Exam 2 Flashcards
Adrenal medulla releases
Epi and norepi
Sympathomimetic
Mimic SNS
Epi and norepi released from adrenal medulla
Catecholamines
Epi and norepi act on which receptors?
Alpha 1 beta 1&2 adrenergic receptors
Released from adrenal cortex
Mineralcorticoids (aldosterone)
Glucocorticoids (cortisol)
Gonadocorticoids (androgens, estrogen)
Primary disorder
Something wrong with the gland itself
Secondary disorder
Something wrong with a different gland or organ that affects the endocrine gland
Cortisol
Regulates metabolism
Increases blood glucose
Stress response
Cushing syndrome
High levels of cortisol in the blood
Can also affect aldosterone and androgens
Cushing syndrome causes
Chronic exposure to excess corticosteroids particularly glucocorticoids
Exogenous corticosteroid administration like prednisone
Cushing disease
More serious
Pituitary Cushing disease or adrenal Cushing disease
High levels of cortisol all the time
Pituitary Cushing disease
Over secretion of act in pituitary usually from pituitary adenoma
Causes adrenals to over secrete cortisol
Adrenal Cushing disease
Excess glucocorticoids caused by a problem in the adrenal cortex such as an adrenal adenoma which is usually benign
Usually only occurs in one adrenal gland
Cushing’s syndrome manifestations
Weight gain with trunkle obesity and thin arms and legs due to muscle wasting and weakness
Moon face and buffalo hump
Hyperglycemia
Osteoporosis due to cortisol interfering with osteoblast formation
Loss of collagen leading to stretch marks also known as striae
Immunosuppression and increased risk for infection
psychosocial changes such as irritability anxiety euphoria and psychosis
Mineral corticoid excess in Cushing’s syndrome
Salt and water retention, hypertension, and bounding pulse
Adrenal androgen excess in Cushing’s syndrome
Acne, amenorrhea, virilization in women (developing male characteristics) and hirsutism
Care of Cushing syndrome patients
Vital signs, watching for fluid overload
Mental status
Laboratory tests: glucose, cortisol, acth, potassium
Cushing syndrome priority nursing diagnoses
- fluid overload
- Risk for injury related to skin thinning poor wound healing and bone density loss
- Risk for infection
Addison’s disease
Primary cause of adrenocortical insufficiency
lack of glucocorticoids and or mineral corticoids and or androgens
Addison’s disease primary causes
Autoimmune (aids, tb)
Bilateral adrenalectomy
Addison’s disease secondary causes
Pituitary or hypothalamus problem
Abrupt discontinuance of long-term steroids
Addison’s disease clinical manifestations
Hypotension due to insufficient aldosterone Dizziness due to hypotension Progressive weakness Fatigue and confusion Weight loss and anorexia Hyperpigmentation of skin Hypovolemia Hypoglycemia Hyponatremia Hyperkalemia Irritability and depression
Addison’s disease treatment
Hormone therapy
Hydrocortisone has glucocorticoid and mineralo corticoid properties
Prednisone
Possible sex hormone replacement
Given in divided doses at the same time each day to mimic the way the body releases hormones throughout the day
during times of illness or stress they may need to increase dosage temporarily
Addison’s disease nursing interventions
Correct fluid and electrolyte imbalance and monitor weight daily
Administer corticosteroids
Cardiac monitoring necessary due to hyperkalemia
assess for manifestations of addisonian crisis or Cushing syndrome
Educate patient to manage stress, high sodium low potassium diet, be careful of heat because sweating can lead to sodium loss, take medications at the same time everyday
Addisonian crisis AKA acute adrenal insufficiency
Life-threatening condition emergency! Coma and death can result!
need for cortisol and aldosterone is greater than available supply
occurs in response to a stressful event or sudden sharp decrease in these hormones (adrenalectomy)
Addisonian crisis signs and symptoms
Fluid volume deficit, hypoglycemia, hyponatremia, hyperkalemia
Shock (bp, HR)
Lethargy which can lead to coma and death
Addisonian crisis treatment
Manage symptoms of shock
Give high dose of hydrocortisone replacement
IV fluids with dextrose
Electrolyte replacement
High doses of IV glucocorticoids example solu- cortef
Long-term corticosteroid therapy risks
Increased risk for infection, osteoporosis, GI ulceration, fluid and electrolyte imbalances
Risk of Cushing’s syndrome
Abrupt discontinuation may lead to adrenal insufficiency
Hyperaldosteronism (Conn’s syndrome)
Excessive secretion of aldosterone
Can be caused by tumor on adrenal glands
Hyperaldosteronism (Conn’s syndrome) can cause
Hypernatremia
Hypokalemia
Metabolic alkalosis
Hyperaldosteronism (Conn’s syndrome) interventions
Adrenalectomy Spironolactone (aldosterone antagonist) therapy if unable to perform surgery
Pheochromocytoma
Tumor in adrenal medulla
Causes excess production of catecholamines, epinephrine and norepinephrine
Pheochromocytoma symptoms
Severe episodic hypertension with classic triad of associated symptoms:
Severe pounding headache, tachycardia with palpitations and profuse sweating, unexplained abdominal or chest pain
Pheochromocytoma diagnostic tests
24 hour urine for metanephrines and vanillymandelic (VMA)
CT or MRI
Pheochromocytoma treatment
Primary treatment is surgery to remove tumor
Post-op care similar to adrenalectomy
May be put on CCB, BB, alpha blockers
HRT
If surgery is not an option medication can be given to decrease catecholamine production by tumor
