clinicalMedEndocrine

• Decrease secretion of adenohypophyseal hormones.
• May be congenital or may occur during life.
• The effects are related to the deficit in 1 or more of the following hormones
• -- Adrenocorticotropic hormone (ACTH): stimulates the adrenal gland to release cortiso which helps to maintain blood pressure and blood sugar
• -- Antidiuretic hormone (ADH): controls water loss by the kidneys
• -- Follicle stimulating hormone (FSH): controls sexual function and fertility in males and females
• -- Growth hormone (GH): stimulates growth of tissues and bone
• -- Luteinizing hormone (LH): controls sexual function and fertility in males and females
• -- Oxytocin: stimulates the uterus to contract during labor and the breasts to release milk
• -- Prolactin: stimulates female breast development and milk production
• -- Thyroid stimulating hormone (TSH): stimulates the thyroid gland to release hormones that affect the body's metabolism

• variations in ADH secretion causing diabetes insipidus
• In ¼ of cases it is associated w/brain tumor requiring surgical
• treatment. If not it can be treated by insufflating (sniffing/inhaling) a small amount of synthetic vasopressin.

tendency to be dehydrated (due to inability to concentrate urine) & to “wash out” electrolytes from body fluids (polyuria, thirst, polydipsia)

• thyrotoxicosis, graves' disease
• A hypermetabolic state produced by increased thyroid hormones.
• Sudden release of excessive amounts of thyroid hormones (thyroid storm) is emergency that can progress to coma.

manifested by hyperkinesias, emotional lability, increased appetite, but decreased weight, muscle weakness w/fine tremors, heat intolerance, warm moist skin, sweating, tachycardia, cardiac arrhythmias, exopthalmos.

• thyroid hormones deficiency
• primary hypothyroidism: result from increase in serum TSH in thyroid disease
• or
• secondary hypothyroidism: from a deficiency in TSH caused by pituitary or hypothalamic disease.

• Adults: myxedema (muccopolysaccardies deposition in connective tissue), apathy, tiredness, dry skin & hair,dilated hrt
• Infants: mental retardation, impaired growth

• (Addison’s disease)
• dec adrenocortical hormones: due to atrophy / TB related destruction of adrenal cortex
• dec cortisol: impaired gluconeogensis
• dec aldosterone: no retention of Na, no excretion of K

• due to dec in adrenocortical hormones: fatigue, anorexia, weight loss, nausea & vomiting.
• dec cortisol: altered bld glucose levels, fat & protein metabolism
• dec aldosterone: hypotension, serum decrease in Na+, Cl- HCO3 & increase in K+ (hyperkalemia)

• (Cushing’s disease)
• associated w/abnormal amounts of cortisol.
• Increased blood glucose level is due to enhanced gluconeogenesis & if it lasts for many months it may “burn out” insulin products on cells & cause “adrenal diabetes.”

“moon faces,” “buffalo hump,” truncal obesity, osteoporosis, menstrual disorders, susceptibility to infection, muscle weakness

• (conn's disease)
• Extracellular fluid volume is increased with hypokalemia.
• Opposite of Hyperadrenalism.

• acute renal shutdown
• chronic renal insufficiency
• pyelonephritis
• nephrotic syndrome

• acute glomerulonephritis
• acute damage to the tubules and necrosis

• causes acute renal shutdown
• results from an antigen-antibody reaction in which the glomeruli become inflamed (from streptococci A)
• inflammatory reaction causing total or partial blockage of large # of glomeruli & those that are not blocked develop increased permeability of glomerular membrane, allowing large amounts of protein & RBCs to leak into Glomerular Filtrate (GF).
• Acute form frequently becomes chronic.

• (common cause of acute renal shutdown)
• Poisons: carbon tetrachloride & mercuric ions have specific nephrotoxic action
• Severe Acute Renal Ischemia: usually a result of severe circulatory shock when heart fails to pump sufficient amounts of blood to body
• Transfusion reaction: where hemolysis of large amounts of RBCs releases Hg (that precipitate in the nephron) & vasoconstriction agent diminishing renal blood flow

decreased number of nephrons

• Chronic glomerulonephritis & polynephritis
• Traumatic or congenital absence of a kidney: decreases nephrons by ½
• Congenital polycystic disease: when large cycsts develop in kidneys & destroy surrounding nephrons by compression Urinary tract obstruction: caused by renal stones
• Arteriosclerosis: when small arteries supplying portions of kidneys become blocked

• an infectious and inflammatory process that usually begins in the renal prelvis and extends progressively into renal parencyma.
• invading infection results in progressive destruction of the functional renal tissue usually affecting more medulla of the kidney.
• patients have reasonably normal renal functions with inability to concentrate urine.

• loss of large quantities of plasma proteins into the urine due to increased permeability of the glomerular membrane, causing fall in colloid osmotic pressure & serious edema.
• usually associated w/renal insufficiency caused by
• -- Chronic glomerulonephritis
• -- Amyloidosis
• -- Syphilis
• -- Systemic lupus erythematosus