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Adrenal/Pituitary Disorders

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Androgen functions
Production off estrogen, sexual differentiation of the male during fetal development, male muscle mass and inhibition of fat deposits. influence of human behavior with links to human aggression and libido. KEY TO MALE SPERMATOGENESIS
Primary glucocorticoid
Cortisol which is a potent metabolic regulatory hormone. Necessary to maintain normal concentration of glucose. Stimulates appetite. Affects carbohydrate, fat, and protein metabolism. AKA hydrocortisone.
Primary mineralocorticoid
aldosterone. critical role in concentrations of minerals in ECF. Sodium, potassium. Keep heart rhythm normal. Maintains normal cardiac output.
Disorders of adrenal cortex
Addison's Disease, Addisonian Crisis, Cushing's syndrome
Addison's disease
Primary adrenal insufficiency. Results from atrophy/destruction of adrenal glands. Autooimmune process/disease. Rare disorder. Common in AIDS pts, TB, metastases of breast, GI tract, melanoma or lymphomas. Result of adrenalectomy and hemorrhagic infarction w/necrotic adrenal gland.
Addison's disease risk factors
Hx of other endocrine disorders, Taking glucocorticoids for more than 3 weeks, then sudden cessation. Taking glucocorticoids more than once QOD. Adrenalectomy. Tuberculosis. Appropriate tx results in little/no effect on life expectancy.
Addison's disease pathophysiology
Autoimmunity is most common cause. Lymphocytic infiltration of adrenal cortex. Frequently w/other immune disorders. Gradual destruction resulting in chronic adrenal insufficiency. Cortical tissue loss correlates w/deficiency of mineralocorticoids and glucocorticoids. Decreased levels of aldosterone, cortisol, and androgens.
Adissons disease manifestations
Intensify as disorder progresses = Fatigue, irratibility, weight loss, N/V, postural hypotension.
Addisons disease diagnosis
primarily with blood and/or urine tests. Cortisol level, ACTH, serum sodium, serum potassium, blood glucose level, CBC.
Cortisol level diagnostics
Normal - nearly undetectable to 25 mcg/dl. Low levels - suggest Addison's disease. Preferred testing is blood. can use 24-hour "free cortisol" urine screen. Consider diurnal variations. Later in day should be 1/3 to 2/3 less than morning results.
ACTH diagnostics
Elevated ACTH suggests Addisons disease.
Labs suggestive of Addison's disease
Low sodium, high potassium, LOW blood sugar, Decreased hemoglobin- RBCs (anemia), Decreased Hematocrit (anemia). Radiology studies = CT scan and MRI.
Addison's disease medical mgmt
Can live normal lives if receive replacement therapeis. Mineralocorticoid replacement - usu - QD Fludrocortisone or Florinef. Tx of symptoms/chronic syncope. Glucocorticoid replacement-usu-BID hydrocortisone or Hydrocortone (short acting) or Dexamethasone (Decadron) which is long acting.
Hypercortisolism: LT therapy effects
Increased blood sugar, abnormal fat deposits (classic moon face and "buffalo hump". Decreased extremity size, sodium/water retention, HTN, euphoria, psychosis, thinned skin w/purpura, glaucoma, osteoporosis.
Addison's crisis
Life-threatening adrenal insufficiency requiring monitoring in CCU and fatal if untreated. Precipitated by stress: pregnancy, surgery,infection/sepsis, dehydration, anorexia, fever, emotional upheaval.
Clinical manifestations/Addison's crisis
Related to DEGREE of hormone deficiency and electrolyte imbalance. Sudden/penetrating back/abdomen/leg pain. Depressed/changed mentation. Volume depletion, hypotension, hyperpyrexia followed by hypothermia, renal failure, LOC/coma, shock, death.
Medical mgmt / Addison's crisis
Correct FVD and monitor electrolytes. Isotonic solutions, kayexelate (oral or rectal; resin reducing potassium levels). Correct hypoglycemia (IV gluccose). Replace steroids (glucocorticoid and mineralocorticoid replacements)
Nursing care of addisons crisis
frequent VS, rehydration, monitor skin integrity, maintain strict I&O, monitor labs, assess for glucocorticoid overdose, pt education, infection (stressors to pt), monitor for URI and UTI. Labs = cortisol, ACTH, NA, K, and blood glucose.. Minotor H&H. Assess radiological studies (CT/MRI).
Pt education for addison's crisis
self-care, healthcare maintenance importance, medical alert bracelet encouraged, emergency kit with dexamethasone prepared syringe/alcohol wipes. written info about dx and needs. Medication needs = steroids self administration, importance of TAKING MEDICATION EVERY DAY, WHEN TO CALL DOCTOR!
Cushing's syndrome
Hypercortisolism. Hyper function of the adrenal cortex (excessive cortisol). Rare/incidence is unknown. Mainly females 20-40 years of age.
Cushing's syndrome pathophysiology
Pituitary hyper secretions and tumors on pituitary gland. Long-term use of corticosteroids. ABout 30% have tumor on adrenal gland. Causes r/t other malignancy (lung, pancreas, thymus, ovary)
Cushing's Syndrome manifestations
Persistent elevated blood glucose, muscle wasting and wkns, capillary fragility leading to ecchymosis, osteoporosis may result in kyphosis, low potassium levels. Persistent sodium/water retention. HTN. Abnormal fat distribution (Moon shape face/dorsocervical fat pad on back of neck/buffalo hump). thin skin, pink/purple striate. Increased susceptibility to infection. Possible virilism (masculine features) in females. Mental changes (memory loss, poor concentration/cognition, euphoria, depression/suicidal, steroid psychosis (hallucinations/delusions).
diagnosis of cushing's syndrome
Elevated blood glucose, low potassium level, elevated cortisol level (diurnal, normal is undetectable to 25 mcg/dl). ACTH: adrenocorticotropic hormone. LOW: Points to adrenal tumor. NORMAL/ELEVATED: Points to ectopic ACTH producing tumor. Pituitary tumor can also cause alterations in ACTH.
petrosal sinus sampling
used to diagnose cushings syndrome. Located near the petrous part of the temporal bone. Isolates source of ACTH secretion. Radiologic test. Catheter threaded from femoral vein into inferior petrosal sinuses. Blood samples drawn from both right and left petrosal sinuses. ACTH values are compaired w/each other and w/ a peripheral blood sample
Surgical mgmt of cushing's syndrome
Tx of choice. Adrenalectomy/adrenal tumor. Ectopic tumor/remove metastatic tumor or perform bilateral adrenalectomy. Pituitary tumor - transphenoidal hypophysectomy. can also perform hemi-hypophysectomy (removal of half the pituitary gland). MOST physical manifestations will resolve after surgery.
Pre-op nursing care of Cushing's patient
Risk for injury (fx's related to osteoporosis, HTN, diabetes). Deficient knowledge (disease, diet)
s/p adrenalectomy
pt requires life-long glucocorticoid and mineralocorticoid replacement.
s/p transsphenoidal hypophyseectomy (for removal of pituitary tumor)
pt requires replacement hormones for 12-24 months.
postop care of cushing's patient
risk for injury (r/t complications of procedure and manifestations of shock r/t hemorrhage). Risk for injury (monitor for Addisonian crisis and monitor for infection)
radiation therapy / cushing's syndrome
internal therapy (implant). external therapy - difficult tx for pituitary tumors d/t proximity of optic nerve
medical mgmt of cushing's syndrome
for pt's with inoperable tumors and pt's with metastasis. GOAL - PALLIATIVE comfort not cure. Includes radiation therapy and meds to block/reduce ACTH production
medication therapy of cushing's syndrome
ACTH reducing agents used to treat the hyper secreation from the pituitary that results in increased ACTH. Cyproheptadine/periactin = an antihistamine used off label for Cushing's. Bromocriptine (Parlodel) lowers growth hormone. Mitotane (Lysodren) = cytotoxic anti-hormonal agent. Aminoglutethimide (Cytadren) = blocks synthesis of glucocorticoids and adrenal steroids.
hyperaldosteronism
aldosterone function...aldosterone excess. Na and Hydrogen ions. Primary = Conn's Syndrome (NO risk factors) excessive aldosterone production. Secondary = Risk factors include chronic HG, cirrhosis w/ascites, nephrotic syndrome and HTN with renal artery disease.
HTN, renin suppression, hypernatremia, hypokalemia, visual disturbances, HF, renal failure, stroke
treatment of hyperaldosteronism
control of causative disease process
diagnosis of hyperaldosteronism
low serum K, alkalosis, elevated urinary or plasma aldosterone levels. Low plasma renin levels. Radiographic - cardiac hypertrophy.
Hyperaldosteronism manifestations
untreated HTN, hypernatremia, hypokalemia. Excess urinary excretion/muscsle wasting, paralysis, cardiac dysrhythmias. Tetany and respiratory suppression. RARELY edematous ESCAPE PHENOMENON (kidneys "escape" Na and H2O retention)
Myperaldosteronism management
Surgical = unilateral or bilateral adrenalectomy. Medical = aldactone (increasing Na excretion), amiloride, pre and postop mgmt for hypercortisolism
adrenomedullary disorder pheochromocytoma
tumor of adrenal medulla (secreting catecholamine) causing HYPERACTIVITY. Unknown etiology (may be familial) Most common in middle age. Rarely after age 50. Can lead to sudden blindness, cerebral hemorrhage, or heart failure unless corrected
risk factors influencing catecholamine release
Paroxysm (sporadic or episodic) influences. Smoking, micturition, abdominal displacement, certain drugs, emotional stressors.
pheochromocytoma
elevated blood glucose, glucosuria, HTN (principal symptom), sympathetic overactivity, N/V, weight loss
diagnosis of pheochromocytoma
H&P = HTN, elevated heart rate, dyspnea, edema, kidney damage (albuminuria, proteinuria, increased serum BUN). Urine = catecholamines, metanephrines and vanillymandelic acid (VMA). Blood = Catecholamines. X-ra, blood glucose level, glycosuria.
Pheochromocytoma surgical mgmt
Treatment of choice is removal of one or both adrenal glands depending on unilateral or bilateral tumor. Complications may delay surgery = HTN, nephropathy, retinopathy, stroke, HF, myocarditis, increased platelet agregation. Pt may need tx for complications before surgery.
Nursing mgmt of pheochromocytoma
Pre-op = Risk for injury r/t HTN. Postop = Risk for injury r/t shock and risk for injury r/t adrenal insufficiency.
Pituitary gland
Small extension suspended from hypothalamus at the sella turcica. Connected to the hypothalamus by the hypophyseal stalk. Three sections - two of which secrete hormones = anterior pituitary and posterior pituitary.
anterior pituitary functions
growth hormone, prolactin, other hormones, cause other endocrine glands to secrete their hormones. Hormones = Growth hormone, prolactin, follicule stimulating hormone, luteinizing hormone, thyroid stimulating hormone, adrenocorticotropic hormone.
posterior pituitary
hypothalamus responsible for production of oxytocin and antidiuretic hormone. These are then transported to the posterior pituitary gland for secretion.
Hypopituitarism
Deficiency of one or more hormones produced by ANTERIOR lobe of the pituitary. Rare disorder. Nine I's.
Clinical manifestations of hypopituitarism
depends on what anterior pituitary hormone is deficient. Onset gradual. Hormone loss. First hormone isusually GH and last is PRL. Short stature, sexual/reproductive disorders, hypothyroidism, prolactin deficiency.
Diagnosis of hypopituitarism
Poor growth, hypoglycemia, delayed puberty, polyuria, impaired libido, fatigue. Labs = ACTH, cortisol, thyroid hormone, TSH, sex steroids, FSH, LH. Radiology = Skull x-ray showing possible enlargement of sella turcica, erosion of sphenoid bone, calcification of a mass in sella turcica area. CT scan/MRI with focus on sella turcica area.
medical/surgical mgmt of hypopituitarism
surgical = removal of tumor. medical = permanent replacement of hormones not secreted.
hyperpituitarism
over secretion of one or more of the hormones of pituitary gland. usually caused by pituitary tumor (benign adenoma). Overproduction of hormones (GH and PRL)
Clinical manifestations of hyperpituitarism
Too much GH = gigantism, acromegal. Too much PRL = hyperprolactinemia
acromegaly
hormone disorder. pituitary gland produces too much GH. Syndrome of hyperpituitarism. Benign adenoma on pituitary gland that causes increased amts of GH. Prior to closure of epiphysis = gigantism. If occurs after closure of epiphysis = acromegaly. middlle aged adults affected. Serious illness or death. Dx can be missed for many years. Progresses slowly (1-10 years).
hallmark of acromegaly
progressive coarsening of facial features d/t bones increasing in thickness and soft tissue growth.
Acromegaly diagnosis
Blood tests - all will show oversecretion....GH, TSH, FSH, LH, ACTH, PRL. Radiology - MRI with focuse on sella turcica.
Surgical mgmt of hyperpituitarism
surgical removal of pituitary tumor. Usually transphenoidal hypophysectomy.
transsphenoidal hypophysectomy complications
Adrenal insufficiency, increased intracranial pressure, diabetes incipidus, meningitis
nursing mgmt of transsphenoidal surgery
Monitor mustache dressing (or drip pad) for bleeding or drainage. Assess for rhinorrhea. Educate to report postnasal drainage. Teach preop to avoid sneezing, coughing, bending over.
diabetes insipidus
uncommon. kidneys not able to to conserve water. Major disorder of posterior pituitary gland. Deficiency of ADH. ADH is produced by hypothalamus. Stored/released by pituitary gland. Role is to regulate fluid balance.
causes of diabetes insipidus
surgery on posterior pituitary, head injury, tumors especially on posterior pituitary, brain infections or inflammation. drugs, alcohol, meds.
clinical manifestations/diagnosis of diabetes insipidus
H&P = Dry, cool skin/dry mucous membranes. tachycardia, polyuria, polydipsia, weight loss, neurologic and mentation changes. UA = Urine specific gravity is decreased. Urine osmolality is decreased. Blood work = Serum osmolality is increased. Serum sodium increased.
medical and surgical mgmt of diabetes incipidus
SURGICAL= transphenoidal hypophysectomy - remove posterior pituitary tumor. MEDICAL= ADH replacement (vasopressin replacement). Desmopressin (DDAVP)
Risk factors for diabetes incipidus
posterior pituitary surgery, head injury, tumors on posterior pituitary, brain infections/inflammation, medications, drugs, alcohol.
patient education for diabetes insipidus
daily weights is priority, meds, tx, manifestations
ADH
produced by hypothalamus. Stored/released by pituitary gland. Role is to regulate fluid balance. Too much = retain fluid. Too little = massive diuresis.
syndrome of inappropriate antidiuretic hormone (SAIDH)
Over secretion of ADH. Causes water retention/low sodium/low serum osmolality. Caused by malignant conditions (lung cancer, lymphoma of duodenum, brain, bladder, pancreatic cancer, prostate cancer), head injuries, pituitary tumors, encephalitis, poliomyelitis, myxedema, viral or bacterial pneumonia, certain meds.
Meds that can cause SAIDH
Chlorpropamide (Diabinese), cyclophosphamide (Cytoxan), carbamazepine (Tegretol), SSRI's, MDMA (Ecstasy, analgesics.
clinical manifestations of SAIDH
H&P = Decreased DTRs, fatigue, headache, anorexia, decreased GI motility, decreased mental status, weight gain (without edema), JVD, tachycardia, tachypnea, rales, water retention, hyponatremia, hypo osmolality of the blood/serum, hyper osmolality of the urine.
Diagnosis of SAIDH
Serum sodium - decreased. Urine sodium (24 hr) - increased. BUN - increased. Serum osmolality - Decreased. Urine osmolality - increased.
mgmt of SAIDH
There is no surgical mgmt. MEDICAL = Hypertonic IV fluid, sodium restriction, fluid restriction, diuretics, monitor electroolytes, meds (demeclocycline)
Nursing mgmt of SIADH
Monitor lab values. Sodium - raise level slowl Assess neurologic status. Monitor daily weights. I&O. Administer Demeclocycline as ordered. Monitor for fluid overcorrection. Place all of these patients on SEIZURE PRECAUTIONS especially if sodium is below 129 and have oral airway and suction equipment available.
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