspnea

b. Increase dosage gradually, especially in clients with

cardiac complication

3. Provide comfortable and warm environment: due to cold

intolerance

4. Provide a low calorie diet

5. Avoid the use of sedatives; reduce the dose of any

sedatives, narcotics, or anesthetic agent by half as

ordered

6. Provide meticulous skin care: to prevent skin

breakdown

7. Increase fluid & food high in fiber: to prevent

constipation; administer stool softener as ordered

8. Observe for signs of myxedema coma; provide

appropriate nursing care

a. Administer medication as ordered

b. Maintain vital functions:

Correct hypothermia

Maintain adequate ventilation

9. Myxedema coma:

A complication of hypothyroidism & an emergency

case

A severe form of hypothyroidism is characterized

by:

Severe hypotension

Bradycardia

Bradypnea

Hypoventilation

Hyponatremia

Hypoglycemia

Hypothermia

Leading to progressive stupor and coma

Nursing Management for Myxedema Coma

1. Assist in mechanical ventilation

2. Administer thyroid hormones as ordered

3. Administer IVF replacement isotonic fluid solution as

ordered / Force fluids

10. Provide client health teaching and discharge planning

concerning:

a. Thyroid hormone replacement

b. Importance of regular follow-up care

c. Need in additional protection in cold weather

d. Measures to prevent constipation

e. Avoid precipitating factors leading to myxedema

coma & hypovolemic shock

f. Stress & infection

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g. Use of anesthetics, narcotics, and sedatives

Hyperthyroidism

Secretion of excessive amounts of thyroid hormone in the

blood causes an increase in metabolic process

Increase in T3 and T4

Grave’s Disease or Thyrotoxicosis

Increase in all V/S except wt & menses


1. More often seen in women between ages 30 & 50

2. Autoimmune: involves release of long acting thyroid

stimulator causing exopthalmus (protrusion of eyeballs)

enopthalmus (late sign of dehydration among infants)

3. Excessive iodine intake

4. Related to hyperplasia (increase size of TG)

S/sx

1. Increase appetite (hyperphagia): but there is weight loss

2. Heat intolerance

3. Weight loss

4. Diarrhea: increase motility

5. Increased in all V/S: except wt & menses

a. Tachycardia

b. Increase systolic BP

c. Palpitation

6. Warm smooth skin

7. Fine soft hair

8. Pliable nails

9. CNS involvement

a. Irritability & agitation

b. Restlessness

c. Tremors

d. Insomnia

e. Hallucinations

f. Sweating

g. Hyperactive movement

10. Goiter

11. PS: Exopthalmus (protrusion of eyeballs)

12. Amenorrhea

Dx

1. Serum T3 and T4: is increased

2. RAIU (Radio Active Iodine Uptake): is increased

3. Thyroid Scan: reveals an enlarged thyroid gland

Medical Management

1. Drug Therap:

a. Anti-thyroid drugs: Propylthiouracil (PTU) &

methimazole (Tapazole): blocke synthesis of thyroid

hormone; toxic effect include agranulocytosis

b. Adrenergic Blocking Agent: Propranolol (Inderal):

used to decrease sympathetic activity & alleviate

symptoms such as tachycardia

2. Radioactive Iodine Therapy

a. Radioactive isotope of iodine (ex. 131I): given to

destroy the thyroid gland, thereby decreasing

production of thyroid hormone

b. Used in middle-aged or older clients who are

resistant to, or develop toxicity from drug therapy

c. Hypothyroidism is a potential complication

3. Surgery: Thyroidectomy performed in younger client for

whom drug therapy has not been effective


1. Monitor strictly V/s & I&O, daily weight

2. Administer anti-thyroid medications as ordered:

a. Propylthiouracil (PTU)

b. Methimazole (Tapazole)

3. Provide for period of uninterrupted rest:

a. Assign a private room away from excessive activity

b. Administer medication to promote sleep as ordered

4. Provide comfortable and cold environment

5. Minimized stress in the environment

6. Encourage quiet, relaxing diversional activities

7. Provide dietary intake that is high in CHO, CHON,

calories, vitamin & minerals with supplemental feeding

between meals & at bedtime; omit stimulant

8. Observe for & prevent complication

a. Exophthalmos: protects eyes with dark glasses &

artificial tears as ordered

b. Thyroid Storm


10. Maintain side rails

11. Provide bilateral eye patch to prevent drying of the eyes

12. Assist in surgical procedures subtotal Thyroidectomy:


concerning:

a. Need to recognized & report S/sx of agranulocytosis

(fever, sore throat, skin rash): if taking anti-thyroid

drugs

b. S/sx of hyperthyroidism & hypothyroidism

Thyroid Storm

Uncontrolled & potentially life-threatening hyperthyroidism

caused by sudden & excessive release of thyroid hormone

into the bloodstream

Precipitating Factors

1. Stress

2. Infection

3. unprepared thyroid surgery

S/sx

1. Apprehension

2. Restlessness

3. Extremely high temp (up to 106 F / 40.7 C)

4. Tahchycardia

5. HF

6. Respiratory Distress

7. Delirium

8. Coma


1. Maintain patent airway & adequate ventilation;

administer O2 as ordered

2. Administer IV therapy as ordered


a. Anti-thyroid drugs

b. Corticosteroids

c. Sedatives

d. Cardiac Drugs

Thyroidectomy

Partial or total removal of thyroid gland

Indication:

Subtotal Thyroidectomy: hyperthyroidism

Total Thyroidectomy: thyroid cancer


1. Ensure that the client is adequately prepared for

surgery

a. Cardiac status is normal

b. Weight & nutritional status is normal

2. Administer anti-thyroid drugs as ordered: to suppressed

the production of thyroid hormone & to prevent thyroid

storm

3. Administer iodine preparation Lugol’s Solution (SSKI) or

Potassium Iodide Solution: to decrease vascularity of the

thyroid gland & to prevent hemorrhage.

Nursing Intervention Post-Op

1. Monitor V/S & I&O

2. Check dressing for signs of hemorrhage: check for

wetness behind the neck

3. Place client in semi-fowlers position & support head with

pillow

4. Observe for respiratory distress secondary to

hemorrhage, edema of glottis, laryngeal nerve damage,

or tetany: keep tracheostomy set, O2 & suction nearby

5. Assess for signs of tetany: due to hypocalcemia: due to

secondary accidental removal of parathyroid glands:

keep Calcium Gluconate available:

Watch out for accidental removal of parathyroid

which may lead to hypocalcemia (tetany)

Classic S/sx of Tetany

Positive trousseu’s sign

Positive chvostek sign

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24

TRIAD SIGNS

Observe for arrhythmia, seizure: give Calcium

Gluconate IV slowly as ordered

6. Ecourage clients voice to rest:

a. Some hoarseness is common

b. Check every 30-60 min for extreme hoarseness or

any accompanying respiratory distress

7. Observe for signs of thyroid storm / thyrotoxicosis: due

to release of excessive amount of thyroid hormone

during surgery

Agitation

Hyperthermia

Tachycardia

Administer medications as ordered:

Anti Pyretics

Beta-blockers

Monitor strictly vital signs, input and output and

neuro check.

Maintain side rails

Offer TSB

8. Administer IV fluids as ordered: until the client is

tolerating fluids by mouth

9. Administer analgesics as ordered: for incisional pain

10. Relieve discomfort from sore throat:

a. Cool mist humidifier to thin secretions

b. Administer analgesic throat lozenges before meals

prn as ordered

11. Encourage coughing & deep breathing every hour

12. Assist the client with ambulation: instruct the client to

place the hands behind the neck: to decrease stress on

suture line if added support is necessary

13. Hormonal replacement therapy for lifetime

14. Watch out for accidental laryngeal damage which may

lead to hoarseness of voice: encourage client to

talk/speak immediately after operation and notify

physician

15. Provide client teaching& discharge planning concerning:

a. S/sx of hyperthyroidism & hypothyroidism

b. Self administration of thyroid hormone: if total

thyroidectomy is performed

c. Application of lubricant to the incision once suture is

removed

d. Perform ROM neck exercise 3-4 times a day

e. Importance of follow up care with periodic serum

calcium level

Hypoparathyroidism

Disorder characterized by hypocalcemia resulting from a

deficiency of parathormone (PTH) production

Decrease secretion of parathormone: leading to

hypocalcemia: resulting to hyperphospatemia

If calcium decreases phosphate increases


1. May be hereditary

2. Idiopathic

3. Caused by accidental damage to or removal of

parathyroid gland during thyroidectomy surgery

4. Atrophy of parathyroid gland due to: inflammation,

tumor, trauma

S/sx

1. Acute hypocalcemia (tetany)

a. Paresthesia: tingling sensation of finger & around lip

b. Muscle spasm

c. laryngospasm/broncospasm

d. Dysphagia

e. Seizure: feared complications

f. Cardiac arrhythmia: feared complications

g. Numbness

h. Positive trousseu’s sign: carpopedal spasm

i. Positive chvostek sign

2. Chronic hypocalcemia (tetany)

a. Fatigue

b. Weakness

c. Muscle cramps

d. Personality changes

e. Irritability

f. Memory impairment

g. Agitation

h. Dry scaly skin

i. Hair loss

j. Loss of tooth enamel

k. Tremors

l. Cardiac arrhythmias

m. Cataract formation

n. Photophobia

o. Anorexia

p. N/V

Diagnostic Procedures

1. Serum Calcium level: decreased (normal value: 8.5 – 11

mg/100 ml)

2. Serum Phosphate level: increased (normal value: 2.5 –

4.5 mg/100 ml)

3. Skeletal X-ray of long bones: reveals a increased in bone

density

4. CT Scan: reveals degeneration of basal ganglia

Nursing Management

1. Administer medications as ordered such as:

a. Acute Tetany: Calcium Gluconate slow IV drip as

ordered

b. Chronic Tetany:

Oral calcium preparation: Calcium Gluconate,

Calcium Lactate, Calcium Carbonate (Os-Cal)

Large dose of vitamin D (Calciferol): to help

absorption of calcium

CHOLECALCIFEROL ARE DERIVED FROM

Drug Diet (Calcidiol)

Sunlight (Calcitriol)

Phosphate Binder: Aluminum Hydroxide Gel

(Amphogel) or aluminum carbonate gel, basic

(basaljel): to decrease phosphate levels

ANTACID

A.A.C

MAD

Aluminum

Magnesium Containing

Containing

Antacids

Antacids

Aluminum

Hydroxide

Gel

Side Effect: Constipation

Side Effect: Diarrhea

2. Institute seizure & safety precaution

3. Provide quite environment free from excessive stimuli

4. Avoid precipitating stimulus such as glaring lights and

noise

5. Monitor signs of hoarseness or stridor; check for signs

for Chvostek’s & Trousseau’s sign

6. Keep emergency equipment (tracheostomy set,

injectable Calcium Gluconate) at bedside: for presence

of laryngospasm

7. For tetany or generalized muscle cramp: may use

rebreathing bag or paper bag to produce mild

respiratory acidosis: to promote increase ionized Ca

levels

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25

8. Monitor serum calcium & phosphate level

9. Provide high-calcium & low-phosphorus diet


concerning:

a. Medication regimen: oral calcium preparation & vit

D to be taken with meal to increase absorption

b. Need to recognized & report S/sx of

hypo/hypercalcemia

c. Importance of follow-up care with periodic serum

calcium level

d. Prevent complications

e. Hormonal replacement therapy for lifetime

Hyperparathyroidism

Increase secretion of PTH that results in an altered state of

calcium, phosphate & bone metabolism

Decrease parathormone

Hypercalcemia: bone demineralization leading to bone

fracture (calcium is stored 99% in bone and 1% blood)

Kidney stones


1. Most commonly affects women between ages 35 & 65

2. Primary Hyperparathyroidism: caused by tumor &

hyperplasia of parathyroid gland

3. Secondary Hyperparathyroidism: cause by

compensatory over secretion of PTH in response to

hypocalcemia from:

a. Children: Ricketts

b. Adults: Osteomalacia

c. Chronic renal disease

d. Malabsorption syndrome

S/sx

1. Bone pain (especially at back); Bone demineralization;

Pathologic fracture

2. Kidney stones; Renal colic; Polyuria; Polydipsia; Cool

moist skin

3. Anorexia; N/V; Gastric Ulcer; Constipation

4. Muscle weakness; Fatigue

5. Irritability / Agitation; Personality changes; Depression;

Memory impairment

6. Cardiac arrhythmias; HPN

Dx

1. Serum Calcium: is increased

2. Serum Phosphate: is decreased

3. Skeletal X-ray of long bones: reveals bone

demineralization


1. Administer IV infusions of normal saline solution & give

diuretics as ordered:

2. Monitor I&O & observe fluid overload & electrolytes

imbalance

3. Assist client with self care: Provide careful handling,

Moving, Ambulation: to prevent pathologic fracture

4. Monitor V/S: report irregularities

5. Force fluids 2000-3000 L/day: to prevent kidney stones

6. Provide acid-ash juices (ex. Cranberry, orange juice): to

acidify urine & prevent bacterial growth

7. Strain urine: using gauze pad: for stone analysis

8. Provide low-calcium & high-phosphorus diet

9. Provide warm sitz bath: for comfort

10. Administer medications as ordered: Morphine Sulfate

(Demerol)

11. Maintain side rails

12. Assist in surgical procedure: Parathyroidectomy


concerning:

a. Need to engage in progressive ambulatory activities

b. Increase fluid intake

c. Use of calcium preparation & importance of high-

calcium diet following a parathyroidectomy

d. Prevent complications: renal failure

e. Hormonal replacement therapy for lifetime

f. Importance of follow up care

Addison’s Disease

Primary adrenocortical insufficiency; hypofunction of the

adrenal cortex causes decrease secretion of the

mineralcorticoids, glucocorticoids, & sex hormones

Hyposecretion of adrenocortical hormone leading to:

Metabolic disturbance: Sugar

Fluid and electrolyte imbalance: Na, H2O, K

Deficiency of neuromascular function: Salt, Sex


1. Relatively rare disease caused by:

Idiopathic atrophy of the adrenal cortex: due to an

autoimmune process

Destruction of the gland secondary to TB or fungal

infections

S/sx

1. Fatigue, Muscle weakness

2. Anorexia, N/V, abdominal pain, weight loss

3. History of hypoglycemic reaction / Hypoglycemia:

tremors, tachycardia, irritability, restlessness, extreme

fatigue, diaphoresis, depression

4. Hyponatremia: hypotension, signs of dehydration,

weight loss, weak pulse

5. Decrease tolerance to stress

6. Hyperkalemia: agitation, diarrhea, arrhythmia

7. Decrease libido

8. Loss of pubic and axillary hair

9. Bronze like skin pigmentation

Dx

1. FBS: is decreased (normal value: 80 – 100 mg/dl)

2. Plasma Cortisol: is decreased

3. Serum Sodium: is decrease (normal value: 135 – 145

meq/L)

4. Serum Potassium: is increased (normal value: 3.5 – 4.5

meq/L)


1. Administer hormone replacement therapy as ordered:

a. Glucocorticoids: stimulate diurnal rhythm of cortisol

release, give 2/3 of dose in early morning & 1/3 of

dose in afternoon

Corticosteroids: Dexamethasone (Decadrone)

Hydrocortisone: Cortisone (Prednisone)

b. Mineralocorticoids:

Fludrocortisone Acetate (Florinef)

Nursing Management when giving steroids

1. Instruct client to take 2/3 dose in the morning and

1/3 dose in the afternoon to mimic the normal

diurnal rhythm

2. Taper dose (withdraw gradually from drug)

3. Monitor side effects:

Hypertension

Edema

Hirsutism

Increase susceptibility to infection

Moon face appearance

2. Monitor V/S

3. Decrease stress in the environment

4. Prevent exposure to infection

5. Provide rest period: prevent fatigue

6. Weight daily

7. Provide small frequent feeding of diet: decrease in K,

increase cal, CHO, CHON, Na: to prevent hypoglycemia,

& hyponatremia & provide proper nutrition

8. Monitor I&O: to determine presence of addisonian crisis

(complication of addison’s disease)



concerning:

a. Disease process: signs of adrenal insufficiency

b. Use of prescribe medication for lifelong replacement

therapy: never omit medication

c. Need to avoid stress, trauma & infection: notify the

physician if these occurs as medication dosage may

need to be adjusted

d. Stress management technique

e. Diet modification

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f. Use of salt tablet (if prescribe) or ingestion of salty

foods (potato chips): if experiencing increase

sweating

g. Importance of alternating regular exercise with rest

periods

h. Avoidance of strenuous exercise especially in hot

weather

i. Avoid precipitating factor: leading to addisonian

crisis: stress, infection, sudden withdrawal to

steroids

j. Prevent complications: addisonian crisis,

hypovolemic shock

k. Importance of follow up care

Addisonian Crisis

Severe exacerbation of addison’s diseasecaused by acute

adrenal insufficiency


1. Strenuous activity

2. Stress

3. Trauma

4. Infection

5. Failure to take prescribe medicine

6. Iatrogenic:

Surgery of pituitary gland or adrenal gland

Rapid withdrawal of exogenous steroids in a

client on long-term steroid therapy

S/sx

1. Generalized muscle weakness

2. Severe hypotension

3. Hypovolemic shock: vascular collapse

4. Hyponatremia: leading to progressive stupor and

coma



2. Administer IV fluids (5% dextrose in saline, plasma)

as ordered: to treat vascular collapse

3. Administer IV glucocorticoids: Hydrocortisone (Solu-

Cortef) & vasopressors as ordered

4. Force fluids

5. If crisis precipitate by infection: administer

antibiotics as ordered

6. Maintain strict bed rest & eliminate all forms of

stressful stimuli

7. Monitor V/S, I&O & daily weight

8. Protect client from infection


concerning: same as addison’s disease

Cushing Syndrome

Condition resulting from excessive secretion of

corticosteroids, particularly glucocorticoid cortisol

Hypersecretion of adrenocortical hormones


1. Primary Cushing’s Syndrome: caused by adrenocortical

tumors or hyperplasia

2. Secondary Cushing’s Syndrome (also called Cushing’s

disease): caused by functioning pituitary or nonpituitary

neoplasm secreting ACTH, causing increase secretion of

glucocorticoids

3. Iatrogenic: cause by prolonged use of corticosteroids

4. Related to hyperplasia of adrenal gland

5. Increase susceptibility to infections

S/sx

1. Muscle weakness

2. Fatigue

3. Obese trunk with thin arms & legs

4. Muscle wasting

5. Irritability

6. Depression

7. Frequent mood swings

8. Moon face

9. Buffalo hump

10. Pendulous abdomen

11. Purple striae on trunk

12. Acne

13. Thin skin

14. Signs of masculinization in women: menstrual

dysfunction, decrease libido

15. Osteoporosis

16. Decrease resistance to infection

17. Hypertension

18. Edema

19. Hypernatremia

20. Weight gain

21. Hypokalemia

22. Constipation

23. U wave upon ECG (T wave hyperkalemia)

24. Hirsutis

25. Easy bruising

Dx

1. FBS: is increased

2. Plasma Cortisol: is increased

3. Serum Sodium: is increased

4. Serum Potassium: is decreased


1. Maintain muscle tone

a. Provide ROM exercise

b. Assist in ambulation

2. Prevent accidents fall & provide adequate rest

3. Protect client from exposure to infection

4. Maintain skin integrity

a. Provide meticulous skin care

b. Prevent tearing of the skin: use paper tape if

necessary

5. Minimize stress in the environment

6. Monitor V/S: observe for hypertension & edema

7. Monitor I&O & daily weight: assess for pitting edema:

Measure abdominal girth: notify physician

8. Provide diet low in Calorie & Na & high in CHON, K, Ca,

Vitamin D

9. Monitor urine: for glucose & acetone; administer insulin

as ordered

10. Provide psychological support & acceptance

11. Prepare client for hypophysectomy or radiation: if

condition is caused by a pituitary tumor

12. Prepare client for Adrenalectomy: if condition is caused

by an adrenal tumor or hyperplasia

13. Restrict sodium intake

14. Administer medications as ordered: Spironolactone

(Aldactone): potassium sparring diuretics


concerning:

a. Diet modification

b. Importance of adequate rest

c. Need to avoid stress & infection

d. Change in medication regimen (alternate day

therapy or reduce dosage): if caused of condition is

prolonged corticosteroid therapy

e. Prevent complications (DM)

f. Hormonal replacement for lifetime: lifetime due to

adrenal gland removal: no more corticosteroid!

g. Importance of follow up care

Diabetes Mellitus (DM)

Represent a heterogenous group of chronic disorders

characterized by hyperglycemia

Hyperglycemia: due to total or partial insulin deficiency or

insensitivity of the cells to insulin

Characterized by disorder in the metabolism of CHO, fats,

CHON, as well as changes in the structure & function of

blood vessels

Metabolic disorder characterized by non utilization of

carbohydrates, protein and fat metabolism

Pathophysiology

Lack of insulin causes hyperglycemia (insulin is necessary for the

transport of glucose across the cell membrane) = Hyperglycemia

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27

leads to osmitic diuresis as large amounts of glucose pass through

the kidney result polyuria & glycosuria = Diuresis leads to cellular

dehydration & F & E depletion causing polydipsia (excessive thirst)

= Polyphagia (hunger & increase appetite) result from cellular

starvation = The body turns to fat & CHON for energy but in the

absence of glucose in the cell fat cannot be completely metabolized

& ketones (intermediate products of fat metabolism) are produced

= This leads to ketonemia, ketonuria (contributes to osmotic

diuresis) & metabolic acidosis (ketones are acid bodies) = Ketone

sacts as CNS depressants & can cause coma = Excess loss of F & E

leads to hypovolemia, hypotension, renal failure & decease blood

flow to the brain resulting in coma & death unless treated.

MAIN FOODSTUFF ANABOLISM CATABOLISM

1. CHO

2. CHON

3. Fats

Glucose

Amino Acids

Fatty Acids

Glycogen

Nitrogen

Free Fatty Acids

: cholesterol

: ketones

HYPERGLYCEMIA

Increase osmotic diuresis

Glycosuria

Polyuria

Cellular starvation: weight loss Cellular dehydration

Stimulates the appetite / satiety center

Stimulates the thirst center

(Hypothalamus)

(Hypothalamus)

Polyphagia

Polydypsia

* liver has glycogen that undergo glycogenesis/glycogenolysis

GLUCONEOGENESIS

Formation of glucose from non-CHO sources

Increase protein formation

Negative Nitrogen balance

Tissue wasting (Cachexia)

INCREASE FAT CATABOLISM

Free fatty acids

Cholesterol

Ketones

Atherosclerosis Diabetic

Keto Acidosis

Hypertension Acetone Breath

Kussmaul’s Respiration odor

MI CVA

DeathDiabetic Coma

Classification Of DM

1. Type I Insulin-dependent Diabetes Mellitus (IDDM)

Secondary to destruction of beta cells in the islets of

langerhans in the pancreas resulting in little of no

insulin production

Non-obese adults

Requires insulin injection

Juvenile onset type (Brittle disease)

Incidence Rate

1. 10% general population has Type I DM


1. Autoimmune response

2. Genetics / Hereditary (total destruction of pancreatic

cells)

3. Related to viruses

4. Drugs: diuretics (Lasix), Steroids, oral contraceptives

5. Related to carbon tetrachloride toxicity

S/sx

1. Polyuria

2. Polydipsia

3. Polyphagia

4. Glucosuria

5. Weight loss

6. Fatigue

7. Anorexia

8. N/V

9. Blurring of vision

10. Increase susceptibility to infection

11. Delayed / poor wound healing

Dx

1. FBS:

a. A level of 140 mg/dl of greater on at two occasions

confirms DM

b. May be normal in Type II DM

2. Postprandial Blood Sugar: elevated

3. Oral Glucose Tolerance Test (most sensitve test):

elevated

4. Glycosolated Hemoglobin (hemoglobin A1c): elevated

Medical Management

1. Insulin therapy

2. Exercise

3. Diet:

a. Consistency is imperative to avoid hypoglycemia

b. High-fiber, low-fat diet also recommended

4. Drug therapy:

a. Insulin:

Short Acting: used in treating ketoacidosis;

during surgery, infection, trauma; management

of poorly controlled diabetes; to supplement

long-acting insulins

Intermediate: used for maintenance therapy

Long Acting: used for maintenance therapy in

clients who experience hyperglycemia during

the night with intermediate-acting insulin

b. Insulin preparation can consist of mixture of pure

pork, pure beef, or human insulin. Human insulin is

the purest insulin & has the lowest antigenic effect

c. Human Insulin: is recommended for all newly

diagnosed Type I & Type II DM who need short-term

insulin therapy; the pregnant client & diabetic client

with insulin allergy or severe insulin resistance

d. Insulin Pumps: externally worn device that closely

mimic normal pancreatic functioning

5. Exercise: helpful adjunct to therapy as exercise

decrease the body’s need for insulin

Characteristics of Insulin Preparation

Drug Synonym Appearance Onset Peak

Duration Compatible Mixed

Rapid Acting

Insulin InjectionRegular Ins Clear ½-1 2-4 6-8

All insulin prep

except lente

Insulin, Zinc Semilente Ins Cloudy ½-1 4-6 12-

16 Lente prep

suspension,

prompt

Intermediate Acting

Isophane Ins NPH Ins Cloudy 1-1 ½ 8-12 18-

24 Regular Ins

injection

injection

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28

Insulin Zinc Lente Ins Cloudy 1-1 ½ 8-12 18-

24 Regular Ins &

Suspension

semilente prep

Long Acting

Insulin Zinc Ultralente Ins Cloudy 4-8 16-20 30-

36 Regular Ins &

suspension,

semilente prep

extended

Complication

1. Diabetic Ketoacidosis (DKA)

2. Type II Non-insulin-dependent Diabetes Mellitus (NIDDM)

May result to partial deficiency of insulin production &/or

an insensitivity of the cells to insulin

Obese adult over 40 years old

Maturity onset type

Incidence Rate

1. 90% of general population has Type II DM


1. Genetics

2. Obesity: because obese persons lack insulin receptor

binding sites

S/sx

1. Usually asymptomatic

2. Polyuria

3. Polydypsia

4. Polyphagia

5. Glycosuria

6. Weight gain / Obesity

7. Fatigue

8. Blurred Vision


10. Delayed / poor wound healing

Dx

5. FBS:

c. A level of 140 mg/dl of greater on at two occasions

confirms DM

d. May be normal in Type II DM

6. Postprandial Blood Sugar: elevated

7. Oral Glucose Tolerance Test (most sensitve test):

elevated

8. Glycosolated Hemoglobin (hemoglobin A1c): elevated

Medical Management

1. Ideally manage by diet & exercise

2. Oral Hypoglycemic agents or occasionally insulin: if diet

& exercise are not effective in controlling hyperglycemia

3. Insulin is needed in acute stress: ex. Surgery, infection

4. Diet: CHO 50%, CHON 30% & Fats 20%

a. Weight loss is important since it decreases insulin

resistance

b. High-fiber, low-fat diet also recommended

5. Drug therapy:

a. Occasional use of insulin

b. Oral hypoglycemic agent:

Used by client who are not controlled by diet &

exercise

Increase the ability of islet cells of the pancreas

to secret insulin; may have some effect on cell

receptors to decrease resistance to insulin

6. Exercise: helpful adjunct to therapy as exercise

decrease the body’s need for insulin

Oral Hypoglycemic Agent

Drug Onset Peak Duration

Comments

Oral Sulfonylureas

Acetohexamide (Dymelor) 1 4-6 12-

24

Chlorpropamide (Diabinase) 1 4-6 40-60

Glyburide (Micronase, Diabeta) 15 min- 1 hr 2-8 10-24

Oral Biguanides

Metformin (Glucophage) 2-2.5 10-

16 :Decrease glucose

production in liver

:Decrease intestinal

absorption of glucose &

improves insulin sensitivity

Oral Alpha-glucosidose Inhibitor

Acarbose (Precose) Unknown 1 Unknown

:Delay glucose absorption

& digestion of CHO,

lowering blood sugar

Miglitol (Glyset) 2-3

Troglitazone (Rezulin) Rapid 2-3 Unknown

:Reduce plasma glucose &

insulin

:Potetiates action of insulin

in skeletal muscle &

decrease glucose

production in liver

Complications

1. Hyper Osmolar Non-Ketotic Coma (HONKC)


1. Administer insulin or oral hypoglycemic agent as

ordered: monitor hypoglycemia especially during period

of drug peak action

2. Provide special diet as ordered:

a. Ensure that the client is eating all meals

b. If all food is not ingested: provide appropriate

substitute according to the exchange list or give

measured amount of orange juice to substitute for

leftover food; provide snack later in the day

3. Monitor urine sugar & acetone (freshly voided

specimen)

4. Perform finger sticks to monitor blood glucose level as

ordered (more accurate than urine test)

5. Observe signs of hypo/hyperglycemia

6. Provide meticulous skin care & prevent injury

7. Maintain I&O; weight daily

8. Provide emotional support: assist client in adapting

change in lifestyle & body image

9. Observe for chronic complications & plan of care

accordingly:

a. Atherosclerosis: leads to CAD, MI, CVA & Peripheral

Vascular Disease

b. Microangiopathy: most commonly affects eyes &

kidneys

c. Kidney Disease

Recurrent Pyelonephritis

Diabetic Nephropathy

d. Ocular Disorder

Premature Cataracts

Diabetic Retinopathy

e. Peripheral Neuropathy

Affects PNS & ANS

Cause diarrhea, constipation, neurogenic

bladder, impotence, decrease sweating


concerning:

a. Disease process

b. Diet

Client should be able to plan a meal using

exchange lists before discharge

29

29

Emphasize importance of regularity of meals;

never skip meals

c. Insulin

How to draw up into syringe

Use insulin at room temp

Gently roll the vial between palms

Draw up insulin using sterile technique

If mixing insulin, draw up clear insulin,

before cloudy insulin

Injection technique

Systematically rotate the site: to prevent

lipodystrophy: (hypertrophy or atrophy of

tissue)

Insert needle at a 45 (skinny clients) or 90

(fat or obese clients) degree angle

depending on amount of adipose tissue

May store current vial of insulin at room

temperature; refrigerate extra supplies

Somogyi’s phenomenon: hypoglycemia followed

by periods of hyperglycemia or rebound effect

of insulin.

Provide many opportunities for return

demonstration

d. Oral hypoglycemic agent

Stress importance of taking the drug regularly

Avoid alcohol intake while on medication: it can

lead to severe hypoglycemia reaction

Instruct the client to take it with meals: to

lessen GIT irritation & prevent hypoglycemia

e. Urine testing (not very accurate reflection of blood

glucose level)

May be satisfactory for Type II diabetics since

they are more stable

Use clinitest, tes-tape, diastix, for glucose

testing

Perform test before meals & at bedtime

Use freshly voided specimen

Be consistent in brand of urine test used

Report results in percentage

Report result to physician if results are greater

that 1%, especially if experiencing symptoms of

hyperglycemia

Urine testing for ketones should be done by

Type I diabetic clients when there is persistent

glycosuria, increase blood glucose level or if the

client is not feeling well (acetest, ketostix)

f. Blood glucose monitoring

Use for Type I diabetic client: since it gives

exact blood glucose level & also detects

hypoglycemia

Instruct client in finger stick technique: use of

monitor device (if used), & recording &

utilization of test results

g. General care

Perform good oral hygiene & have regular

dental exam

Have regular eye exam

Care for “sick days” (ex. Cold or flu)

Do not omit insulin or oral hypoglycemic

agent: since infection causes increase blood

sugar

Notify physician

Monitor urine or blood glucose level & urine

ketones frequently

If N/V occurs: sip on clear liquid with simple

sugar

h. Foot care

Wash foot with mild soap & water & pat dry

Apply lanolin lotion to feet: to prevent drying &

cracking

Cut toenail straight across

Avoid constrictive garments such as garters

Wear clean, absorbent socks (cotton or wool)

Purchase properly fitting shoes & break new

shoes in gradually

Never go barefoot

Inspect foot daily & notify physician: if cut,

blister, or break in skin occurs

i. Exercise

Undertake regular exercise; avoid sporadic,

vigorous exercise

Food intake may need to be increased before

exercising

Exercise is best performed after meals when the

blood sugar is rising

j. Complication

Learn to recognized S/sx of hypo/hyperglycemia:

for hypoglycemia (cold and clammy skin), for

hyperglycemia (dry and warm skin): administer

simple sugars

Eat candy or drink orange juice with sugar

added for insulin reaction (hypoglycemia)

Monitor signs of DKA & HONKC

k. Need to wear a Medic-Alert bracelet

Diabetic Ketoacidosis (DKA)

Acute complication of DM characterized by hyperglycemia &

accumulation of ketones in the body: cause metabolic

acidosis

Acute complication of Type I DM: due to severe

hyperglycemia leading to severe CNS depression

Occurs in insulin-dependent diabetic clients

Onset slow: maybe hours to days


1. Undiagnosed DM

2. Neglect to treatment

3. Infection

4. cardiovascular disorder

5. Hyperglycemia

6. Physical & Emotional Stress: number one precipitating

factor

S/sx

1. Polyuria

2. Polydipsia

3. Polyphagia

4. Glucosuria

5. Weight loss

6. Anorexia

7. N/V

8. Abdominal pain

9. Skin warm, dry & flushed

10. Dry mucous membrane; soft eyeballs


12. PS: Acetone breath odor

13. PS: Kussmaul’s Respiration (rapid shallow breathing) or

tachypnea

14. Alteration in LOC

15. Hypotension

16. Tachycardia

17. CNS depression leading to coma

Dx

1. FBS: is increased

2. Serum glucose & ketones level: elevated

3. BUN (normal value: 10 – 20): elevated: due to

dehydration

4. Creatinine (normal value: .8 – 1): elevated: due to

dehydration

5. Hct (normal value: female 36 – 42, male 42 – 48):

elevated: due to dehydration

6. Serum Na: decrease

7. Serum K: maybe normal or elevated at first

8. ABG: metabolic acidosis with compensatory respiratory

alkalosis


1. Maintain patent airway


3. Maintain F&E balance:

a. Administer IV therapy as ordered:

Normal saline (0.9% NaCl), followed by

hypotonic solutions (.45% NaCl) sodium

chloride: to counteract dehydration & shock

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30

When blood sugar drops to 250 mg/dl: may add

5% dextrose to IV

Potassium will be added: when the urine output

is adequate

b. Observe for F&E imbalance, especially fluid

overload, hyperkalemia & hypokalemia

4. Administer insulin as ordered: regular acting

insulin/rapid acting insulin

a. Regular insulin IV (drip or push) & / or

subcutaneously (SC)

b. If given IV drip: give small amount of albumin since

insulin adheres to IV tubing

c. Monitor blood glucose level frequently


a. Sodium Bicarbonate: to counteract acidosis

b. Antibiotics: to prevent infection

6. Check urine output every hour

7. Monitor V/S, I&O & blood sugar levels

8. Assist client with self-care

9. Provide care for unconscious client if in a coma

10. Discuss with client the reasons ketosis developed &

provide additional diabetic teaching if indicated

Hyperglycemic Hyperosmolar Non-Ketotic Coma (HHNKC)

Characterized by hyperglycemia & a hyperosmolar state

without ketosis

Occurs in non-insulin-dependent diabetic or non-diabetic

persons (typically elderly clients)

Hyperosmolar: increase osmolarity (severe dehydration)

Non-ketotic: absence of lypolysis (no ketones)


1. Undiagnosed diabetes

2. Infection or other stress

3. Certain medications (ex. dilantin, thiazide, diuretics)

4. Dialysis

5. Hyperalimentation

6. Major burns

7. Pancreatic disease

S/sx

1. Polyuria

2. Polydipsia

3. Polyphagia

4. Glucosuria

5. Weight loss

6. Anorexia

7. N/V

8. Abdominal pain

9. Skin warm, dry & flushed

10. Dry mucous membrane; soft eyeballs


12. Hypotension

13. Tachycardia

14. Headache and dizziness

15. Restlessness

16. Seizure activity

17. Alteration / Decrease LOC: diabetic coma

Dx

1. Blood glucose level: extremely elevated

2. BUN: elevated: due to dehydration

3. Creatinine: elevted: due to dehydration

4. Hct: elevated: due to dehydration

5. Urine: (+) for glucose


1. Maintain patent airway


3. Maintain F&E balance:

a. Administer IV therapy as ordered:

Normal saline (0.9% NaCl), followed by

hypotonic solutions (.45% NaCl) sodium

chloride: to counteract dehydration & shock

When blood sugar drops to 250 mg/dl: may add

5% dextrose to IV

Potassium will be added: when the urine output

is adequate

b. Observe for F&E imbalance, especially fluid

overload, hyperkalemia & hypokalemia

4. Administer insulin as ordered:

a. Regular insulin IV (drip or push) & / or

subcutaneously (SC)

b. If given IV drip: give small amount of albumin since

insulin adheres to IV tubing

c. Monitor blood glucose level frequently


a. Antibiotics: to prevent infection

6. Check urine output every hour

7. Monitor V/S, I&O & blood sugar levels

8. Assist client with self-care

9. Provide care for unconscious client if in a coma

10. Discuss with client the reasons ketosis developed &

provide additional diabetic teaching if indicated

Overview of Anatomy & Physiology of Hematologic System

The structure of the hematological of hematopoietic system

includes the blood, blood vessels, & blood forming organs

(bone marrow, spleen, liver, lymph nodes, & thymus gland).

The major function of blood: is to carry necessary materials

(O2, nutrients) to cells & remove CO2 & metabolic waste

products.

The hematologic system also plays an important role in

hormone transport, the inflammatory & immune responses,

temperature regulation, F&E balance & acid-base balance.

HEMATOLOGICAL SYSTEM

I. Blood II. Blood VesselsIII. Blood Forming Organs

1. Arteries 1. Liver 55% Plasma 45% Formed 2. Veins

2. Thymus (Fluid) cellular elements 3. Capillaries 3. Spleen

4. Lymphoid Organ Serum Plasma CHON 5. Lymph Nodes

(formed in liver) 6. Bone Marrow

1. Albumin2. Globulins3. Prothrombin and Fibrinogen

Bone Marrow

Contained inside all bones, occupies interior of spongy

bones & center of long bones; collectively one of the largest

organs in the body (4-5% of total body weight)

Primary function is Hematopoiesis: the formation of blood

cells

All blood cells start as stem cells in the bone marrow; these

mature into different, specific types of cells, collectively

referred to as Formed Elements of Blood or Blood

Components:

1. Erythrocytes

2. Leukocytes

3. Thrombocytes

Two kinds of Bone Marrow:

1. Red Marrow

Carries out hematopoiesis; production site of

erythroid, myeloid, & thrombocytic component of

blood; one source of lymphocytes & macrophages

Found in the ribs, vertebral column, other flat bones

2. Yellow Marrow

Red marrow that has changed to fats; found in long

bone; does not contribute to hematopoiesis

Blood

Composed of plasma (55%) & cellular components (45%)

Hematocrit

1. Reflects portion of blood composed of red blood cells

31

31

2. Centrifugation of blood results in separation into top

layer of plasma, middle layer of leukocytes & platelets,

& bottom layer of erythrocytes

3. Majority of formed elements is erythrocytes; volume of

leukocytes & platelets is negligible

Distribution

1. 1300 ml in pulmonary circulation

a. 400 ml arterial

b. 60 ml capillary

c. 840 ml venous

2. 3000 ml in systemic circulation

a. 550 ml arterial

b. 300 ml capillary

c. 2150 ml venous

Plasma

Liquid part of the blood; yellow in color because of pigments

Consists of serum (liquid portion of plasma) & fibrinogen

Contains plasma CHON such as albumin, serum, globulins,

fibrinogen, prothrombin, plasminogen

1. Albumin

Largest & numerous plasma CHON

Involved in regulation of intravascular plasma

volume

Maintains osmotic pressure: preventing edema

2. Serum Globulins

a. Alpha: role in transport steroids, lipids, bilirubin &

hormones

b. Beta: role in transport of iron & copper

c. Gamma: role in immune response, function of

antibodies

3. Fibrinogens, Prothrombin, Plasminogens: clotting factors

to prevent bleeding

Cellular Components or Formed Elements

1. Erythrocytes (RBC)

a. Normal value: 4 – 6 million/mm3

b. No nucleus, Biconcave shape discs, Chiefly sac of

hemoglobin

c. Call membrane is highly diffusible to O2 & CO2

d. Responsible for O2 transport via hemoglobin (Hgb)

Two portion: iron carried on heme portion; second

portion is CHON

Normal blood contains 12-18 g Hgb/100 ml blood;

higher (14-18 g) in men than in women (12-14 g)

e. Production

Start in bone marrow as stem cells, release as

reticulocytes (immature cells), mature into

erythrocytes

Erythropoietin stimulates differentiation; produced

by kidneys & stimulated by hypoxia

Iron, vitamin B12, folic acid, pyridoxine vitamin B6,

& other factors required for erythropoiesis

f. Hemolysis (Destruction)

Normal life span of RBC is 80 – 120 days and is

killed in red pulp of spleen

Immature RBCs destroyed in either bone marrow or

other reticuloendothelial organs (blood, connective

tissue, spleen, liver, lungs and lymph nodes)

Mature cells remove chiefly by liver and spleen

Bilirubin (yellow pigment): by product of Hgb (red

pigment) released when RBCs destroyed, excreted

in bile

Biliverdin (green pigment)

Hemosiderin (golden brown pigment)

Iron: feed from Hgb during bilirubin formation;

transported to bone marrow via transferring and

and reclaimed for new Hgb production

Premature destruction: may be caused by RBC

membrane abnormalities, Hgb abnormalities,

extrinsic physical factors (such as the enzyme

defects found in G6PD)

Normal age RBCs may be destroyed by gross

damage as in trauma or extravascular hemolysis (in

spleen, liver, bone marrow)

g. Hemoglobin: normal value female 12 – 14 gms% male

14 – 16 gms%

h. Hematocrit red cell percentage in wholeblood (normal

value: female 36 – 42% male 42 – 48%)

i. Substances needed for maturation of RBC:

a. Folic acid

b. Iron

c. Vitamin c

d. Vitamin b12 (Cyanocobalamin)

e. Vitamin b6 (Pyridoxine)

f. Intrinsic factor

2. Leukocytes (WBC)

a. Normal value: 5000 – 10000/mm3

b. Granulocytes and mononuclear cells: involved in the

protection from bacteria and other foreign substances

c. Granulocytes:

Polymorphonuclear Neutrophils

- 60 – 70% of WBC

- Involved in short term phagocytosis for acute

inflammation

- Mature neutrophils: polymorphonuclear

leukocytes

- Immature neutrophils: band cells (bacterial

infection usually produces increased numbers of

band cells)

Polymorphonuclear Basophils

- For parasite infections

- Responsible for the release of chemical

mediation for inflammation

- Involved in prevention of clotting in

microcirculation and allergic reactions

Polymorphonuclear Eosinophils

- Involved in phagocytosis and allergic reaction

Eosinophils & Basophils: are reservoirs of histamine,

serotonin & heparin

d. Non Granulocytes

Mononuclear cells: large nucleated cells

a. Monocytes:

Involved in long-term phagocytosis for

chronic inflammation

Play a role in immune response

Macrophage in blood

Largest WBC

Produced by bone marrow: give rise to

histiocytes (kupffer cells of liver),

macrophages & other components of

reticuloendothelial system

b. Lymphocytes: immune cells; produce

substances against foreign cells; produced

primarily in lymph tissue (B cells) & thymus (T

cells)

Lymphocytes

B-cell T-cell Natural killer cell- bone marrow - thymus - anti-viral and anti-tumor property

for immunity

HIV

c. Thrombocytes (Platelets)

Normal value: 150,000 – 450,000/mm3

Normal life span of platelet is 9 – 12 days

Fragments of megakaryocytes formed in

bone marrow

Production regulated by thrombopoietin

Essential factors in coagulation via

adhesion, aggregation & plug formation

Release substances involved in coagulation

Promotes hemostasis (prevention of blood

loss)

Consist of immature or baby platelets or

megakaryocytes which is the target of

dengue virus

Signs of Platelet Dysfunction

1. Petechiae

2. Echhymosis

3. Oozing of blood from venipunctured site

Blood Groups

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32

Erythrocytes carry antigens, which determine the different

blood group

Blood-typing system are based on the many possible

antigens, but the most important are the antigens of the

ABO & Rh blood groups because they are most likely to be

involved in transfusion reactions

1. ABO Typing

a. Antigens of systems are labeled A & B

b. Absence of both antigens results in type O blood

c. Presence of both antigen is type AB

d. Presence of either type A or B results in type A & type B,

respectively

e. Type O: universal donor

f. Antibodies are automatically formed against ABO

antigens not on persons own RBC

2. Rh Typing

a. Identifies presence or absence of Rh antigens (Rh + or

Rh -)

b. Anti-Rh antibodies not automatically formed in Rh (-)

persons, but if Rh (+) blood is given, antibody formation

starts & second exposure to Rh antigen will trigger a

transfusion reaction

c. Important for Rh (-) woman carrying Rh (+) baby; 1st

pregnancy not affected, but subsequent pregnancy with

an Rh (+) baby, mother’s antibodies attack baby’s RBC

Complication of Blood Transfusion

Type Causes Mechanism Occurrence S/sx

Intervention

Hemolytic ABO Antibodies in Acute:

Headache, Stop transfusion.

Incompatibility; recipient plasma first 5 min

lumbar or continue saline IV

Rh react w/ antigen after

completion sternal pain, send blood unit &

Incompatibility; in donor cells. of transfusion

diarrhea, fever, client blood

Use of dextrose Agglutinated cell

chills, flushing, sample to lab.

solutions; block capillary Delayed:

heat along vein, Watch for

Wide temp blood flow to days to 2

restlessness, hemoglobinuria.

fluctuation organs. weeks after

anemia, jaundice, Treat or prevent

Hemolysis (Hgb

dyspnea, signs shock, DIC, &

into plasma & of

shock, renal renal shutdown

urine)

shutdown, DIC

Complication of Blood Transfusion

Type Causes Mechanism Occurrence S/sx

Intervention

Allergic Transfer of an Immune Within 30 min

Uticaria, larygeal Stop transfusion.

antigen & sensitivity to start of

edema, wheezing Administer

antibody from foreign serum transfusion

dyspnea, antihistamine &

donor to CHON

bronchospasm, or epinephrine.

recipient;

headache, Treat

Allergic donor

anaphylaxis life-threatening

reaction

_____________________________________________________________________

__________________

Pyrogenic Recipient Leukocytes Within 15-90

Fever, chills, Stop transfusion.

possesses agglutination min after

flushing, Treat temp.

antibodies bacterial initiation of

palpitation, Transfuse with

directed against organism transfusion

tachycardia, leukocytes-poor

WBC; bacterial

occasional blood of washed

contamination;

lumbar pain RBC.

Multitransfused

Administer

client;

antibiotics prn

multiparous

client

_____________________________________________________________________

__________________

Circulatory Too rapid Fluid volume During & after

Dyspnea, Slow infusion rate

Overload infusion in overload

transfusion increase BP, Used packed cells

Susceptible

tachycardia, instead of whole

Client

orthopnea, blood.

cyanosis, anxiety Monitor CVP

t

hro

ug

h a

separate line.

_____________________________________________________________________

__________________

Air Embolism Blood given Bolus of air Anytime

Dyspnea, Clamp tubing.

under air blocks pulmonary

increase pulse, Turn client on

pressure artery outflow

wheezing, chest left side

following severe

pain, decrease BP,

blood loss

apprehension

_____________________________________________________________________

__________________Thrombo- Used of large Platelets

When large Abnormal Assess for signs

cytopenia amount of deteriorate amount of blood

bleeding of bleeding.

banked blood rapidly in stored given over

24 hr Initiate bleeding

blood

precautions.

Use fresh blood.

_____________________________________________________________________

__________________

Citrate Large amount Citrate binds After large

Neuromascular Monitor/treat

Intoxication of citrated blood ionic calcium amount of

irritability hypocalcemia.

in client with banked blood

Bleeding due to Avoid large

decrease liver

decrease calcium amounts of

function

citrated blood.

Monitor liver fxn

_____________________________________________________________________

__________________

Hyperkalemia Potassium level Release of In client with

Nausea, colic, Administer blood

increase in potassium into renal

diarrhea, muscle less than 5-7

stored blood plasma with insufficiency

spasm, ECG days old in client

33

33

red cell lysis

changes (tall with impaired

peaked T-waves, potassium

short Q-T excretion

seg

ments)

Blood Coagulation

Conversion of fluid blood into a solid clot to reduce blood

loss when blood vessels are ruptured

System that Initiating Clotting

1. Intrinsic System: initiated by contact activation following

endothelial injury (“intrinsic” to vessel itself)

a. Factor XII: initiate as contact made between damaged

vessel & plasma CHON

b. Factors VIII, IX & XI activated

2. Extrinsic System:

a. Initiated by tissue thromboplastins released from injured

vessels (“extrinsic” to vessel)

b. Factor VII activated

Common Pathways: activated by either intrinsic or extrinsic

pathways

1. Platelet factor 3 (PF3) & calcium react with factor X & V

2. Prothrombin converted to thrombin via thromboplastin

3. Thrombin acts on fibrinogens, forming soluble fibrin

4. Soluble fibrin polymerized by factor XIII to produce a stable,

insoluble fibrin clot

Clot Resolution: takes place via fibrinolytic system by plasmin &

proteolytic enzymes; clots dissolves as tissue repairs.

Spleen

Largest Lymphatic Organ: functions as blood filtration

system & reservoir

Vascular bean shape; lies beneath the diaphragm, behind &

to the left of the stomach; composed of fibrous tissue

capsule surrounding a network of fiber

Contains two types of pulp:

a. Red Pulp: located between the fibrous strands,

composed of RBC, WBC & macrophages

b. White Pulp: scattered throughout the red pulp, produces

lymphocytes & sequesters lymphocytes, macrophages,

& antigens

1%-2% of red cell mass or 200 ml blood/minute stored in the

spleen; blood comes via splenic artery to the pulp for

cleansing, then passes into splenic venules that are lined

with phagocytic cells & finally to the splenic vein to the liver.

Important hematopoietic site in fetus; postnatally

procedures lymphocytes & monocytes

Important in phagocytosis; removes misshapen

erythrocytes, unwanted parts of erythrocytes

Also involved in antibody production by plasma cells & iron

metabolism (iron released from Hgb portion of destroyed

erythrocytes returned to bone marrow)

In the adult functions of the spleen can be taken over by the

reticuloendothelial system.

Liver

Involved in bile production (via erythrocyte destruction &

bilirubin production) & erythropoeisis (during fetal life &

when bone marrow production is insufficient).

Kupffer cells of liver have reticuloendothelial function as

histiocytes; phagocytic activity & iron storage.

Liver also involved in synthesis of clotting factors, synthesis

of antithrombins.

Blood Tranfusion

Purpose

1. RBC: Improve O2 transport

2. Whole Blood, Plasma, Albumin: volume expansion

3. Fresh Frozen Plasma, Albumin, Plasma Protein Fraction:

provision of proteins

4. Cryoprecipitate, Fresh Frozen Plasma, Fresh Whole

Blood: provision of coagulation factors

5. Platelet Concentration, Fresh Whole Blood: provision of

platelets

Blood & Blood Products

1. Whole Blood: provides all components

a. Large volume can cause difficulty: 12-24 hr for Hgb

& Hct to rise

b. Complications: volume overload, transmission of

hepatitis or AIDS, transfusion reacion, infusion of

excess potassium & sodium, infusion of

anticoagulant (citrate) used to keep stored blood

from clotting, calcium binding & depletion (citrate)

in massive transfusion therapy

2. Red Blood Cell (RBC)

a. Provide twice amount of Hgb as an equivalent

amount of whole blood

b. Indicate in cases of blood loss, pre-op & post-op

client & those with incipient congestive failure

c. Complication: transfusion reaction (less common

than with whole blood: due to removal of plasma

protein)

3. Fresh Frozen Plasma

a. Contains all coagulation factors including V & VIII

b. Can be stored frozen for 12 months; takes 20

minutes to thaw

c. Hang immediately upon arrival to unit (loses its

coagulation factor rapidly)

4. Platelets

a. Will raise recipient’s platelet count by 10,000/mm3

b. Pooled from 4-8 units of whole blood

c. Single-donor platelet transfusion may be necessary

for clients who have developed antibodies;

compatibilities testing may be necessary

5. Factor VIII Fractions (Cryoprecipitate): contains factor

VIII, fibrinogens & XIII

6. Granulocytes

a. Do not increase WBC: increase marginal pool (at

tissue level) rather than circulating pool

b. Premedication with steroids, antihistamine &

acetaminophen

c. Respiratory distress with shortness of breath,

cyanosis & chest pain may occur; requires cessation

of transfusion & immediate attention

d. Shaking chills or rigors common, require brief

cessation of therapy, administration of meperdine IV

until rigors are diminished & resumption of

transfusion when symptoms relieved

7. Volume Expander: albumin; percentage concentration

varies (50-100 ml/unit); hyperosmolar solution should

not be used in dehydrated clients

Goals / Objectives

1. Replace circulating blood volume

2. Increase the O2 carrying capacity of blood

3. Prevent infection: if there is a decrease in WBC

4. Prevent bleeding: if there is platelet deficiency

Principles of blood transfusion

1. Proper refrigeration

a. Expiration of packed RBC is 3-6 days

b. Expiration of platelet is 3-5 days

2. Proper typing and cross matching

a. Type O: universal donor

b. Type AB: universal recipient

c. 85% of population is RH positive

3. Aseptically assemble all materials needed for BT

a. Filter set

b. Gauge 18-19 needle

c. Isotonic solution (0.9 NaCl / plain NSS): to prevent

hemolysis

4. Instruct another RN to re check the following

a. Client name

b. Blood typing & cross matching

c. Expiration date

d. Serial number

5. Check the blood unit for bubbles cloudiness, sediments

and darkness in color because it indicates bacterial

contamination

34

34

a. Never warm blood: it may destroy vital factors in

blood.

b. Warming is only done: during emergency situation &

if you have the warming device

c. Emergency rapid BT is given after 30 minutes & let

natural room temperature warm the blood.

6. BT should be completed less than 4 hours because

blood that is exposed at room temperature more than 2

hours: causes blood deterioration that can lead to

bacterial contamination

7. Avoid mixing or administering drugs at BT line: to

prevent hemolysis

8. Regulate BT 10-15 gtts/min or KVO rate or equivalent to

100 cc/hr: to prevent circulatory overload

9. Monitor strictly vital signs before, during & after BT

especially every 15 minutes for first hour because

majority of transfusion reaction occurs during this period

a. Hemolytic reaction

b. Allergic reaction

c. Pyrogenic reaction

d. Circulatory overload

e. Air embolism

f. Thrombocytopenia

g. Cytrate intoxication

h. Hyperkalemia (caused by expired blood)

S/sx of Hemolytic reaction


2. Dyspnea

3. Diarrhea / Constipation

4. Hypotension

5. Flushed skin

6. Lumbasternal / Flank pain

7. Urine is color red / portwine urine

Nursing Management

1. Stop BT

2. Notify physician

3. Flush with plain NSS

4. Administer isotonic fluid solution: to prevent shock and

acute tubular necrosis

5. Send the blood unit to blood bank for re-examination

6. Obtain urine & blood sample & send to laboratory for re-

examination

7. Monitor vital signs & I&O

S/sx of Allergic reaction

1. Fever

2. Dyspnea

3. Broncial wheezing

4. Skin rashes

5. Urticaria

6. Laryngospasm & Broncospasm

Nursing Management

1. Stop BT

2. Notify physician



a. Anti Histamine (Benadryl): if positive to hypotension,

anaphylactic shock: treat with Epinephrine

5. Send the blood unit to blood bank for re examination


examination

7. Monitor vital signs and intake and output

S/sx Pyrogenic reactions

1. Fever and chills

2. Headache

3. Tachycardia

4. Palpitations

5. Diaphoresis

6. Dyspnea

Nursing Management

1. Stop BT

2. Notify physician



a. Antipyretic

b. Antibiotic

5. Send the blood unit to blood bank for re examination


examination

7. Monitor vital signs & I&O

8. Render TSB

S/sx of Circulatory reaction

1. Orthopnea

2. Dyspnea

3. Rales / Crackles upon auscultation

4. Exertional discomfort

Nursing Management

1. Stop BT

2. Notify physician


a. Loop diuretic (Lasix)

Nursing Care

1. Assess client for history of previous blood transfusions &

any adverse reaction

2. Ensure that the adult client has an 18-19 gauge IV

catheter in place

3. Use 0.9% sodium chloride

4. At least two nurse should verify the ABO group, RH type,

client & blood numbers & expiration date

5. Take baseline V/S before initiating transfusion

6. Start transfusion slowly (2 ml/min)

7. Stay with the client during the first 15 min of the

transfusion & take V/S frequently

8. Maintain the prescribed transfusion rate:

a. Whole Blood: approximately 3-4 hr

b. RBC: approximately 2-4 hr

c. Fresh Frozen Plasma: as quickly as possible

d. Platelet: as quickly as possible

e. Cryoprecipitate: rapid infusion

f. Granulocytes: usually over 2 hr

g. Volume Expander: volume-dependent rate

9. Monitor for adverse reaction

10. Document the following:

a. Blood component unit number (apply sticker if

available)

b. Date of infusion starts & end

c. Type of component & amount transfused

d. Client reaction & vital signs

e. Signature of transfusionist

HIV

- 6 months – 5 years incubation period

- 6 months window period

- western blot opportunistic

- ELISA

- drug of choice AZT (Zidon Retrovir)

2 Common fungal opportunistic infection in AIDS

1. Kaposis Sarcoma

2. Pneumocystic Carini Pneumonia

Blood Disorder

Iron Deficiency Anemia (Anemias)

A chronic microcytic anemia resulting from inadequate

absorption of iron leading to hypoxemic tissue injury

Chronic microcytic, hypochromic anemia caused by either

inadequate absorption or excessive loss of iron

Acute or chronic bleeding principal cause in adults (chiefly

from trauma, dysfunctional uterine bleeding & GI bleeding)

May also be caused by inadequate intake of iron-rich foods

or by inadequate absorption of iron

In iron-deficiency states, iron stores are depleted first,

followed by a reduction in Hgb formation

Incidence Rate

1. Common among developed countries & tropical zones

(blood-sucking parasites)

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35

2. Common among women 15 & 45 years old & children

affected more frequently, as are the poor

3. Related to poor nutrition


1. Chronic blood loss due to:

a. Trauma

b. Heavy menstruation

c. Related to GIT bleeding resulting to hematemasis

and melena (sign for upper GIT bleeding)

d. Fresh blood per rectum is called hematochezia

2. Inadequate intake or absorption of iron due to:

a. Chronic diarrhea

b. Related to malabsorption syndrome

c. High cereal intake with low animal CHON digestion

d. Partial or complete gastrectomy

e. Pica

3. Related to improper cooking of foods

S/sx

1. Usually asymptomatic (mild cases)

2. Weakness & fatigue (initial signs)

3. Headache & dizziness

4. Pallor & cold sensitivity

5. Dyspnea

6. Palpitations

7. Brittleness of hair & nails, spoon shape nails

(koilonychias)

8. Atrophic Glossitis (inflammation of tongue)

a. Stomatitis PLUMBER

VINSON’S SYNDROME

b. Dysphagia

9. PICA: abnormal appetite or craving for non edible foods

Dx

1. RBC: small (microcytic) & pale (hypochromic)

2. RBC: is decreased

3. Hgb: decreased

4. Hct: moderately decreased

5. Serum iron: decreased

6. Reticulocyte count: is decreased

7. Serum ferritin: is decreased

8. Hemosiderin: absent from bone marrow


1. Monitor for s/sx of bleeding through hematest of all

elimination including urine, stool & gastrict content

2. Enforce CBR / Provide adequate rest: plan activities so

as not to over tire the client

3. Provide thorough explanation of all diagnostic exam

used to determine sources of possible bleeding: help

allay anxiety & ensure cooperation

4. Instruct client to take foods rich in iron

a. Organ meat

b. Egg yolk

c. Raisin

d. Sweet potatoes

e. Dried fruits

f. Legumes

g. Nuts

5. Instruct the client to avoid taking tea and coffee:

because it contains tannates which impairs iron

absorption

6. Administer iron preparation as ordered:

a. Oral Iron Preparations: route of choice

Ferrous Sulfate

Ferrous Fumarate

Ferrous Gluconate

Nursing Management when taking oral iron

preparations

Instruct client to take with meals: to lessen GIT

irritation

Dilute in liquid preparations well & administer

using a straw: to prevent staining of teeth

When possible administer with orange juice as

vitamin C (ascorbic acid): to enhance iron

absorption

Warn clients that iron preparations will change

stool color & consistency (dark & tarry) & may

cause constipation

Antacid ingestion will decrease oral iron

effectiveness

b. Parenteral: used in clients intolerant to oral

preparations, who are noncompliant with therapy or

who have continuing blood losses

Nursing Management when giving parenteral

iron preparation

Use one needle to withdraw & another to

administer iron preparation as tissue staining &

irritation are a problem

Use Z-track injection technique: to prevent

leakage into tissue

Do not massage injection site but encourage

ambulation as this will enhance absorption;

advice against vigourous exercise & constricting

garments

Observe for local signs of complication:

Pain at the injection site

Development of sterile abscesses

Lymphadenitis

Fever & chills

Headache

Urticaria

Pruritus

Hypotension

Skin rashes

Anaphylactic shock

Medications administered via straw

Lugol’s Solution

Iron

Tetracycline

Nitrofurantoin (Macrodentin)

7. Administer with Vitamin C or orange juice for absorption

8. Monitor & inform client of side effects

a. Anorexia

b. N/V

c. Abdominal pain

d. Diarrhea / constipation

e. Melena

9. If client can’t tolerate / no compliance administer

parenteral iron preparation

a. Iron Dextran (IM, IV)

b. Sorbitex (IM)

10. Provide dietary teaching regarding food high in iron

11. Encourage ingestion of roughage & increase fluid intake:

to prevent constipation if oral iron preparation are being

taken

Pernicious Anemia

Chronic progressive, macrocytic anemia caused by a

deficiency of intrinsic factor; the result is abnormally large

erythrocytes & hypochlorhydria (a deficiency of hydrochloric

acid in gastric secretion)

Chronic anemia characterized by a deficiency of intrinsic

factor leading to hypochlorhydria (decrease hydrochloric

acid secretion)

Characterized by neurologic & GI symptoms; death usually

resuls if untreated

Lack of intrinsic factor is caused by gastric mucosal atrophy

(possibly due to heredity, prolonged iron deficiency, or an

autoimmune disorder); can also results in clients who have

had a total gastrctomy if vitamin B12 is not administer

Pathophysiology

1. Intrinsic factor is necessary for the absorbtion of vitamin

B12 into small intestines

2. B12 deficiency diminished DNA synthesis, which results

in defective maturation of cell (particularly rapidly

dividing cells such as blood cells & GI tract cells)

3. B12 deficiency can alter structure & function of

peripheral nerves, spinal cord, & the brain

STOMACH

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Pareital cells/Argentaffin or Oxyntic cells

Produces intrinsic factors

Secretes hydrochloric acid

Promotes reabsorption of Vit B12

Aids in digestion

Promotes maturation of RBC


1. Usually occurs in men & women over age of 50 with an

increase in blue-eyed person of Scandinavian decent

2. Subtotal gastrectomy

3. Hereditary factors

4. Inflammatory disorders of the ileum

5. Autoimmune

6. Strictly vegetarian diet

S/sx

1. Anemia

2. Weakness & fatigue


4. Pallor & cold sensitivity

5. Dyspnea & palpitations: as part of compensation

6. GIT S/sx:

a. Mouth sore

b. PS: Red beefy tongue

c. Indigestion / dyspepsia

d. Weight loss

e. Constipation / diarrhea

f. Jaundice

7. CNS S/sx:

a. Tingling sensation

b. Numbness

c. Paresthesias of hands & feet

d. Paralysis

e. Depression

f. Psychosis

g. Positive to Romberg’s test: damage to cerebellum

resulting to ataxia

Dx

1. Erythrocytes count: decrease

2. Blood Smear: oval, macrocytic erythrocytes with a

proportionate amount of Hgb

3. Bilirubin (indirect): elevated unconjugated fraction

4. Serum LDH: elevated

5. Bone Marrow:

a. Increased megaloblasts (abnormal erythrocytes)

b. Few normoblasts or maturing erythrocytes

c. Defective leukocytes maturation

6. Positive Schilling’s Test: reveals inadequate / decrease

absorption of Vitamin B12

a. Measures absorption of radioactive vitamin B12

bothe before & after parenteral administration of

intrinsic factor

b. Definitive test for pernicious anemia

c. Used to detect lack of intrinsic factor

d. Fasting client is given radioactive vitamin B12 by

mouth & non-radioactive vitamin B12 IM to permit

some excretion of radioactive vitamin B12 in the

urine if it os absorbed

e. 24-48 hour urine collection is obtained: client is

encourage to drink fluids

f. If indicated, second stage schilling test performed 1

week after first stage. Fasting client is given

radioactive vitamin B12 combined with human

intrinsic factor & test is repeated

7. Gastric Analysis: decrease free hydrochloric acid

8. Large number of reticulocytes in the blood following

parenteral vitamin B12 administration

Medical Management

1. Drug Therapy:

a. Vitamin B12 injection: monthly maintenance

b. Iron preparation: (if Hgb level inadequate to meet

increase numbers of erythrocytes)

c. Folic Acid

Controversial

Reverses anemia & GI symptoms but may

intensify neurologic symptoms

May be safe if given in small amounts in

addition to vitamin B12

2. Transfusion Therapy


1. Enforce CBR: necessary if anemia is severe

2. Adminster Vitamin B12 injections at monthly intervals for

lifetime as ordered

Never given orally because there is possibility of

developing tolerance

Site of injection for Vitamin B12 is dorsogluteal and

ventrogluteal

No side effects

3. Provide a dietary intake that is high in CHON, vitamin c

and iron (fish, meat, milk / milk product & eggs)

4. Avoid highly seasoned, coursed, or very hot foods: if

client has mouth sore

5. Provide safety when ambulating (especially when

carrying hot item)

6. Instruct client to avoid irritating mouth washes instead

use soft bristled toothbrush

7. Avoid heat application to prevent burns


concerning:

a. Dietery instruction

b. Importance of lifelong vitamin B12 therapy

c. Rehabilitation & physical therapy for neurologic

deficit, as well as instruction regarding safety

Aplastic Anemia

Stem cell disorder leading to bone marrow depression

leading to pancytopenia

Pancytopenia or depression of granulocytes, platelets &

erythrocytes production: due to fatty replacement of the

bone marrow

Bone marrow destruction may be idiopathic or secondary

PANCYTOPENIA

Decrease RBC Decrease WBC Decrease Platelet

(anemia) (leukopenia)

(thrombocytopenia)


1. Chemicals (Benzene and its derivatives)

2. Related to radiation / exposure to x-ray

3. Immunologic injury

4. Drugs:

a. Broad Spectrum Antibiotics: Chloramphenicol

(Sulfonamides)

b. Cytotoxic agent / Chemotherapeutic Agents:

Methotrexate (Alkylating Agent)

Vincristine (Plant Alkaloid)

Nitrogen Mustard (Antimetabolite)

Phenylbutazones (NSAIDS)

S/sx

1. Anemia

a. Weakness & fatigue

b. Headache & dizziness

c. Pallor & cold sensitivity

d. Dyspnea & palpitations

2. Leukopenia

a. Increase susceptibility to infection

3. Thrombocytopenia

a. Petechiae (multiple petechiae is called purpura)

b. Ecchymosis

c. Oozing of blood from venipunctured sites

Dx

1. CBC: reveals pancytopenia

2. Normocytic anemia, granulocytopenia,

thrombocytopenia

3. Bone marrow biopsy: aspiration (site is the posterior

iliac crest): marrow is fatty & contain very few

developing cells; reveals fat necrosis in bone marrow

Medical Management

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1. Blood transfusion: key to therapy until client’s own

marrow begins to produce blood cells

2. Aggressive treatment of infection

3. Bone marrow transplantation

4. Drug Therapy:

a. Corticosteroids & / or androgens: to stimulate bone

marrow function & to increase capillary resistance

(effective in children but usually not in adults)

b. Estrogen & / or progesterone: to prevent

amenorrhea in female clients

5. Identification & withdrawal of offending agent or drug


1. Removal of underlying cause

2. Administer Blood Transfusion as ordered

3. Administer O2 inhalation

4. Enforce CBR

5. Institute reverse isolation

6. Provide nursing care for client with bone marrow

transplant


a. Corticosteroids: caused by immunologic injury

b. Immunosuppressants: Anti Lymphocyte Globulin

Given via central venous catheter

Given 6 days to 3 weeks to achieve maximum

therapeutic effect of drug

8. Monitor for signs of infection & provide care to minimize

risk:

a. Monitor neuropenic precautions

b. Encourage high CHON, vitamin diet: to help reduce

incidence of infection

c. Provide mouth care before & after meals

d. Fever

e. Cough

9. Monitor signs of bleeding & provide measures to

minimize risk:

a. Use soft toothbrush when brushing teeth & electric

razor when shaving: prevent bleeding

b. Avoid IM, subcutaneous, venipunctured sites:

Instead provide heparin lock

c. Hematest urine & stool

d. Observe for oozing from gums, petechiae or

ecchymoses


concerning:

a. Self-care regimen

b. Identification of offending agent & importance of

avoiding it (if possible) in future

Disseminated Intravascular Coagulation (DIC)

Diffuse fibrin deposition within arterioles & capillaries with

widespread coagulation all over the body & subsequent

depletion of clotting factors

Acute hemorrhagic syndrome characterized by wide spread

bleeding and thrombosis due to a deficiency of prothrombin

and fibrinogen

Hemorrhage from kidneys, brain, adrenals, heart & other

organs

May be linked with entry of thromboplasic substance into

the blood

Mortality rate is high usually because underlying disease

cannot be corrected

Pathophysiology

1. Underlying disease (ex. toxemia of pregnancy, cancer)

cause release of thromboplastic substance that promote

the deposition of fibrin throughout the microcirculation

2. Microthrombi form in many organs, causing

microinfarcts & tissue necrosis

3. RBC are trapped in fibrin strands & are hemolysed

4. Platelets, prothrombin & other clotting factors are

destroyed, leading to bleeding

5. Excessive clotting activates the fibrinolytic system,

which inhibits platelet function, causing futher bleeding.


1. Related to rapid blood transfusion

2. Massive burns

3. Massive trauma

4. Anaphylaxis

5. Septecemia

6. Neoplasia (new growth of tissue)

7. Pregnancy

S/sx

1. Petechiae & Ecchymosis on the skin, mucous

membrane, heart, eyes, lungs & other organs

(widespread and systemic)

2. Prolonged bleeding from breaks in the skin: oozing of

blood from punctured sites

3. Severe & uncontrollable hemorrhage during childbirth or

surgical procedure

4. Hemoptysis

5. Oliguria & acute renal failure (late sign)

6. Convulsion, coma, death

Dx

1. PT: prolonged

2. PTT: usually prolonged

3. Thrombin Time: usually prolonged

4. Fibrinogen level: usually depressed

5. Fibrin splits products: elevated

6. Protamine Sulfate Test: strongly positive

7. Factor assay (II, V, VII): depressed

8. CBC: reveals decreased platelets

9. Stool occult blood: positive

10. ABG analysis: reveals metabolic acidosis

11. Opthamoscopic exam: reveals sub retinal hemorrhages

Medical Management

1. Identification & control the underlying disease is key

2. Blood Tranfusions: include whole blood, packed RBC,

platelets, plasma, cryoprecipitites & volume expanders

3. Heparin administration

a. Somewhat controversial

b. Inhibits thrombin thus preventing further clot

formation, allowing coagulation factors to

accumulate


1. Monitor blood loss & attemp to quantify

2. Monitor for signs of additional bleeding or thrombus

formation

3. Monitor all hema test / laboratory data including stool

and GIT

4. Prevent further injury

a. Avoid IM injection

b. Apply pressure to bleeding site

c. Turn & position the client frequently & gently

d. Provide frequent nontraumatic mouth care (ex. soft

toothbrush or gauze sponge)

5. Administer isotonic fluid solution as ordered: to prevent

shock

6. Administer oxygen inhalation

7. Force fluids


a. Vitamin K

b. Pitressin / Vasopresin: to conserve fluids

c. Heparin / Comadin is ineffective

9. Provide heparin lock

10. Institute NGT decompression by performing gastric

lavage: by using ice or cold saline solution of 500-1000

ml

11. Monitor NGT output

12. Prevent complication

a. Hypovolemic shock: Anuria (late sign of

hypovolemic shock)

13. Provide emotional support to client & significant other

14. Teach client the importance of avoiding aspirin or

aspirin-containing compounds

Overview of the Structure & Functions of the Heart

Cardiovascular system consists of the heart, arteries, veins

& capillaries. The major function are circulation of blood,

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SA NODE

AV NODE

BUNDLE OF HIS

JLJLJLJJLJLJL

delivery of O2 & other nutrients to the tissues of the body &

removal of CO2 & other cellular products metabolism

Heart

Muscular pumping organ that propel blood into the arerial

system & receive blood from the venous system of the

body.

Located on the left mediastinum

Resemble like a close fist

Weighs approximately 300 – 400 grams

Covered by a serous membrane called the pericardium

Heart Wall / Layers of the Heart

Pericardium

Composed of fibrous (outermost layer) & serous pericardium

(parietal & visceral); a sac that function to protect the heart

from friction

In between is the pericardial fluid which is 10 – 20 cc:

Prevent pericardial friction rub

2 layers of pericardium

Parietal: outer layer

Visceral: inner layer

Epicardium

Covers surface of the heart, becomes continuous with

visceral layer of serous pericardium

Outer layer

Myocardium

Middle muscular layer

Myocarditis can lead to cardiogenic shock and rheumatic

heart disease

Endocardium

Thin, inner membrabous layer lining the chamber of the

heart

Inner layer

Papillary Muscle

Arise from the endocardial & myocardial surface of the

ventricles & attach to the chordae tendinae

Chordae Tendinae

Attach to the tricuspid & mitral valves & prevent eversion

during systole

Chambers of the Heart

Atria

2 chambers, function as receiving chambers, lies above the

ventricles

Upper Chamber (connecting or receiving)

Right Atrium: receives systemic venous blood through

the superior vena cava, inferior vena cava & coronary

sinus

Left Atrium: receives oxygenated blood returning to the

heart from the lungs trough the pulmonary veins

Ventricles

2 thick-walled chambers; major responsibility for forcing

blood out of the heart; lie below the atria

Lower Chamber (contracting or pumping)

Right Ventricle: contracts & propels deoxygenated blood

into pulmonary circulation via the aorta during

ventricular systole; Right atrium has decreased pressure

which is 60 – 80 mmHg

Left Ventricle: propels blood into the systemic

circulation via aortaduring ventricular systole; Left

ventricle has increased pressure which is 120 – 180

mmHg in order to propel blood to the systemic

circulation

Valves

To promote unidimensional flow or prevent backflow

Atrioventricular Valve

Guards opening between

Mitral Valve: located between the left atrium & left

ventricle; contains 2 leaflets attached to the chordae

tandinae

Tricuspid Valve: located between the right atrium &

right ventricle; contains 3 leaflets attached to the

chordae tandinae

Functions

Permit unidirectional flow of blood from specific atrium to

specific ventricle during ventricular diastole

Prevent reflux flow during ventricular systole

Valve leaflets open during ventricular diastole; Closure of AV

valves give rise to first heart sound (S1 “lub”)

Semi-lunar Valve

Pulmonary Valve

Located between the left ventricle & pulmonary artery

Aortic Valve

Located between left ventricle & aorta

Function

Pemit unidirectional flow of the blood from specific ventricle

to arterial vessel during ventricular diastole

Prevent reflux blood flow during ventricular diastole

Valve open when ventricle contract & close during

ventricular diastole; Closure of SV valve produces second

heart sound (S2 “dub”)

Extra Heart Sounds

S3: ventricular gallop usually seen in Left Congestive Heart

Failure

S4: atrial gallop usually seen in Myocardial Infarction and

Hypertension

Coronary Circulation

Coronary Arteries

Branch off at the base of the aorta & supply blood to the

myocardium & the conduction system

Arises from base of the aorta

Types of Coronary Arteries

Right Main Coronary Artery

Left Main Coronary Artery

Coronary Veins

Return blood from the myocardium back to the right atrium

via the coronary sinus

Conduction System

Sinoatrial Node (SA node or Keith Flack Node)

Located at the junction of superior vena cava and right

atrium

Acts as primary pacemaker of the heart

Initiates the cardiac impulse which spreads across the atria

& into AV node

Initiates electrical impulse of 60-100 bpm

Atrioventricular Node (AV node or Tawara Node)

Located at the inter atrial septum

Delays the impulse from the atria while the ventricles fill

Delay of electrical impulse for about .08 milliseconds to

allow ventricular filling

Bundle of His

Arises from the AV node & conduct impulse to the bundle

branch system

Located at the interventricular septum

Right Bundle Branch: divided into anterior lateral &

posterior; transmits impulses down the right side of the

interventricular myocardium

Left Bundle Branch: divided into anterior & posterior

Anterior Portion: transmits impulses to the anterior

endocardial surface of the left ventricle

Posterior Portion: transmits impulse over the

posterior & inferior endocardial surface of the left

ventricle

Purkinje Fibers

Transmit impulses to the ventricle & provide for

depolarization after ventricular contraction

Located at the walls of the ventricles for ventricular

contraction

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39

PURKINJE FIBERS

Electrical activity of heart can be visualize by attaching electrodes

to the skin & recording activity by ECG

Electrocadiography (ECG) Tracing

P wave (atrail depolarization) contraction

QRS wave (ventricular depolarization)

T wave (ventricular repolarization)

Insert pacemaker if there is complete heart block

Most common pacemaker is the metal pacemaker and lasts

up to 2 – 5 years

Abnormal ECG Tracing

Positive U wave: Hypokalemia

Peak T wave: Hyperkalemia

ST segment depression: Angina Pectoris

ST segment elevation: Myocardial Infarction

T wave inversion: Myocardial Infarction

Widening of QRS complexes: Arrythmia

Vascular System

Major function of the blood vessels isto supply the tissue

with blood, remove wastes, & carry unoxygenated blood

back to the heart

Types of Blood Vessels

Arteries

Elastic-walled vessels that can stretch during systole &

recoil during diastole; they carry blood away from the heart

& distribute oxygenated blood throughout the body

Arterioles

Small arteries that distribute blood to the capillaries &

function in controlling systemic vascular resistance &

therefore arterial pressure

Capilliaries

The following exchanges occurs in the capilliaries

O2 & CO2

Solutes between the blood & tissue

Fluid volume transfer between the plasma & interstitial

space

Venules

Small veins that receive blood from capillaries & function as

collecting channels between the capillaries & veins

Veins

Low-pressure vessels with thin small & less muscles than

arteries; most contains valves that prevent retrograde blood

flow; they carry deoxygenated blood back to the heart.

When the skeletal surrounding veins contract, the veins are

compressed, promoting movement of blood back to the

heart.

Cardiac Disorders

Coronary Arterial Disease / Ischemic Heart Disease

Stages of Development of Coronary Artery Disease

1. Myocardial Injury: Atherosclerosis

2. Myocardial Ischemia: Angina Pectoris

3. Myocardial Necrosis: Myocardial Infarction

ATHEROSCLEROSIS

ATHEROSCLEROSIS ARTERIOSCLEROSIS

Narrowing of artery

Lipid or fat deposits

Tunica intima

Hardening of artery

Calcium and protein

deposits

Tunica media


1. Sex: male

2. Race: black

3. Smoking

4. Obesity

5. Hyperlipidemia



8. Hypothyroidism

9. Diet: increased saturated fats


S/sx

1. Chest pain

2. Dyspnea

3. Tachycardia

4. Palpitations

5. Diaphoresis

Treatment

P - Percutaneous

T - Transluminal

C - Coronary

A – Angioplasty

C - Coronary

A - Arterial

B - Bypass

A - And

G - Graft

S - Surgery

Objectives

1. Revascularize myocardium

2. To prevent angina

3. Increase survival rate

4. Done to single occluded vessels

5. If there is 2 or more occluded blood vessels CABG is done

3 Complications of CABG

1. Pneumonia: encourage to perform deep breathing, coughing

exercise and use of incentive spirometer

2. Shock

3. Thrombophlebitis

Angina Pectoris

Transient paroxysmal chest pain produced by insufficient

blood flow to the myocardium resulting to myocardial

ischemia

Clinical syndrome characterized by paroxysmal chest pain

that is usually relieved by rest or nitroglycerine due to

temporary myocardial ischemia


1. Sex: male

2. Race: black

3. Smoking

4. Obesity

5. Hyperlipidemia



8. Hypertension

9. CAD: Atherosclerosis

10. Thromboangiitis Obliterans

11. Severe Anemia

12. Aortic Insufficiency: heart valve that fails to open & close

efficiently

13. Hypothyroidism



Precipitating Factors

4 E’s of Angina Pectoris

1. Excessive physical exertion: heavy exercises, sexual activity

2. Exposure to cold environment: vasoconstriction

3. Extreme emotional response: fear, anxiety, excitement,

strong emotions

4. Excessive intake of foods or heavy meal

S/sx

1. Levine’s Sign: initial sign that shows the hand clutching the

chest

2. Chest pain: characterized by sharp stabbing pain located at

sub sterna usually radiates from neck, back, arms, shoulder

and jaw muscles usually relieved by rest or taking

nitroglycerine (NTG)

3. Dyspnea

4. Tachycardia

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5. Palpitations

6. Diaphoresis

Dx

1. History taking and physical exam

2. ECG: may reveals ST segment depression & T wave

inversion during chest pain

3. Stress test / treadmill test: reveal abnormal ECG during

exercise

4. Increase serum lipid levels

5. Serum cholesterol & uric acid is increased

Medical Management

1. Drug Therapy: if cholesterol is elevated

Nitrates: Nitroglycerine (NTG)

Beta-adrenergic blocking agent: Propanolol

Calcium-blocking agent: nefedipine

Ace Inhibitor: Enapril

2. Modification of diet & other risk factors

3. Surgery: Coronary artery bypass surgery

4. Percutaneuos Transluminal Coronary Angioplasty (PTCA)


1. Enforce complete bed rest

2. Give prompt pain relievers with nitrates or narcotic

analgesic as ordered


a. Nitroglycerine (NTG): when given in small doses will act

as venodilator, but in large doses will act as vasodilator

Give 1st dose of NTG: sublingual 3-5 minutes

Give 2nd dose of NTG: if pain persist after giving 1st

dose with interval of 3-5 minutes

Give 3rd & last dose of NTG: if pain still persist at 3-5

minutes interval

Nursing Management when giving NTG

1. NTG Tablets (sublingual)

Keep the drug in a dry place, avoid moisture and

exposure to sunlight as it may inactivate the drug

Relax for 15 minutes after taking a tablet: to

prevent dizziness

Monitor side effects:

Orthostatic hypotension

Transient headache & dizziness: frequent side

effect

Instruct the client to rise slowly from sitting position

Assist or supervise in ambulation

2. NTG Nitrol or Transdermal patch

Avoid placing near hairy areas as it may decrease

drug absorption

Avoid rotating transdermal patches as it may

decrease drug absorption

Avoid placing near microwave ovens or during

defibrillation as it may lead to burns (most

important thing to remember)

b. Beta-blockers

Propanolol: side effects PNS

Not given to COPD cases: it causes bronchospasm

c. ACE Inhibitors

Enalapril

d. Calcium Antagonist

Nefedipine


5. Place client on semi-to high fowlers position

6. Monitor strictly V/S, I&O, status of cardiopulmonary fuction

& ECG tracing

7. Provide decrease saturated fats sodium and caffeine


Avoidance of 4 E’s

Prevent complication (myocardial infarction)

Instruct client to take medication before indulging into

physical exertion to achieve the maximum therapeutic

effect of drug

Reduce stress & anxiety: relaxation techniques & guided

imagery

Avoid overexertion & smoking

Avoid extremes of temperature

Dress warmly in cold weather

Participate in regular exercise program

Space exercise periods & allow for rest periods

The importance of follow up care

9. Instruct the client to notify the physician immediately if pain

occurs & persists despite rest & medication administration

Myocardial Infarction

Death of myocardial cells from inadequate oxygenation,

often caused by sudden complete blockage of a coronary

artery

Characterized by localized formation of necrosis (tissue

destruction) with subsequent healing by scar formation &

fibrosis

Heart attack

Terminal stage of coronary artery disease characterized by

malocclusion, necrosis & scarring.

Types

1. Transmural Myocardial Infarction: most dangerous type

characterized by occlusion of both right and left coronary

artery

2. Subendocardial Myocardial Infarction: characterized by

occlusion of either right or left coronary artery

The Most Critical Period Following Diagnosis of Myocardial Infarction

6-8 hours because majority of death occurs due to

arrhythmia leading to premature ventricular contractions

(PVC)


1. Sex: male

2. Race: black

3. Smoking

4. Obesity

5. CAD: Atherosclerotic

6. Thrombus Formation

7. Genetic Predisposition

8. Hyperlipidemia



11. Hypothyroidism



S/sx

1. Chest pain

Excruciating visceral, viselike pain with sudden onset

located at substernal & rarely in precordial

Usually radiates from neck, back, shoulder, arms, jaw &

abdominal muscles (abdominal ischemia): severe

crushing

Not usually relieved by rest or by nitroglycerine

2. N/V

3. Dyspnea

4. Increase in blood pressure & pulse, with gradual drop in

blood pressure (initial sign)

5. Hyperthermia: elevated temp

6. Skin: cool, clammy, ashen

7. Mild restlessness & apprehension

8. Occasional findings:

Pericardial friction rub

Split S1 & S2

Rales or Crackles upon auscultation

S4 or atrial gallop

Dx

1. Cardiac Enzymes

CPK-MB: elevated

Creatinine phosphokinase (CPK): elevated

Heart only, 12 – 24 hours

Lactic acid dehydrogenase (LDH): is increased

Serum glutamic pyruvate transaminase (SGPT): is

increased

Serum glutamic oxal-acetic transaminase (SGOT): is

increased

2. Troponin Test: is increased

3. ECG tracing reveals

ST segment elevation

T wave inversion

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Widening of QRS complexes: indicates that there is

arrhythmia in MI

4. Serum Cholesterol & uric acid: are both increased

5. CBC: increased WBC


Goal: Decrease myocardial oxygen demand

1. Decrease myocardial workload (rest heart)

Establish a patent IV line

Administer narcotic analgesic as ordered: Morphine

Sulfate IV: provide pain relief (given IV because after an

infarction there is poor peripheral perfusion & because

serum enzyme would be affected by IM injection as

ordered)

Side Effects: Respiratory Depression

Antidote: Naloxone (Narcan)

Side Effects of Naloxone Toxicity: is tremors

2. Administer oxygen low flow 2-3 L / min: to prevent

respiratory arrest or dyspnea & prevent arrhythmias

3. Enforce CBR in semi-fowlers position without bathroom

privileges (use bedside commode): to decrease cardiac

workload

4. Instruct client to avoid forms of valsalva maneuver

5. Place client on semi fowlers position

6. Monitor strictly V/S, I&O, ECG tracing & hemodynamic

procedures

7. Perform complete lung / cardiovascular assessment

8. Monitor urinary output & report output of less than 30 ml /

hr: indicates decrease cardiac output

9. Provide a full liquid diet with gradual increase to soft diet:

low in saturated fats, Na & caffeine

10. Maintain quiet environment

11. Administer stool softeners as ordered: to facilitate bowel

evacuation & prevent straining

12. Relieve anxiety associated with coronary care unit (CCU)

environment


a. Vasodilators: Nitroglycirine (NTG), Isosorbide Dinitrate,

Isodil (ISD): sublingual

b. Anti Arrythmic Agents: Lidocaine (Xylocane), Brithylium

Side Effects: confusion and dizziness

c. Beta-blockers: Propanolol (Inderal)

d. ACE Inhibitors: Captopril (Enalapril)

e. Calcium Antagonist: Nefedipine

f. Thrombolytics / Fibrinolytic Agents: Streptokinase,

Urokinase, Tissue Plasminogen Activating Factor (TIPAF)

Side Effects: allergic reaction, urticaria, pruritus

Nursing Intervention: Monitor for bleeding time

g. Anti Coagulant

Heparin

Antidote: Protamine Sulfate

Nursing Intervention: Check for Partial Thrombin

Time (PTT)

Caumadin (Warfarin)

Antidote: Vitamin K

Nursing Intervention: Check for Prothrombin

Time (PT)

h. Anti Platelet: PASA (Aspirin): Anti thrombotic effect

Side Effects: Tinnitus, Heartburn, Indigestion /

Dyspepsia

Contraindication: Dengue, Peptic Ulcer Disease,

Unknown cause of headache

14. Provide client health teaching & discharge planning

concerning:

a. Effects of MI healing process & treatment regimen

b. Medication regimen including time name purpose,

schedule, dosage, side effects

c. Dietary restrictions: low Na, low cholesterol, avoidance

of caffeine

d. Encourage client to take 20 – 30 cc/week of wine,

whisky and brandy: to induce vasodilation

e. Avoidance of modifiable risk factors

f. Prevent Complication

Arrhythmia: caused by premature ventricular

contraction

Cardiogenic shock: late sign is oliguria

Left Congestive Heart Failure

Thrombophlebitis: homan’s sign

Stroke / CVA

Dressler’s Syndrome (Post MI Syndrome): client is

resistant to pharmacological agents: administer

150,000-450,000 units of streptokinase as ordered

g. Importance of participation in a progressive activity

program

h. Resumption of ADL particularly sexual intercourse: is 4-

6 weeks post cardiac rehab, post CABG & instruct to:

Make sex as an appetizer rather than dessert

Instruct client to assume a non weight bearing

position

Client can resume sexual intercourse: if can climb or

use the staircase

i. Need to report the ff s/sx:

Increased persistent chest pain

Dyspnea

Weakness

Fatigue

Persistent palpitation

Light headedness

j. Enrollment of client in a cardiac rehabilitation program

k. Strict compliance to mediation & importance of follow

up care

Congestive Heart Failure

Inability of the heart to pump an adequate supply of blood

to meet the metabolic needs of the body

Inability of the heart to pump blood towards systemic

circulation

Types of Heart Failure

1. Left Sided Heart Failure

2. Right Sided Heart Failure

3. High-Output Failure

Left Sided Heart Failure

Left ventricular damage causes blood to back up through

the left atrium & into the pulmonary veins: Increased

pressure causes transudation into interstitial tissues of the

lungs which result pulmonary congestion.


1. 90% is mitral valve stenosis due to RHD: inflammation of

mitral valve due to invasion of Group A beta-hemolytic

streptococcus

2. Myocardial Infarction

3. Ischemic heart disease

4. Hypertension

5. Aortic valve stenosis

S/sx

1. Dyspnea

2. Paroxysmal nocturnal dyspnea (PND): client is awakened at

night due to difficulty of breathing

3. Orthopnea: use 2-3 pillows when sleeping or place in high

fowlers

4. Tiredness

5. Muscle Weakness

6. Productive cough with blood tinged sputum

7. Tachycardia

8. Frothy salivation

9. Cyanosis

10. Pallor

11. Rales / Crackles

12. Bronchial wheezing

13. Pulsus Alternans: weak pulse followed by strong bounding

pulse

14. PMI is displaced laterally: due to cardiomegaly

15. Possible S3: ventricular gallop

Dx

1. Chest X-ray (CXR): reveals cardiomegaly

2. Pulmonary Arterial Pressure (PAP): measures pressure in

right ventricle or cardiac status: increased

3. Pulmonary Capillary Wedge Pressure (PCWP): measures end

systolic and dyastolic pressure: increased

4. Central Venous Pressure (CVP): indicates fluid or hydration

status

Increase CVP: decreased flow rate of IV

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Decrease CVP: increased flow rate of IV

5. Swan-Ganz catheterization: cardiac catheterization

6. Echocardiography: shows increased sized of cardiac

chamber (cardiomyopathy): dependent on extent of heart

failure

7. ABG: reveals PO2 is decreased (hypoxemia), PCO2 is

increased (respiratory acidosis)

Right Sided Heart Failure

Weakened right ventricle is unable to pump blood into he

pulmonary system: systemic venous congestion occurs as

pressure builds up


1. Right ventricular infarction

2. Atherosclerotic heart disease

3. Tricuspid valve stenosis

4. Pulmonary embolism

5. Related to COPD

6. Pulmonic valve stenosis

7. Left sided heart failure

S/sx

1. Anorexia

2. Nausea

3. Weight gain

4. Neck / jugular vein distension

5. Pitting edema

6. Bounding pulse

7. Hepatomegaly / Slenomegaly

8. Cool extremities

9. Ascites

10. Jaundice

11. Pruritus

12. Esophageal varices

Dx

1. Chest X-ray (CXR): reveals cardiomegaly

2. Central Venous Pressure (CVP): measure fluid status:

elevated

Measure pressure in right atrium: 4-10 cm of water

If CVP is less than 4 cm of water: Hypovolemic shock:

increase IV flow rate

If CVP is more than 10 cm of water: Hypervolemic

shock: Administer loop diuretics as ordered

Nursing Intervention:

When reading CVP patient should be flat on bed

Upon insertion place client in trendelendberg

position: to promote ventricular filling and prevent

pulmonary embolism

3. Echocardiography: reveals increased size of cardiac

chambers (cardiomyopathy)

4. Liver enzymes: SGPT & SGOT: is increased

5. ABG: decreased pO2

Medical Management

1. Determination & elimination / control of underlying cause

2. Drug therapy: digitalis preparations, diuretics, vasodilators

3. Sodium-restricted diet: to decrease fluid retention

4. If medical therapies unsuccessful: mechanical assist devices

(intra-aortic balloon pump), cardiac transplantation, or

mechanical heart may be employed

5. Treatment for Left Sided Heart Failure Only:

M – Morphine SO4

A – Aminophylline

D – Digitalis

D – Diuretics

O – O2

G – Gases


Goal: Increase cardiac contractility thereby increasing cardiac

output of 3-6 L / min

1. Monitor respiratory status & provide adequate ventilation

(when HF progress to pulmonary edema)

a. Administer O2 therapy: high inflow 3-4 L / min delivered

via nasal cannula

b. Maintain client in semi or high fowlers position:

maximize oxygenation by promoting lung expansion

c. Monitor ABG

d. Assess for breath sounds: noting any changes

2. Provide physical & emotional rest

a. Constantly assess level of anxiety

b. Maintain bed rest with limited activity

c. Maintain quiet & relaxed environment

d. Organized nursing care around rest periods

3. Increase cardiac output

a. Administer digitalis as ordered & monitor effects

Cardiac glycosides: Digoxin (Lanoxin)

Action: Increase force of cardiac contraction

Contraindication: If heart rate is decreased do not

give

b. Monitor ECG & hemodynamic monitoring

c. Administer vasodilators as ordered

Vasodilators: Nitroglycerine (NTG)

d. Monitor V/S

4. Reduce / eliminate edema

a. Administer diuretics as ordered

Loop Diuretics: Lasix (Furosemide)

b. Daily weight

c. Maintain accurate I&O

d. Assess for peripheral edema

e. Measure abdominal girth daily

f. Monitor electrolyte levels

g. Monitor CVP & Swan-Ganz reading

h. Provide Na restricted diet as ordered

i. Provide meticulous skin care

5. If acute pulmonary edema occurs: For Left Sided Heart

Failure only

a. Administer Narcotic Analgesic as ordered

Narcotic analgesic: Morphine SO4

Action: to allay anxiety & reduce preload & afterload

b. Administer Bronchodilator as ordered

Bronchodilators: Aminophylline IV

Action: relieve bronchospasm, increase urinary

output & increase cardiac output

c. Administer Anti-arrythmic as ordered

Anti-arrythmic: Lidocaine (Xylocane)

6. Assist in bloodless phlebotomy: rotating tourniquet, rotated

clockwise every 15 minutes: to promote decrease venous

return or reducing preload


a. Need to monitor self daily for S/sx of Heart Failure

(pedal edema, weight gain, of 1-2 kg in a 2 day period,

dyspnea, loss of appetite, cough)

b. Medication regimen including name, purpose, dosage,

frequency & side effects (digitalis, diuretics)

c. Prescribe diet plan (low Na, cholesterol, caffeine: small

frequent meals)

d. Need to avoid fatigue & plan for rest periods

e. Prevent complications

Arrythmia

Shock

Right ventricular hypertrophy

MI

Thrombophlebitis

f. Importance of follow-up care

Peripheral Vascular Disorder

Arterial Ulcer

1. Thromboangiitis Obliterans (Buerger’s Disease)

2. Raynaud’s Phenomenon

Venous Ulcer

1. Varicose Veins

2. Thrombophlebitis (deep vein thrombosis)

Thromboangiitis Obliterans (Buerger’s Disease)

Acute inflammatory disorder affecting the small / medium

sized arteries & veins of the lower extremities

Occurs as focal, obstructive, process; result in occlusion of a

vessel with a subsequent development of collateral

circulation


1. High risk groups - men 25-40 years old

2. High incident among smokers

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S/sx

1. Intermittent claudication: leg pain upon walking

2. Cold sensitivity & changes in skin color 1st white (pallor)

changing to blue (cyanosis) then red (rubor)

3. Decreased or absent peripheral pulses (posterior tibial &

dorsalis pedis)

4. Trophic changes

5. Ulceration & Gangrene formation (advanced)

Dx

1. Oscillometry: may reveal decrease in peripheral pulse

volume

2. Doppler (UTZ): reveals decrease blood flow to the affected

extremity

3. Angiography: reveals location & extent of obstructive

process

Medical Management

1. Drug Therapy

a. Vasodilators: to improve arterial circulation

(effectiveness ?)

Papaverine

Isoxsuprine HCL (Vasodilan)

Nylidrin HCL (Arlidin)

Nicotinyl Alcohol (Roniacol)

Cyclandelate (Cyclospasmol)

Tolazoline HCL (Priscoline)

b. Analgesic: to relieve ischemic pain

c. Anti-coagulant: to prevent thrombus formation

2. Surgery

a. Bypass Grafting

b. Endarterectomy

c. Balloon Catheter Dilation

d. Lumbar Sympathectomy: to increase blood flow

e. Amputation: may be necessary


1. Encourage a slow progressive physical activity

Walking at least 2 times / day

Out of bed at least 3-4 times / day


Analgesics

Vasodilators

Anti-coagulants

3. Foot care management:

Need to avoid trauma to the affected extreminty

4. Importance of stop smoking

5. Need to maintain warmth especially in cold weather

6. Prepare client for surgery: below knee amputation (BKA)

7. Importance of follow-up care

Raynaud’s Phenomenon

Intermittent episodes of arterial spasm most frequently

involving the fingers or digits of the hands


1. High risk group: female between the teenage years & age

40 years old & above

2. Smoking

3. Collagen diseases

a. Systemic Lupus Erythematosus (SLE): butterfly rash

b. Rheumatoid Arthritis

4. Direct hand trauma

a. Piano playing

b. Excessive typing

c. Operating chainsaw

S/sx

1. Coldness

2. Numbness

3. Tingling in one or more digits

4. Pain: usually precipitated by exposure to cold, Emotional

upset & Tobacco use

5. Intermittent color changes: pallor (white), cyanosis (blue),

rubor (red)

6. Small ulceration & gangrene a tips of digits (advance)

Dx

1. Doppler UTZ: decrease blood flow to the affected extremity

2. Angiography: reveals site & extent of malocclusion

Medical Management


a. Catecholamine-depliting antihypertinsive drugs:

Reserpine

Guanethidine Monosulfate (Ismelin)

b. Vasodilators


1. Importance of stop smoking

2. Need to maintain warmth especially in cold weather

3. Need to wear gloves when handling cold object / opening a

freezer or refrigerator door

Varicose Veins

Dilated veins that occurs most often in the lower extremities

& trunk. As the vessel dilates the valves become stretched

& incompetent with result venous pooling / edema

Abnormal dilation of veins of lower extremities and trunks

due to incompetent valve resulting to increased venous

pooling resulting to venous stasis causing decrease venous

return


1. Hereditary

2. Congenital weakness of the veins

3. Thrombophlebitis

4. Cardiac disorder

5. Pregnancy

6. Obesity

7. Prolonged standing or sitting

S/sx

1. Pain after prolonged standing: relieved by elevation

2. Swollen dilated tortuous skin veins

3. Warm to touch

4. Heaviness in legs

Dx

1. Venography

2. Trendelenburg Test: veins distends quickly in less than 35

seconds

3. Doppler Ultrasound: decreased or no blood flow heard after

calf or thigh compression

Medical Management

1. Vein Ligation: involves ligating the saphenous vein where it

joins the femoral vein & stripping the saphenous vein

system fro groin to ankles

2. Sclerotherapy: can recur & only done in spider web

varicosities & danger of thrombosis (2-3 years for embolism)


1. Elevate legs above heart level: to promote increased venous

return by placing 2-3 pillows under the legs

2. Measure the circumference of ankle & calf muscle daily: to

determine if swollen

3. Apply anti-embolic / knee-length stockings

4. Provide adequate rest


a. Analgesics: for pain

6. Prepare client for vein ligation if necessary

a. Provide routine pre-op care: usually OPD

b. In addition to routine post-op care:

Keep affected extremity elevated above the level of

the heart: to prevent edema

Apply elastic bandage & stockings which should be

removed every 8 hours for short periods & reapplied

Assist out of bed within 24 hours ensuring the

elastic stockings is applied

Assess for increase of bleeding particularly in groin

area


Thrombophlebitis (Deep vein thrombosis)

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Inflammation of the vessel wall with formation of clot

(thrombus), may affect superficial or deep veins

Inflammation of the veins with thrombus formation

Most frequent veins affected are the saphenous, femoral &

popliteal

Can result in damage to the surrounding tissue, ischemia &

necrosis


1. Obesity

2. Smoking

3. Related to pregnancy

4. Severe anemia

5. Prolong use of oral contraceptives: promotes lipolysis

6. Prolonged immobility

7. Trauma

8. Dehydration

9. Sepsis

10. Congestive heart failure

11. Myocardial infarction

12. Post-op complication: surgery

13. Venous cannulation: insertion of various cardiac catheter

14. Increase in saturated fats in the diet.

S/sx

1. Pain in the affected extremity

2. Superficial vein: Tenderness, redness induration along

course of the vein

3. Deep vein:

Swelling

Venous distention of limb

Tenderness over involved vein

Positive homan’s sign: pain at the calf or leg muscle

upon dorsi flexion of the foot

Cyanosis

Dx

1. Venography (Phlebography): increased uptake of radioactive

material

2. Doppler ultrasonography: impairment of blood flow ahead of

thrombus

3. Venous pressure measurement: high in affected limb until

collateral circulation is developed

Medical Management

1. Anti-coagulant therapy

a. Heparin

Action: block conversion of prothrombin to thrombin

& reduces formation or extension of thrombus

Side effects:

Spontaneous bleeding

Injection site reaction

Ecchymoses

Tissue irritation & sloughing

Reversible transient alopecia

Cyanosis

Pan in the arms or legs

Thrombocytopenia

b. Warfarin (Coumadin)

Action: block prothrombin synthesis by interfering

with vit. K synthesis

Side effects:

GI:

Anorexia

N/V

Diarrhea

Stomatitis

Hypersensitivity:

Dermatitis

Urticaria

Pruritus

Fever

Other:

Transient hair loss

Burning sensation of feet

Bleeding complication

2. Surgery

a. Vein ligation & stripping

b. Venous thrombectomy: removal of cloth in the

iliofemoral region

c. Plication of the inferior vena cava: insertion of an

umbrella-like prosthesis into the lumen of the vena

cava: to filter incoming cloth


1. Elevate legs above heart level: to promote increase venous

return & decreased edema

2. Apply warm moist pack: to reduce lymphatic congestion

3. Administer anti-coagulant as ordered:

a. Heparin

Monitor PTT: dosage should be adjusted to keep PTT

between 1.5-2.5 times normal control level

Use infusion pump to administer heparin

Ensure proper injection technique

Use 26 or 27 gauge syringe with ½-5/8 inch

needle, inject into fatty layer of abdomen above

iliac crest

Avoid injecting within 2 inches of umbilicus

Insert needle at 45-90o to skin

Do not withdraw plunger to assess blood return

Apply gentle pressure after removal of needle:

avoid massage

Assess for increased bleeding tendencies

(hematuria, hematemesis, bleeding gums, petechiae

of soft palate, conjunctiva retina, ecchymoses,

epistaxis, bloody spumtum, melena) & instruct the

client to observe for & report these

Have antidote (Protamine Sulfate) available

Instruct the client to avoid aspirin, antihistamines 7

cough preparations containing glyceryl guaiacolate

& obtain MD permission before using other OTC

drugs

b. Warfarin (Coumadin)

Assess PT daily: dosage should be adjusted to

maintain PT at 1.5-2.5 times normal control level;

INR of 2

Obtain careful medication history (there are many

drug-drug interaction)

Advise client to withhold dose & notify MD

immediately if bleeding occur

Have antidote (Vitamin K) available

Alert client to factors that may affect the

anticoagulant response (high-fat diet or sudden

increased in vit. K-rich food)

Instruct the client to wear medic-alert bracelet

4. Assess V/S every 4 hours

5. Monitor chest pain or shortness of breath: possible

pulmonary embolism

6. Measure thigh, calves, ankles & instep every morning


a. Need to avoid standing, sitting for long period,

constrictive clothing, crossing legs at the knee, smoking,

oral contraceptives

b. Importance of adequate hydration: to prevent

hypercoagubility

c. Use elastic stockings when ambulatory

d. Importance of planned rest periods with elevation of the

feet

e. Drug regimen

f. Plan for exercise / activity

Begin with dorsiflexion of the feet while sitting or

lying down

Swim several times weekly

Gradually increased walking distance

g. Importance of weight reduction: if obese

h. Monitor for signs of complications

a. Pulmonary Embolism

Sudden sharp chest pain

Unexplained dyspnea

Tachycardia

Palpitations

Diaphoresis

Restlessness

Overview of Anatomy & Physiology of the Respiratory System

Upper Respiratory System

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Structure of the respiratory system, primarily an air

conduction system, include the nose, pharynx & larynx. Air

is filtered warmed & humidified in the upper airway before

passing to lower airway.

Nose

1. External nose is a frame work of bone & cartilage , internally

divided into two passages or nares (nasal cavity) by the

septum: air enters the system through the nares

2. The septum is covered with mucous membrane, where the

olfactory receptors are located. Turbinates, located

internally, assist in warming & moistening the air

3. The major function of the nose are warming, moistening &

filtering air.

4. Consist of anastomosis of capillaries known as Keissel Rach

Plexus: the site of nose bleeding

Pharynx

1. A muscular passageway commonly called the throat

2. Air passes through the nose to the pharynx

3. Serves as a muscular passageway for both food and air

Composed of three section

1. Nasopharynx: located above the soft palate of the mouth,

contains the adenoids & opening to the eustachian tubes

2. Oropharynx: located directly behind the mouth & tongue,

contains the palatine tonsils; air & food enter the body

through oropharynx

3. Laryngopharynx: extends from the epiglotitis to the sixth

cervical level

Larynx

1. Sometimes called “voice Box” connects upper & lower

airways

2. Framework is formed by the hyoid bone, epiglotitis &

thyroid, cricoid & arytenoids cartilages

3. Larynx opens to allow respiration & closes to prevent

aspiration when food passes through the pharynx

4. Vocal cords of larynx permit speech & are involved in the

cough reflex

5. For phonation (voice production)

Glottis

1. Opening of larynx

2. Opens to allow passage of air

3. Closes to allow passage of food going to the esophagus

4. The initial sign of complete airway obstruction is the

inability to cough

Lower Respiratory System

Consist of trachea, bronchi & branches, & the lungs &

associated structures

For gas exchange

Trachea

AKA “Windpipe”

Air move from the pharynx to larynx to trachea (length 11-

13 cm, diameter 1.5-2.5 cm in adult)

Extend from the larynx to the second costal cartilage, where

it bifurcates & is supported by 16-20 C-shaped cartilage

rings

The area where the trachea divides into two branches is

called the carina

Consist of cartilaginous rings

Serves as passageway of air going to the lungs

Site of tracheostomy

Bronchi

Right main bronchus

Larger & straighter than the left

Divided into three lobar branches (upper, middle &

lower bronchi) to supply the three lobes of right lung

Left main bronchus

Divides into the upper & lower lobar bronchi to supply

the left lobes

Bronchioles

In the bronchioles, airway patency is primarily dependent

upon elastic recoil formed by network of smooth muscles

The tracheobronchial tree ends at the terminal bronchials.

Distal to the terminal bronchioles the major function is no

longer air conduction but gas exchange between blood &

alveolar air

The respiratory bronchioles serves as the transition to the

alveolar epithelium

Lungs

Right lung (consist of 3 lobes, 10 segments)

Left lung (consist of 2 lobes, 8 segments)

Main organ of respiration, lie within the thoracic cavity on

either side of the heart

Broad area of lungs resting on diaphragm is called the base

& the narrow superior portion called the apex

Pleura

Serous membranes covering the lungs, continuous with the

parietal pleura that lines the chest wall

Parietal Pleura

Lines the chest walls & secretes small amounts of

lubricating fluid into the intrapleural space (space between

the parietal pleura & visceral pleura) this fluid holds the

lungs & chest wall together as a single unit while allowing

them to move separately

Chest Wall

Includes the ribs cage, intercostal muscles & diaphragm

Chest is a C shaped & supported by 12 pairs of ribs & costal

cartilages, the ribs have several attached muscles

Contraction of the external intercostal muscles raises

the ribs cage during inspiration & helps increase the size

of the thoracic cavity

The internal intercoastal muscles tends to pull ribs down

& in & play a role in forced expiration

Diaphragm

A major muscle of ventilation (the exchange of air between

the atmosphere & the alveoli).

Alveoli

Are functional cellular unit of the lungs; about half arise

directly from alveolar ducts & are responsible for about 35%

of alveolar gas exchange

Produces surfactants

Site of gas exchange (CO2 and O2)

Diffusion (Dalton’s law of partial pressure of gases)

Surfactant

A phospholipids substance found in the fluid lining the

alveolar epithelium

Reduces surface tension & increase stability of the alveoli &

prevents their collapse

Alveolar Ducts

Arises from the respiratory bronchioles & lead to the alveoli

Alveolar Sac

Form the last part of the airway

Functionally the same as the alveolar ducts they are

surrounded by alveoli & are responsible for the 65% of the

alveolar gas exchange

Type II Cells of Alveoli

Secretes surfactant

Decrease surface tension

Prevent collapse of alveoli

Composed of lecithin and spingomyelin

Lecitin / Spingomyelin ratio: to determine lung maturity

Normal Lecitin / Spingomyelin ratio: is 2:1

In premature infants: 1:2

Give oxygen of less 40% in premature: to prevent

atelectasis and retrolental fibroplasias

Retinopathy & blindness: in premature

Pulmonary Circulation

Provides for reoxygenation of blood & release of CO2

Gas transfers occurs in the pulmonary capillary bed

Respiratory Distress Syndrome

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Decrease oxygen stimulates breathing

Increase carbon dioxide is a powerful stimulant for

breathing

Pneumonia

Inflammation of the alveolar spaces of the lungs, resulting in

consolidation of lung tissue as the alveoli fill with exudates

Inflammation of the lung parenchyma leading to pulmonary

consolidation as the alveoli is filled with exudates

Etiologic Agents

1. Streptococcus Pneumonae: causing pneumococal

pneumonia

2. Hemophylus Influenzae: causing broncho pneumonia

3. Diplococcus Pneumoniae

4. Klebsella Pneumoniae

5. Escherichia Pneumoniae

6. Pseudomonas

High Risk Groups

1. Children below 5 years old

2. Elderly


1. Smoking

2. Air pollution

3. Immuno compromised

4. Related to prolonged immobility (CVA clients): causing

hypostatic pneumonia

5. Aspiration of food: causing aspiration pneumonia

S/sx

1. Productive cough with greenish to rusty sputum

2. Rapid shallow respiration with expiratory grunt

3. Nasal flaring

4. Intercostal rib retraction

5. Use of accessory muscles of respiration

6. Dullness to flatness upon auscultation

7. Possible pleural friction rub

8. High-pitched bronchial breath sound

9. Rales / crackles (early) progressing to coarse (later)

10. Fever

11. Chills

12. Anorexia

13. General body malaise

14. Weight loss


16. Cyanosis

17. Chest pain

18. Abdominal distention leading to paralytic ileus (absence of

peristalsis)

Dx

1. Sputum Gram Staining & Culture Sensitivity: positive to

cultured microorganisms

2. Chest x-ray: reveals pulmonary consolidation over affected

area

3. ABG analysis: reveals decrease PO2

4. CBC: reveals increase WBC, erythrocyte sedimentation rate

is increased


1. Facilitate adequate ventilation

Administer O2 as needed & assess its effectiveness: low

inflow

Place client semi fowlers position

Turn & reposition frequently client who are immobilized

Administer analgesic as ordered: DOC: codeine: to

relieve pain associated with breathing

Auscultate breath sound every 2-4 hour

Monitor ABG

2. Facilitate removal of secretions

General hydration

Deep breathing & coughing exercise: tends to promote

expectoration

Tracheobronchial suctioning as needed

Administer Mucolytic or Expectorant as ordered

Aerosol treatment via nebulizer

Humidification of inhaled air

Chest physiotherapy (Postural Drainage): tends to

promote expectoration

3. Observe color characteristics of sputum & report any

changes: encourage client to perform good oral hygiene

after expectoration

4. Provide adequate rest & relief control of pain

Enforce CBR with limited activity

Limit visits & minimized conversation

Plan for uninterrupted rest periods

Maintain pleasant & restful environment

5. Administer antibiotic as ordered: monitor effects & possible

toxicity

Broad Spectrum Antibiotic

Penicillin

Tetracycline

Microlides (Zethromax)

Azethromycin: Side Effect: Ototoxicity

6. Prevent transmission: respiratory isolation client with

staphylococcal pneumonia

7. Control fever & chills:

Monitor temperature A

Administer antipyretic as ordered

Increased fluid intake

Provide frequent clothing & linen changing

8. Assist in postural drainage: uses gravity & various position

to stimulate the movement of secretions

Nursing Management for Postural Drainage

a. Best done before meals or 2-3 hours: to prevent gastro

esophageal reflux

b. Monitor vital signs

c. Encourage client deep breathing exercises

d. Administer bronchodilators 20-30 minutes before

procedure

e. Stop if client cannot tolerate procedure

f. Provide oral care after procedure

g. Contraindicated with

Unstable V/S

Hemoptysis

Clients with increase intra ocular pressure (Normal

IOP 12 – 21 mmHg)

Increase ICP

9. Provide increase CHO, calories, CHON & vitamin C


a. Medication regimen / antibiotic therapy

b. Need for adequate rest, limited activity, good nutrition,

with adequate fluid intake & good ventilation

c. Need to continue deep breathing & coughing exercise

for at least 6-8 weeks after discharge

d. Availability of vaccines

e. Need to report S/sx of respiratory infection

Persistent or recurrent fever

Changes in characteristics color of sputum

Chills

Increased pain

Difficulty in breathing

Weight loss

Persistent fatigue

f. Avoid smoking

g. Prevent complications

Atelectasis

Meningitis

h. Importance of follow up care

Histoplasmosis

Systemic fungal disease caused by inhalation of dust

contaminated by histoplasma capsulatum which is

transmitted to bird manure

Acute fungal infection caused by inhalation of contaminated

dust or particles with histoplasma capsulatum derived from

birds manure

S/sx

1. Similar to PTB or Pneumonia

2. Productive cough

3. Fever, chills, anorexia, general body malaise

4. Chest and joint pains

5. Dyspnea

6. Cyanosis

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7. Hemoptysis

8. Sometimes asymptomatic

Dx

1. Chest X-ray: often appears similar to PTB

2. Histoplasmin Skin Test: positive

3. ABG analysis: PO2 decrease

Medical Management

1. Anti-fungal Agent: Amphotericin B (Fungizone)

Very toxic: toxicity includes anorexia, chills, fever,

headaches & renal failure

Acetaminophen, Benadryl & Steroids is given with

Amphotericin B: to prevent reaction


1. Monitor respiratory status

2. Enforce CBR



a. Antifungal: Amphotericin B (Fungizone)

Observe severe side effects:

Fever: acetaminophen given prophylactically

Anaphylactic reaction: Benadryl & Steroids

given prophylactically

Abnormal renal function with hypokalemia &

azotemia: Nephrotoxicity, check for BUN and

Creatinine, Hypokalemia

5. Force fluids to liquefy secretions

6. Nebulize & suction as needed

7. Prevent complications: bronchiectasis

8. Prevent the spread of infection by spraying of breeding

places

Chronic Obstructive Pulmonary Disease (COPD)

Chronic Bronchitis

Excessive production of mucus in the bronchi with

accompanying persistent cough

Characteristic include hypertrophy / hyperplasia of the

mucus secreting gland in the bronchi, decreased ciliary

activity, chronic inflammation & narrowing of the airway

Inflammation of bronchus resulting to hypertrophy or

hyperplasia of goblet mucous producing cells leading to

narrowing of smaller airways

AKA “Blue Bloaters”


1. Smoking

2. Air pollution

S/sx

1. Productive copious cough (consistent to all COPD)

2. Dyspnea on exertion

3. Use of accessory muscle of respiration

4. Scattered rales / rhonchi

5. Feeling of gastric fullness

6. Slight Cyanosis

7. Distended neck veins

8. Ankle edema

9. Prolonged expiratory grunt

10. Anorexia and generalized body malaise

11. Pulmonary hypertension

a. Leading to peripheral edema

b. Cor Pulmonale (right ventricular hypertrophy)

Dx

1. ABG analysis: reveals PO2 decrease (hypoxemia): causing

cyanosis, PCO2 increase

Bronchial Asthma

Immunologic / allergic reaction results in histamine release

which produces three mainairway response: Edema of

mucus membrane, Spasm of the smooth muscle of bronchi

& bronchioles, Accumulation of tenacious secretions

Reversible inflammatory lung condition due to

hypersensitivity to allergens leading to narrowing of smaller

airways

Predisposing Factors (Depending on Types)

1. Extrinsic Asthma (Atopic / Allergic)

Causes

Pollen

Dust

Fumes

Smoke

Gases

Danders

Furs

Lints

2. Intrinsic Asthma (Non atopic / Non allergic)

Causes

Hereditary

Drugs (aspirin, penicillin, beta blocker)

Foods (seafoods, eggs, milk, chocolates, chicken)

Food additives (nitrates)

Sudden change in temperature, air pressure and

humidity

Physical and emotional stress

3. Mixed Type: 90 – 95%

S/sx

1. Cough that is non productive

2. Dyspnea

3. Wheezing on expiration

4. Cyanosis

5. Mild Stress or apprehension

6. Tachycardia, palpitations

7. Diaphoresis

Dx

1. Pulmonary Function Test Incentive spirometer: reveals

decrease vital lung capacity

2. ABG analysis: PO2 decrease

3. Before ABG test for positive Allens Test, apply direct

pressure to ulnar & radial artery to determine presence of

collateral circulation

Medical Management

1. Drug Therapy

a. Bronchodilators: given via inhalation or metered dose

inhaler or MDI for 5 minutes

b. Steroids: decrease inflammation: given 10 min after

bronchodilator

c. Mucomysts (acetylceisteine): at bed side put suction

machine

d. Mucolytics / expectorants

e. Anti histamine

2. Physical Therapy

3. Hyposensitization

4. Execise


1. Enforce CBR

2. O2 inhalation: low flow 2-3 L/min: to prevent respiratory

distress


4. Force fluids 2-3 L/day

5. Semi fowlers position: to promote lung expansion

6. Nebulize & suction when needed


concerning

a. Avoidance of precipitating factor

b. Prevent complications

Emphysema

Status Asthmaticus: severe attack of asthma which

cause poor controlled asthma

DOC: Epinephrine

Steroids

Bronchodilators

c. Regular adherence to medications: to prevent

development of status asthmaticus

d. Importance of follow up care

Bronchiectasis

Permanent abnormal dilation of the bronchi with destruction

of muscular & elastic structure of the bronchial wall

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Abnormal permanent dilation of bronchus leading to

destruction of muscular and elastic tissues of alveoli


1. Caused by bacterial infection

2. Recurrent lower respiratory tract infections

3. Chest trauma

4. Congenital defects (altered bronchial structure)

5. Related to presence of tumor (lung tumor)

6. Thick tenacious secretion

Sx

1. Productive cough with mucopurulent sputum

2. Dyspnea in exertion

3. Cyanosis

4. Anorexia & generalized body malaise

5. Hemoptysis (only COPD with sign)

6. Wheezing

7. Weight loss

Dx

1. CBC: elevation in WBC

2. ABG: PO2 decrease

3. Bronchoscopy: reveals sources & sites of secretion: direct

visualization of bronchus using fiberscope

Nursing Management before Bronchoscopy

1. Secure inform consent and explain procedure to client

2. Maintain NPO 6-8 hours prior to procedure

3. Monitor vital signs & breath sound

Post Bronchoscopy

1. Feeding initiated upon return of gag reflex

2. Avoid talking, coughing and smoking, may cause irritation

3. Monitor for signs of gross

4. Monitor for signs of laryngeal spasm: prepare tracheostomy

set

Medical Management

1. Surgery

Pneumonectomy: 1 lung is removed & position on

affected side

Segmental Wedge Lobectomy: promote re-expansion of

lungs

Unaffected lobectomy: facilitate drainage

Emphysema

Enlargement & destruction of the alveolar, bronchial &

bronchiolar tissue with resultant loss of recoil, air tapping,

thoracic overdistension, sputum accumulation & loss of

diaphragmatic muscle tone

These changes cause a state of CO2 retention, hypoxia &

respiratory acidosis

Irreversible terminal stage of COPD characterized by

Inelasticity of alveoli

Air trapping

Maldistribution of gases

Overdistention of thoracic cavity (barrel chest)


1. Smoking

2. Inhaled irritants: air pollution

3. Allergy or allergic factor

4. High risk: elderly

5. Hereditary: it involves deficiency of Alpha 1 anti-trypsin: to

release elastase for recoil of alveoli

S/sx

1. Productive cough

2. Sputum production

3. Anorexia & generalized body malaise

4. Weight loss

5. Flaring of nostrils (alai nares)

6. Use of accessory muscles

7. Dyspnea at rest

8. Increased rate & depth of breathing

9. Decrease respiratory excursion

10. Resonance to hyper resonance

11. Decrease or diminished breath sounds with prolong

expiration

12. Decrease tactile fremitus

13. Prolong expiratory grunt

14. Rales or rhonchi


16. Barrel chest

17. Purse lip breathing: to eliminates excess CO2 (compensatory

mechanism)

Dx

1. Pulmonary Function Test: reveals decrease vital lung

capacity

2. ABG analysis: reveals

Panlobular/centrilobular

Decrease PO2 (hypoxemia leading to chronic

bronchitis, “Blue Bloaters”)

Decrease ph

Increase PCO2

Respiratory acidosis

Panacinar/centriacinar

Increase PO2 (hyperaxemia, “Pink Puffers”)

Decrease PCO2

Increase ph

Respiratory alkalosis


1. Enforce CBR

2. Administer oxygen inhalation via low inflow


a. Bronchodilators: used to treat bronchospam

Aminophylline

Isoproterenol (Isuprel)

Terbutalin (Brethine)

Metaproterenol (Alupent)

Theophylline

Isoetharine (Bronkosol)

b. Corticosteroids:

Prednisone

c. Anti-microbial / Antibiotics: to treat bacterial infection

Tetracycline

Ampicilline

d. Mucolytics / expectorants

4. Facilitate removal of secretions:

a. Force fluids at least 3 L/day

b. Provide chest physiotherapy, coughing & deep

breathing

c. Nebulize & suction when needed

d. Provide oral hygiene after expectoration of sputum

5. Improve ventilation

a. Position client to semi or high fowlers

b. Instruct the client diaphragmatic muscles to breathe

c. Encourage productive cough after all treatment (splint

abdomen to help produce more expulsive cough)

d. Employ pursed-lip breathing techniques (prolonged slow

relaxed expiration against pursed lips)

e. Institute pulmonary toilet

6. Institute PEEP (positive end expiratory pressure) in

mechanical ventilation promotes maximum alveolar lung

expansion

7. Provide comfortable & humid environment

8. Provide high carbohydrates, protein, calories, vitamins and

minerals

9. Provide client teachings and discharge planning concerning

a. Prevention of recurrent infection

Avoid crowds & individual with known infection

Adhere to high CHON, CHO & increased vit C diet

Received immunization for influenza & pneumonia

Report changes in characteristic & color of sputum

immediately

Report of worsening of symptoms (increased

tightness of chest, fatigue, increased dyspnea)

b. Control of environment

Use home humidifier at 30-50%

Wear scarf over nose & mouth in cold weather: to

prevent bronchospasm

Avoid smoking & contact with environmental smoke

Avoid abrupt change in temperature

c. Avoidance of inhaled irritants

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Stay indoor: if pollution level is high

Use air conditioner with efficiency particulate air

filter: to remove particles from air

d. Increase activity tolerance

Start with mild exercise: such as walking & gradual

increase in amount & duration

Used breathing techniques: (pursed lip,

diaphragmatic) during activities / exercise: to

control breathing

Have O2 available as needed to assist with activities

Plan activities that require low amount of energy

Plan rest period before & after activities

e. Prevent complications

Atelectasis

Cor Pulmonale: R ventricular hypertrophy

CO2 narcosis: may lead to coma

Pneumothorax: air in the pleural space

f. Strict compliance to medication

g. Importance of follow up care

Oncology Nursing

Pathophysiology & Etiology of Cancer

Evolution of Cancer Cells All cells constantly change through growth, degeneration,

repair, & adaptation. Normal cells must divide & multiply to

meet the needs of the organism as a whole, & this cycle of

cell growth & destruction is an integral part of life

processes. The activities of the normal cell in the human

body are all coordinated to meet the needs of the organism

as a whole, but when the regulatory control mechanisms of

normal fail, & growth continues in excess of the body needs,

neoplasia results.

The term neoplasia refers to both benign & malignant

growths, but malignant cells behave very differently from

normal cells & have special features characteristics of the

cancer process.

Since the growth control mechanism of normal cells is

not entirely understood, it is not clear what allows the

uncontrolled growth, therefore no definitive cure has

been found.

Characteristics of Malignant Cells

Cancer cells are mutated stem cells that have undergone

structural changes so that they are unable to perform the

normal functions of specialized tissues.

They may function is a disorderly way to crease normal

function completely, only functioning for their own survival

& growth.

The most undifferentiated cells are also called anaplastic.

Rate of Growth

Cancer cells have uncontrolled growth or cell division

Rate at which a tumor grows involves both increased cell

division & increased survival time of cells.

Malignant cells do not form orderly layers, but pile on top of

each other to eventually form tumors.

Pre-disposing Factors

G – Genetics

Some cancers shows familial pattern

Maybe caused by inherited genetics defects

I – Immunologic

Failure of the immune system to respond & eradicate

cancer cells

Immunosuppressed individuals are more susceptible to

cancer

V – Viral

o Viruses have been shown to be the cause of certain

tumors in animals

o Viruses ( HTLV-I, Epstein Barr Virus, Human

Papilloma Virus) linked to human tumors

o Oncovirus (RNA – Type Viruses) thought to be culprit

E – Environmental

o Majority (over 80%) of human cancer related to

environmental carcinogens

o Types:

Physical

Radiation: X – ray, radium, nuclear

explosion & waste, UV

Trauma or chronic irritation

Chemical

Nitrates, & food additives, polycyclic

hydrocarbons, dyes, alkylating

agents

Drugs: arsenicals, stilbestol,

urethane

Cigarette smoke

hormones

Classification of Cancer

Tissue Typing:

Carcinoma – arises from surface, glandular, or parenchymal

epithelium

1. Squamous Cell Carcinoma – surface epithelium

2. Adenocarcinoma – glandular or parenchymal tissue

Sarcoma – arises from connective tissue

Leukemia – from blood

Lymphoma – from lymph glands

Multiple Myeloma – from bone marrow

Stages of Tumor Growth

A. Staging System:

TNM System: uses letters & numbers to designate the

extent of tumors

o T– stands for primary growth; 1-4 with increasing

size; T1S indicates carcinoma in situ

o N – stands for lymph nodes involvement: 0-4

indicates progressively advancing nodal disease

o M – stands for metastasis; 0 indicates no distant

metastases, 1 indicates presence of metastases

Stages 0 – IV: all cancers divided into five stages

incorporating size, nodal involvement & spread

B. Cytologic Diagnosis of Cancer

1. Involves in the study of shed cells (ex. Pap smear)

2. Classified by degree of cellular abnormality

Normal

Probably normal (slight changes)

Doubtful (more severe changes)

Probably cancer or precancerous

Definitely cancer

Client Factors

1. Seven warning signs of cancer

2. BSE – breast self – examination

3. Importance of retal exam for those over age 40

4. Hazards of smoking

5. Oral self – examination as well as annual exam of mouth

& teeth

6. Hazards of excess sun exposure

7. Importance of pap smear

8. P.E. with lab work – up: every 3 years ages 20-40; yearly

for age 40 & over

9. TSE – testicular self – examination

Testicular Cancer

i. Most common cancer in men between

the age of 15 & 34

Warning signs that men should look for:

i. Painless swelling

ii. Feeling of heaviness

iii. Hard lump (size of a pea)

iv. Sudden collection fluid in the scrotum

v. Dull ache in the lower abdomen or in the

groin

vi. Pain in the testicle or in the scrotum

vii. Enlargement or tenderness of the

breasts

7 Warning Signs of Cancer

C: change in bowel or bladder habits

A: a sore that doesn’t heal

U: unusual bleeding or discharge

T: thickening of lump in breast or elsewhere

I: indigestion or dysphagia

O: obvious change in wart or mole

N: nagging cough or hoarseness

Treatment of Cancer

Therapeutic Modality

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Chemotherapy

Ability of the drug to kill cancer cells; normal cells may also

be damaged, producing side effects.

Different drug act on tumor cell in different stages of the cell

growth cycle.

Types of Chemotherapeutic Drugs

1. Antimetabolites

o Foster cancer cell death by interfering with cellular

metabolic process.

2. Alkylating Agent

o act with DNA to hinder cell growth & division.

3. Plant Alkaloids

o obtained from periwinkle plant.

o makes the host’s body a less favorable environment

for the growth of cancer cells.

4. Antitumor Antibiotics

o affect RNA to make environment less favorable for

cancer growth.

5. Steroids & Sex Hormones

o alter the endocrine environment to make it less

conducive to growth of cancer cells.

Major Side Effects & Nursing Intervention

A. GI System

Nausea & Vomiting

o Administer antiemetics routinely q 4-6 hrs as well as

prophylactically before chemotherapy is initiated.

o Withhold food/fluid 4-6 hrs before chemotherapy

o Provide bland food in small amounts after treatment

Diarrhea

o Administer antidiarrheals.

o Maintain good perineal care.

o Give clear liquids as tolerated.

o Monitor K, Na, Cl levels.

Stomatitis (mouth sore)

o Provide & teach the client good oral hygiene,

including avoidance of commercial mouthwashes.

o Rinse with viscous lidocaine before meals to provide

analgesic effect.

o Perform a cleansing rinse with plain H2O or dilute a

H2O soluble lubricant such as hydrogen peroxide

after meal.

o Apply H2O lubricant such as K-Y jelly to lubricate

cracked lips.

o Advice client to suck on Popsicles or ice chips to

provide moisture.

B. Hematologic System

Thrombocytopenia

o Avoid bumping or bruising the skin.

o Protect client from physical injury.

o Avoid aspirin or aspirin products.

o Avoid giving IM injections.

o Monitor blood counts carefully.

o Assess for signs of increase bleeding tendencies

(epistaxis, petechiae, ecchymoses)

Leukopenia

o Use careful handwashing technique.

o Maintain reverse isolation if WBC count drops below

1000/mm

o Assess for signs of respiratory infection

o Avoid crowds/persons with known infection

Anemia

o Provide adequate rest period

o Monitor hemoglobin & hematocrit

o Protect client from injury

o Administer O2 if needed

C. Integumentary System

Alopecia

o Explain that hair loss is not permanent

o Offer support & encouragement

o Scalp tourniquets or scalp hypothermia via ice pack

may be ordered to minimize hair loss with some

agent

o Advice client to obtain wig before initiating

treatment

D. Renal System

Encourage fluid & frequent voiding to prevent accumulation

of metabolites in bladder; R: may cause direct damage to

kidney by excretion of metabolites.

Increased excretion of uric acid may damage kidney

Administer allopurinol (Zyloprim) as ordered; R: to prevent

uric acid formation; encourage fluids when administering

allopurinol

E. Reproductive System

Damage may occur to both men & women resulting

infertility &/or mutagenic damage to chromosomes

Banking sperm often recommended for men before

chemotherapy

Clients & partners advised to use reliable methods of

contraception during chemotherapy

F. Neurologic System

Plant alkaloids (vincristine) cause neurologic damage with

repeated doses

Peripheral neuropathies, hearing loss, loss of deep tendon

reflex, & paralytic ileus may occur.

Radiation Therapy

Uses ionizing radiation to kill or limit the growth of cancer

cells, maybe internal or external.

It not only injured cell membrane but destroy & alter DNA so

that the cell cannot reproduce.

Effects cannot be limited to cancer cells only; all exposed

cells including normal cells will be injured causing side

effects.

Localized effects are related to the area of the body being

treated; generalized effects maybe related to cellular

breakdown products.

Types of Energy Emitted

Alpha – particles cannot passed through skin, rarely used.

Beta – particle cannot passed through skin, more

penetrating than alpha, generally emitted from radioactive

isotopes, used for internal source.

Gamma – penetrate more deeper areas of the body, most

common form of external radiotherapy (ex. Electromagnetic

or X-ray)

Methods of Delivery

External Radiation Therapy – beams high energy rays

directly to the affected area. Ex. Cobalt therapy

Internal Radiation Therapy – radioactive material is injected

or implanted in the client’s body for designated period of

time.

o Sealed Implants – a radioisotope enclosed in a

container so it does not circulate in the body;

client’s body fluids should not be contaminated.

o Unsealed source – a radioisotope that is not encased

in a container & does circulate in the body &

contaminate body fluids.

Factors Controlling Exposure

Half-life – time required for half of radioactive atoms to

decay.

1. Each radioisotope has different half-life.

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2. At the end of half-life the danger from exposure

decreases.

Time – the shorter the duration the less the exposure.

Distance – the greater the distance from the radiation

source the less the exposure.

Shielding – all radiation can be blocked; rubber gloves for

alpha & usually beta rays; thick lead or concrete stop

gamma rays.

Side Effects of Radiation Therapy & Nursing Intervention

A. Skin - itching, redness, burning, oozing, sloughing.

Keep skin free from foreign substances.

Avoid use of medicated solution, ointment, or powders that

contain heavy metals such as zinc oxide.

Avoid pressure, trauma, infection to skin; use bed cradle.

Wash affected areas with plain H2O & pat dry; avoid soap.

Use cornstarch, olive oil for itching; avoid talcum powder.

If sloughing occurs, use sterile dressing with micropore tape

Avoid exposing skin to heat, cold, or sunlight & avoid

constricting irritating clothing.

B. Anorexia, N/V

Arrange meal time so they do not directly precede or

follow therapy.

Encourage bland foods.

Provide small attractive meals.

Avoid extreme temperature.

Administer antiemetics as ordered before meals.

C. Diarrhea

Encourage low residue, bland, high CHON food.

Administer antidiarrheal as ordered.

Provide good perineal care.

Monitor electrolytes particularly Na, K, Cl

D. Anemia, Leukopenia, Thrombocytopenia

Isolate from those with known infection.

Provide frequent rest period.

Encourage high CHON diet.

Avoid injury.

Assess for bleeding.

Monitor CBC, WBC, & platelets.

Burns

direct tissue injury caused by thermal, electric, chemical &

smoke inhaled (TECS)

Type:

1. Thermal

2. Smoke Inhalation

3. Chemical

4. Electrical

Classification

Partial Thickness

1. Superficial partial thickness (1st degree)

Depth: epidermis only

Causes: sunburn, splashes of hot liquid

Sensation: painful

Characteristics: erythema, blanching on

pressure, no vesicles

2. Deep Partial Thickness (2nd degree)

Depth: epidermis & dermis

Causes: flash, scalding, or flame burn

Sensation: very painful

Characteristics: fluid filled vesicles; red,

shinny, wet after vesicles ruptures

Full Thickness (3rd & 4th degree)

1. Depth: all skin layers & nerve endings; may involve

muscles, tendons & bones

2. Causes: flames, chemicals, scalding, electric current

3. Sensation: little or no pain

4. Characteristics: wound is dry, white, leathery, or

hard

Overview Of Anatomy & Physiology Of Musculoskeletal System

Consist of bones, muscles, joints, cartilages, tendons,

ligaments, bursae

To provide a structural framework for the body

To provide a means for movement

Bones

Function of Bones

Provide support to skeletal framework

Assist in movement by acting as levers for muscles

Protect vital organ & soft tissue

Manufacture RBC in the red bone marrow

(hematopoiesis)

Provide site for storage of calcium & phosphorus

1. Types of Bones

Long Bones

Central shaft (diaphysis) made of compact bone &

two end (epiphyses) composed of cancellous bones

(ex. Femur & humerus)

Short Bones

Cancellous bones covered by thin layer of compact

bone (ex. Carpals & tarsals)

Flat Bones

Two layers of compact bone separated by a layer of

cancellous bone (ex. Skull & ribs)

Irregular Bones

Sizes and shapes vary (ex. Vertebrae & mandible)

Joints

Articulation of bones occurs at joints

Movable joints provide stabilization and permit a variety of

movements

Classification

1. Synarthroses: immovable joints

2. Amphiarthroses: partially movable joints

3. Diarthroses (synovial): freely movable joints

Have a joint cavity (synovial cavity) between the

articulating bone surfaces

Articular cartilage covers the ends of the bones

A fibrous capsule encloses the joint

Capsule is lined with synovial membrane that secretes

synovial fluid to lubricate the joint and reduce friction.

Muscles

Functions of Muscles

Provide shape to the body

Protect the bones

Maintain posture

Cause movement of body parts by contraction

Types of Muscles

Cardiac: involuntary; found only in heart

Smooth: involuntary; found in walls of hollow structures

(e.g. intestines)

Striated (skeletal): voluntary

1. Characteristics of skeletal muscles

Muscles are attached to the skeleton at the point of

origin and to bones at the point of insertion.

Have properties of contraction and extension, as

well as elasticity, to permit isotonic (shortening and

thickening of the muscle) and isometric (increased

muscle tension) movement.

Contraction is innervated by nerve stimulation.

Cartilage

A form of connective tissue

Major functions are to cushion bony prominences and offer

protection where resiliency is required

Tendons and Ligaments

Composed of dense, fibrous connective tissue

Functions

1. Ligaments attach bone to bone

2. Tendons attach muscle to bone

Rheumatoid Arthritis (RA)

Chronic systemic disease characterized by inflammatory

changes in joints and related structures.

Joint distribution is symmetric (bilateral): most commonly

affects smaller peripheral joints of hands & also commonly

involves wrists, elbows, shoulders, knees, hips, ankles and

jaw.

If unarrested, affected joints progress through four stages of

deterioration: synovitis, pannus formation, fibrous ankylosis,

and bony ankylosis.

Cause

1. Cause unknown or idiopathic

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2. Maybe an autoimmune process

3. Genetic factors

4. Play a role in society (work)

Predisposing factors

1. Occurs in women more often than men (3:1) between the

ages 35-45.

2. Fatigue

3. Cold

4. Emotional stress

5. Infection

S/sx

1. Fatigue

2. Anorexia & body malaise

3. Weight loss

4. Slight elevation in temperature

5. Joints are painful: warm, swollen, limited in motion, stiff in

morning & after a period of inactivity & may show crippling

deformity in long-standing disease.

6. Muscle weakness secondary to inactivity

7. History of remissions and exacerbations

8. Some clients have additional extra-articular manifestations:

subcutaneous nodules; eye, vascular, lung, or cardiac

problems.

Dx

1. X-rays: shows various stages of joint disease

2. CBC: anemia is common

3. ESR: elevated

4. Rheumatoid factor positive

5. ANA: may be positive

6. C-reactive protein: elevated

Medical Management

1. Drug therapy

a. Aspirin: mainstay of treatment: has both analgesic and

anti-inflammatory effect.

b. Nonsteroidal anti-inflammatory drugs (NSAIDs): relieve

pain and inflammation by inhibiting the synthesis of

prostaglandins.

Ibuprofen (Motrin)

Indomethacin (Indocin)

Fenoprofen (Nalfon)

Mefenamic acid (Ponstel)

Phenylbutazone (Butazolidin)

Piroxicam (Feldene)

Naproxen (Naprosyn)

Sulindac (Clinoril)

c. Gold compounds (Chrysotherapy)

Injectable form: given IM once a week; take 3-6

months to become effective

Sodium thiomalate (Myochrysine)

Aurothioglucose (Solganal)

SI: monitor blood studies & urinalysis

frequently

Proteinuria

Mouth ulcers

Skin rash

Aplastic anemia.

Oral form: smaller doses are effective; take 3-6

months to become effective

Auranofin (Ridaura)

SI: blood & urine studies should be

monitored.

Diarrhea

d. Corticosteroids

Intra-articular injections: temporarily suppress

inflammation in specific joints.

Systemic administration: used only when client does

not respond to less potent anti-inflammatory drugs.

e. Methotrexate: given to suppress immune response

Cytoxan

SI: bone marrow suppression.

2. Physical therapy: to minimize joint deformities.

3. Surgery: to remove severely damaged joints (e.g. total hip

replacement; knee replacement).


1. Assess joints for pain, swelling, tenderness & limitation of

motion.

2. Promote maintenance of joint mobility and muscle strength.

a. Perform ROM exercises several times a day: use of heat

prior to exercise may decrease discomfort; stop exercise

at the point of pain.

b. Use isometric or other exercise to strengthen muscles.

3. Change position frequently: alternate sitting, standing &

lying.

4. Promote comfort & relief / control of pain.

a. Ensure balance between activity & rest.

b. Provide 1-2 scheduled rest periods throughout day.

c. Rest & support inflamed joints: if splints used: remove

1-2 times/day for gentle ROM exercises.

5. Ensure bed rest if ordered for acute exacerbations.

a. Provide firm mattress.

b. Maintain proper body alignment.

c. Have client lie prone for ½ hour twice a day.

d. Avoid pillows under knees.

e. Keep joints mainly in extension, not flexion.

f. Prevent complications of immobility.

6. Provide heat treatments: warm bath, shower or whirlpool;

warm, moist compresses; paraffin dips as ordered.

a. May be more effective in chronic pain.

b. Reduce stiffness, pain & muscle spasm.

7. Provide cold treatments as ordered: most effective during

acute episodes.

8. Provide psychologic support and encourage client to

express feelings.

9. Assists clients in setting realistic goals; focus on client

strengths.

10. Provide client teaching & discharge planning & concerning.

a. Use of prescribed medications & side effects

b. Self-help devices to assist in ADL and to increase

independence

c. Importance of maintaining a balance between activity &

rest

d. Energy conservation methods

e. Performance of ROM, isometric & prescribed exercises

f. Maintenance of well-balanced diet

g. Application of resting splints as ordered

h. Avoidance of undue physical or emotional stress

i. Importance of follow-up care

Osteoarthritis

Chronic non-systemic disorder of joints characterized by

degeneration of articular cartilage

Weight-bearing joints (spine, knees and hips) & terminal

interphalangeal joints of fingers most commonly affected

Incident Rate

1. Women & men affected equally

2. Incidence increases with age


1. Most important factor in development is aging (wear & tear

on joints)

2. Obesity

3. Joint trauma

S/sx

1. Pain: (aggravated by use & relieved by rest) & stiffness of

joints

2. Heberden’s nodes: bony overgrowths at terminal

interphalangeal joints

3. Decreased ROM with possible crepitation (grating sound

when moving joints)

Dx

1. X-rays: show joint deformity as disease progresses

2. ESR: may be slightly elevated when disease is inflammatory


1. Assess joints for pain & ROM.

2. Relieve strain & prevent further trauma to joints.

a. Encourage rest periods throughout day.

b. Use cane or walker when indicated.

c. Ensure proper posture & body mechanics.

d. Promote weight reduction: if obese

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53

e. Avoid excessive weight-bearing activities & continuous

standing.

3. Maintain joint mobility and muscle strength.

a. Provide ROM & isometric exercises.

b. Ensure proper body alignment.

c. Change client’s position frequently.

4. Promote comfort / relief of pain.

a. Administer medications as ordered:

Aspirin & NSAID: most commonly used

Corticosteroids (Intra-articular injections): to relieve

pain & improve mobility.

b. Apply heat or ice as ordered (e.g. warm baths,

compresses, hot packs): to reduce pain.

5. Prepare client for joint replacement surgery if necessary.

6. Provide client teaching and discharge planning concerning

a. Used of prescribed medications and side effects

b. Importance of rest periods

c. Measures to relieve strain on joints

d. ROM and isometric exercises

e. Maintenance of a well-balanced diet

f. Use of heat/ice as ordered.

Gout

A disorder of purine metabolism; causes high levels of uric

acid in the blood & the precipitation of urate crystals in the

joints

Inflammation of the joints caused by deposition of urate

crystals in articular tissue

Incident Rate

1. Occurs most often in males

2. Familial tendency

S/sx

1. Joint pain

2. Redness

3. Heat

4. Swelling

5. Joints of foot (especially great toe) & ankle most commonly

affected (acute gouty arthritis stage)

6. Headache

7. Malaise

8. Anorexia

9. Tachycardia

10. Fever

11. Tophi in outer ear, hands & feet (chronic tophaceous stage)

Dx

1. CBC: uric acid elevated

Medical Management

1. Drug therapy

a. Acute attack:

Colchicine IV or PO: discontinue if diarrhea occurs

NSAID: Indomethacin (Indocin)

Naproxen (Naprosyn)

Phenylbutazone (Butazolidin)

b. Prevention of attacks

Uricosuric agents: increase renal excretion of uric

acid

Probenecid (Benemid)

Sulfinpyrazone (Anturanel)

Allopurinal (Zyloprim): inhibits uric acid formation

2. Low-purine diet may be recommended

3. Joint rest & protection

4. Heat or cold therapy


1. Assess joints for pain, motion & appearance.

2. Provide bed rest & joint immobilization as ordered.

3. Administer anti-gout medications as ordered.

4. Administer analgesics as ordered: for pain

5. Increased fluid intake to 2000-3000 ml/day: to prevent

formation of renal calculi.

6. Apply local heat or cold as ordered: to reduce pain

7. Apply bed cradle: to keep pressure of sheets off joints.


a. Medications & their side effects

b. Modifications for low-purine diet: avoidance of shellfish,

liver, kidney, brains, sweetbreads, sardines, anchovies

c. Limitation of alcohol use

d. Increased in fluid intake

e. Weight reduction if necessary

f. Importance of regular exercise

Systemic Lupus Erythematosus (SLE)

Chronic connective tissue disease involving multiple organ

systems

Incident Rate

1. Occurs most frequently in young women


1. Cause unknown

2. Immune

3. Genetic & viral factors have all been suggested

Pathophysiology

1. A defect in body’s immunologic mechanisms produces

autoantibodies in the serum directed against components of

the client’s own cell nuclei.

2. Affects cells throughout the body resulting in involvement of

many organs, including joints, skin, kidney, CNS &

cardiopulmonary system.

S/sx

1. Fatigue

2. Fever

3. Anorexia

4. Weight loss

5. Malaise

6. History of remissions & exacerbations

7. Joint pain

8. Morning stiffness

9. Skin lesions

Erythematous rash on face, neck or extremities may

occur

Butterfly rash over bridge of nose & cheeks

Photosensitivity with rash in areas exposed to sun

10. Oral or nasopharyngeal ulcerations

11. Alopecia

12. Renal system involvement

Proteinuria

Hematuria

Renal failure

13. CNS involvement

Peripheral neuritis

Seizures

Organic brain syndrome

Psychosis

14. Cardiopulmonary system involvement

Pericarditis

Pleurisy


Dx

1. ESR: elevated

2. CBC: RBC anemia, WBC & platelet counts decreased

3. Anti-nuclear antibody test (ANA): positive

4. Lupus Erythematosus (LE prep): positive

5. Anti-DNA: positive

6. Chronic false-positive test for syphilis

Medical Management

1. Drug therapy

a. Aspirin & NSAID: to relieve mild symptoms such as fever

& arthritis

b. Corticosteroids: to suppress the inflammatory response

in acute exacerbations or severe disease

c. Immunosuppressive agents: to suppress the immune

response when client unresponsive to more

conservative therapy

Azathioprine (Imuran)

Cyclophosphamide (Cytoxan)

2. Plasma exchange: to provide temporary reduction in

amount of circulating antibodies.

3. Supportive therapy: as organ systems become involved.

54

54


1. Assess symptoms to determine systems involved.

2. Monitor vital signs, I&O, daily weights.

3. Administer medications as ordered.

4. Institute seizure precautions & safety measures: with CNS

involvement.

5. Provide psychologic support to client / significant others.

6. Provide client teaching & discharge planning concerning

a. Disease process & relationship to symptoms

b. Medication regimen & side effects.

c. Importance of adequate rest.

d. Use of daily heat & exercises as prescribed: for arthritis.

e. Need to avoid physical or emotional stress

f. Maintenance of a well-balanced diet

g. Need to avoid direct exposure to sunlight: wear hat &

other protective clothing

h. Need to avoid exposure to persons with infections

i. Importance of regular medical follow-up

j. Availability of community agencies

Osteomyelitis

Infection of the bone and surrounding soft tissues, most

commonly caused by S. aureus.

Infection may reach bone through open wound (compound

fracture or surgery), through the bloodstream, or by direct

extension from infected adjacent structures.

Infections can be acute or chronic; both cause bone

destruction.

S/sx

1. Malaise

2. Fever

3. Pain & tenderness of bone

4. Redness & swelling over bone

5. Difficulty with weight-bearing

6. Drainage from wound site may be present.

Dx

1. CBC: WBC elevated

2. Blood cultures: may be positive

3. ESR: may be elevated


1. Administer analgesics & antibiotics as ordered.

2. Use sterile techniques during dressing changes.

3. Maintain proper body alignment & change position

frequently: to prevent deformities.

4. Provide immobilization of affected part as ordered.

5. Provide psychologic support & diversional activities

(depression may result from prolonged hospitalization)

6. Prepare client for surgery if indicated.

Incision & drainage: of bone abscess

Sequestrectomy: removal of dead, infected bone &

cartilage

Bone grafting: after repeated infections

Leg amputation


Use of prescribed oral antibiotic therapy & side effects

Importance of recognizing & reporting signs &

complications (deformity, fracture) or recurrence

FRACTURES

A. General information

1.

B. Medical management

C. Assessment findings

D. Nursing interventions

Overview of Anatomy & Physiology Gastro Intestinal Track System

The primary function of GIT are the movement of food,

digestion, absorption, elimination & provision of a

continuous supply of the nutrients electrolytes & H2O.

Upper alimentary canal: function for digestion

Mouth

Consist of lips & oral cavity

Provides entrance & initial processing for nutrients &

sensory data such as taste, texture & temperature

Oral Cavity: contains the teeth used for mastication &

the tongue which assists in deglutition & the taste

sensation & mastication

Salivary gland: located in the mouth produce secretion

containing pyalin for starch digestion & mucus for

lubrication

Pharynx: aids in swallowing & functions in ingestion by

providing a route for food to pass from the mouth to the

esophagus

Esophagus

Muscular tube that receives foods from the pharynx &

propels it into the stomach by peristalsis

Stomach

Located on the left side of the abdominal cavity occupying

the hypochondriac, epigastric & umbilical regions

Stores & mixes food with gastric juices & mucus producing

chemical & mechanical changes in the bolus of food

The secretion of digestive juice is stimulated by

smelling, tasting & chewing food which is known as

cephalic phase of digestion

The gastric phase is stimulated by the presence of food

in the stomach & regulated by neural stimulation via

PNS & hormonal stimulation through secretion of gastrin

by the gastric mucosa

After processing in the stomach the food bolus called

chyme is released into the small intestine through the

duodenum

Two sphincters control the rate of food passage

Cardiac Sphincter: located at the opening between the

esophagus & stomach

Pyloric Sphincter: located between the stomach &

duodenum

Three anatomic division

Fundus

Body

Antrum

Gastric Secretions:

Pepsinogen: secreted by the chief cells located in the

fundus aid in CHON digestion

Hydrocholoric Acid: secreted by parietal cells, function

in CHON digestion & released in response to gastrin

Intrinsic Factor: secreted by parietal cell, promotes

absorption of Vit B12

Mucoid Secretion: coat stomach wall & prevent auto

digestion

1st half of duodenum

Middle Alimentary canal: Function for absorption; Complete

absorption: large intestine

Small Intestines

Composed of the duodenum, jejunum & ileum

Extends from the pylorus to the ileocecal valve which

regulates flow into the large intestines to prevent reflux to

the into the small intestine

Major function: digestion & absorption of the end product of

digestion

Structural Features:

Villi (functional unit of the small intestines): finger like

projections located in the mucous membrane;

containing goblet cells that secrets mucus & absorptive

cells that absorb digested food stuff

Crypts of Lieberkuhn: produce secretions containing

digestive enzymes

Brunner’s Gland: found in the submucosaof the

duodenum, secretes mucus

2nd half of duodenum

Jejunum

Ileum

1st half of ascending colon

Lower Alimentary Canal: Function: elimination

Large Intestine

Divided into four parts:

55

55

Cecum (with appendix)

Colon (ascending, transverse, descending, sigmoid)

Rectum

Anus

Serves as a reservoir for fecal material until defecation

occurs

Function: to absorb water & electrolytes

MO present in the large intestine: are responsible for small

amount of further breakdown & also make some vitamins

Amino Acids: deaminated by bacteria resulting in

ammonia which is converted to urea in the liver

Bacteria in the large intestine: aid in the synthesis of

vitamin K & some of the vitamin B groups

Feces (solid waste): leave the body via rectum & anus

Anus: contains internal sphincter (under involuntary

control) & external sphincter (voluntary control)

Fecal matter: usually 75% water & 25% solid wastes

(roughage, dead bacteria, fats, CHON, inorganic matter)

a. 2nd half of ascending colon

b. Transverse

c. Descending colon

d. Sigmoid

e. Rectum

Accessory Organ

Liver

Largest internal organ: located in the right hypochondriac &

epigastric regions of the abdomen

Liver Loobules: functional unit of the liver composed of

hepatic cells

Hepatic Sinusoids (capillaries): are lined with kupffer cells

which carry out the process of phagocytosis

Portal circulation brings blood to the liver from the stomach,

spleen, pancreas & intestines

Function:

Metabolism of fats, CHO & CHON: oxidizes these

nutrient for energy & produces compounds that can be

stored

Production of bile

Conjugation & excretion (in the form of glycogen, fatty

acids, minerals, fat-soluble & water-soluble vitamins) of

bilirubin

Storage of vitamins A, D, B12 & iron

Synthesis of coagulation factors

Detoxification of many drugs & conjugation of sex

hormones

Salivary gland

Verniform appendix

Liver

Pancreas: auto digestion

Gallbladder: storage of bile

Biliary System

Consist of the gallbladder & associated ductal system (bile

ducts)

Gallbladder: lies under the surface of the liver

Function: to concentrate & store bile

Ductal System: provides a route for bile to reach the

intestines

Bile: is formed in the liver & excreted into hepatic duct

Hepatic Duct: joins with the cystic duct (which drains

the gallbladder) to form the common bile duct

If the sphincter of oddi is relaxed: bile enters the duodenum,

if contracted: bile is stored in gallbladder

Pancreas

Positioned transversely in the upper abdominal cavity

Consist of head, body & tail along with a pancreatic duct

which extends along the gland & enters the duodenum via

the common bile duct

Has both exocrine & endocrine function

Function in GI system: is exocrine

Exocrine cells in the pancreas secretes:

Trypsinogen & Chymotrypsin: for protein digestion

Amylase: breakdown starch to disacchardes

Lipase: for fat digestion

Endocrine function related to islets of langerhas

Physiology of Digestion & Absorption

Digestion: physical & chemical breakdown of food into

absorptive substance

Initiate in the mouth where the food mixes with saliva &

starch is broken down

Food then passes into the esophagus where it is

propelled into the stomach

In the stomach food is processed by gastric secretions

into a substance called chyme

In the small intestines CHO are hydrolyzed to

monosaccharides, fats to glycerol & fatty acid & CHON

to amino acid to complete the digestive process

When chymes enters the duodenum, mucus is

secreted to neutralized hydrocholoric acid, in

response to release secretin, pancreas releases

bicarbonate to neutralized acid chyme

Cholecystokinin & Pancreozymin (CCKPZ)

Are produced by the duodenal mucosa

Stimulate contraction of the gallbladder along

with relaxation of the sphincter of oddi (to allow

bile flow from common bile duct into the

duodenum) & stimulate release of the

pancreatic enzymes

Salivary Glands

1. Parotid – below & front of ear

2. Sublingual

3. Submaxillary

- Produces saliva – for mechanical digestion

- 1200 -1500 ml/day - saliva produced

Disorder of the GIT

Peptic Ulcer Disease (PUD)

Gastric Ulcer

Ulceration of the mucosal lining of the stomach

Most commonly found in the antrum

Excoriation / erosion of submucosa & mucosal lining due to:

Hypersecretion of acid: pepsin

Decrease resistance to mucosal barrier

Caused by bacterial infection: Helicobacter Pylori

Doudenal Ulcer

Most commonly found in the first 2 cm of the duodenum

Characterized by gastric hyperacidity & a significant rate of

gastric emptying

Predisposing factor

Smoking: vasoconstriction: effect GIT ischemia

Alcohol Abuse: stimulates release of histamine: Parietal cell

release Hcl acid = Ulceration

Emotional Stress

Drugs:

Salicylates (Aspirin)

Steroids

Butazolidin

S/sx

Gastric Ulcer

Duodenal Ulcer

Site Antrum or lesser

curvature

Duodenal bulb

Pain 30 min-1 hr

after eating

Left

epigastrium

Gaseous &

burning

Not usually

relieved by

food &

antacid

2-3 hrs after

eating

Mid

epigastrium

Cramping &

burning

Usually

relieved by

food &

antacid

12 MN –

3am pain

Hypersecreti

on

Normal

gastric acid

secretion

Increased

gastric acid

secretion

Vomiting Common Not

common

56

56

Hemorrhage Hematemeis Melena

Weight Weight loss Weight gain

Complication

s

Stomach

cause

Hemorrhage

Perforation

High Risk 60 years old 20 years old

Dx

Hgb & Hct: decrease (if anemic)

Endoscopy: reveals ulceration & differentiate ulceration

from gastric cancer

Gastric Analysis: normal gastric acidity

Upper GI series: presence of ulcer confirm

Medical Management

1. Supportive:

Rest

Bland diet

Stress management

2. Drug Therapy:

Antacids: neutralizes gastric acid

Aluminum hydroxide: binds phosphate in the GIT &

neutralized gastric acid & inactivates pepsin

Magnesium & aluminum salt: neutralized gastric

acid & inactivate pepsin if pH is raised to >=4

Aluminum containing Antacids Magnesium

containing Antacids

Ex. Aluminum OH gel (Amphojel) Ex. Milk of Magnesia

SE: Constipation SE: Diarrhea

Maalox

SE: fever

Histamines (H2) receptor antagonist: inhibits gastric

acid secretion of parietal cells

Ranitidine (Zantac): has some antibacterial action

against H. pylori

Cimetidine (Tagamet)

Famotidine (Pepcid)

Anticholinergic:

Atropine SO4: inhibit the action of acetylcholine at

post ganglionic site (secretory glands) results

decreases GI secretions

Propantheline: inhibit muscarinic action of

acetylcholine resulting decrease GI secretions

Proton Pump Inhibitor: inhibit gastric acid secretion

regardless of acetylcholine or histamine release

Omeprazole (Prilosec): diminished the accumulation

of acid in the gastric lumen & healing of duodenal

ulcer

Pepsin Inhibitor: reacts with acid to form a paste that

binds to ulcerated tissue to prevent further destruction

by digestive enzyme pepsin

Sucralfate (Carafate): provides a paste like subs that

coats mucosal lining of stomach

Metronidazole & Amoxacillin: for ulcer caused by

Helicobacter Pylori

3. Surgery:

Gastric Resection

Anastomosis: joining of 2 or more hollow organ

Subtotal Gastrectomy: Partial removal of stomach

Before surgery for BI or BII

Do Vagotomy (severing or cutting of vagus

nerve) & Pyloroplasty (drainage) first

Billroth I (Gastroduodenostomy)

Removal of ½ of

stomach &

anastomoses of gastric

stump to the

duodenum.

Billroth II (Gastrojejunostomy)

Removal of ½ -3/4 of

stomach & duodenal bulb

& anastomostoses of

gastric stump to jejunum.

Nursing Intervention Post op

1. Monitor NGT output

Immediately post op should be bright red

Within 36-42 hrs: output is yellow green

After 42 hrs: output is dark red

2. Administer medication

Analgesic

Antibiotic

Antiemetics

3. Maintain patent IV line

4. Monitor V/S, I&O & bowel sounds

5. Complications:

Hemorrhage: Hypovolemic shock: Late signs: anuria

Peritonitis

Paralytic ileus: most feared

Hypokalemia

Thromobphlebitis

Pernicious anemia



2. Diet: bland, non irritating, non spicy

3. Avoid caffeine & milk / milk products: Increase gastric acid

secretion


a. Medical Regimen

Take medication at prescribe time

Have antacid available at all times

Recognized situation that would increase the need

for antacids

Avoid ulcerogenic drugs: salicylates, steroids

Know proper dosage, action & SE

b. Proper Diet

Bland diet consist of six meals / day

Eat slowly

Avoid acid producing substance: caffeine, alcohol,

highly seasoned food

Avoid stressfull situation at mealtime

Plan rest period after meal

Avoid late bedtime snacks

c. Avoidance of stress-producing situation & development

of stress production methods

Relaxation techniques

Exercise

Biofeedback

Dumping syndrome

Abrupt emptying of stomach content into the intestine

Rapid gastric emptying of hypertonic food solutions

Common complication of gastric surgery

Appears 15-20 min after meal & last for 20-60 min

Associated with hyperosmolar CHYME in the jejunum which

draws fluid by osmosis from the extracellular fluid into the

bowel. Decreased plasma volume & distension of the bowel

stimulates increased intestinal motility

S/sx

1. Weakness

2. Faintness

3. Feeling of fullness

4. Dizziness

5. Diaphoresis

6. Diarrhea

7. Palpitations


1. Avoid fluids in chilled solutions

2. Small frequent feeding: six equally divided feedings

3. Diet: decrease CHO, moderate fats & CHON

4. Flat on bed 15-30 min after q feeding

Disorders of the Gallbladder

Cholecystitis / Cholelithiasis

Cholecystitis:

Acute or chronic inflammation of the gallbladder

Most commonly associated with gallstones

Inflammation occurs within the walls of the gallbladder

& creates thickening accompanied by edema

Consequently there is impaired circulation, ischemia &

eventually necrosis

Cholelithiasis:

Formation of gallstones & cholesterol stones

Inflammation of gallbladder with gallstone formation.

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57

Predisposing Factor:

1. High risk: women 40 years old

2. Post menopausal women: undergoing estrogen therapy

3. Obesity


5. Hyperlipidemia

6. Neoplasm

S/sx:

1. Severe Right abdominal pain (after eating fatty food):

Occurring especially at night

2. Intolerance of fatty food

3. Anorexia

4. N/V

5. Jaundice

6. Pruritus

7. Easy bruising

8. Tea colored urine

9. Steatorrhea

Dx

1. Direct Bilirubin Transaminase: increase

2. Alkaline Phosphatase: increase

3. WBC: increase

4. Amylase: increase

5. Lipase: increase

6. Oral cholecystogram (or gallbladder series): confirms

presence of stones

Medical Management

1. Supportive Treatment: NPO with NGT & IV fluids

2. Diet modification with administration of fat soluble vitamins

3. Drug Therapy

Narcotic analgesic: DOC: Meperdipine Hcl (Demerol): for

pain

(Morpine SO4: is contraindicated because it causes

spasm of the Sphincter of Oddi)

Antocholinergic: (Atrophine SO4): for pain

(Anticholinergic: relax smooth muscles & open bile

ducts)

Antiemetics: Phenothiazide (Phenergan): with anti

emetic properties

4. Surgery: Cholecystectomy / Choledochostomy


1. Administer pain medication as ordered & monitor effects

2. Administer IV fluids as ordered

3. Diet: increase CHO, moderate CHON, decrease fats

4. Meticulous skin care: to relieved priritus

Disorders of the Pancreas

Pancreatitis

An inflammatory process with varying degrees of pancreatic

edema, fat necrosis or hemorrhage

Proteolytic & lipolytic pancreatic enzymes are activated in

the pancreas rather than in the duodenum resulting in

tissue damage & auto digestion of pancreas

Acute or chronic inflammation of pancreas leading to

pancreatic edema, hemorrhage & necrosis due to auto

digestion

Bleeding of Pancreas: Cullen’s sign at umbilicus

Predisposing factors:

1. Chronic alcoholism

2. Hepatobilary disease

3. Trauma

4. Viral infection

5. Penetrating duodenal ulcer

6. Abscesses

7. Obesity

8. Hyperlipidemia

9. Hyperparathyroidism

10. Drugs: Thiazide, steroids, diuretics, oral contraceptives

S/Sx:

1. Severe left upper epigastric pain radiates from back & flank

area: aggravated by eating with DOB

2. N/V

3. Tachycardia

4. Palpitation: due to pain

5. Dyspepsia: indigestion

6. Decrease bowel sounds

7. (+) Cullen’s sign: ecchymosis of umbilicus

Hemorrhage

8. (+) Grey Turner’s spots: ecchymosis of flank area

9. Hypocalcemia

Dx

1. Serum amylase & lipase: increase

2. Urinary amylase: increase

3. Blood Sugar: increase

4. Lipids Level: increase

5. Serum Ca: decrease

6. CT Scan: shows enlargement of the pancreas

Medical Management

1. Drug Therapy

Narcotic Analgesic: for pain

Meperidine Hcl (Demerol)

Don’t give Morphine SO4: will cause spasm of

Sphincter of Oddi

Smooth muscle relaxant: to relieve pain

Papaverine Hcl

Anticholinergic: to decrease pancreatic stimulation

Atrophine SO4

Propantheline Bromide (Profanthene)

Antacids: to decrease pancreatic stimulation

Maalox

H2 Antagonist: to decrease pancreatic stimulation

Ranitidin (Zantac)

Vasodilators: to decrease pancreatic stimulation

Nitroglycerine (NTG)

Ca Gluconate: to decrease pancreatic stimulation

2. Diet Modification

3. NPO (usually)

4. Peritoneal Lavage

5. Dialysis



2. Withhold food & fluid & eliminate odor: to decrease

pancreatic stimulation / aggravates pain

3. Assist in Total Parenteral Nutrition (TPN) or

hyperalimentation

Complication of TPN

Infection

Embolism

Hyperglycemia

4. Institute non-pharmacological measures: to decrease pain

Assist client to comfortable position: Knee chest or fetal

like position

Teach relaxation techniques & provide quiet, restful

environment


Dietary regimen when oral intake permitted

High CHO, CHON & decrease fats

Eat small frequent meal instead of three large ones

Avoid caffeine products

Eliminate alcohol consumption

Maintain relaxed atmosphere after meals

Report signs of complication

Continued N/V

Abdominal distension with feeling of fullness

Persistent weight loss

Severe epigastric or back pain

Frothy foul smelling bowel movement

Irritability, confusion, persistent elevation of

temperature (2 day)

Apendicitis

Inflammation of the appendix that prevents mucus from

passing into the cecum

Inflammation of verniform appendix

If untreated: ischemia, gangrene, rupture & peritonitis

May cause by mechanical obstruction (fecalith, intestinal

parasites) or anatomic defect

May be related to decrease fiber in the diet

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Predisposing factor:

1. Microbial infection

2. Feacalith: undigested food particles like tomato seeds,

guava seeds etc.

3. Intestinal obstruction

S/Sx:

1. Pathognomonic sign: (+) rebound tenderness

2. Low grade fever

3. N/V

4. Decrease bowel sound

5. Diffuse pain at lower Right iliac region

6. Late sign: tachycardia: due to pain

Dx

1. CBC: mild leukocytosis: increase WBC

2. PE: (+) rebound tenderness (flex Right leg, palpate Right

iliac area: rebound)

3. Urinalysis: elevated acetone in urine

Medical Management

Surgery: Appendectomy 24-45 hrs


1. Administer antibiotics / antipyretic as ordered

2. Routinary pre-op nursing measures:

Skin prep

NPO

Avoid enema, cathartics: lead to rupture of appendix

3. Don’t give analgesic: will mask pain

Presence of pain means appendix has not ruptured

4. Avoid heat application: will rupture appendix

5. Monitor VS, I&O bowel sound

Nursing Intervention post op

1. If (+) Pendrose drain (rubber drain inserted at surgical

wound for drainage of blood, pus etc): indicates rupture of

appendix

2. Position the client semi-fowlers or side lying on right: to

facilitate drainage

3. Administer Meds:

Analgesic: due post op pain

Antibiotics: for infection

Antipyretics: for fever (PRN)

4. Monitor VS, I&O, bowel sound

5. Maintain patent IV line

6. Complications: Peritonitis, Septicemia

Liver Cirrhosis

Chronic progressive disease characterized by inflammation,

fibrosis & degeneration of the liver parenchymal cell

Destroyed liver cell are replaced by scar tissue, resulting in

architectural changes & malfunction of the liver

Lost of architectural design of liver leading to fat necrosis &

scarring

Types

Laennec’s Cirrhosis:

Associated with alcohol abuse & malnutrition

Characterized by an accumulation of fat in the liver cell

progressing to widespread scar formation

Postnecrotic Cirrhosis

Result in severe inflammation with massive necrosis as a

complication of viral hepatitis

Cardiac Cirrhosis

Occurs as a consequence of right sided heart failure

Manifested by hepatomegaly with some fibrosis

Biliary Cirrhosis

Associated with biliary obstruction usually in the common bile

duct

Results in chronic impairment of bile excretion

S/sx

Fatigue

Anorexia

N/V

Dyspepsia: Indigestion

Weight loss

Flatulence

Change (Irregular) bowel habit

Ascites

Peripheral edema

Hepatomegaly: pain located in the right upper quadrant

Atrophy of the liver

Fetor hepaticus: fruity, musty odor of chronic liver

disease

Aterixis: flapping of hands & tremores

Hard nodular liver upon palpation

Increased abdominal girth

Changes in moods

Alertness & mental ability

Sensory deficits

Gynecomastia

Decrease of pubic & axilla hair in males

Amenorrhea in female

Jaundice

Pruritus or urticaria

Easy bruising

Spider angiomas on nose, cheeks, upper thorax &

shoulder

Palmar erythema

Muscle atrophy

Dx

Liver enzymes: increase

SGPT (ALT)

SGOT (AST)

LDH Alkaline Phosphate

Serum cholesterol & ammonia: increase

Indirect bilirubin: increase

CBC: pancytopenia

PT: prolonged

Hepatic Ultrasonogram: fat necrosis of liver lobules


CBR with bathroom privileges

Encourage gradual, progressive, increasing activity with

planned rest period

Institute measure to relieve pruritus

Do not use soap & detergent

Bathe with tepid water followed by application of emollient

lotion

Provide cool, light, non-constrictive clothing

Keep nail short: to avoid skin excoriation from scratching

Apply cool, moist compresses to pruritic area

Monitor VS, I & O

Prevent Infection

Prevent skin breakdown: by turning & skin care

Provide reverse isolation for client with severe leukopenia:

handwashing technique

Monitor WBC

Diet:

Small frequent meals

Restrict Na!

High calorie, low to moderate CHON, high CHO, low fats with

supplemental Vit A, B-complex, C, D, K & folic acid

Monitor / prevent bleeding

Measure abdominal girth daily: notify MD

With pt daily & assess pitting edema

Administer diuretics as ordered

Provide client teaching & discharge planning

Avoidance of hepatotoxicity drug: sedative, opiates or OTC

drugs detoxified by liver

How to assess weight gain & increase abdominal girth

Avoid person with upper respiratory infection

Reporting signs of reccuring illness (liver tenderness, increase

jaundice, increase fatigue, anorexia)

Avoid all alcohol

Avoid straining stool vigorous blowing of nose & coughing: to

decrease incidence of bleeding

Complications:

Ascites: accumolation of free fluid in abdominal cavity


Meds: Loop diuretics: 10-15 min effect

Assist in abdominal paracentesis: aspiration of fluid

Void before paracentesis: to prevent accidental puncture of

bladder as trochar is inserted

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Bleeding esophageal varices: Dilation of esophageal veins


Administer meds:

Vit K

Pitrisin or Vasopresin (IM)

NGT decompression: lavage

Give before lavage: ice or cold saline solution

Monitor NGT output

Assist in mechanical decompression

Insertion of sengstaken-blackemore tube

3 lumen typed catheter

Scissors at bedside to deflate balloon.

Hepatic encephalopathy


Assist in mechanical ventilation: due coma

Monitor VS, neuro check

Siderails: due restless

Administer meds

Laxatives: to excrete ammonia

Overview of Anatomy & Physiology Of GUT System

GUT: Genito-urinary tract

GUT includes the kidneys, ureters, urinary bladder, urethra & the

male & female genitalia

Function:

Promote excretion of nitrogenous waste products

Maintain F&E & acid base balance

Kidneys

Two of bean shaped organ that lie in the retroperitonial

space on either side of the vertebral column

Retroperitonially (back of peritoneum) on either side of

vertebral column

Adrenal gland is on top of each kidneys

Encased in Bowmans’s capsule

Renal Parenchyma

Cortex

Outermost layer

Site of glomeruli & proximal & distal tubules of nephron

Medulla

Middle layer

Formed by collecting tubules & ducts

Renal Sinus & Pelvis

Papillae

Projection of renal tissues located at the tip of the renal

pyramids

Calices

Minor Calyx: collects urine flow from collecting ducts

Major Calyx: directs urine from renal sinus to renal pelvis

Urine flows from renal pelvis to ureters

Nephron

Functional unit of the kidney

Basic living unit

Renal Corpuscle (vascular system of nephron)

Bowman’s Capsule:

Portion of the proximal tubule surrounds the glomerulus

Glomerulus:

Capillary network permeable to water, electrolytes,

nutrients & waste

Impermeable to large CHON molecules

Filters blood going to kidneys

Renal Tubule

Divided into proximal convoluted tubule, descending

loop of Henle, acending loop of Henle, distal

convoluted tubule & collecting ducts

Ureters

Two tubes approximately 25-35 cm long

Extend from the renal pelvis to the pelvic cavity where they

enter the bladder, convey urine from the kidney to the

bladder

Passageway of urine to bladder

Ureterovesical valve: prevent backflow of urine into ureters

Bladder

Located behind the symphisis pubis

Composed of muscular elastic tissue that makes it distensible

Serve s as reservoir of urine (capable of holding 1000-1800 ml &

500 ml moderately full)

Internal & external urethral sphincter controls the flow of urine

Urge to void stimulated by passage of urine past the internal

sphincter (involuntary) to the upper urethra

Relaxation of external sphincter (voluntary) produces emptying

of the bladder (voiding)

Urethra

Small tube that extends from the bladder to the exterior of

the body

Passage of urine, seminal & vaginal fluids.

Females: located behind the symphisis pubis & anterior

vagina & approximately 3-5 cm

Males: extend the entire length of the penis &

approximately 20 cm

Function of kidneys

Kidneys remove nitrogenous waste & regulates F & E

balance & acid base balance

Urine is the end product

Urine formation: 25 % of total cardiac output is received by kidneys

Glomerular Filtration

Ultrafiltration of blood by the glomerulus, beginning of urine

formation

Requires hydrostatic pressure & sufficient circulating volume

Pressure in bowman’s capsule opposes hydrostatic pressure &

filtration

If glomerular pressure insufficient to force substance out of the

blood into the tubules filtrate formation stops

Glomerular Filtration Rate (GFR)

Amount of blood filtered by the glomeruli in a given time

Normal: 125 ml / min

Filtrate formed has essentially same composition as blood

plasma without the CHON; blood cells & CHON are

usually too large to pass the glomerular membrane

Tubular Function

Tubules & collecting ducts carry out the function of

reabsorption, secretion & excretion

Reabsorption of H2O & electrolytes is controlled by

anitdiuretics hormones (ADH) released by the

pituitary & aldosterone secreted by the adrenal

glands

Proximal Convoluted Tubule

Reabsorb the ff:

80% of F & E

H2O

Glucose

Amino acids

Bicarbonate

Secretes the ff:

Organic substance

Waste

Loop of Henli

Reabsorb the ff:

Na & Chloride in the ascending limb

H2O in the descending limb

Concentrate / dilutes urine

Distal Convoluted Tubule

Secretes the ff:

Potassium

Hydrogen ions

Ammonia

Reabsorb the ff:

H2O

Bicarbonate

Regulate the ff:

Ca

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Phosphate concentration

Collecting Ducts

Received urine from distal convoluted tubules & reabsorb H2O

(regulated by ADH)

Normal Adult: produces 1 L /day of urine

Regulation of BP

Through maintenance of volume (formation / excretion of urine)

Rennin-angiotensin system is the kidneys controlled mechanism

that can contribute to rise the BP

When the BP drops the cells of the glomerulus release rennin

which then activates angiotensin to cause vasoconstriction.

Filtration – Normal GFR/ min is 125 ml of blood

Tubular reabsorption – 124ml of ultra infiltrates (H2O & electrolytes

is for reabsorption)

Tubular secretion – 1 ml is excreted in urine

Regulation of BP:


Ex CS – hypovolemia – decrease BP going to kidneys

Activation of RAAS

Release of Renin (hydrolytic enzyme) at

juxtaglomerular apparatus

Angiotensin I mild vasoconstrictor

Angiotensin II vasoconstrictor

Adrenal cortex increase CO increase PR

Aldosterone

Increase BP

Increase Na &

H2O reabsorption

Hypervolemia

Color – amber

Odor – aromatic

Consistency – clear or slightly turbid

pH – 4.5 – 8

Specific gravity – 1.015 – 1.030

WBC/ RBC – (-)

Albumin – (-)

E coli – (-)

Mucus thread – few

Amorphous urate (-)

UTI

CYSTITIS

Inflammation of bladder due to bacterial infection


Microbial invasion: E. coli

High risk: women

Obstruction

Urinary retention

Increase estrogen levels

Sexual intercourse

S/Sx:

Pain: flank area

Urinary frequency & urgency

Burning pain upon urination

Dysuria

Hematuria

Nocturia

Fever

Chills

Anorexia

Gen body malaise

Dx

Urine culture & sensitivity: (+) to E. coli


Force fluid: 3000 ml

Warm sitz bath: to promote comfort

Monitor & assess urine for gross odor, hematuria & sediments

Acid Ash Diet: cranberry, vit C: OJ: to acidify urine & prevent

bacterial multiplication

Administer Medication as ordered:

Systemic Antibiotics

Ampicillin

Cephalosporin

Aminoglycosides

Sulfonamides

Co-trimaxazole (Bactrim)

Gantrism (Gantanol)

Antibacterial

Nitrofurantoin (Macrodantin)

Methenamine Mandelate (Mandelamine)

Nalixidic Acid (NegGram)

Urinary Tract Anagesic

Urinary antiseptics: Mitropurantoin (Macrodantin)

Urinary analgesic: Pyridium

Provide client teachings & discharge planning

Importance of Hydration

Void after sex: to avoid stagnation

Female: avoids cleaning back & front (should be front to

back)

Bubble bath, Tissue paper, Powder, perfume

Complications: Pyelonephritis

Pyelonephritis

Acute / chronic inflammation of 1 or 2 renal pelvis of

kidneys leading to tubular destruction & interstitial

abscess formation

Acute: infection usually ascends from lower urinary tract

Chronic: a combination of structural alteration along

with infection major cause is ureterovesical reflux

with infected urine backing up into ureters & renal

pelvis

Recurrent infection will lead to renal parenchymal

deterioration & Renal Failure


Microbial invasion

E. Coli

Streptococcus

Urinary retention /obstruction

Pregnancy

DM

Exposure to renal toxins

S/sx:

Acute Pyelonephritis

Severe flank pain or dull ache

Costovertibral angle pain / tenderness

Fever

Chills

N/V

Anorexia

Gen body malaise

Urinary frequency & urgency

Nocturia

Dsyuria

Hematuria

Burning sensation on urination

Chronic Pyelonephritis: client usually not aware of

disease

Bladder irritability

Slight dull ache over the kidney

Chronic Fatigue

Weight loss

Polyuria

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Polydypsia

HPN

Atrophy of the kidney

Medical Management

Urinary analgesic: Peridium

Acute

Antibiotics

Antispasmodic

Surgery: removal of any obstruction

Chronic

Antibiotics

Urinary Antiseptics

Nitrofurantoin (macrodantin)

SE: peripheral neuropathy

GI irritation

Hemolytic anemia

Staining of teeth

Surgery: correction of structural abnormality if possible

Dx

Urine culture & sensitivity: (+) E. coli & streptococcus

Urinalysis: increase WBC, CHON & pus cells

Cystoscopic exam: urinary obstruction


Provide CBR: acute phase

Monitor I & O

Force fluid

Acid ash diet

Administer medication as ordered

Chronic: possibility of dialysis & transplant if has renal

deterioration

Complication: Renal Failure

Nephrolithiasis / Urolithiasis

Presence of stone anywhere in the urinary tract

Formation of stones at urinary tract

Frequent composition of stones

Calcium

Oxalate

Uric acid

Calcium Oxalate Uric Acid

Milk Cabbage Anchovies

Cranberries Organ meat

Nuts tea Nuts

Chocolates Sardines


Diet: increase Ca & oxalate

Increase uric acid level

Hereditary: gout or calculi

Immobility

Sedentary lifestyle

Hyperparathyroidism

S/sx

Abdominal or flank pain

Renal colic

Cool moist skin (shock)

Burning sensation upon urination

Hematuria

Anorexia

N/V

Dx

Intravenous Pyelography (IVP): identifies site of obstruction &

presence of non-radiopaque stones

KUB: reveals location, number & size of stone

Cytoscopic Exam: urinary obstruction

Stone Analysis: composition & type of stone

Urinalysis: indicates presence of bacteria, increase WBC, RBC &

CHON

Medical Management

Surgery

Percutaneous Nephrostomy:

Tube is inserted through skin & underlying tissue into renal

pelvis to remove calculi

Percutaneous Nephrostolithotomy

Delivers ultrasound wave through a probe placed on the

calculus

Extracorporeal Shockwave Lithotripsy:

Non-invasive

Delivers shockwaves from outside of the body to the stone causing

pulverization

Pain management & diet modification


Force fluid: 3000-4000 ml / day

Strain urine using gauze pad: to detect stones & crush all cloths

Encourage ambulation: to prevent stasis

Warm sitz bath: for comfort

Administer narcotic analgesic as ordered: Morphine SO4: to

relieve pain

Application warm compress at flank area: to relieve pain

Monitor I & O

Provide modified diet depending upon the stone consistency

Calcium Stones

Limit milk & dairy products

Provide acid ash diet (cranberry or prune juice, meat, fish,

eggs, poultry, grapes, whole grains): to acidify urine

Take vitamin C

Oxalate Stone

Avoid excess intake of food / fluids high in oxalate

(tea, chocolate, rhubarb, spinach)

Maintain alkaline-ash diet (milk, vegetable, fruits

except cranberry, plums & prune): to alkalinize

urine

Uric Acid Stone

Reduce food high in purine (liver, brain, kidney, venison,

shellfish, meat soup, gravies, legumes)

Maintain alkaline urine

Administer Allopurinol (Zyloprim) as ordered: to decrease uric

acid production: push fluids when giving allopurinol


Prevention of urinary stasis: increase fluid intake especially

during hot weather & illness

Mobility

Voiding whenever the urge is felt & at least twice during night

Adherence to prescribe diet

Complications: Renal Failure

Benign Prostatic Hypertrophy (BPH)

Mild to moderate glandular enlargement, hyperplsia & over

growth of the smooth muscles & connective tissue

As the gland enlarges it compresses the urethra: resulting to

urinary retention

Enlarged prostate gland leading to

Hydroureters: dilation of urethers

Hydronephrosis: dilation of renal pelvis

Kidney stones

Renal failure


High risk: 50 years old & above & 60-70 (3-4x at risk)

Influence of male hormone

S/sx

Urgency, frequency & hesitancy

Nocturia

Enlargement of prostate gland upon palpation by digital

rectal exam

Decrease force & amount of urinary stream

Dysuria

Hematuria

Burning sensation upon urination

Terminal bubbling

Backache

Sciatica: severe pain in the lower back & down the back

of thigh & leg

Dx

Digital rectal exam: enlarged prostate gland

KUB: urinary obstruction

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Cystoscopic Exam: reveals enlargement of prostate gland &

obstruction of urine flow

Urinalysis: alkalinity increase

Specific Gravity: normal or elevated

BUN & Creatinine: elevated (if longstanding BPH)

Prostate-specific Antigen: elevated (normal is < 4 ng /ml)


Prostate message: promotes evacuation of prostatic

fluid

Force fluid intake: 2000-3000 ml unless contraindicated

Provide catheterization

Administer medication as ordered:

Terazosine (Hytrin): relaxes bladder sphincter & make it

easier to urinate

Finasteride (Proscar): shrink enlarge prostate gland

Surgery: Prostatectomy

Transurethral Resection of Prostate (TURP): insertion of a

resectoscope into urethra to excise prostatic tissue

Assist in cystoclysis or continuous bladder irrigation.


Monitor symptoms of infection

Monitor symptoms gross / flank bleeding. Normal

bleeding within 24h

Maintain irrigation or tube patent to flush out clots: to

prevent bladder spasm & distention

Acute Renal Failure

Sudden inability of the kidney to regulate fluid & electrolyte

balance & remove toxic products from the body

Sudden immobility of kidneys to excrete nitrogenous waste

products & maintain F&E balance due to a decrease in GFR

(N 125 ml/min)

Causes

Pre-renal cause: interfering with perfusion & resulting in

decreased blood flow & glomerular filtrate

Inter-renal cause: condiion that cause damage to the nephrons

Post-renal cause: mechanical obstruction anywhere from the

tubules to the urethra

Pre renal cause: decrease blood flow & glomerular filtrate

Ischemia & oliguria

Cardiogenic shock

Acute vasoconstriction

Septicemia

Hypovolemia Decrease

flow to kidneys

Hypotension

CHF

Hemorrhage

Dehydration

Intra-renal cause: involves renal pathology: kidney problem

Acute tubular necrosis

Endocarditis

DM

Tumors

Pyelonephritis

Malignant HPN

Acute Glomerulonephritis

Blood transfision reaction

Hypercalemia

Nephrotoxin (certain antibiotics, X-ray, dyes, pesticides,

anesthesia)

Post renal cause: involves mechanical obstruction

Tumors

Stricture

Blood cloths

Urolithiasis

BPH

Anatomic malformation

S/sx

Oliguric Phase: caused by reduction in glomerular filtration rate

Urine output less than 400 ml / 24 hrs; duration 1-2 weeks

S/sx

Hypernatremia

Hyperkalemia

Hyperphosphotemia

Hypermagnesemia

Hypocalcemia

Metabolic acidosis

Dx

BUN & Creatinine: elevated

Diuretic Phase: slow gradual increase in daily urine output

Diuresis may occur (output 3-5 L / day): due to partially

regenerated tubules inability to concentrate urine

Duration: 2-3 weeks

S/sx

Hyponatremia

Hypokalemia

Hypovolemia

Dx

BUN & Creatinine: elevated

Recovery or Covalescent Phase: renal function stabilized with

gradual improvement over next 3-12 mos


Monitor / maintain F&E balance

Obtain baseline data on usual appearance & amount of

client’s urine

Measure I&O every hour: note excessive losses

Administer IV F&E supplements as ordered

Weight daily

Monitor lab values: assess / treat F&E & acid base

imbalance as needed

Monitor alteration in fluid volume

Monitor V/S. PAP, PCWP, CVP as needed

Monitor I&O strictly

Assess every hour fro hypervolemia

Maintain ventilation

Decrease fluid intake as ordered

Administer diuretics, cardiac glycosides &

hypertensive agent as ordered

Assess every hour for hypovolemia: replace fluid as

ordered

Monitor ECG

Check urine serum osmolality / osmolarity & urine

specific gravity as ordered

Promote optimal nutrition

Administer TPN as ordered

Restrict CHON intake

Prevent complication from impaired mobility

Pulmonary Embolism

Skin breakdown

Contractures

Atelectesis

Prevent infection / fever

Assess sign of infection

Use strict aseptic technique for wound & catheter care

Take temperature via rectal

Administer antipyretics as ordered & cooling blankets

Support clients / significant others: reduce level of anxiety

Provide care for client receiving dialysis


Adherence to prescribed dietary regime

S/sx of recurrent renal disease

Importance of planned rest period

Use of prescribe drugs only

S/sx of UTI or respiratory infection: report to MD

Chronic Renal Failure

Progressive, irreversible destruction of the kidneys that

continues until nephrons are replaced by scar tissue

Loss of renal function gradual

Irreversible loss of kidney function


DM

HPN

Recurrent UTI/ nephritis

Urinary Tract obstruction

Exposure to renal toxins

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Stages of CRF

Diminished Reserve Volume – asymptomatic

Normal BUN & Crea, GFR < 10 – 30%

2. Renal Insufficiency

3. End Stage Renal disease

S/Sx:

N/V

Diarrhea / constipation

Decreased urinary output

Dyspnea

Stomatitis

Hypotension (early)

Hypertension (late)

Lethargy

Convulsion

Memory impairment

Pericardial Friction Rub

HF

Urinary System

Polyuria

Nocturia

Hematuria

Dysuria

Oliguria

Metabolic Disturbance

Azotemia (increase BUN

& Creatinine)

Hyperglycemia

Hyperinsulinemia

CNS

Headache

Lethargy

Disorientation

Restlessness

Memory impairment

GIT

N/V

Stomatitis

Uremic breath

Diarrhea /

constipation

Respiratory

Kassmaul’s resp

Decrease cough

reflex

Hematological

Normocytic anemia

Bleeding tendencies

Fluid & Electrolytes

Hyperkalemia

Hypernatermia

Hypermagnese

mia

Hyperposphate

mia

Hypocalcemia

Metabolic

acidosis

Integumentary

Itchiness /

pruritus

Uremic frost

Dx

Urinalysis: CHON, Na & WBC: elevated

Specific gravity: decrease

Platelets: decrease

Ca: decrease

Medical Management

Diet restriction

Multivitamins

Hematinics

Aluminum Hydroxide Gels

Antihypertensive


Prevent neurologic complication

Monitor for signs of uremia

Fatigue

Loss of appetite

Decreased urine output

Apathy

Confusion

Elevated BP

Edema of face & feet

Itchy skin

Restlessness

Seizures

Monitor for changes in mental functioning

Orient confused client to time, place, date & person

Institute safety measures to protect the client from

falling out of bed

Monitor serum electrolytes, BUN & creatinine as ordered

Promote optimal GI function

Provide care for stomatitis

Monitor N/V & anorexia: administer antiemetics as

ordered

Monitor signs of GI bleeding

Monitor & prevent alteration in F&E balance

Monitor for hyperphosphatemia: administer aluminum

hydroxides gel (amphojel, alternagel) as ordered

Paresthesias

Muscle cramps

Seizures

Abnormal reflex

Maintenance of skin integrity

Provide care for pruritus

Monitor uremic frost (urea crystallization on the skin): bathe

in plain water

Monitor for bleeding complication & prevent injury to client

Monitor Hgb, Hct, platelets, RBC

Hematest all secretions

Administer hematinics as ordered

Avoid IM injections

Maintain maximal cardiovascular function

Monitor BP

Auscultate for pericardial friction rub

Perform circulation check routinely

Administer diuretics as ordered & monitor I&O

Modify digitalis dose as ordered (digitalis is excreted in

kidneys)

Provide care for client receiving dialysis

Disequilibrium syndrome: from rapid removal of urea &

nitrogenous waste prod leading to:

N/V

HPN

Leg cramps

Disorientation

Paresthes

Enforce CBR

Monitor VS, I&O

Meticulous skin care. Uremic frost – assist in bathing

pt

4. Meds:

a.) Na HCO3 – due Hyperkalemia

b.) Kagexelate enema

c.) Anti HPN – hydralazine

d.) Vit & minerals

e.) Phosphate binder

(Amphogel) Al OH gel - S/E constipation

f.) Decrease Ca – Ca gluconate

5. Assist in hemodialysis

Consent/ explain procedure

Obtain baseline data & monitor VS, I&O, wt,

blood exam

Strict aseptic technique

Monitor for signs of complications:

B – bleeding

E – embolism

D – disequilibrium syndrome

S – septicemia

S – shock – decrease in tissue perfusion

Disequilibrium syndrome – from rapid removal of urea &

nitrogenous waste prod leading to:

n/v

HPN

Leg cramps

Disorientation

Paresthesia

Avoid BP taking, blood extraction, IV, at side of shunt or

fistula. Can lead to compression of fistula.

Maintain patency of shunt by:

Palpate for thrills & auscultate for bruits if (+)

patent shunt!

Bedside- bulldog clip

- If with accidental removal of fistula to prevent

embolism.

- Infersole (diastole) – common dialisate used

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7. Complication

- Peritonitis

- Shock

8. Assist in surgery:

Renal transplantation : Complication – rejection.

Reverse isolation

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Medical Surgical Nursing Pinoy

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Transcript of Medical Surgical Nursing Pinoy