PITUITARY GLAND

HYPOPITUITARISM
decreased secretion of one or more of the eight hormones produced by the pituitary gland Panhypopituitarism most hormones ETIOLOGIC CAUSES: disease of the pituitary gland itself disease of the hypothalamus can result from radiation therapy (head and neck area) total destruction from trauma, tumor/vascular lesion which removes all stimuli DWARFISM GENERALIZED LIMITED GROWTH CATEGORIES: Disproportionate small body but other parts are of average size or above average size example: Dagul Proportionate everything is proportionate but small in nature example: Mahal and Mura TYPES: Genetic or Mid-parental height boys height: (+ 5in to mothers height) + fathers height = total / 2 girls height: ( - 5in from fathers height) + mothers height = total / 2 Constitutional Stature short in nature Psychosocial Dwarfism due to an emotional problem Catch-up Growth present during puberty stage CLINICAL MANIFESTATIONS: approximately 4ft in height average size trunk short arms and legs short fingers limited mobility progressive development of bowed legs progressive development of swayed lower back (Kyphotic) NURSING INTERVENTION: provide emotional support to the family encourage client and family to express feelings administer prescribed GH DIABETES INSIPIDUS HYPOSECRETION OF ADH DISORDER OF WATER

ETIOLOGIC FACTORS: Primary idiopathic

Secondary

METABOLISM

CAUSED DI)

BY

DEFICIENCY OF ADH SECRETED BY PPG OR INABILITY OF THE KIDNEY TO RESPOND TO ADH

(NEPHROGENIC

DEFICIENCY ADH MAY BE PARTIAL /COMPLETE DI MAY BE PERMANENT / TRANSIENT

tumor), aneurysms, conditions that ICP, surgical removal of posterior pituitary tumor, CNS infections Nephrotic Diabetes Insipidus failure of renal tubules to respond to ADH longstanding renal disease (r/t hypokalemia, hypercalcemia) and other meds DIAGNOSTIC TESTS: Fluid deprivation test withholding fluid for 8-12 hours/until 3-5% body weight is lost Plasma and urine osmolality studie inability to SG and osmolality = DI Na level Plasma levels, desmopressin (synthetic vasopressin), IV infusion (hypertonic) CLINICAL MANIFESTATION: marked polyuria (4L/day) USG: 1.001 - 1.005 polydipsia (2-20L), craves cold water dehydration muscle pain and weakness postural hypotension and tachycardia urine is like water MEDICAL MANAGEMENT: GOALS: replace ADH, adequate fluid replacement, correct underlying intracranial pathology Desmopressin without vascular effects of natural ADH = fewer adverse effects administered intranasally via calibrated plastic tube Vasopressin causes vasoconstriction; used cautiously with CAD IM administration of ADH if intranasal route is not possible done every 24 96 hours vial of med should be shaken rotation of injection to prevent lipodystrophy Clofibrate (Atromid-S) hypolipidemic agent with antidiuretic effect on px with DI Chlorpropamide (Diabinese) and thiazide diuretics used in mild forms as it potentiate the actions of Vasopressin Tx for nephrogenic DI thiazide diuretics mild salt depletion prostaglandin inhibitors and indomethacin

head trauma, neurosurgery (brain

 NURSING MANAGEMENT: demonstrate correct med administration provide s/sx of hyponatremia instruct px to wear medical bracelet

HYPERPITUITARISM
ETIOLOGIC CAUSES: Sheehans syndrome Postpartum pituitary necrosis severe blood loss, hypovolemia, HPN ACROMEGALY AFTER CLOSURE OF THE EPIPHYSEAL PLATE CLINICAL MANIFESTATION: local or systemic effects growth large and thick hands visual disturbances HTN hyperglycemia organomegaly LAB ASST: CT scan MRI MEDICAL MANAGEMENT: Transphenoidal Hypophysectomy removal of pituitary gland post-op: avoid sneezing watch out for bleeding (racoons eyes, hematoma under ear). CSF leak, infection, hypopituitarism Bromocriptine (Parlodel) SE: drowsiness AE: fainting, depression NURSING MANAGEMENT: emotional support skin care prepare patient for surgery GIGANTISM BEFORE CLOSURE OF THE EPIPHYSEAL MEDICAL MANAGEMENT: Octreotide Lanreotide Parlodel Radiation therapy Surgery SYNDROME

ADRENAL GLANDS
HYPOFUNCTION

CNS disorders (head injury, brain surgery/tumor, infection) CLINICAL MANIFESTATION: hypervolemia mental status change abnormal weight gain MEDICAL MANAGEMENT: GOAL: eliminate underlying cause NURSING MANAGEMENT: monitor VS, neuro status, I&O, daily weight, provide safe environment restrict fluid intake administer diuretics (Furosemide) and IVF carefully with fluid restriction to treat severe hyponatremia administer prescribed Demeclemycin

OF ADRENAL GLANDS

PLATE

OF

INCREASED

ADH

(SIADH)
HYPERSECRETION OF ADH ETIOLOGIC CAUSES: nonendocrine origin: bronchogenic carcinoma malignant lung cells synthesize and release ADH severe pneumonia, pneumothorax, and other lung disorders direct stimulation of pituitary gland

ADDISONS DISEASE HYPERCOTISOLISM HYPOFUNCTION OF ADRENAL GLANDS ETIOLOGIC FACTORS: idiopathic surgical removal of both adrenal glands infection of adrenal glands TB, histoplasmosis inadequate secretion of ACTH therapeutic use of corticosteroids sudden cessation of ACTH therapy CLINICAL MANIFESTATIONS: muscle weakness fatigue weight loss appetite GI disturbances hyponatremia hypoglycemia dehydration and hypovolemia /dark skin pigmentation anorexia emaciation (too thin) hypotension hyperkalemia mental status changes (apathy, confusion) NURSING MANAGEMENT: less stress fluid monitor VS, especially BP monitor weight monitor blood glucose level and potassium level administer hormone agents as prescribed (glucocorticoids) ADDISONIANS/HYPOTENSIVE CRISIS LIFE-THREATENING DISORDER CAUSED BY ACUTESEVERE ADRENAL INSUFFICIENCY

CAUSES: severe stress infection trauma/surgery CLINICAL MANAGEMENT:

severe headache severe abdominal pain severe weakness severe hypotension signs of shock pallor apprehension rapid and weak pulse rapid respiration hypotension other signs: nausea diarrhea cyanosis

NURSING MANAGEMENT: administer hydrocortisone monitor VS frequently monitor I&O, neuro status, electrolyte imbalance and blood glucose administer IVF maintain bed rest maintain antibiotics

adrenal hypertrophy PHARMACOLOGICAL MANAGEMENT: Metyrapone test function of pituitary glands Mitotane ability to stress NURSING MANAGEMENT: risk for injury risk for infection prepare patient for surgery encouraging rest and activity promoting skin integrity (meticulous) improving body image use ketonazole for production of excess cortisol improving thought process (for emotional instability) monitor lab values (glucose, Na, K, Ca) administer aminoglutamide provide CHO, Na, CHON CONNS DISEASE HYPERALDOSTEROIDISM MINERALOCORTICOIDS DIAGNOSTIC TEST: USG very serum K serum Na urinary aldosterone NURSING MANAGEMENT: monitor VS, I&O, USG monitor serum, K, Na provide K-rich foods administer diuretics (Spironolactone) maintain sodium-restricted diet PHEOCHROMOCYTOMA

radiation of pituitary gland adrenalectomy of primary

HYPERFUNCTION

OF ADRENAL

GLANDS CUSHINGS DISEASE

DIURNAL PATTERN OF CORTISOL IS LOST EXCESSIVE ADRENOCORTICAL ACTIVITY HYPERSECRETION OF GLUCOCORTICOIDS
ADRENAL CORTEX

FROM

ETIOLOGIC FACTORS: adrenal tumor overuse of corticosteroids pituitary tumor ectopic production of ACTH by malignancies abuse of steroids DIAGNOSTIC TEST: serum cortisol CLINICAL MANIFESTATIONS: arrest of growth obesity, musculoskeletal changes, central-type obesitya buffalo hump in neck, heavy trunk w/ thin extremities thin and fragile skin development of bruises and striae (ecchymoses) moon-faced kyphosis, compression fractures backache osteoporosis, muscle wasting hypertension, heart failure hyperglycemia/overt DM oiliness of skin/acne disturbed sleep lost libido mood changes visual disturbances d/t pituitary tumor slow healing of wounds weight gain MEDICAL MANAGEMENT: surgical removal of tumor by transphenoidal hypophysectomy

ACTH SECRETION
MEDULLA

OF EPINEPHRINE AND NOREPINEPHRINE BY

ADRENERGIC

HORMONES

CLINICAL MANIFESTATIONS: hypertension severe headache palpitation tachycardia profuse sweating sweating and flushing weight loss, tremors hyperglycemia, glycosurics NURSING MANAGEMENT: monitor BP monitor hypertensive crisis (TOP priority) avoid stimulation (regulate BP) administer antihypertensive (check BP) prepare phentolamine monitor blood glucose provide adequate rest caloric food prepare surgery (adrenalectomy) depletion of water in body monitor s/sx of shock

 IVF lifelong replacement

glucocorticoids

Fine-needle Aspiration Biopsy

THYROID GLANDS
ASSESSMENT
AND

DIAGNOSTIC FINDINGS

inspection and palpation

swelling and asymmetry: extend neck

slightly and swallow size, consistency, shape, symmetry, and presence of tenderness hands encircle patients neck soft texture = Graves disease, firmness = Hashimotos, tenderness = thyroiditis auscultation localized audible vibration of a bruit = blood flow through thyroid gland (hyperthyroidism) Serum Thyroid-Stimulating Hormone used for monitoring thyroid hormone replacement therapy distinguishing disorders of thyroid and pituitary/hypothalamus Serum Free T4 to confirm abnormal TSH direct measurement of free thyroxine N: 0.9 1.7ng/dL (11.5 21.8 pmol/L) Serum T3 and T4 includes protein bond and free hormone levels that occur in response to TSH secretion CI: serious systemic illnesses, meds (oral contraceptives, corticosteroids, phenytoin, salicylates), protein wasting (result of nephrosis), androgen use N (T4): 4.5 11.5 ug/dL (58.5 150 nmol/L) N (T3): 70 220 ng/dL (1.15 3.10 nmol/L) T3 Resin Uptake Test indirect measure of unsaturated TBG; to determine the amount of thyroid hormone bound to TBG and the number of available binding sites useful in evaluation of thyroid hormone levels in px who have received diagnostic/therapeutic doses of iodine free binding sites = T3 reuptake > 35% = hyperthyroidism free binding sites = T3 reuptake < 25% = hypothyroidism CI: estrogen, androgen, salicylates, phenytoin, anticoagulants, corticosteroids Thyroid Antibodies RIA techniques for antithyroid antibodies 90 % = chronic autoimmune thyroid disease; 100 % = Hashimotos; 80% = Graves disease Radioactive Iodine Uptake measures rate of iodine uptake by the thyroid gland and counts the gamma rays released from the breakdown of iodine in the thyroid CI: intake of iodine

use of small-gauge needle to sample thyroid tissue negative = benign; positive = malignant; indetermine = suspicious; inadequate = nondiagnostic Thyroid Scan, Radioscan, Scintiscan a scintillation detector or gamma camera which moves back and forth across the area visual image is being made of the distribution of radioactivity in the area being scanned determine size, location, shape and anatomic function hot and cold areas Serum Thyroglobulin RIA to detect persistence or recurrence of thyroid carcinoma

HYPOTHYROIDISM
inadequate amount; underactive thyroid Cretenism (children); Myxedema (adult) TYPES: PRIMARY/THYROIDAL dysfunction of thyroid gland itself SECONDARY/PITUITARY entirely a pituitary disorder TERTIARY/HYPOTHALMIC disorder of the hypothalamus resulting in adequate secretion of TSH d/t stimulation of TRH CENTRAL failure of the pituitary gland, hypothalamus, or both CRETENISM thyroid deficiency present at birth HYPOTHYROIDISM

ETIOLOGIC FACTORS:
fails to secrete several hormones medications (Lithium, iodine

compounds, anti-thyroid meds) infiltrate diseases of the thyroid atrophy of thyroid with aging iodide insufficiency and excess thyroidectomy autoimmune response radiation therapy RISK FACTORS: 50 years above (woman) 60 years above (man) family history of thyroid problems CLINICAL MANIFESTATION: extreme fatigue hair loss, brittle nails, dry skin, and numbness/tingling of fingers husky voice and hoarseness menstrual disturbances severe hypothyroidism (subnormal temp and PR, wt gain, cachexia debilitated states) thickened skin, alopecia, expressionless/masklike facial features

tongue, hands and feet; constipation ( GI motility); possible deafness advanced hypothyroidism: pleural effusion, pericardial effusion, and respiratory muscle weakness MEDICAL MANAGEMENT: GOAL: restore metabolic state by replacing missing hormone Synthetic levothyroxine (Synthroid or Levothroid) 6 weeks dosage is based on patients serum TSH concentration prevention of cardiac dysfunction long term hypothyroidism = cholesterol, atherosclerosis, and CAD angina occurrence = oxygen needs of the myocardium exceeded its blood supply prevention of med interactions may blood glucose levels; adjust insulin levels pharma effects of digitalis glycosides, anticoagulants, indomethacim phenytoin and tricyclic antidepressants drug effects of thyroid bone loss and osteoporosis may occur hypnotic and sedative effects may cause respiratory depression supportive therapy measure ABG to determine CO2 retention pulse oximetry to monitor O2 saturations fluids are administered cautiously d/t danger of water intoxication NURSING DIAGNOSIS: alveolar ventilation leading to bradycardia activity intolerance r/t fatigue and depressed cognitive process participation in activities and independence risk for imbalanced body temp maintenance of body temp constipation r/t depressed GI function return to normal bowel function deficient knowledge about the therapeutic regimen for lifelong thyroid replacement therapy knowledge and acceptance of the prescribed therapeutic regimen ineffective breathing pattern r/t depressed ventilation improved respi status and maintenance of normal breathing pattern

cold intolerance subdued emotional responses slowed speech; enlarged

thought processes r/t depressed metabolism and altered CV and respi status improved thought process NURSING MANAGEMENT: avoid heating techniques calorie diet encourage activity to constipation; drink 6-8 glasses of water; fiberintake maintain patient airway administer oxygen IVF monitor I&O m PATHOPHYSIOLOGY: inadequate thyroid hormones general slowing of all physical and mental processes general depression of most cellular enzyme systems metabolic activities of all cells oxygen demand oxidation of less body heat nutrients hypoxia risk for energy hyponatremia hyperventilation bradycardia cold intolerance MYXEDEMA COMA

disturbed

ACCUMULATION

OF

MUCOPOLYSACCHARIDES

IN

SUBCUTANEOUS AND OTHER INTERSTITIAL TISSUE

MOST EXTREME, SEVERE STAGE OF HIGH MORTALITY CARBON DIOXIDE RETENTION,

THROIDISM

HYPOTHYROIDISM NARCOSIS ,

AND

CARDIOVASCULAR COLLAPSE AND SCHOCK INTENSIVE THERAPY IF PATIENT SURVIVE ETIOLOGICAL FACTORS: infection/other systemic disease use of sedatives CLINICAL MANIFESTATION: initially: depression, cognitive status, lethargy, somnolence hypotension bradycardia unresponsive hypoventilation hypovolemia convulsions hypothermia cerebral hypoxia MEDICAL MANAGEMENT: restore normal metabolic state by replacing missing hormone (TSH) primary object

 oxygen therapy T4 to T3 (Cytomel); Proloid (T4 to T3)

dieresis because of edema muscle tone metabolic activity slight fever s/sx hypothyroidism in 3-12 weeks TSH level NURSING MANAGEMENT: VS monitoring administer hormone replacement calorie, cholesterol, fat manage constipation appropriately provide warm environment avoid sedatives and narcotics report chest pain promptly HASHIMOTOS THYROIDITIS COMMON WITH WOMEN (MULTIPLE PREGNANCY WITH BLEEDING ) ETIOLOGIC FACTOR: idiopathic CLINICAL MANIFESTATIONS: firm enlargement of thyroid glands no gross nodules BMR DIAGNOSTIC TEST: T3, T4 normal to abnormal amounts TSH MEDICAL MANAGEMENT: suppression of TSH surgical resection of goiter if tracheal compression, cough/hoarseness management of hypocalcemia

controls nervousness SURGICAL MANAGEMENT: Thyroidectomy can be all/part of the thyroid gland patient who cannot tolerate antithyroid glands PTU administered before surgery Iodism iodine toxicity NURSING MANAGEMENT: assess cardiac respiratory function signs for thyroid storms administer oxygen to avoid hypoxia cool, comfortable temperature improve nutritional status reduce diarrhea provide quiet atmosphere record weight enhance coping measures reduce stress improve self-esteem provide eye protection

PARATHYROID GLANDS
ANATOMY-PHYSIOLOGY
mobilization of Ca from bone

osteoclast activity; Ca level absorption of Ca from small intestine Vitamin D suppression of Ca loss in urine rate of which Ca are loss in the urine stimulate PO4 ions
enhancing

HYPERTHYROIDISM
hypermetabolic condition characterized by excessive amounts of thyroid by abnormal stimulation of thyroid gland HYPERTHYROIDISM: ETIOLOGIC FACTORS: medical conditions age gender (men are prone) genetic factors ethnic background other factors CLINICAL MANIFESTATIONS enlarged thyroid nervousness heat intolerance MEDICAL MANAGEMENT: PTU and Methimazole associated with Graves disease SE: rash itching Radioactive iodine therapy destroys overactive thyroid cells common treatment in elderly patients hyperthyroidism will subside in 3-5 weeks Potassium Iodide, Lugols solution Beta-adrenergic blocking agents (Propanolol)

HYPOPARATHYROIDISM
inadequate parathyroid hormones TYPES:

ACUTE

iatrogenic caused by accidental damage due to

removal of parathyroid aglands CHRONIC idiopathic lethargy, thin, patchy hair PSEUDOHYPOPARATHYROIDISM Albrights hereditary osteodystrophy HYPOPARATHYROIDISM: ETIOLOGIC FACTORS: occurs more in women than men CLINICAL MANIFESTATIONS: Latent tetany numbness tingling stiffness cramp Overt tetany (occurs after surgery) bronchospasm laryngeal spasm hypocalcemia anxiety irritability depression delirium

 ECG changes hypotension carpopedal spasm dysphagia photophobia cardiac dysrhythmias seizures DIAGNOSTIC TESTS: Positive Trosseaus sign: carpopedal spasm use of BP cuff by applying 3050ammHg (applying hypoxia) result: stiffening of wrists, and adduction of fingers Positive Chvoteks sign: touching the earlobe result: twitching of mouth and nose Ca levels of 5-6mg/dl or lower PHARMACOLOGICAL MANAGEMENT: Oral Ca Carbonate tabs Vitamin D which can help absorb Ca and eliminate phosphorus MEDICAL MANAGEMENT: Parenteral Parathormone for treatment for acute hypoparathyroidism monitor for allergic reactions and changes in serum level Sedative agents for neuromuscular irritability/seizures Aluminum hydroxide gel and Aluminum carbonate which should be taken after meals Phenobarbital for seizures NURSING MANAGEMENT: assess client at risk numbness/tingling monitor lab values, VS, I&O administer Ca gluconate slowly and cautiously encourage fluid intake provide health teaching Ca diet (green leafy vegetables) keep Ca gluconate and tracheostomy set hand washing provide stress-free environment spinach is avoided (contains oxalate) Vitamin D preparation to Ca care of post-op patient trach set or mechanical ventilation Ca gluconate

renal failure, phenytoin) TERTIARTY

osteomalacia

(d/t

HYPERPARATHYROIDISM: CLINICAL MANIFESTATIONS: apathy, muscle weakness, n/v, constipation, hypertension, cardiac dysrythmia, cardiac contraction musculoskeletal sx skeletal pain/tenderness peptic ulcer and pancreatitis renal damage shortening of bone irritability renal system polyuria nephrocalcinosis pain in weight bearing shortening of body stature fatigue, muscle tone, muscle weakness abdominal pain ranging to the back ASSESSMENT: radioimmunoassay (RIA) x-ray (bone changes) concentrations of parathormone serum Ca levels spectrophotometry ultrasound, MRI biopsy (for cysts, adenoma, hyperplasia) MEDICAL MANAGEMENT: Parathyroidectomy < 50 years old serum Ca 1.0 mg/dl urinary Ca level 400 mg/day 30% in renal function Mobility bed rest is discouraged due to Ca excretion; when an individual moves, the Ca is stored in the bones rather than in the bloodstream Hydration therapy 2000 ml/day cranberry juice urinary pH Diet and meds avoid a diet with restricted/excess Ca anorexia is common Pharmacotherapy Calcimimetic therapy NURSING MANAGEMENT: airway patency, dehydration, immobility, diet fluid intake (3-4L/day) acid-ash fruit juices (prune and cranberry juice) protect from injury to prevent fracture NS IV ( Na) Ca excretion is promoted by Na excretion mobility

HYPERPARATHYROIDISM
excessive parathyroid secretion TYPES: PRIMARY one or more parathyroid glands affected SECONDARY destruction of the one that sends problem dietary from cause: rickets from vitamin D deficiency, chronic

 bed rest Ca
diet/meds

Ca diet administer antacids those with peptic ulcer thiazide diuretics must be avoided (as it promotes Ca reabsorption)