May be due to over activity of the gland or the result of an adenoma • Characterized by: excessive serum concentration of pituitary hormone ( GH, AGH, PRL) morphologic and functional changes in the anterior pituitary • GROWTH HORMONE HYPERSECRETION • Gigantism – prior to closure of epiphyses; proportional growth • Acromegaly – after closure of the epiphyses; disproportional growth • CLINICAL MANIFESTATIONS: Arthritis Chest barreled shape Rough facial features Odd sensations: hands and feet Muscle weakness & fatigue Enlargement of organs Growth of course hair Amenorrhea; breast milk production Loss of vision; headaches Impotence; increased perspiration Snoring • Management: o Medication: Bromocriptine cabergoline -dopamine agonist GH hypersecretion and prolactinoma Ocreotide sematostatin -GH hypersecretion Radiation: Indicated for larger tumors o Surgery: trans-sphenoidal hypophysectomy o •

post-surgery nursing care semi to high fowler’s position protect from infection and stressful situation Hormone replacement Constant neurologic checks Monitor I&O to check for diabetes Incipidus Encourage deep breathing but not coughing Institute measures to prevent constipation Watch out for CSF leak

Medication: hormonal substitution ( maybe for life) Corticosteroids Levothyroxine Androgen/estrogen Growth hormone o o Radiation: Indicated for larger tumors Surgery: trans-sphenoidal hypophysectomy

• • Characterized by massive polyuria due to either lack of ADH or rnal insensitivity CENTRAL DI - due to deficiency in ADH production


Deficiency of one or more anterior pituitary hormones Causes: Infections/inflammatory disorsers Autoimmune diseases Tumors Surgery/radiation theraphy SIMMOND’S DISEASE - Panhypopituitarism - Complete absence of pituitary hormones CACHEXIA - most prominent feature follows destruction of the pituitary by surgery, infection, injury or tumor SHEEHAN’S SYNDROME -post partum pituitary necrosis - a complication of delivery results from severe blood loss and hypovolemia CLINICAL MANIFESTATIONS: HYPO-thermia, glycemia, tension Loss of vision, strength, libido & secondary sexual characteristics MANAGEMENT

NEPHROGENIC DI - due to defect in the kidney tubules that interferes with H2O absorption - polyuria is unresponsive to ADH, which is secreted normally
DIAGNOSTIC Fluid deprivation test Administration of desmopressin 24-h urine collection for volume, glucose and creatinine Serum for glucose, urea, nitrogen, calcium, uric acid, potassium and sodium. MANAGEMENT: CENTRAL DI Desmopressin, lypressin (intranasal) Vassopresine tannate in oil (IM) NEPHROGENIC DI Indomethacin -hydrochlorothiazide -desmopressin -amiloride Clofibrate chlorpropamide

stressful illness. thyroid surgery.increased ICP • DIAGNOSTIC Low serum sodium Low serum osmolality High urine osmolality High urine sodium excretion Normal renal function • MANAGEMENT Maintain fluid balance MIOW Fluid restriction Loop diuretic Lithium or democlocycline Maintain Na balance Increased Na intake Emergency treatment of 3% NaCl followed by furosimide Excessive rapid correction of hyponatremia: central pontine myelinolysis Increased basal metabolic rate THROID DISORDERS • Function test Fine needle aspiration biopsy -Sampling of thyroid tissue to detect malignancy.RAI Increased systemic adrenergic activity severe hypermetabolism MANAGEMENT o Anti-thyroid drugs o Prophylthiouracil (PTU). SSKl (Lugol’s) Adjuct to other anti-thyroid drugs in preparation for thyroidectomy Treatment for thyroroxic crisis Inhibits release and synthesis of TH MEDICATIONS: Digitalis. tell patient that radiation is only minimal HYPERTHYROIDISM CAUSES: o Grave’s disease o Initial manifestation of thyroiditis o TSH-screening pituitary tumor o Toxic adenoma o Factitious thyrotoxicosis o Amiodarone theraphy CLINICAL MSNIFESTATION o GI Hypermotility o Rapid weight loss o Apphrehension o Volume deficit. Initial test for evaluation of thyroid masses NURSING INTERVENTION o Determine whether the patient has taken medications or argents that contains iodine because they may alter the test results o Assess allergy to iodine or shellfish o For scans. erratic menses o Systolic BP elevated.voracious appetite o Exopthalmos.proprandol (inderal)Phenobarbital Well balance.• SYNDROME OF INNAPROPRIATE ADH • Disorder due to excessive ADH release • CLINICAL MANIFESTATION Persistent excretion of concentrated urine Signs of fluid overload Hyponatremia LOC changes.sweating o TSH decreased in primary disease o Increased in secondary disease TYROID STORM/ THYROTOXIC CRISIS o Marked delirium o Severe tachycardia o Vomiting o Diarrhea o Dehydration o High fever -occurs in patient with exsisting but unrecognized thyrotoxicosis. methimazole o Blocks thyroid hormones synthesis • Use for pregnant women and patients who have refused surgery or RA1 treatment o During pregnancy. o 1% of infants born to mothers on antithyroid theraphy will be hypothyroid o WOF agranulocytosis RAI (131I). PTU is DOC. K or Na iodide. high calorie diet with vitamin and mineral supplement Subtotal or total thyroidectomy NURSING IMPLICATION o NPO post midnight o Initial dose: o Urine and saliva slightly radioactive o 24h vomitus highly radioactive x 6-8h o Institute full radiation precations o Instruct the patient to use appropriate disposal methods when coughing and expectorating o Dilute oral doses in water or fruit juices and give witm meals to prevent gastric irritation o LUGOL’s Solution o Decreased vascularity of thyroid gland o Discoloration of the teeth provide straw for the patient when drinking o Encourage for increased H2O intake o May caused tyrotoxic crisis HYPOTHYROIDISM o State of low serum thyroid hormone in the blood resistance to TH Autoimmune Developmental o .

anorexia. anemia Increased weight.Dietary Iodine Oncologic Drugs induce Iatrogenic Nonthyroidal Endocrine o COMMON CAUSES: o Autoimmune hypothyroiditis aka hashimoto disease o Failure of the hypothalamus o Failure of the pituitary gland o Inborn errors of EH synthesis o History of thyroidectomy o Expose to radiation o Antithyroid theraphy o COMMON CAUSE: iron Deficiency CLASSIFICATIONS o CRETINISM – in infants and young children o LYMPHOCYTIC THYROIDITIS – self limiting and appears after 6 yrs of age and peak during adolescent o HYPOTHYROIDISM W/O MYXEDEMA. dry course skin Edema in periorbital Reduce BMR Apathy. intolerance to food Lethargy. loss of libido Enlarged tongue Drooling saliva TSH increased in primary Decreased in secondary MYXEDEMA COMA o Decreased all body function o Decreased v/s o Precipitating Factors: Acute illness Rapid withdrawal to medication anesthesia Thyroidectomy Opiod use MANAGEMENT Prevention Prophylaxis Hormonal replacement Levothyroxine (syncroid) Liothyronine (cytomel) Liothrix (thyrolar) Doses increased every 2-3 weeks Watch out for: o Chest pain o Palpitation o Profuse sweating o Nervousness o Drink meds at exact time each day o May develop insomia if taken at night o Monitor bp and apical pulse o If pulse morethan 100 bpm-stop NURSING IMPLICATION o Low calorie o Warm environment o Stool softener o Maintain patent airway HYPERPARATHYROIDISM Primary o Single adenoma o Genetic disorders o Multiple endocrine neoplasias Secondary o Rickets o Vit. chvostek sign Trousseau sign. tetany MANAGEMENT o IV calcium gluconate-drug of choice o Oral calcium salts o Vit d supplementation o Elevated serum phosphate o Low calcium o Trousseau & chvostek sign o Elevated serum phosphate o Low calcium o Akalosis/arrhythmias o Narrowing of airways o Irritability . dysrrhytmia Extremities tingling Fhotophobia Increased bone density Cramps. D deficiency o Chronic renal failure o Phenitoin or laxative abuse CLINICAL MANIFESTATION o Constipation o Apathy o Lordosis o Cardiac dysthemia o Upset GI tract o Low energy level Increased BP SYMPTOMS o Increased calcium o Increased parathyroid hormone MANAGEMENT o Decreased calcium intake o Increased phosphorus intake o Calcitonin o Surgery to remove adenoma o Furosemides o Biphosponates HYPOPARATHYROIDISM Auto immune Injury to the parathyroid theraphy Ischemic thyroid surgery CLINICAL MANIFESTATION Dypsnea.mild thyroid failure common in older children and adult CLINICAL MANIFESTATION Dry brittle hair.

trunkal obesity ACTH is elevated Loss of muscle mass Over extended skin Hypertension. hypernatrimia Urinary cortisol elevated Menstrual irregularity Pourosity of the bone MANAGEMENT o Remove steroids o Irradiation o Hypophesectomy o Adrenalectomy o DRUGS o Cyproheptadine (perjactine) o Nysodrine o Aminoglutethamine ( cytadrin) o Monitor V/S o Monitor I & O o Stress reduction . nausea o Low sodium o Decreased potassium o Decreased bp MANAGEMENT o Replacement of hormones:hydrocortisone o Increased carbohydrate and protein o Potassium o Sodium o Monitor v/s 4x a day o Monitor I & O o Monitor Weight and glucose o 24h urine specimen collection o Bronze skin discoloration o Avoid stress o Avoid contacts CUSHING SYNDROME Enlargement of adrenal gland Increased stimulation CLINICAL MANIFESTATION Buffalo hump Unusual behavior Facial features. moon facesfat.o Cramps o Parathormone injection o High calcium diet-spinach o Low phosphate PHEOCHROMOCYTOMA Adrenal tumor Increased epinephrine and norepinephrine Tumor in the adrenal corex which is responsible for the regulation of BP CLINICAL MANIFESTATION Headache Anxiety Nausea Eye disturbances Sever hypertension Dilate blood vessels by nitroprussside Monitor bp Monitor I & o Fluid replacement Decreased environment stimulation Stress Maintain dosage of steroids Follow up check up ADDISON’S DISEASE Hyposecretion of adenocortical hormones Idiophatic atrophy SIGNS AND SYMPTOMS o Weakness o Excess stress o Anorexia. vomiting.

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