Endocrppt 1216137284642326-8
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Transcript of Endocrppt 1216137284642326-8
METABOLISM
ENDOCRINE
SYSTEM
ENDOCRINE GLANDSENDOCRINE GLAND
HORMONES FUNCTIONS
PITUITARY
ANTERIOR
TSH Thyroid to release hormones
LOBE ACTH Adrenal cortex to release hormones
FSH,LH Growth, maturation & function of sex organs
GH/
SOMATOTROPIN
Growth of body tissues & bones
PROLACTIN/
LTH
Development of mammary glands & lactation
ENDOCRINE GLANDS
ENDOCRINE GLAND
HORMONE FUNCTION
PITUITARY
POSTERIOR
LOBE
ADH Regulates water metabolism
OXYTOCIN Stimulate uterine contractions
release of milk
INTERME-
DIATE LOBE
MSH Affects skin pigmentation
ENDOCRINE GLANDSENDOCRINE GLAND
HORMONES FUNCTION
ADRENAL CORTEX
ALDOSTERONE Fluid & electrolyte balance;
Na reabsorption;
K excretion
CORTISOL Glycogenolysis;
Gluconeogenesis
Na & water reabsorption
Antiinflammatory
Stress hormone
SEX
HORMONES
Slightly significant
ENDOCRINE GLANDS
ENDOCRINE
GLAND
HORMONE FUNCTION
ADRENAL MEDULLA
EPINEPHRINE
NOR-
EPINEPHRINE
Increase heart rate & BP
Bronchodilation,
Glycogenolysis
Stress hormone
ENDOCRINE GLANDSENDOCRINE GLAND
HORMONE FUNCTION
THYROID T3 & T4’ Regulate metabolic rate
P,C,F metabolism
Regulate physical & mental growth & development
THYRO-
CALCITONIN
Decrease serum Ca by increasing bone deposition
PARA-
THYROID
PTH Increase serum calcium by promoting bone decalcification
ENDOCRINE GLANDSENDOCRINE
GLAND
HORMONE FUNCTION
PANCREAS
BETA
CELLS
INSULIN Decrease blood glucose by:
Glucose diffusion across cell membrane;
Converts glucose to glycogen
ALPHA
CELLS
GLUCAGON Increase blood glucose by:
Gluconeogenesis
Glycogenolysis
ENDOCRINE GLANDS
ENDOCRINE
GLAND
HORMONES FUNCTION
OVARIES ESTROGEN &
PROGES-
TERONE
Development of secondary sex charac in female
Maturation of sex organs
Sexual functioning
Maintenance of pregnancy
TESTES TESTOS-
TERONE
Development of secondary sex charac in male
Maturation of sex organs
Sexual functioning
HORMONE REGULATIONNEGATIVE FEEDBACK MECHANISM
CHANGING OF BLOOD LEVELS OF CERTAIN SUBSTANCES (e..g CALCIUM & GLUCOSE)
RHYTHMIC PATTERNS OF SECRETION (e.g. CORTISOL, FEMALE REPRODUCTIVE HORMONES)
AUTONOMIC & C.N.S. CONTROL(PITUITARY-HYPOTHALAMIC AXIS,
ADRENAL MEDULLA HORMONES)
NEGATIVE FEEDBACK MECHANISM
DECREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)
PITUITARY GLAND RELEASE OF STIMULATING HORMONE (e.g. TSH)
STIMULATION OF TARGET ORGANS TO PRODUCE & RELEASE HORMONE
(e.g. Thyroid gland release of Thyroxine)
RETURN OF THE NORMAL CONCENTRATION OF HORMONE
NEGATIVE FEEDBACK MECHANISM
INCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)
PITUITARY GLAND IS INHIBITED TORELEASE STIMULATING HORMONE (e.g. TSH)
DECREASED PRODUCTION & SECRETION OF TARGET ORGAN OF THE HORMONE (e.g. Thyroid gland release of Thyroxine)
RETURN OF THE NORMAL CONCENTRATION OF HORMONE
CASE STUDYKatie, an elderly, came in because of palpitations.
VS revealed: 37.9o , 120, 25, 140/ 90
She expressed hyperactivty, sweating, increased appetite & weight loss
CASE STUDY
She claimed history of goiter since her 30’s but no follow-up was done.
What are your nursing plans?
PLANNINGHEALTH PROMOTION IODIZED SALTCONTROLLING WEIGHT
HEALTH MAINTENANCE & RESTORATIONSTEROID THERAPY
STEROID THERAPY
STEROID LEVELS
PITUITARY GLAND IS INHIBITED TO REALEASE ACTH
ENDOGENOUS CORTISOL
PRODUCTION & RELEASE BY ADRENAL MEDULLA
ADRENAL ATROPHY
STEROID THERAPYPHARMACOLOGIC CONSIDERATIONS:
PEPTIC ULCER IN SHORT TERM, HIGH DOSE STEROID TX
ADMINISTER DRUG: HIGHER DOSE IN THE MORNING, TAPERING TO LOWER ONES IN THE AFTERNOON
LAST DOSE @ MEAL TIME TO AVOID INSOMNIA
PALLIATIVE EFFECT
STEROID THERAPYASSESSMENT:
BASELINE STEROID LEVEL IS ASSESSED BEFORE PROLONGED THERAPY IS STARTED TO DETERMINE THE DOSE REQUIRED
STEROID WITHDRAWAL (LOW STRESS TOLERANCE) EXHAUSTION WEAKNESS LETHARGY
STEROID THERAPYASSESSMENT:
ACUTE ADRENAL CRISIS RESTLESSNESS WEAKNESS HEADACHE DHN N/V FALLING BP TO SHOCK
PSYCHOLOGICAL CXS MOOD ELEVATION, FRANK EUPHORIA THEN, DEPRESSION
STEROID THERAPYIMPORTANT FACTS:
MAJOR UNTOWARD EFFECTS: MASKS INFECTION DEFENSE AGAINST INFECTION FROM
LYMPHOPENIASLOW WOUND HEALING FROM ITS
ANTIINFLAMMATORY EFFECTP.U.D. ACTIVATION/ REACTIVATION SERUM SODIUM SERUM POTASSIUM
STEROID THERAPYIMPORTANT FACTS:
MINOR UNTOWARD EFFECTS:PIGMENTATIONACNEFACIAL HAIRMOON-FACIE
STEROID THERAPYIMPORTANT FACTS:
PROBLEMS OF LONG TERM THERAPY:GROWTH RETARDATIONOBESITYGASTRITIS TO P.U.D.OSTEOPOROSISHPNRENAL CALCULIADRENAL ATROPHY
STEROID THERAPY
STEROID LEVELS
PITUITARY GLAND IS INHIBITED TO REALEASE ACTH
ENDOGENOUS CORTISOL
PRODUCTION & RELEASE BY ADRENAL MEDULLA
ADRENAL ATROPHY
STEROID THERAPYIMPLEMENTATION
DECREASE Na IN THE DIETCALORIC RESTRICTIONFOODS HIGH IN POTASSIUMGIVE MEDS WITH ANTACIDS OR WITH FOODTEST STOOLS OR EMESIS FOR BLOODREPORT ANY EVIDENCE OF GI BLEEDINGLYMPHOPENIC PRECAUTION
ANTERIOR PITUITARY DISTURBANCES
HYPOPITUITARISM
HYPERPITUITARISM
HYPOPITUITARISMANTERIOR LOBE
PANHYPOPITUITARISM
(SIMMOND’S DSE)DECREASED SECRETION OF ALL
ANTERIOR LOBE HORMONES
HYPERPITUITARISMANTERIOR LOBE
EOSINOPHILIC TUMOR INCREASED GROWTH HORMONE AND
PROLACTIN
BASOPHILIC TUMOR INCREASED TSH, FSH, LH, MSH, INCREASED ACTH (CUSHING’S DSE)
CHROMOPHOBE TUMOR INCREASED ACTH & GROWTH
HORMONE
PITUITARY ANTERIOR LOBEHORMONE HYPO FXN HYPER FXN
GH Dwarfism – young
Cachexia - adult
Gigantism – young
Acromegaly - adult
ACTH Atrophy of adrenal cortex
Cushing’s dse
TSH Atrophy & depressed thyroid fxn
Grave’s dse
FSH Atrophy & infertility Exaggerated fxn of sex organs
PROLACTIN Underdevelopment of mammary glands
Decreased milk production
MANAGEMENT
HYPOPITUITARISM SURGICAL REMOVAL / IRRADIATION REPLACEMENT THERAPY
THYROID HORMONES STEROIDS SEX HORMONES GONADOTROPINS (restore fertility)
HYPERPITUITARISM SURGICAL REMOVAL / IRRADIATION MONITOR FOR HYPERGLYCEMIA &
CARDIOVASCULAR PROBLEMS
POSTERIOR PITUITARY DISTURBANCES
DIABETES INSIPIDUS
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN
CAUSE:
TUMOR
TRAUMA
VASCULAR DSE
INFLAMMATION
PITUITARY SURGERY
S/SX:
POLYURIA 15-29L/ DAY
POLYDIPSIA
SG OF URINE IS
<1.010
S/SX OF DHN
SHOCK
DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN
MANAGEMENTHORMONAL REPLACEMENT – FOR LIFE VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR NASAL
SPRAY
NON-HORMONAL THERAPY CHLORPROPRAMIDE – INCREASE RESPONSE OF THE BODY
TO DECREASED VASOPRESSIN
SALT & P RESTRICTED DIET, INCREASE FLUIDSMONITOR I&OMAINTAIN FLUID & ELECTROLYTE BALANCE
SYNDROME OF INAPPROPRIATE ADH
ELEVATED ADH
CAUSES:BRONCHOGENIC CANONENDOCRINE TUMORS
S/SX:DECREASED SERUM SODIUM CX IN LOC TO UNCONSCIOUSNESS SEIZURES
WATER INTOXICATION N/V MENTAL CONFUSION
SYNDROME OF INAPPROPRIATE ADH
MANAGEMENT:WATER INTAKE RESTRICTION
ADMINISTER AS ORDERED:NaClDiureticsDemeclocycline (declamycin) – a
tetracycline analogue that interferes with the action of ADH on the collecting tubules
Mission possible
THYROID GLAND
STIMULATED BY THYROID STIMULATING
HORMONE (TSH)NEEDS IODINE TO SYNTHESIZE HORMONE
SECRETES:THYROXINE (T4)TRIIODOTHYRONINE (T3)
THYROID DISTURBANCESDIAGNOSTIC TESTS:
B.M.R.- AMT OF O2 USED BY A PERSON @ A GIVEN TIME
PBI – MEASURE IODINE LIBERATED IN THE BLOOD WITH THYROID DAMAGE
SERUM THYROXINE (T4), SERUM TRIIODOTHYRONINE (T3), SERUM TSHBLOOD SERUM CHOLESTEROLRADIOACTIVE IODINE TESTS: T3 RED CELL UPTAKE RADIOACTIVE IODINE UPTAKE (I131 THYROID SCAN
THYROID DISTURBANCES
HYPOTHYROIDISM HYPERTHYROIDISM
CRETINISM- infants, young children
HYPOTHYROIDISM WITHOUT MYXEDEMA- atrophy/ destruction of thyroid gland
MYXEDEMA –adults
GRAVE’S DSE or Exophthalmic goiter
EFFECTS
HYPOTHYROIDISM HYPERTHYROIDISM
Reduction in HEAT PRODUCTION
Failure of MENTAL & PHYSICAL GROWTH
increased storage of C, P & F
Abnormal collection of WATER
Increase heat
Deranged C metabolism, glycosuria
Increase use of F & P as fuel
HYPOTHYROIDISM HYPERTHYROIDISM
SERUM
CHOLESTEROL:INCREASED
BMR:DECREASED
SKIN:THICK, PUFFY, DRY
HAIR:DRY, BRITTLE
DECREASED
INCREASED
WARM, MOIST, FLUSHED
SOFT, SILKY
HYPOTHYROIDISM HYPERTHYROIDISM
NERVOUS SYSTEM:APATHETIC
LETHARGIC
MAYBE HYPERIRRITABLE
SLOW CEREBRATION
WEIGHT:INCREASED
APPETITE:DECREASED
HYPERACTIVE
LABILE MOOD
HYPERSENSITIVE
TENSED
DECREASED
INCREASED
MANAGEMENTHYPOTHYROIDISM HYPERTHYROIDISM
MEDICAL:
HORMONE REPLACEMENT
DESSICATED THYROID
THYROGLOBULIN
Na LEVOTHYROXINE
Na LYOTHYRONINE
MEDICAL:
REST
ANTITHYROID DRUGS:
LUGOL’S SOLUTION
THIOUREA DERIVATIVES
RADIOACTIVE IODINE
BETA-BLOCKERS
SURGICAL:SUBTOTAL
THYROIDECTOMY
ANTITHYROID MEDICATIONSLUGOL’S SOLUTION
(POTASSIUM IODIDE) DECREASE THYROID VASCULARITY INHIBIT IODINE RELEASE DILUTED IN MILK / JUICE STAINS THE TEETH- USE STRAW
THIOUREA & DERIVATIVES(PTU,METHIMAZOLE) BLOCK THYROID HORMONE RELEASE TOXIC SIGNS: FEVER, SORETHROAT, LEUKOPENIA
RADIOACTIVE IODINE PATIENT IS ISOLATED FOR 3 DAYS
BETA BLOCKERS PROPANOLOL
SUBTOTAL THYROIDECTOMYREMAINING TISSUE PROVIDES ENOUGH HORMONES FOR
NORMAL FXN
PRE OP NURSING CARE:PATIENT EDUCATION ON POST OP: LITTLE HOARSENESS DIFFICULTY OF SWALLOWING
POST OP NURSING CARE:SEMIFOWLER’SAVOID HYPEREXTENSION OF THE NECKBE ASKED TO SPEAK @ 40 MIN INTERVAL – ASSESS RECURRENT NERVE INJURYWATCH OUT FOR COMPLICATIONS.
SUBTOTAL THYROIDECTOMYCOMPLICATIONS:
RECURRENT LARYNGEAL NERVE INJURY HOARSENESS
HEMORRHAGE 12-24 HRS POST OP OBSERVE FOR IRREGULAR BREATHING, CHOKING
SIGNS TRACHEOSTOMY SET @ BEDSIDE
TETANY
RESPIRATORY OBSTRUCTION
THYROID STORM
TETANYDEPENDS UPON THE NUMBER OF PARATHYROID GLANDS
REMOVED
S/SX:
1ST – TINGLING TOES & FINGERS2ND – CHEVOSTEK’S SIGN (TAPPING THE FACIAL MUSCLES)
3RD – TROUSSEAU’S SIGN (CARPO-PEDAL SPASM WITH OCCLUSION OF CIRCULATION WITH A BP CUFF)
MANAGEMENT:
CALCIUM REPLACEMENT: CaGluconate IV
THYROID STORM / CRISISS/SX:
HYPERTHERMIA > 41C
TACHYCARDIAAPPREHENSIONRESTLESSNESSIRRITABILITYDELIRIUMCOMA
MANAGEMENT:DECREASE TEMP
ANTITHYROID DRUGS
GLUCOSE
DIGITALIS
STEROIDS TO
DECREASE ACTH
THYROID STORM / CRISISINCREASED AMOUNT OF THYROID HORMONES
POST OP
AFTER RADIOACTIVE IODINE ADMINISTRATION
TOO SHORT PERIOD OF PRE OP TX
CAUSES:EMOTIONAL STRESS
PHYSICAL STRESS
VARIANTS OF HYPERTHYROIDISM
GRAVE’S DSE
THYROIDITIS
GOITER
GRAVE’S DISEASE
CAUSE:UNKNOWN AUTOIMMUNE WITH LONG-ACTING THYROID STIMULATOR
S/SX: TRIAD OF SYMPTOMS:HYPERTHYROIDISMOPHTHALMOPATHYDERMOPATHY
OPHTHALMOPATHY
EXOPHTHALMOS – ACCUMULATION OF FLUID IN THE FAT PADS BEHIND HE EYEBAL
LID LAG – PROMINENT PALPEBRAL FISSURE WHEN THE PATIENT LOOKS DOWN
THYROID STARE (DARYMPLE’S SIGN) – INFREQUENT EYE BLINKING
DERMOPATHYPRETIBIAL MYXEDEMA
@ THE DORSUM OF THE LEG
RAISED, THICKENED, PRURITIC, HYPERPIGMENTED SKIN
CLUBBING OF FINGERS & TOES
OSTEOARTHROPATHY
THYROIDITIS
CLASSIFICATION:
SUBACUTE, NONSUPPURATIVE UNKNOWN CAUSE ASSOC. WITH VIRAL URT INFECTIONS
CHRONIC, HASHIMOTO’S IMMUNOLOGICAL FACTORS PRESENCE OF IMMUNOGLOBULINS &
ANTIBODIES DIRECTED AGAINST THE THYROID
GOITER
ENLARGEMENT OF THE THYROID GLAND.
TYPES:TOXIC NODULAR
NONTOXIC
TOXIC NODULAR GOITER
COMMON IN ELDERLY
FROM LONG STANDING SIMPLE GOITER
NODULES FUNCTIONING TISSUE SECRETES THYROXINE
AUTONOMOUSLY FROM TSH
NON-TOXIC GOITER(SIMPLE/ COLLOID/ EUTHYROID)
CAUSE :IODINE DEFICIENCYINTAKE OF GOITROGENIC SUBSTANCES/ DRUGS: CASSAVA, CABBAGE, CAULIFLOWER, CARROTS RADDISH TURNIPS RED SKIN OF PEANUTS IODINE COBALT LITHIUM
NON-TOXIC GOITER
IMPAIRED THYROID HORMONE SYNTHESIS
SERUM THYROXINE
PITUITARY SECRETE TSH
THYROID GLAND ENLARGES
TO COMPENSATE FOR THE REDUCED LEVEL OF THYROXINE
IODINE DEFICIENCY OR INTAKE OF GOITROGENIC SUBSTANCES
NON-TOXIC GOITER
COMMON IN WOMEN:ADOLESCENT
PREGNANT
LACTATING
MENOPAUSE
TREATMENT:IODIZED OIL IM
IODINE TABLETS
SALT FORTIFICATION WITH IODINE
EDUCATE ABOUT INTAKE OF: SEAWEEDS SHELLFISH FISH- TAMBAN, HITO,
DALAG
MYXEDEMA COMA
MEDICAL EMERGENCY
OCCURS IN SEVERE & UNTREATED MYXEDEMA
HIGH MORTALTY RATE
S/SX:INTENSIFIED HYPOTHYROIDISM
NEUROLOGIC IMPAIRMENT COMA
MYXEDEMA COMA
PRECIPITATING FACTORS:
FAILURE TO TAKE MEDSINFECTIONTRAUMAEXPOSURE TO COLDUSE OF SEDATIVES, NARCOTICS, ANESTHETICS
MYXEDEMA COMA
MANAGEMENT:
IV THYROID HORMONES
CORRECTION OF HYPOTHERMIA
MAINTAIN VITAL FXNS
TREAT PRECIPITATING CAUSES
PARATHYROID GLAND4 GLANDS
SECRETES PARATHORMONE (PTH) IN RESPONSE TO SERUM Ca & Ph LEVELS
REGULATE CALCIUM & PHOSPHORUS METABOLISM
ORGANS AFFECTED:BONES - RESORPTION
KIDNEYS Ca REABSORPTION Ph EXCRETION
GIT – ENHANCES Ca ABSORPTION
PARATHYROID DISORDERS
DIAGNOSTIC TESTS:HEMATOLOGICALSERUM CALCIUMSERUM PHOSPHORUSSERUM ALKALINE PHOSPHATASE
URINARY STUDIESURINARY CALCIUMURINARY PHOSPHATE - TUBULAR
REABSORPTION OF PHOSPHATE
HYPOPARATHYROIDISM
DECREASED PTH PRODUCTION
HYPOCALCEMIA
CALCIUM IS: DEPOSITED IN THE BONE EXCRETED
CAUSE:
HEREDITARY
IDIOPATHIC
SURGICAL
HYPOPARATHYROIDISM
S/SX:
ACUTE HYPOCALCEMIA TINGLING OF THE FINGERS CHEVOSTEK’S, TROUSSEAU’S
CHRONIC HYPOCALCEMIA FATIGUE, WEAKNESS PERSONALITY CHANGES LOSS OF TOOTH ENAMEL, DRY SCALY SKIN CARDIAC ARRHYTHMIA CATARACT
HYPOPARATHYROIDISMXRAY: INCREASED BONE DENSITY
MANAGEMENT:Ca SUPPLEMENTVIT D SUPPLEMENT – LIQ FORM: WITH WATER, JUICE OR MILK, pc
SEIZURE prec
LISTEN FOR STRIDOR OR HOARSENESSTRACHEOSTOMY SET @ BEDSIDE
CaGLUCONATE @ BEDSIDE
HYPERPARATHYROIDISMINCREASED PTH PRODUCTION
HYPERCALCEMIA
HYPOPHOSPHATEMIA
PRIMARY – TUMOR OR HYPERPLASIA OF THE PARATHYROID GLAND
SECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM: CHRONIC RENAL DSE RICKETS MALABSORPTION SYNDROME OSTEOMALACIA
HYPERPARATHYROIDISMS/SX:
BONE PAIN : ESP @ THE BACK, PATHOLOGIC FRUCTURESTUBULAR CALCIUM DEPOSITS - KIDNEY STONES, RENAL COLIC, POLYURIA, POLYDIPSIAMUSCLE WEAKNESSPERSONALITY CX, DEPRESSIONCARDIAC ARRHYTHMIAS, HPN
XRAY: BONE DEMINERALIZATION
HYPERPARATHYROIDISMMANAGEMENT:
TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC TISSUE
IV PNSS 5L/ DAY WITH DIURETICSCRANBERRY JUICE (ACID-ASH)
LOW Ca, HIGH Ph DIET NO MILK, CAULIFLOWER & MOLASSESSTRAIN URINE FOR STONESCARE FOR PARATHYROIDECTOMY
ADRENAL GLAND
STIMULATED BY ACTH
HORMONE PRECURSOR: CHOLESTEROL
SECRETES: CORTISOL ALDOSTERONE SEX HORMONES : ANDROGEN, ESTROGEN
ADRENAL GLANDHORMONE FUNCTION
ALDOSTERONE Renal : Na & Cl reabsorption; K excretion
GI : Na absorption
GLUCO-
CORTICOIDS
increase serum glucose by gluconeogenesis & glycogenolysis esp during STRESS
Blocks inflammation
Counteracts effect of histamine
SEX HORMONE Physiologically insignificant
Becomes useful during menopause in women
SYMPTOMATOLOGY
ALDOSTERONE DEFICIENCY
DECREASE IN PLASMA VOLUME LEADING TO DEHYDRATON
HYPOTENSION TO SHOCK
INCREASED K
METABOLIC ACIDOSIS
SYMPTOMATOLOGY
CORTISOL DEFICIENCY
ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS, LETHARGY
HYPOGLYCEMIA
HYPOTENSION
INCREASED K, WEAK PULSE
PIGMENTATION
IMPAIRED STRESS TOLERANCE
SYMPTOMATOLOGY
SEX HORMONE DEFICIENCY
LOSS OF BODY HAIR
LOSS OF LIBIDO OR IMPOTENCE
MENSTRUAL & FERTILITY DISORDER
ADRENAL CORTEX DISORERS
ADRENAL INSUFFICIENCY
ADRENAL CRISIS
CUSHING’S SYNDROME
ALDOSTERONISM
ADRENAL INSUFFICIENCYADDISON’S DISEASE
INCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO STRESS
ADRENAL CRISIS
ACUTE EPISODES FROM STRESS THAT TAXES THE ADRENAL CORTICAL FUNCTION BEYOND ITS CAPABILITIES
POSSIBLE COMPLICATION OF ADDISON’S DISEASE
ADRENAL CRISIS
PRECIPITATING CAUSES:
ABDOMINAL DISCOMFORT
INFECTION
TRAUMA
HIGH TEMP
EMOTIONAL UPSET
ANTICOAGULANT DRUGS
ADRENAL CRISIS
S/SX:
HYPOTENSION
FLUID LOSS
HYPONATREMIA
ADRENAL CRISISLAB:
SERUM ELEC: DECREASED Na
INCREASED K
S. BUN :
S. GLUCOSE:
ADRENAL HORMONE ASSAY : HYDROXYCORTICOID & 17 KETOSTEROID IN 24-
HR URINE DET.
ADRENAL CRISIS
GOALS OF CARE:TO REVERSE SHOCK
RESTORE BLOOD CIRCULATION
REPLENISH NEEDED STEROID
ADRENAL CRISIS
TREATMENT:D5NSS
ADRENAL CORTICAL HORMONE REPLACEMENT: INJECTABLE
NEOSYNEPHRINE - SHOCK
HIGH SALT DIET
ANTIBIOTICS
CUSHING’S SYNDROME
CAUSE:SUSTAINED OVER-PRODUCTION OF GLUCOCORTICOIDS BY ADRENAL GLAND FROM
ACTH BY PITUITARY TUMOR
EXCESSIVE GLUCORTICOID ADMINISTRATION
CUSHING’S SYNDROME
S/SX:TRUNCAL OBESITY
BUFFALO HUMP
MOON-FACIE
WT GAIN
SODIUM RETENTIONTHINNING OF EXTREMITIES – FROM LOSS OF MUSCLE TISSUE DUE TO PROTEIN CATABOLISM
CUSHING’S SYNDROME
PURPLE STRIAE – FROM THINNING OF SKINECHYMOSIS FROM SLIGHT TRAUMAANDROGENIC EFFECTS:
OLIGOMENORRHEA
HIRSUTISMGYNECOMASTIA
HYPERTENSION FROM S. Na
CUSHING’S SYNDROME
TREATMENT & NURSING CARE:
PSYCHOLOGICAL SUPPORTPREVENT INFECTION – INFLAM & IMMUNE RESPONSE ARE SUPPRESSED
PROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMY
ALDOSTERONISM
HYPERSECRETION OF ALDOSTERONE
PRIMARY – CONN’S SYNDROME
SECONDARY
CONN’S SYNDROMEPRIMARY ALDOSTERONISM
CAUSE:ADRENAL ADENOMA
S/SX:HYPOKALEMIAFATIGUEHYPERNATREMIA, HPN, TETANY
MANAGEMENT:
SURGERYALDACTONE – ALDOSTERONE ANTAGONIST
SECONDARY ALDOSTERONISM
THE PROBLEM IS OUTSIDE THE ADRENAL GLAND:
e.g. RENIN – ANGIOTENSIN SYSTEM
ADRENAL MEDULLA
HORMONES : EPINEPHRINE
NOREPINEPHRINE
EFFECTS
PHEOCHROMOCYTOMA
TUMOR OF ADRENAL MEDULLASECRETES INCREASED AMOUNT OF CATECHOLAMINES
S/SX:HPNHYPERGLYCEMIACARDIAC ARRHYTHMIA & CHF
DIAGNOSTIC TEST : VMA IN 24H URINE
VMA IN 24H URINE
END PRODUCT OF CATECHOLAMINE METABOLISM
DRUGS & FOOD TO BE WITHHELD 24H B4 THE TEST:COFFEE & TEABANANAVANILLACHOCOLATES
PHEOCHROMOCYTOMA
MANAGEMENT:SURGERYMEDICAL : ADRENERGIC BLOCKING AGENTS: PHENTOLAMINE
NURSING CARE:MONITOR BP IN SUPINE & STANDINGMONITOR URINE FOR GLUC & ACETONE
PANCREAS
HORMONES:
INSULIN BY BETA CELLS
GLUCAGON BY ALPHA CELLS
DIABETES MILLETUS
CAUSE:
INSUFFICIENCY OF INSULIN
LACK OF INSULIN
EFFECT:
HYPERGLYCEMIA
DIABETES MILLETUS
PATHOPHYSIOLOGYREDUCED /NO INSULINREDUCED /NO INSULIN
HYPERGLYCEMIAHYPERGLYCEMIA
GLUCOSURIAGLUCOSURIA
WEIGHT LOSSWEIGHT LOSS
OSMOTICDIURESISOSMOTICDIURESIS
POLYURIAPOLYURIA
CELLULAR HUNGER
CELLULAR HUNGER
POLYPHAGIAPOLYPHAGIA
POLYDIPSIAPOLYDIPSIA
LIPOLYSISLIPOLYSIS
OSMOTICDEHYDRATION
OSMOTICDEHYDRATION
DIABETES MILLETUS
S/SX:
3 – P’s
WEIGHT LOSS
STAGES:
PREDIABETES
SUSPECTED
CHEMICAL
CLINICAL / OVERT
DIABETES MILLETUS
PREDIABETES / POTENTIAL:
CONCEPTIONCONCEPTION
EVIDENCE OF GLUCOSE METABOLISMALTERATION
EVIDENCE OF GLUCOSE METABOLISMALTERATION
DIABETES MILLETUS
SUSPECTED/ SUBCLINICAL/ LATENT:
PREDIABETESPREDIABETES
NO STRESS STRESSSTRESS
NORMAL GLUCOSEMETABOLISM
OVERT DIABETESOVERT DIABETES
DIABETES MILLETUSCHEMEICAL:
SUBCLINICALSUBCLINICAL
GTT IS ABNORMALGTT IS ABNORMAL
NO STRESSNO STRESS STRESSSTRESS
ASYMPTOMATICASYMPTOMATIC SYMPTOMATICSYMPTOMATIC
DIABETES MILLETUSCLINICAL / OVERT:
CHEMICALCHEMICAL
PERSISTENT INCREASED FBSPERSISTENT INCREASED FBS
WITH OR WITHOUT STRESSWITH OR WITHOUT STRESS
SYMPTOMATICSYMPTOMATIC
DIABETES MILLETUSTYPES:
TYPE I JUVENILE ONSET BEFORE 15 YO LEAN/ NORMAL
WEIGHT ABSOLUTE INSULIN
DEFICIENCY INSULIN -DEPENDENT PRONE TO DKA
TYPE II – MATURITY ONSET AFTER AGE 40 OBESE REDUCED INSULIN
RECEPTOR NONINSULIN
DEPENDENT PRONE TO HHONK
DIABETES MILLETUS
DIAGNOSTIC EXAMS:
FBS
2 HR- POSTPRANDIAL
OGTT
GLYCOSYLATED HGB
DEXTROSTRIP
URINE TESTS: BENEDICT’S CLINITEST TAB ACETONE TEST
2 HR POSTPRANDIAL BLOOD SUGAR
INTAKE OF 100GM GLUCOSE, 2 HRS BEFORE THE TEST
TEST FOR ABILITY TO DISPOSE GLUCOSE LOAD
OGTT
CONFIRMATORY, WHEN OTHER BLOOD TESTS ARE BORDERLINE
3 DAYS OF NORMAL ACITIVITY & 150MG OF CARB DIETNPO 10-12HRS BEFORE THE TEST
BASELINE BLOOD SUGAR TAKENGLUCOSE LOAD IS GIVEN, P.O. OR IV
BLOOD & URINE SPECS TAKEN 30 MIN, 1HR, 2HRS, 3 HRS, AFTER GLUCOSE LOADING
GLYCOSYLATED HEMOGLOBIN
MEASURES GLUCOSE METABOLISM FOR THE PAST 3 MONTHS
USEFUL TO CHECK:COMPLIANCE WITH THERAPYHISTORY OF SUBCLINICAL OR
CHEMICAL DIABETES
DIABETES MILLETUS
PLANNING & IMPLEMENTATION:CLIENT’S ACTIVITYDIET : C,F,P – 50, 30, 20 LOW SATURATED FATS, HIGH FIBER
DRUGS: ORAL HYPOGLYCEMICS
BIGUANIDE SULFONYLUREAS CONTRAINDICATED - PREGNANCY
INSULIN
DIABETES MILLETUS
INSULIN THERAPY
DISPENSED IN “U”/ml : eg 100, 80
REFRIGERATE
GIVEN @ ROOM TEMP
GENTLY ROTATED, NOT SHAKEN
ROUTE : SQ (MTC); IM OR IV
SYRINGE: 5/8 INCH ; SAME BRAND
DIABETES MILLETUS
INSULIN THERAPY:
SITE OF INJECTION:ABDOMENANTERIOR THIGHARM UPPER BACK BUTTOCKS
DIABETES MILLETUS
INSULIN THERAPY REACTIONS:
LOCAL: STNGING INDURATION ITCHING
LIPODYSTROPHY
GENERALIZED: HIVES URTICARIA ANTIHISTAMINES
30 MIN B4 DESENSITIZATION
LIPODYSTROPHY
CAUSE:FAULTY TECHNIQUETRAUMAINJECTION OF REFRIGERATED INSULIN
MANAGEMENT:ROTATING SITES: 1 AREA IS NOT USED MORE THAN ONCE EVERY 3 WKS
INSULIN THERAPY & HORMONAL ACTIVITY
GLUCORTICOIDS & EPINEPHRINE CAUSES HYPERGLYCEMIA DURING: PHYSICAL TRAUMA STRESS INFECTION ANXIETY ANGER FEAR CHANGE IN LIFESTYLE
INCREASE IN INSULIN DOSE IS NEEDED
SURPRISE!!!
ACUTE COMPLICATIONS OF DIABETES MILLETUS
DIABETIC KETO-ACIDOSIS (DKA)
INSULIN SHOCK
HYPERGLYCEMIC, HYPEROSMOLAR,
NONKETOTIC (HHONK) COMA
SOMOGYI EFFECT
D.K.A.PATHOPHYSIOLOGY
NO INSULINNO INSULIN
MARKED HYPERGLYCEMIAMARKED HYPERGLYCEMIA
GLUCOSURIAGLUCOSURIA
WEIGHT LOSS
WEIGHT LOSS
OSMOTICDIURESIS
OSMOTICDIURESIS
POLYURIAPOLYURIA
CELLULAR HUNGER
CELLULAR HUNGER
POLYPHAGIAPOLYPHAGIA
POLYDIPSIAPOLYDIPSIA
LIPOLYSISLIPOLYSIS
OSMOTICDEHYDRATION
OSMOTICDEHYDRATION
KETOACIDOSISKETOACIDOSIS
D.K.A.
S/SX:S/SX OF DM +KETONURIAMETABOLIC ACIDOSISKUSSMAUL’S RESPIRATIONACETONE BREATHDHNFLUSHED FACETACHYCARDIA
CIRCULATORY COLLAPSE COMA DEATH
D.K.A.
MANAGEMENT:
ADEQUATE VENTILATION
FLUID REPLACEMENT
INSULIN – RAPID ACTING
ECG – ELEC IMB
INSULIN SHOCK
LOW BLOOD SUGAR
CAUSE:OVERDOSE OF EXOGENOUS INSULIN
EATING LESS
OVEREXERTION WITHOUT ADDITIONAL CALORIE INTAKE
INSULIN SHOCKS/SX:
PARASYMPATHETIC HUNGER NAUSEA HYPORTENSION BRADYCARDIA
CEREBRAL LETHARGY, YAWNING SENSORIUM CX
SYMPATHETIC IRRITABILITY SWEATING TREMBLING TACHYCARDIA PALLOR
INSULIN SHOCK
CLINICAL FINDING : BLOOD GLUCOSE BELOW 55-60 mg%
TREATMENT:GLUCOSE PO ( SUGAR, ORANGE JUICE OR CANDY) or IV
ADMINISTRATION OF GLUCAGON IM, IV OR SQ
HHONKPATHOPHYSIOLOGY
Very insufficient INSULINVery insufficient INSULIN
MARKED HYPERGLYCEMIAMARKED HYPERGLYCEMIA
GLUCOSURIAGLUCOSURIA
WEIGHT LOSS
WEIGHT LOSS
OSMOTICDIURESISOSMOTICDIURESIS
POLYURIAPOLYURIA
CELLULAR HUNGER
CELLULAR HUNGER
POLYPHAGIAPOLYPHAGIA
POLYDIPSIAPOLYDIPSIA
LIPOLYSISWithoutKETOSIS
LIPOLYSISWithoutKETOSIS
SEVEREOSMOTIC
DEHYDRATION
SEVEREOSMOTIC
DEHYDRATION
HHONK
S/SX:
S/SX OF DKA WITHOUT:KAUSMAUL’S BREATHINGACETONE BREATHMETABOLIC ACIDOSISKETONURIA
LACTIC ACIDOSIS
SEVERE TISSUE ANOXIASEVERE TISSUE ANOXIA
LACTIC ACID PRODUCTIONLACTIC ACID PRODUCTION
AGGRAVATION OF EXISTING
METABOLIC ACIDOSISAGGRAVATION OF EXISTING
METABOLIC ACIDOSIS
SOMOGYI EFFECTTOO MUCH INSULINTOO MUCH INSULIN
HYPOGLYCEMIAHYPOGLYCEMIA
GLUCAGON IS RELEASEDGLUCAGON IS RELEASED
LIPOLYSISGLUCONEOGENESISGLYCOGENOLYSIS
LIPOLYSISGLUCONEOGENESISGLYCOGENOLYSIS
REBOUNDHYPERGLYCEMIA
+KETOSIS
REBOUNDHYPERGLYCEMIA
+KETOSIS
CHRONIC COMPLICATIONS OF DIABETES MILLETUS
DEGENERATIVE CHANGES IN THE VASCULAR SYSTEM UNDERNOURISHMENT ATHEROSCLEROSIS
NEUROPATHY FROM: VASCULAR INSUFFICIENCY VIT B DEFICIENCY HYPERGLYCEMIA
EYE COMPLICATIONS FROM ANOXIA CATARACT DIABETIC RETINOPATHY RETINAL DETACHMENT
CHRONIC COMPLICATIONS OF DIABETES MILLETUS
NEPHROPATHY DAMAGE & OBLITERATION OF CAPILLARIES
SUPPLYING THE KIDNEY
HEART DISEASE MI FROM ATHEROSCLEROSIS
SKIN CHANGES DIABETIC DERMOPATHY – HYPERPIGMENTED &
SCALY PRETIBIAL AREAS
LIVER CHANGES ENLARGEMENT & FATTY INFILTRATION
Ms A, 45 y.o., has a simple goiter. She’s being seen by the community health nurse for teaching & follow-up regarding nutritional deficiencies related to her goiter. Ms A’s problem is almost associated with what nutritional deficiency?
a. Calcium
b. Iodine
c. Iron
d. Sodium