Dennis Christopher D. So Chan RNTUA-SLCN

Endocrine System The endocrine system

integrates body functions by the synthesis and release of hormones

The functions of the endocrine and the nervous system are interrelated.

Hypothalamus: link between the nervous system and the endocrine system.

Endocrine Glands Pituitary Gland Adrenal Glands Thyroid Glands Parathyroid Glands Gonads

Endocrine SystemEndocrine Glands

secrete their products directly to the blood stream

different from exocrine glands

Exocrine glands: secrete through ducts onto epithelial surfaces or into the GI tract

Overview of the Endocrine SystemThe body’s second great controlling system

which influences metabolic activities of cells by means of hormones, which are produced by endocrine glands Endocrine glands: pituitary, thyroid,

parathyroid, adrenal, pineal, and thymus The pancreas and gonads produce both

hormones and exocrine productsThe hypothalamus has both neural functions and

releases hormonesOther tissues and organs that produce

hormones: adipose cells, pockets of cells in the walls of the small intestine, stomach, kidneys, and heart

Functions of Endocrine System1. Metabolism and tissue maturation2. Ion regulation3. Water Balance4. Immune system regulation5. Heart rate and blood pressure regulation6. Control of blood glucose and other

nutrients7. Control of reproductive function8. Uterine contractions and milk release

Hormones Are chemical substances that are secreted by

the endocrine glands. Can travel moderate to long distances or very

short distances. Acts only to cells or tissues that have

receptors for the specific hormone. Target organ: the cell or tissue that responds

to a particular hormone.

Hormones are dissolved in plasma or bind to plasma proteins

Water-soluble hormonesProteins, epinephrine, and norepinephrineDo not bind to plasma proteins or readily diffuse out of

the bloodThey are quickly broken down by enzymes or are taken

up by tissuesThese hormones regulate activities that have a rapid

onset and a short durationLipid-soluble hormones and thyroid hormones

Not quickly removed from the bloodProduce a prolonged effect

Hormones leave the blood to reach target tissues or are excreted by the kidneys or liver

Hormone Transport and Excretion

Regulation of Hormones If the client is healthy, the concentration or

hormones is maintained at a constant level. When the hormone concentration rises,

further production of that hormone is inhibited.

When the hormone concentration falls, the rate of the production of that hormone increases.

Diseases of the Endocrine System Primary Disease- problem in target gland;

autonomous

Secondary Disease-problem outside the target gland; most often due to a problem in pituitary gland

HypopituitarismHyperpituitatism

Hypopituitarism Caused by low levels of one or more anterior

pituitary hormones.

Lack of the hormone leads to loss of function in the gland or organ that it controls.

Causes of Primary Hypopituitarism Pituitary tumors Inadequate blood supply to the pituitary gland

o e.g. Sheehan’s syndrome Infections and or inflammatory diseases

o sarcoidosiso amyloidosis

Radiation therapy Surgical removal of pituitary tissue Autoimmune diseases Congenital absence

Causes of 2° Hypopituitarism Tumors of the hypothalamus Inflammatory disease Head injuries Surgical damage to the pituitary and/or blood

vessels or nerves leading to it.

Signs and Symptoms Tumor: bitemporal

hemianopsia on visual confrontation

Varying signs of hormonal disturbances depending on which hormones are being under secreted

Signs and Symptoms Gonadotropin Deficiency

Congenital Onset Delayed or absent secondary sexual

characteristics May have micropenis, cryptorchidism

Acquired Loss of body hair Infertility, decrease libido, impotence in males,

amenorrhea in females Prolactin Deficiency

Failure to lactate

Signs and Symptoms TSH (Thyroid Stimulating hormone) Deficiency

causes hypothyroidism with manifesations such as fatigue, weakness, weight change, and hyperlipidemia

Adrenocorticotropic (ACTH) hormone deficiency

• results in diminished cortisol secretion.• symptoms include weakness, fatigue, weight

loss, and hypotension

Signs and Symptoms

Growth hormone (GH) deficiency

In childhood: failure to grow

In adulthood: mild to moderate central obesity, increased systolic BP and increases in LDL cholesterol

Diagnostics X-ray, MRI or CT

scan: pituitary tumor

Plasma hormone levels: decreased

Therapeutics Hormonal Substitution: may be for life

corticosteroids levothyroxine androgen for males estrogen for females Growth hormone

Radiation therapy for tumorsSurgery for tumors: Transphenoidal Hypophysectomy

Hyperpituitarism Hyperfunction of the anterior pituitary

gland=oversecretion of one or more of the pituitary hormones

Usually caused by benign pituitary adenoma 2 most common hormones affected:

Prolactin growth hormone

Prolactinoma vs.Somatotropinoma

Prolactinoma Female: galactorrhea menstrual

disturbances, infertility, signs of estrogen deficit (vaginal mucosal atrophy, decreased vaginal lubrication and libido)

Male: Decreased libido and possible impotence, reduced sperm count and infertility, gynecomastia

Growth Hormone Hypersecretion Gigantism: GH hypersecretion prior to

closure of epiphyses; proportional growth

Acromegaly: GH hypersecretion after closure of epiphyses; disproportional growth

Gigantism vs. Acromegaly

Growth Homone Hypersecretion:Signs and Symptoms Enlarged hand and feet; carpal tunnel syndrome

common Coarsening of features esp. in Acromegaly;

prominent mandible, tooth spacing widens, Macroglossia leading to OSA Hypertension, cardiomegaly, heart failure Insulin resistance leading to type 2 DM Visual field defects: bitemporal hemianopsia-

>complete blindness Headaches Arthritis Hypogonadism

Therapeutics Medication

bromocriptine and cabergoline (dopamine agonist) For prolactinoma and GH hypersecretion

Octreotide (somatostatin) for GH hypersecretion Sx

surgical remission is achieved in about 70% of patients followed over 3 years

Growth hormone levels fall immediately; diaphoresis and carpal tunnel syndrome often improve within a day post-Sx

Radiation Therapy for large tumors Diet

Nursing Interventions Provide emotional support=striking body

change can cause psychological stress. Perform or assist with range of motion

exercises to promote maximum joint mobility and prevent injury.

Evaluate muscle weakness, especially in the patient with late stage Acromegaly.

Keep the skin dry. Avoid using an oily lotion because the skin is already oily.

Nursing Interventions Be aware that pituitary tumor cause visual

problems. If there is hemianopsia, stand where he can see you.

Warn relatives that hyperpituitarism can cause inexplicable mood changes.

If the patient is a child, explain to the parents that surgery prevents permanent soft-tissue deformities but won’t correct bone changes that have already occurred.

After an operation, emphasize the importance of continuing hormone replacement therapy.

Transphenoidal Hypophysectomy

Endoscopic, transnasal, transsphenoidal pituitary microsurgery.

Removal of adenoma while preserving anterior pituitary function in most patients.

Surgery is usually well tolerated, but complication occur in about 10%.

Postoperative care WOF: Bleeding

operative site is patched with muscle or fat-> sutures easily disrupted.

keep the patient on bed rest for 24 hours after surgery and encourage ambulation thereafter

keep the head of bed elevated (30°) to avoid placing tension or pressure on the suture line.

Instruct the patient not to sneeze, cough, blow his nose, or bend over for several days to avoid disturbing the suture line.

Arrange for visual field testing as soon as possible because visual defects can indicate hemorrhage.

Postoperative Care WOF: CSF leak and infection

reinforce measures to prevent increased ICP oral care, BUT the patient should not brush his

teeth for 2 weeks to avoid suture line disruption Signs of CSF leak

Frequent clearing of the throat and swallowing Presence of halo ring on gauze Test for glucose Signs of infection Fever, headache, nuchal rigidity

Postoperative Care WOF: Post-Op pain

Mild analgesics for headache caused by CSF loss during surgery or paranasal pain.

Paranasal pain typically subsides when the catheters and packing are removed, usually 24 to 72 hours after surgery

Postoperative Care WOF: Diabetes Insipidus

due to inadequate release of ADH usually happens 24 to 48 hours after surgery and

may resolve within 72 hours. be alert for increased thirst and increased specific

gravity. Management I & O, urine sp. Gravity and daily weight monitoring Fluid replacement Aqueous vasopressin, sublingual desmopressin

acetate.

Postoperative Care WOF: S/Sx of hypopituitarism

patient may need hormonal replacement therapy due to decreased pituitary secretion of tropic hormones.

Necessary: cortisol immediate post-op Maintenance hormonal replacement as needed

o Cortisolo Thyroxineo Estrogen or Testosteroneo Vasopressin

Diabetes InsipidusSIADH

Vasopressin or Antidiuretic Hormone

Regulates water metabolism

Released during stress or in response to an increase plasma osmolality to stimulate reabsorption of water and decreased urine output.

Diabetes Insipidus Disorder characterized by massive polyuria

due to either lack of ADH or kidney’s insensitivity to it.

Types:Central DINephrogenic DI

Diabetes Insipidus Central Diabetes Insipidus: Deficiency of

vasopressinPrimary diabetes Insipidus ( without an identifiable

organic lesion noted on MRI of the pituitary and hypothalamus) May be familial, occurring as a dominant trait, or

(“idiopathic”)Secondary diabetes insipidus

Due to damage to the hypothalamus or pituitary stalk by tumor, anoxic encephalopathy, surgical or accidental trauma, infection (encephalitis, tuberculosis, syphilis), sarcoidosis, or multifocal langerhans cell (eosinophilic) granulomatosis (“histiocytosis X”)

Diabetes Insipidus “Nephrogenic Diabetes Insipidus”

Due to defect in the kidney tubules that interferes with water reabsorption

Polyuria is unresponsive to vasopressinPatients have normal secretion of vasopressin

Diabetes InsipidusSigns and Symptoms Polyuria-> enormous daily output of very dilute

urine, water-like urine with specific gravity of 1.001 to 1.005

Intense thirst (patient tends to drink 4 to 40liters of fluid daily), especially with a craving for ice water,

Dehydration-> weight loss, poor tissue turgor, dry mucous membranes, constipation, muscle weakness, dizziness.

Inadequate water replacement results in Hyperosmolality (irritability, mental dullness,

coma, hyperthermia) because of dehydration and hypernatremia

Hypovolemia (hypotension, tachycardia and shock eventually)

Diabetes Insipidus Diagnostics

Fluid deprivation test-> to differentiate between psychogenic polydipsia and DI

Administration of desmopressin->to differentiate between central DI and nephrogenic DI

24 hour urine collection of volume, glucose, and creatinine

Serum for glucose, urea nitrogen, calcium, uric acid, potassium and sodium.

TherapeuticsMedications

For central DI Desmopressin (DDAVP): intranasal Lypressin: intrasanal Vasopressin tannate in oil: IM

For nephrogenic DI: Indomethacin-hydrochlorthiazide (with potassium

supplementation) Indomethacin-demopressin Indomethacin-amiloride

Clofibrate, chlorpropamide and thiazide diuretics (mild DI)

Psychotherapy

DI: Nursing ManagementMaintain fluid and Sodium balance

Record I & O. Weigh patient daily.Maintain fluid intake to prevent dehydration.WOF: dehydration and shockKeep the side rails up and assist with walking if

the patient is dizzy or has muscle weakness.Monitor urine specific gravity between doses.

Watch for decreased specific gravity with increased urine output->need for the next dose or a dosage increase.

DI: Nursing Management Add more bulk foods and fruit juices to the diet-

>to prevent constipation. Laxative (milk of magnesia PRN).

Provide meticulous skin and mouth care, and apply a lubricant to cracked or sore lips.

Diet: low in sodium Carry out drug therapy

caution must be used with administration of vasopressin if coronary artery disease is present->causes vasoconstriction

assist in searching for the underlying pathology

Syndrome of Inappropriate Antiduretic Hormone (SIADH) Disorder due to

excessive ADH release Signs and Symptoms

persistent excretion of concentrated urine

signs of fluid overload change in level of

consciousness NO EDEMA HYPONATREMIA

Causes of SIADH Tumors: bronchogenic carcinoma, lymphoma,

pancreatic cancer, mesothelioma Pulmonary: TB, pneumonia, lung abscess, COPD,

pneumothorax, HIV secretion CNS: meningitis, head injury, subdural hematoma,

subarachnoid hemorrhage, neurosurgery Drugs: some medications (vincristine,

phenotiazines, tricylic antidepressants, thiazide diuretics, and others) and nicotine have been implicated in SIADH; they either directly stimulate the pituitary gland or increase the sensitivity of renal tubules to circulating ADH.

SIADH: diagnostic tests Low serum sodium (<135meqs/L) Low serum osmolality High urine sodium osmolality (urine

osmolality >100 mosmol/kg) High urine sodium excretion (>20 mmol/L) Normal renal function (low

BUN<10mg/dL),absence of hypothyroidism and glucocorticoid deficiency and recent diuretic therapy.

SIADH: Management Maintain fluid balance

Restriction or water intake (<1,000ml/day). (takes 3-10 days to work) If the patient has evidence of fluid

overloading, a history of CHF, or is resistant to treatment, loop diuretics (furosemide) may be added as well.

Chronic treatment: lithium or demeclocycline which inhibit ADH action.

Monitoring of body weight.

SIADH: Management Maintain sodium balance

Increase sodium intake if the serum sodium is below 120 or if the

patient is seizing, emergency treatment: 3% NaCL. May be followed by furosemide.

Excessively rapid correction of hyponatemia may cause central pontine myelinolysis.

Patients with a plasma sodium concentration greater then 125 mmol/L rarely need specific therapy for hyponatremia.

Adrenal InsufficiencyCushing’s SyndromeHyperaldosteronsimPheochromocytoma

Adrenal Cortex Hormones Glucocorticoids

Cortisol, corticosterone Increased blood glucose levels by increasing

the rate of gluconeogenesis. Increase protein catabolism Increasing mobilization of fatty acids promote

Na and H2O retention Anti-inflammatory effect Aid the body in coping with stress

Adrenal Cortex Hormones Mineralocorticoids

Aldosterone, corticosterone, Deoxycorticosterone

Regulate fluid and electrolyte balanceStimulate reabsorption of sodium, chloride and

waterStimulate potassium excretion.

Under the control of the Renin-Angiotensin-aldosterone system

Adrenal cortex hormones Sex hormones

Androgens, EstrogensInfluences the development of sexual

characteristics

Adrenal Medulla Release catecholamines

EpinephrineNorepinephrine

Released during “fight or flight” situations-> SYMPATHETIC effect

Hypercortisolism (Cushing’s Syndrome)Cluster of physical

abnormalities due to excessive cortisol release

Cortisol excess is due either to: Autonomous steroid

release from adrenal Increased ACTH release

from pituitary complication of

exogenous steroid therapy

Pic of hympy dumpty

Hypercortisolism (Cushing’s Syndrome)Altered metabolism of

CHO: hyperglycemiaCHON: muscle wasting, thin, fragile skin,

impaired wound healingFats: central obesity, moon face, buffalo humpNa and water retentionHypokalemia, hypocalcemiaAcne, hirsutism, menstrual changes, decreased

libidoWeakness, emotional lability

Cushing’s Syndrome

Complications Osteoporosis

Peptic Ulcer

Immune and inflammatory response is also compromised

Other complications include HPN, and sexual and psychological complications

Cushing’s Syndrome: Diagnostics ACTH levels-> determine whether the

syndrome is ACTH dependent. 24-hour urine collection for cortisol, midnight

serum cortisol Dexamethasone suppression test-> 1mg

dexamethasone given at 11 pm and serum cortisol taken at 8am the next day.Cortisol level <5ug/dl excludes Cushing’s

syndrome with 98% certainty Radiologic evaluation

Tumor in the pituitary or adrenal gland

Cushing’s Syndorme: Management Transsphenoidal resection of pituitary tumor Medications:

o Aminogluthetimide: adrenal enzyme inhibitoro Metyrapone and ketoconazole: suppress

hypercortisolism in unresectable adrenal tumor Antihypertensives Adrenalectomy as needed

Cushing’s Syndome: Nursing ConsiderationsMonitor VS, WOF for HPNSafety Precaution:

Maintain muscle tone Prevent accidents or falls and provide adequate rest

Protect client from exposure to infection, monitor WBC

Maintain skin integrityMinimize stressProvide diet low in calories, sodium and high

in protein, potassium, calcium and vitamin DMonitor for urine glucose and acetone, administer

insulin if necessaryPrepare client for adrenalectomy if needed

HyperaldosteronismHypersecretion of aldosterone from the

adrenal cortex

Two types: Primary disease of the adrenal cortex Secondary condition due to increased plasma

renin activityCauses:

Excessive reabsorption of sodium and water Excessive renal excretion of potassium

Hyperaldosteronism: CausesPrimary hyperaldosteronism: Autonomous

secretion of aldosterone from the adrenals Benign adrenal adenoma (Conn’s syndrome)

Secondary hyperaldosteronism: High renin state-> stimulating aldosterone release Renal artery stenosis Wilm’s tumor Pregnancy Oral Contraceptive use Nephritic syndrome Cirrhosis with ascites Heart failure

Hyperaldosteronism: signs and sypmtoms Hypertension

Headache and visual disturbance Hypokalemia

Muscle weakness and fatigueParesthesia and ArrhytmiasPolyuria and PolydipsiaTetany from alkalosis

Hypernatremia

Hyperaldosteronism: DiagnosticsHypokalemiaHypernatremiaElevated serum bicarbonate and pHHypomagnesemiaElevated plasma and urinary aldosteroneDecreased Renin in 1° hyperaldosteronismIncreased Renin in 2° hyperaldosteronismLow specific gravity urine (diluted urine)

Hyperaldosteronism: TreatmentPrimary hyperaldosteronism:

Unilateral adrenalectomy After aderenalectomy, WOF: signs of adrenal insufficiency.

• Potassium-sparing diuretic (such as spironolactone or amiloride)-> may lead to decreased libido, gynecomastia, impotence

• Antihypertensives• Aminogluthetimide-> inhibits synthesis of

aldosterone.• Diet: sodium restriction, increased potassium• Treatment of secondary hyperaldosteronism:

include correction of the underlying cause.

Adrenal Insufficiency• 1° adrenal insufficiency: Addison’s disease

The most common form of adrenal hypofunction-> occurs when more than 90% of the adrenal gland is destroyed

Autoimmune process-> decreased secretion of androgen, glucocorticoids, and mineralocorticoids.

• 2 ° adrenal Insufficiency: It may also be caused by a disorder outside the gland Aldosterone secretion frequently continues.Nursing Alert! Adrenal crisis (addisonian crisis) is

a medical emergency requiring immediate, vigorous treatment.

Adrenal Insufficiency:causesAutoimmune destruction of the adrenal gland,

tuberculosis, bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, or fungal infections.

Secondary adrenal hypofunction is caused by Hypopituitarism Abrupt withdrawal of long term corticosteroid

therapy• In a patient with adrenal hypofunction, adrenal

crisis occurs when the body’s stores of glucocorticoids are exhausted by trauma, infection, surgery, or other physiologic stressors.

Adrenal Insufficiency: signs and symptomsWeakness, fatigue

Weight loss, nausea and vomiting, anorexia

Chronic constipation or diarrhea

Cardiovascular abnormalities Postural hypotension, decreased cardiac output Weak, irregular pulse Decreased tolerance for even minor stress

Adrenal Insufficiency: signs and symptomsConspicuous bronze skin coloration,

especially in hand creases and over the metacarpophalangeal joints, elbows, and knees.

Poor coordinationFasting hypoglycemia; and craving for salty

food.AmenorrheaAdrenal crisis

Profound weakness and fatigue, shock, severe nausea and vomiting, hypotension, dehydration and high fever.

POMC: the “Big Momma”MSH is produced when the ACTH production

is increased-> hyperpigmentation

Adrenal Insufficiency

Decreased plasma cortisol levels and serum sodium levels.

Increased ACTH (in addison’s), serum potassium, and BUN level.

Adrenal Insufficiency: TreatmentCorticosteroid replacement, usually with

cortisone or hydrocortisone-> primary lifelong treatment

Fludrocortisone acetate: acts as a mineralocorticoid to prevent dehydration and hypotension.

Adrenal Crisis: prompt IV bolus of corticosteroids, 3 to 5 L of IV fluids, dextrose

Adrenal Insufficiency: Nursing ManagementWOF: adrenal crisis

Hypotension and signs of shock (decreased level of consciousness and urine output)

Watch for hyperkalemia before treatment and for hypokalemia after treatment (from excessive mineralocorticoid effect)

Adrenal Insufficiency: Nursing Management

If patient has diabetes, check blood glucose levels periodically because steroid replacement may necessitate changing the insulin dosage.

Adrenal Insufficiency: Nursing Management Diet: maintain sodium and potassium balance,

high protein and carbohydrates

If the patient is anorexic, suggest six small meals per day to increase calorie intake.

Observe the patient receiving steroids for cushingoid signs, such as fluid retention around the eyes and face.

Adrenal Insufficiency: Nursing Management Instruct on lifelong cortisone replacement

therapy: “ Do not omit medications” Give 2/3 of dose in AM and 1/3 in PM

Instruct the patient that he’ll need to increase the dosage during times of stress.

Warn that infection, injury, or profuse sweating in hot weather may precipitate crisis.

Pheochromocytoma Rare disorder, a chromaffin-cell tumor of the

sympathetic nervous system, usually in the adrenal medulla, secretes an excess of the catecholamines epinephrine and norepinephrine.

This causes episodes of hypotension and symptoms of catecholamine excess.

The tumor is usually benign but may be malignant in as many as 10% of patient.

Pheochromocytoma

Pheochromocytoma: Signs and Symptoms Think sympathetic!!!

Persistent or paroxysmal HPN Palpitations, tachycardia,

headache, visual disturbances, diaphoresis, pallor, warmth or fluting, paresthesia, tremor, and excitation.

Anxiety, fright, nervousness, feelings of impending doom, abdominal or chest pain, tachypnea, N&V, fatigue, wt. loss, constipation, postural hypotension, paradoxical response to antiHPNs(common), hyperglycemia

Pheochromocytoma:Diagnostic tests:

Increased plasma levels of catecholamines, elevated blood sugar, glucosuria

Elevated urinary catecholamines and urinary VMA Nursing considerations! Avoid coffee, nuts,

chocolate, banana, vanilla.

Tumor on CT scan.

Pheochromocytoma: TreatmentSurgical removal of the tumor with sparing of

the normal adrenals, if possible WOF: hypo or hypertension post-op

Anti-hypertensives: Alpha-adrenergic blocker ( phentolamine,

prazosin, or phenoxybenzamines) A beta-blocker (propanolol)

Metyrosine may be used to block catecholamine synthesis.

AdrenalectomyResection or removal of one or both adrenal

glands.

The treatment of choiceFor adrenal hyperfunction and

hyperaldosteronismAdrenal tumors, such as adenomas and

pheochromocytomas.

Adrenalectomy: Pre-opCorrect electrolyte imbalance

Potassium, sodium, calcium

• Manage hypertension

Adrenalectomy: Post-Op careMonitor vital signsWOF: shock and hemorrhageKeep in mind that postoperative hypertension

is common because handling of the adrenal glands stimulates catecholamine release.

WOF: adrenal crisis-> hypotension, hyponatremia, hyperkalemia

Remember, glucocorticoids from the adrenal cortex are essential to life and must be replaced to prevent adrenal crisis until the hypothalamic, pituitary, and adrenal axis resumes functioning.

Adrenalectomy: Nursing interventionsInstruct the patient to take prescribed

medication as directed.

If patient had unilateral adrenalectomy, explain that he may be able to taper his medication in a few months.

Inform patient that sudden withdrawal of steroids can precipitate adrenal crisis.

HyperthyroidismHypothyroidsim

The Thyroid GlandThyroid gland is a butterfly-shaped organ located in the lower neck anterior to the trachea

It consists of two lateral lobes connected by an isthmus

The gland is about 5cm long and 3cm wide and weighs about 30g

It produces 3 hormones: T3, T4, and calcitonin

Functions of Thyroid HormonesT3

T4

Calcitonin

Tests of Thyroid FunctionThyroid-Stimulating Hormone

Single best screening test of thyroid function because of its high sensitivity

Values above the normal range of 0.38 to 6.15 uU/mL are indicative of primary hypothyroidism, and low values indicate hyperthyroidism

If TSH is normal, there is a 98% chance that the free thyroxine (FT4) is also normal.

Used for monitoring thyroid hormone replacement therapy and for differentiating between disorders of the thyroid gland and disorders of the pituitary or hypothalamus.

Tests of Thyroid FunctionSerum Free Thyroxine

Test used to confirm an abnormal TSH is FT4 FT4 is a direct measurement of free (unbound)

thyroxine, the only metabolically active fraction of T4.

Normal value: 0.9 and 1.7ng/L (11.5 to 21.8pmol/L)Serum T3 and T4

Normal range for T4 is between 4.5 and 11.5ug/dL (58.5 to 150 nmol/L)

Although serum T3 and T4 levels generally increase or decrease together, the T3 level appears to be a more accurate indicator of hyperthyroidism, which causes a greater rise in T3 than T4 levels.

Normal range for serum T3 is 70 to 220ng/dL (1.15 to 3.10 nmo/L)

Tests of Thyroid FunctionThyroid scan, Radioscan, or Scintiscan

In a thyroid scan, a scintillation detector or gamma camera moves back and forth across the area to be studied and a visual image is made of the distribution of radioactivity in the area being scanned.

• Isotopes used: 123I->most commonly used isotope. Technetium-99m pertechnetate, thallium,

thallium and americanium Scans are helpful in determining location, size, shape,

and anatomic function of the thyroid gland, particularly when thyroid tissue is substernal or large.

Identifying areas of increased function (“Hot”areas) or decreased function (“cold” areas) can assist in diagnosis.

Tests of Thyroid FunctionRadioactive Iodine Uptake

Measures the rate of iodine uptake by the thyroid gland.

The patient is administered a tracer dose of iodine-123

Measures the proportion of the administered dose present in the thyroid gland at a specific time after its administration.

Affected by the patient’s intake of iodine or thyroid hormone; therefore, a careful preliminary clinical history is essential in evaluating results.

Hyperthyroidism-> high uptake of the 123I Hypothyroidism-> very low uptake.

Tests of Thyroid FunctionFine-Needle

Aspiration Biopsy Sampling Thyroid

Tissue to: detect malignancy

Initial test for evaluation of thyroid masses.

Tests of Thyroid Function

Nursing Implications of Thyroid TestsIt is necessary to determine whether the

patient has taken medications or agents that contain iodine because these alter the results of some of the schedule tests.

Assess for allergy to iodine or shellfishFor the scans, tell patient that radiation is

minimal

Plummer’s nails

HyperthyroidismOr thyrotoxicosisIncreased metabolic rateCauses:

o Grave’s diseaseo Initial manifestations of thyroiditis (hashimoto’s

and subacute thyroiditis)o Toxic adenomao TSH-secreting pituitary tumoro Factitious thyrotoxicosiso Jodbasedow diseaseo Amiodarone-induced

Hyperthyroid: Signs and SymptomsEnlarged thyroid glandTachycardia-> atrial fibrillation, heart failureHypertensionHeat intolerance, diaphoresisSmooth, soft, warm skinFine Soft HairDiarrhea, weight loss inspite of increased appetiteNervousness and fine tremors of hands.Hyperactive reflexes, body weaknessPersonality changes, mood swingsOsteoporosisClubbing and swelling of fingers, Plummer’s nailsMenstrual disturbances, decreased fertility

Signs and Symptom’s of Grave’s DiseaseAll s/s of thyrotoxicosis

Grave’s exopthalmos-> vision loss, diplopia

Pretibial Edema

Hyperthyroidism

Thyroid StormA medical emergency: high mortality

Marked delirium, severe tachycardia, vomiting, diarrhea, dehydration, high fever

Occurs in patients with existing but unrecognized thyrotoxicosis, stressful illness, thyroid surgery, RAI administration

Increased systemic adrenergic activity->epinephrine overproduction and severe hypermetabolism

Hyperthyroidism: DiagnosticsRadioimmunoassay test shows elevated T4

and T3.Thyroid scan reveals increased radioactive

iodine (123I) uptake.↓TSH in 1° hyperthyroidism↑TSH in 2° hyperthyroidismOrbital sonography and CT scan confirm

subclinical ophthalmopathy

Hyperthyroidism: ManagementPropylthiouracil (PTU) and methimazoleUsed for pregnant women and patient who refuse

surgery or 131I treatment.During pregnancy PTU, is the preferred

therapyA few (1%) of the infants born to mothers

receiving antithyroid medication will be hypothyroid.

Mechanism of actionBlocks thyroid hormone synthesis

• WOF: Agranulocytosis

Hyperthyroidism: ManagementRadioactive iodine (131I), potassium or

sodium iodide (Potassium iodide SSKI), strong iodine solution (Lugol’s solution)

Adjunct with other antithyroid drugs in preparation for thyroidectomy

Treatment for thyrotoxic crisis: Inhibits the release and synthesis of thyroid

hormonesDecreases the vascularity of the thyroid glandDecreases thyroidal uptake of radioactive iodine

following radiation emergencies or administration of radioactive isotopes of iodine.

Hyperthyroidism: Nursing ManagementPotassium, or sodium iodide, (potassium iodide

solution, SSKI) strong iodine solution (Lugol’s solution) Category D

Dilute oral doses in water or fruit juice and give with meals to prevent gastric irritation, to hydrate the patient, and to mask the very salty taste

Warn the patient that sudden withdrawal may precipitate thyrotoxicosis

Store in a light-resistant containerGive iodides through a straw to avoid tooth

discolorationForce fluids to prevent fluid volume deficit

Hyperthyroidism: Nursing Management of RAI treatmentRadioactive iodine (sodium iodide or 131I)-cat. X

Food may delay absorption. The patient should fast overnight before administration

After dose for hyperthyroidism, the patient’s urine and saliva are slightly radioactive for 24 hours; vomitus is highly radioactive for 6 to8 hours.

Institute full radiation precautions during this time

Instruct the patient to use appropriate disposal methods when coughing and expectorating.

Hyperthyroidism: Nursing Management of RAI Tx After dose for thyroid cancer, isolate the

patient and observe the following precations:Pregnant personnel shouldn't take care of the

clientDisposable eating utensils and linens should be

usedInstruct the patient to save all urine in lead

containers for 24 to 48 hours so amount of radioactive material excreted can be determined

Or flush the toilet twice after urination

Hyperthyroidism: Nursing Management of RAI Treatment

The patient should drink as much fluid as possible for 48 hours after drug administration to facilitate excretion.

Limit contact with the patient to 30 minutes per shift per person the 1st day; may increase time to 1 hour on 2nd day and longer on the 3rd day.

Hyperthyroidism: Nursing Management of RAI treatment If the patient is discharged less than 7 days

after 131I dose for thyroid cancer, warn patient:To avoid close, prolonged contact with small

childrenNot to sleep in the same room with his spouse

for 7 days after treatment-> increased risk of thyroid cancer in persons exposed to 131I.

Hyperthyroidism B- blockers, Digoxin, anticoagulation Prednisone for opthalmopathy Treatment for thyroid storm:

o PTUo I.V. propanolol to block sympathetic effectso Corticosteroids to replace depleted cortisol

levelso Iodide to block release of thyroid hormone

Hyperthyroidism: ManagementSurgery: ThyroidectomyFor exopthalmos

Suggest sunglasses or eye patches to protect his eyes from light

Moisten the conjunctivae often with artificial tears Warn the patient with severe lid retraction to avoid

sudden physical movement that might cause the lid to slip behind the eyeball.

Elevate the head of bed to reduce periorbital edema Stress the importance of regular medical follow-up

after discharge because hypothyroidism may develop from 2 to 4 weeks pot-op

Drug therapy and 131I therapy require careful monitoring and comprehensive teaching

Hypothyroidism A state of low serum thyroid hormone levels or cellular

resistance to thyroid hormoneCauses May result from thyroidectomy Radiation therapy Chronic autoimmune thyroiditis ( Hashimoto’s Thyroiditis) Inflammatory conditions such as amyloidosis and

sarcoidosis Pituitary failure to produce TSH Hypothalamic failure to produce thyrotropin-releasing

hormone(TRH) Inborn errors of thyroid hormone synthesis An inability to synthesize thyroid hormone because of

iodine deficiency. Use of antithyroid medications such as PTU.

Hypothyroidism Weakness Fatigue Forgetfulness Cold intolerance Unexplained weight gain Constipation Goiter Slow speech Decreasing mental

stability

Cool, dry, coarse, flaky inelastic skin.

HypothyroidismPuffy face, hands and feetDry, sparse hairThick, brittle nailsSlow pulse rateAnorexiaAbdominal distentionMenorrhagia Decreased libidoInfertilityAtaxiaIntentional tremor

Myxedema Coma Manifests as hypotension, bradycardia,

hypothermia, hyponatremia, hypoglycemia, respiratory failure, coma

Can be precipitated by acute illness, rapid withdrawal of thyroid medication, anesthesia, surgery, hypothermia, use of opioids

Hypothyroidism : Diagnostics Radioimmunoassay tests: ↓ T3 & T4 ↑TSH level with 1° hypothyroidism ↓TSH in 2 ° hypothyroidism Serum cholesterol and triglyceride levels are

increased

In myxedema coma Low serum Na levels Respiratory acidosis because of hypoventilation

ManagementPrevention: Prophylactic iodine

supplements to decrease the incidence of iodine deficient goiter

Symptomatic cases:Hormonal replacement: synthroid

(synthetic hormone (levothyroxine))-dosage is increased q 2-3weeks

Nursing Management of replacement therapy Warn the patient (especially the elderly) to

tell the doctor if withChest pain, palpitations, sweating,

nervousness, or other signs or symptoms of overdosage

Signs and symptoms of aggravated cardiovascular disease (chest pain, dyspnea and tachycardia)

Nursing Management of replacement therapy Instruct the patient to take thyroid hormones

at the same time each day to maintain constant hormone levels.

Suggest a morning dosage to prevent insomnia

Monitor apical pulse and BP. If pulse is >100bpm, withhold the drug. Assess to tachyarrhythmia and chest pain.

Nursing Management of Replacement therapy Thyroid hormones alter thyroid function test

results.For 123I uptake studiesD/C levothyroxine 4 weeks before the test.D/C liothyronine 7 to 10 days before the test.

Monitor prothrombin time; a patient taking these hormones usually requires less anticoagulant WOF: unusual bleeding and bruising

Hypothyroidism: Nursing InterventionsDiet: High bulk, low-calorie dietEncourage activityMaintain warm environmentAdminister cathartics and stool softeners, as needed.To prevent myxedema coma, tell the patient to

continue his course of thyroid medication even if his symptoms subside: Maintain patent airway Administer meds-synthroid, glucose, corticosteroids. IV fluid replacement Wrap patient in blanket Treat infection or any underlying illness

HyperparathyroidismCharacterized by

excess activity or one more of the four parathyroid glands, resulting in excessive secretion of parathyroid hormone(PTH)

Maybe primary or secondary

Hyperparathyroidism: causes1° hyperparathyroidism:

Single adenoma, genetic disorders, or MEN

• 2 ° hyperparathyroidism:Rickets, vitamin D deficiency, chronic renal

failure, phenytoin or laxative abuse.

HyperparathyroidismEffect of PTH secretion: ↑Calcium

Through increased bone resorption, increased GI and renal absorption of calcium

• Complications Renal calculi-> renal failure Osteoporosis Pancreatitis Peptic ulcer

HyperparathyroidismTHINK OF HYPERCALCEMIA: CNS: psychomotor and personality disturbances,

loss of memory for recent event, depression, overt psychosis, stupor and possibly, coma.

GI: anorexia, N&V dyspepsia, and constipation.

Neuromuscular: fatigue; marked muscle weakness and atrophy, particularly in the legs.

Hyperparathyroidism:Signs and Symptoms Renal: symptoms of recurring nephrolithiasis-

>renal insufficiency

Skeletal and articular: chronic lower back pain and easy fracturing from bone degeneration, bone tenderness, joint pain

Others: skin pruritus, vision impairment, subcutaneous calcification.

Hyperparathyroidism: Dx ↑ serum PTH levels ↑ serum Ca and decreased Phosphorus

levels. X-rays may show diffuse demineralization of

bones Elevated alkaline phosphatase

Hyperparathyroidism: Treatment Surgery to remove the adenoma Force fluids; limiting dietary calcium intake For life threatening hypercalcemia: promote

sodium and calcium excretion, using normal saline solution (up to 6L in life-threatening situations), furosemide, and administering oral sodium or potassium phosphate, Calcitonin

Postmenopausal women: estrogen supplements

Hypoparathyroidism A deficiency of PTH PTH primarily regulates calcium balance; hypoparathyroidism leads to

hypocalcemia and produces neuromuscular symptoms ranging from paresthesia to tetany.

Hypoparathyroidism Congenital absence or malfunction of the parathyroid

glands. Autoimmune destruction Removal of or injury to one or more parathyroid glands

during neck surgery Rarely, from massive thyroid radiation therapy. Ischemic infarction of the parathyroids during Sx. Diseases, such as amyloidosis or neoplasms Suppression of normal gland function caused by

hypercalcemia(reversible) Hypomagnesemia-induced impairment of hormone

secretion(reversible)

Hypoparathyroidism: Signs and Sypmtoms Neuromuscular irritability Increased deep tendon reflexes, (+) chvostek’s and Trousseau’s

signs Dysphagia Paresthesia Psychosis Mental deficiency in children Tetany seizures Arrhythmias Abdominal pain Dry, lusterless hair, spontaneous hair loss Brittle fingernails that develop ridges or fall out. Dry scaly skin Weakened tooth enamel may cause teeth to stain, crack, and

decay easily.

Hypoparathyroidism

Decreased PTH and serum calcium levels

Elevated serum phosphorus levels

X-rays reveal increased bone density

ECG: prolonged Qti, QRS-complex ST-elevation changes.

Diabetes Mellitus

Hormones of the PancreasInsulin

Decreases blood sugar: Stimulating active transport of glucose into muscle

and adipose tissue Promoting the conversion of glucose to glycogen for

storage Promoting conversion of fatty acids into fat Stimulating protein synthesis

Secreted in response to high blood sugarFound in βcells of the islets of langerhans

Hormones of the PancreasGlucagon

Increases blood glucose by Causing glycogenolysis and gluconeogenesis in the

liver

Secreted in response to low blood sugar Found in the α-cells of the islets of langerhans

Diabetes MellitusChronic disease characterized by

hyperglycemiaIt is due to total or partial insulin deficiency or

insensitivity of the cells to insulin

Characterized by disorders in the metabolism of CHO, FAT and CHON as well changes in the structure and function of blood vessels.

Types of DM Type 1 or IDDM

Usually occurs in children or in non-obese adults

Type 2 or NIDDM Usually occurs in obese adult over age 40

Gestational DM Secondary DM

Induced by trauma, surgery, pancreatic disease or medications

Can be treated as either type 1 or type 2

Comparison Bet Type 1 and Type II Diabetes Mellitus

Type 1 Type 2

Onset- SuddenAge at Onset- Any age

(typically young)Body Habitus- Usually

thinKetosis- commonAutoantibodies-present

in most casesEndogenous insulin- low

or absent

GradualMostly in adults

Frequently obeseRareAbsent

Can be normal, decreased, or increased.

PathophysiologyHyperglycemia Lack of insulin causes

hyperglycemia (insulin is necessary for the transport across the membrane)

Body excretes excess glucose through kidneys ->osmotic diuresis->polyuria->dehydration->polydipsia

Cellular starvation-> polyphagia

Cont. pathophysiology

The body turns to fats and protein for energy; but in the absence of glucose in the cell, fats cannot be completely metabolized and ketones are produced

Chronic Complications

Microangiopathy: retinopathy, nephropathy

Macroangiopathy: peripheral vascular disease: peripheral vascular disease, atheroscelrosis, CAD

Neuropathy

Pathophysiology of Diabetic Nephropathy

Hyperglycemia

↑GFR Microalbuminuria

Proteinuria

↓GFR

ESRD

Diabetic Foot

Instruction in the care of the FeetHygiene of the feet

Wash feet daily with mild soap and lukewarm water. Dry thoroughly between toes by pressure. DO NOT RUB vigorously, as this is apt to break the delicate skin

Rub well with vegetable oil to keep them soft, prevent excess friction, remove scales, and prevent dryness.

If the feet become too soft and tender, rub them with alcohol about once a week.

Instruction in the Care of the FeetHygiene of the feet When rubbing the feet, always rub upward from the

tips of the toes. If varicose veins are present, massage the feet very gently; never massage the legs.

If the toenails are brittle and dry, soften them by soaking for 1 ½ hr each night in lukewarm water containing 1 tsbp of powdered sodium borate (borax) per quart. Clean around nails become too long, file them with an emery board. File them straight across and no shorter than the underlying soft tissue of the toes. Never cut the corner of the nails.

Instruction in the care of the Feet Wear low-heeled shoes of soft leather that fit the

shape of the feet correctly. The shoes should have wide toes that will cause no pressure, fit close in the arch, and grip the heels snugly. Wear new shoes one-half hour on the first day and increase by 1 hour each day following. Wear thick, warm, loose stockings.

Treatment of Corns and Calluses Corns and calluses are due to friction and pressure,

most often from improperly fitted shoes and stockings. Wear shoes that fit properly and cause no friction or pressure.

Instructions in the Care of the Feet To remove excess calluses or corns, soak the

feet in lukewarm (not hot) water, using a mild soap, for about 10 minutes and then rub off the excess tissue with a towel or file. Do not tear it off. Under no circumstances must the skin become irritated.

Do not cut corns or calluses. If they need attention it is safer to see a podiatrist.

Prevent callus formation under the ball of the foot (a) by exercise, such as curling and stretching the toes several times a day; (b) by finishing each step on the toes and not on the ball of the foot. And (c) by wearing shoes that are not too short and that do not have high heels

Diagnostics: FBS, OGTT and RBSNormalGlucoseTolerance

Impaired GlucoseTolerance

DiabetesMellitus

FastingPlasmaGlucose

< 110 mg/dl 11o-125 mg/dl ≥ 126 mg/dl on 2 occassions

2 hours after glucose

< 140 mg/dl ≥ 140 but <200 ≥ 200 mg/dl

Random Blood Glucose

--------- --------- >200 mg/dl plus diabetic symptoms

Diagnostics: Glycosylated HemoglobinNV= 7.5% or less good control

7.6%--8.9% fair control

9% or greater, poor control

Therapeutic interventions Lifestyle changes

Weight control and exercise

Planned diet 50-60% of calories are

complex carbohydrates, high fiber

12-20% of daily calories is protein, 60-85g/day

Fat intake not to exceed 30% of daily calories, more of polyunsaturated/ monounsaturated fats

Basic tools: food exchange groups

Self monitoring of blood glucose

Moderation in alcohol intake

Using artificial sweetener is acceptable

Cont: therapeutic interventionsInsulin administration:

For type 1 and type 2 dm when diet and weight control therapy failed.

Aspirin, alcohol, oral anticoagulants, oral hypoglycemics beta blockers, TCA’s, tetracycline, MAOI’s increase the hypoglycemic effect of insulin

Glucocorticoids, thiazide diuretics, thyroid agents, oral contraceptives increase glucose levels

Illness, infection and stress increase the need for insulin

Insulin Onset Peak Duration

Ultra rapid acting insulin analog(humalog)

10- 15 mins 1 hour 3 hours

Short acting insulin(Human regular insulin)

30 minutes- 1 hour

2-4 hours 4-6 hours

Intermediate acting insulin(Humulin lente, Humulin NPH)

3-4 hours 4-12 hours 16-20 hours

Long acting Insulin(Protamine zinc, humulin ultralente)

6-8 hours 12-16 hours 20-30 hours

Premixed insulin(70% NPH, 30% regular)

30min-1 hour 2-12 hours 18-24 hours

Example Order for Typical Sliding Scale (HR)

CBG Insulin Dose150-200 201-250 251-300301-350351-400>400

2 units4 units6 units8 units10 unitsRefer to MROD, EFOD

or Diabetology Fellow.

Complications of Insulin TherapyLocal allergic reaction, lipodystrophy, insulin

resistance

“Dawn Phenomenon”- increase in blood sugar because of release of GH at around 3am;Tx: give NPH at 10 pm

• “Somogyi effect”-rebound hyperglycemia at 7am after a bout of hypoglycemia at 2-3am.Tx: Decrease the evening dose of intermediate

acting insulin

Diabetes Mellitus: Complication of Insulin

Dawn Phenomenon

Somogyi Phenomenon

S/SxHyperglycemia at dawn

Rebound Hyperglycemia at early morning

Cause Growth hormone release at 3 AM

Hypoglycemia at dawn

Mgt Give IAI at 10 PM (or adjust dose)

Decrease dose of IAI at 10 PM

Complications of insulin therapyHypoglycemia Hypoglycemia

If awake, give 10-15 g of fast acting simple carbohydrate (glucose tablets, fruit juice, and soda)

If unconscious, glucagon SQ or IM

If in the hospital, 25-5o cc of D5050 (50% dextrose in 50cc vial)

Oral Hypoglycemic Agents For DM type 2

May have to be shifted to insulin when sick, under stress, during surgery.

Necessary to shift to insulin when pregnant

Oral Hypoglycemicso Sulfonyureas

Promotes increase insulin secretion from pancreatic beta cells through the stimulation( requires at least 30% normally functioning beta cells)

1st gen-agents: Tolbutamide, acetohexamide, tolzamide,

chlorpropamide2nd gen-agents:

Glypizide, Glyburide

Oral HypoglycemicsBiguanides

Reduces hepatic production of glucose by inhibiting glucogenolysis

Decrease the intestinal absorption of glucose and improves lipid profile

Agents Phenformin, Metformin, Buformin

Oral HypoglycemicsThiazolidinediones-enhances action at the cell

and post receptor site decreasing insulin resistance

Agents: Pioglitazone (actos), Rosiglitazone (avandia)

Acute Complication: DKAo Characterized by hyperglycemia and

accumulation of ketones in the body causing metabolic acidosis

o Occurs in insulin dependent Diabetic cliento Precipitating factors: Undiagnosed DM,

neglect of treatment, infection, other physical or emotional stress

o Onset slow, maybe hours to days

DKA: Signs and Symptoms Polydipsia, polyphagia, polyuria Nausea and vomiting, abdominal pain Skin warm, dry and flushed Dry mucous membranes Kussmaul’s respirations or hyperventilation;

acetone breath Alterations in LOC Hypotension, tachycardia

Hyperglycemic Hyperosmolar Nonketotic Coma (HHNK)Characterized by hyperglycemia and a

hyperosmolar state w/o ketosis

Occurs in NIDDM or non-diabetic persons (typically elderly persons

Precipitating factors: undiagnosed DM, infection or other stress; certain medications, dialysis, hyperalimentation, major burns

Emergency ManagementFor both DKA and HHNK, treat dehydration first

with 0.9% or .45% saline Shift to d5w when glucose levels are down to 250-

300mg/dl WOF too rapid correction, it can cause rapid fluid

shifts (brain edema and increased ICP, ARDS) IV regular insulin 0.1 unit/kg bolus then 0.1 u/kg/hr

drip Correcting electrolyte imbalance. WOF hypoK as a

result of treatment. For severe acidosis (pH <7.1), DKA patients may have to be given NaHCO3

DKA HHNK

Lab Findings

•Hyperglycemia (>250)

•Metabolic Acidosis ph <7.3

•Ketosis

•Hyperglycemia (>600mg/dl)

•Hyperosmolarity(>320 mOsm/L)

•pH >7.3 (no acidosis)

S/sx HyperglycemiaPolyuriaDehydrationAcidosis

HyperglycemiaHyperosmolarityPolyuria (osmotic diuresis)Dehydration

Type of patients DM type I

DM type IIElderlyPatients on TPN, burn

DKA HHNK

Treatment HydrationInsulinNaHCO3

HydrationInsulin

Mortality

rate

5% to 10% 10% to 20%

“Always strive for excellence in everything that you do.”

Thank You Very MuchDCSC RN