Adrenal Cortex

Divided into three zones Zona glomerulosa (outer layer) produces mineralocorticoids, mostly aldosterone.
Aldosterone causes kidneys to reabsorb (keep) sodium and water, and lose potassium and H+. Control is by K+ levels in blood (only mildly by Na+) and by renin-angiotensin- aldosterone pathway.

 Zona Fasciculata (middle layer) produces glucocorticoids, mostly cortisol (hydrocortisone)

Regulate metabolism, esp. of glucose, and resistance to stress. Increase protein breakdown and decrease synthesis, raising blood amino acid levels. Lipolysis promotes breakdown of adipose tissue, increasing use of fatty acids for energy and decreasing use of glucose Gluconeogenesis production of new glucose from other substances, increasing blood glucose

 Resistance to stress increased glucose is available to tissues, and makes blood vessels more sensitive to agents that cause vasoconstriction Anti-inflammatory effects inhibits cells that participate in inflammatory response slower wound healing Depression of the immune response prevents rejection of transplanted organs, but decreases resistance to infection.

 Control : through blood levels of cortisol and ACTH which is controlled by hypothalamus through corticotropin releasing hormone. Hyposecretion leads to Addisons disease Hypersecretion leads to Cushings syndrome

 Zona Reticularis (inner layer) produces androgens (male sex hormones). These are overwhelmed by testosterone in males and so are insignificant. In females, they contribute to the female sex drive, and may be converted into estrogen in other tissues, which is especially important after menopause.

Adrenal gland: A. Adrenal cortex: I. Hyper-corticism (Cushings syndrome): It is clinical picture produced by prolonged increases in plasma glucocoricoids. The caused of increase of glucocorticoids (which either exogenous or endogenous) or due to excess ACTH (which is also either exogenous or endogenous).

The clinical characteristics of the disease will depend on the physiological functions of glucocorticoid: Protein depletion: it will cause protein catabolism and will end to cause the skin and subcutaneous tissues are thinmuscles are poorly developed wounds heals poorlyminor injures causes bruises and ecchymosed hair is thin and scraggly (atrophied), facial hair, and acne. Fat distribution: the extremities are thin, but fat collected in abdominal wall, face, and upper back, where it produces a buffalo hump. As the thin skin of abdomen is stretched by the increased subcutaneous fat depots, the sub-dermal tissue rupture to form prominent reddish-purple striae. Many amino acids liberated from catabolized protein are converted into glucose in the liver, and the result is hyperglycemia.

The excess gluco-corticoid may exert a significant mineralo-corticoid action. About 85% of patients are hypertensive. Bone dissolution: this is due to decrease bone formation and increase bone resorption (osteoporosis) Mental effects: mental aberration ranging from increase appetite, insomnia, and euphoria to psychosis.

HYPER AND HYPOFUNCTION ADRENAL CORTEX HORMONES: Too much: Too little
CUSHINGS Syndrome (TOO MUCH CORTISOL!)

secretion of cortisol from adrenal cortex 4X more frequent in females Usually occurs at 35-50 years of age
*Cushings disease if due to inc ACTH secreting tumor from pituitary

II. Hyper-aldosteronsim: 1.It cause by primary (Conns syndrome: adrenocortical adenoma) or secondary: caused by edema (cirrhosis, nephritic syndrome, cardiac failure). It is characterized clinically by hypertension, Na and water retention, and hypokalemia, often with hypokalemic alkalosis. III. Hypo-corticism (Addisons disease): 1.It either caused by primary which is idiopathic adrenal atrophy or secondary which caused by infection most tuberculosis. It is characterized by hypotension, increased pigmentation of skin; decrease serum Na, Cl, glucose, and bicarbonate; and increased serum K.

Addisons Disease: Etiology/Pathophysiology

Common cause-autoimmune response to adrenal tissue (esp. white females) Susceptibility genes; other endocrine conditions often found Other causes of Addisons disease Tuberculosis (rare in North America) Infarction Fungal infections AIDS Metastatic cancer
Most often occurs in adults <60 years old

Affects both genders equally Disease not evident until 90% of adrenal cortex destroyed- advanced before diagnosis

Addisons Disease: Clinical Manifestations

Primary features
Progressive weakness Fatigue Weight loss Anorexia Skin hyperpigmentation primarily in
Areas exposed to sun Pressure points Over joints

Addisons Disease: Diagnostic Studies

Subnormal levels of serum cortisol Levels fail to rise over basal levels with ACTH stimulation test Latter indicates primary adrenal disease Positive response to ACTH stimulation indicates functioning adrenal gland Abnormal laboratory findings Hyperkalemia Hypochloremia Hyponatremia Hypoglycemia

Addisons Disease-Diagnostic Studies

Abnormal laboratory findings Anemia Low urine cortisol levels ECG Low voltage, vertical QRS axis, peaked T waves from hyperkalemia CT and MRI used to Localize tumors Identify adrenal calcifications or enlargement

HYPERALDOSTERONISM
Usually due to adrenal tumor Too much aldosterone secretion Sodium retention (hypernatremia) Potassium excretion (hypokalemia) Muscle weakness Fatigue Cardiac dysrhythmias Glucose intolerance Metabolic alkalosis Hydrogen ion excretion

(Conn Syndrome)

*Hallmark- hyperaldosteronism Hypertension with hypokalemic alkalosis Usually no edema Headache

Review renin/aldosterone effect!

Hyperaldosteronism Etiology and Pathophysiology

Primary hyperaldosteronism
Usually caused by adrenocortical adenoma

Secondary hyperaldosteronism
Due to renal artery stenosis, renin-secreting tumors, and chronic kidney disease

DIAGNOSIS/INTERVENTIONSHyperaldosteronism
Primary aldosteronism
Plasma aldosterone levels Sodium levels Potassium levels Renin activity

Adenomas are localized by CT or MRI

Preferred treatment of primary hyperaldosteronism is surgical removal of the adenoma (ADRENALECTOMY)

Adrenal Medulla
Made up of hormone producing cells called chromaffin cells, which surround large blood vessels. Sympathetic postganglionic cells that are specialized to secrete hormones which are sympathomimetic. Secretions are 80% epinephrine and 20 % norepinephrine

 Control through nervous impulses that originate in the hypothalamus Not essential for life Tumors are called pheochromocytomas, and produce extended Fight or Flight response. Treated by surgical removal of tumor.

PHEOCHROMOCYTOMA
Rare, benign tumor of the adrenal medulla catecholamines Produces excessive _________ Mostly in young to middle-aged adults Results in severe hypertension If untreated, may lead to Diabetes mellitus Cardiomyopathy Death

Clinical Manifestations
Hallmark-hypertension-200/150 or greater Spells-paroxymal attacks bladder distension,emotional distress, exposure to cold. Norepinephrine and Epinepherine released sporadically Clinical features include Severe, episodic hypertension Severe, headache Tachycardia with palpitations Profuse sweating Abdominal or chest pain Diagnosis is often missed

DIAGNOSIS
Best test- Urinary fractionated metanephrines (catecholamines metabolites) Plasma catecholamines (elevated during an attack) 24 hour urine- (metabolite of Epinepherine) CT/MRI to locate tumor

Pheochromocytoma Treatment
Surgical removal of tumor Medications
Calcium channel blockers control BP nicardipine (Cardene) Sympathetic blocking agents may BP ; Symptoms of catecholamine

excess
Beta blockers to dysrhythmias, BP Inderal

Diet high in vitamin, mineral, calorie, no caffeine Sedatives