• May result from inadequate secrete of ACTH, dysfxn of hypothalamic-pituitary control, direct dysfxn of adrenal gland tissue
• Gradual or quickly with stress
• Acute adrenocortical insufficiency = adrenal crisis
• Life threatening manifestations appear quickly and without warning

• Insufficiency of adrenocortical steroids = loss of aldosterone and cortisol actions
• Low cortisol:
• Decreased gluconeogenesis
• Depletion of liver and muscle glycogen
• Hypoglycemia
• GFR and gastric acid production decrease
• Low aldosterone secretion:
• Hyperkalemia - d/t decreased K excretion
• Hyponatremia and hypovolemia

Adrenal Gland Hypofunction

Acute adrenal insufficiency

• Life threatening
• Usually d/t stress
• Without rapid intervention....
• Sodium falls rapidly
• Potassium increases rapidly
• SEVERE hypotension occurs

Addisonian Crisis

Treatment

• Hormone replacement:
• Rapid infusion of NS or D5NS
• IV bolus of Solu-Cortef
• Solu-Cortef IV drip for 8 hrs
• Hydrocortisone 50 mg IM q 12 hours
• H2 histamine blocker IV for ulcer prevention
• Hyperkalemia Mgmt:
• Insulin with dextrose in NS (shifts K into cells)
• Kayexelate (excrete K in feces)
• Loop or thiazide diuretics
• I/O w/ K restriction
• Cardiac monitoring
• Hypoglycemia Mgmt:
• IV glucose
• Glucagon
• Accuchecks hourly

Adrenal Gland Hypofxn

Assessment

• ACTH stimulation test - most definitive
• Given IV then plasma cortisol lvl checked at 30 min, then 1 hr
• Increased with secondary insufficiency
• Decreased with primary insufficiency
• In Addisonian crisis suspects, tx started without test

Adrenal Gland Hypofunction

Interventions

• Daily weights
• Replacement therapy
• Caution - salt restricition or diuretic therapy may cause adrenal crisis in these patients

• Hypercortisolism - Cushing's
• Hyperaldosteronism
• Excessive androgen production
• Pheochromocytoma - excessive secretion of catecholamines (epi & norepi)

Adrenal Gland Hyperfunction

Hypercortisolism

Cushing's Disease

• Most common cause of Cushing's disease in spituitary adenoma resulting in bilateral adrenal hyperplasia
• May be caused by glucocorticoid therapy
• Excess glucocorticoids affect metabolism and all body systems
• Redistribution of fat - truncal obesity, buffalo hump, moon face

Adrenal Gland Hyperfunction

Hypercortisolism

Causes:

• Most common = pituitary adenoma (bilat adrenal hyperplasia)
• Use of glucocorticoids
• Autoimmune disorders
• Organ transplants

Adrenal Gland Hyperfunction

Hypercortisolism

Assesment:

• Weight gain
• HTN
• Capillary fragility
• Osteoporosis
• Thinning skin
• Increased pigmentation

Hypercortisolism

Assessment:

Weight gain

HTN

Cap fragility

Osteoporosis

Thinning skin

Increased pigmentation

Lab test = Blood, saliva (from cheek), urine

Hypercortisolism

Treatment:

• Hypophysectomy
• Adrenalectomy
• Unilateral or bilateral
• Replacement therapy needed:
• Lifetime for bilateral
• Up to two years for unilateral

Adrenal Gland Hyperfunction

Hyperaldosteronism

HTN

Hypernatremia

Hypokalemia

Metabolic acidosis

Surgery is common tx - must wait for potassium lvl to become normal

Adrenal Gland Hyperfunction

Pheochromocytoma

• Usually benign; produces, stores and releases epi and norepi
• Assess for HTN (hallmark sign); do NOT palpate abdomen
• Tx - surgery; monitor BP closely post op as HTN is the most serious complication post op