Anterior Pituitary - Patho

hypothalamus

sends releasing hormones to anterior pituitary, directly stimulates posterior pituitary, has direct neural control over adrenal medulla to release epinephrine

anterior pituitary aka adenohypophysis

responds to hormonal signals by hypothalamus to send out TSH, GH, ACTH

posterior pituitary aka neurohypophysis

sends out ADH (made by hypothalamus), is directly connected to hypothalamus via nerves

hypofunction etiology

too little hormone due to congenital defects, lack of ingredients to make hormone, destruction or aging, receptor defects

hyperfunction etiology

too much hormone due to excessive stimulation or exogenous administration

thyroid hormone actions

affects almost all cells in the body, revs things up. increases energy, produces heat, stimulates cardiac tissue

follicular cells of thyroid release and store

T3/triiodothyronine and T4/thyroxine

parafollicular cells/C cells or thyroid release

calcitonin

most abundant thyroid hormone

thyroxine/T4

more biologically active thyroid hormone

triiodothyronine/T3

what is necessary to make thyroid hormones?

iodine

thyroid functions tests include

blood levels of T3, T4, TSH, TRH/TRF, thyroid antibodies; iodine uptake test; thyroid scan

hypothyroidism primary etiologies

cretinism, hashimoto’s, non-toxic goiter, thyroidectomy. labs: elevated TSH and low T3 & T4

secondary hypothyroidism etiology

issue with pituitary gland

tertiary hypothyroidism etiology

issue with hypothalamus

cretinism

primary hypothyroidism due to congenital issue, either defective gland or defective T3/T4, newborns are screened for this. sx: sluggish, lack of interest, somnolent, babies won’t suckle. can lead to impaired cognitive development, impaired growth, large protruding tongue (macroglossia), boggy non-pitting edema

hashimoto’s 

most common cause of primary hypothyroidism in the US. autoimmune disorder where antibodies attack the gland = inflammation & gland dysfunction

non-toxic goiter

primary hypothyroidism, enlarged gland due to inadequate iodine intake, doesn’t produce hormones. noncancerous, noninflammatory. elevated TSH levels leads to hyperplasia of gland, main concern is airway. reversible if iodine intake is reestablished quickly

thyroidectomy

primary hypothyroidism due to removal of thyroid gland

clinical manifestations of hypothyroidism

weight gain, low HR, slowed GI motility (easily constipated), cold intolerance, brittle hair, dry skin, flat affect (puffy & expressionless due to mucopolysaccharide accumulation), lethargy, fatigue, can lead to cognitive impairment

myxedema

severe hypothyroidism that can lead to coma and death, usually due to untreated/undiagnosed hypothyroidism. bradycardia, hypothermia, severe lethargy, boggy non-pitting edema periorbitally. tx: IV T3, cardiovascular support

hyperthyroidism occurs more often in…

women

primary hyperthyroidism

grave’s disease (thyrotoxicosis), nodules/toxic goiter. labs: high levels of T3 & T4 with low TSH and TRH

secondary hyperthyroidism

rare, due to adenomas in pituitary

tertiary hyperthyroidism

rare, due to adenomas in hypothalamus

grave’s disesase

most common form of primary hyperthyroidism. autoimmune disorder where autoantibodies activate TSH receptors in thyroid gland = unwanted release of T3 & T4. positive autoantibody test confirms dx

plumber’s disease

benign nodules of thyroid gland that cause primary hyperthyroidism

toxic goiter

primary hyperthyroidism due to cancerous or benign nodules that cause an enlarged overactive thyroid gland

thyroid nodules may be

overactive or underactive

signs and symptoms of hyperthyroidism

revving up - exophthalmos, pretibial myxedema, jitters, increased HR, increased BP, feeling hot, intolerance to warm environments, sudden weight loss

thyroid storm

medical emergency of hyperthyroidism precipitated by trauma to the neck/thyroid surgery. sx: high temp, HR, BP, can result in coma and death. Tx: cooling blankets, beta blockers to decrease HR, antithyroid drugs to quiet the gland

zona glomerulosa of adrenal cortex

produces mineralocorticoids - aldosterone

aldosterone

increases sodium and water reabsorption into the blood at the nephron, causes secretion of K+. Increases blood volume in response to decreased blood osmolarity or hypovolemia.

zona fasciculata of adrenal cortex

produces glucocorticoids - cortisol, corticosterone, cortisone

cortisol

stimulates glucose, protein, fat metabolism, is immunosuppressant. blocks action of insulin, increased gluconeogenesis, inhibits bone formation, anti-inflammatory, inhibits migration of WBCs to sites of inflammation

zona reticularis of adrenal cortex

androgens - role in onset of puberty

flow of adrenal control

hypothalamus receives signals from body → releases corticotropin releasing hormones → signals anterior pituitary to release adrenocorticotropin hormone → signals adrenal cortex to release their steroid substances

hypocortical disorders

addison’s = primary adrenal gland insufficiency, secondary adrenal insufficiency = problem with pituitary, tertiary adrenal insufficiency = problem with hypothalamus

hypercortical disorders

cushing’s disease & syndrome, conn’s syndrome

addison’s disease

primary adrenal insufficiency, autoimmune destruction of adrenal cortex, leads to deficiency of aldosterone, glucocorticosteroids, and androgens

manifestations of addison’s disease

low aldosterone = hyponatremia, hyperkalemia, fluid loss and dehydration, crave salt, low cortisol = hypoglycemia, fatigue, low androgens = low libido, amenorrhea. Hyperpigmentation, low BP, F&E imbalance = N/V and diarrhea. Labs: elevated ACTH and low levels of cortisol and aldosterone

ACTH stimulation test

tests for addison’s disease. give synthetic ACTH, normal response = corresponding increase in cortisol, no increase in cortisol = adrenal gland is not responding to stimulation

Addison’s crisis

medical emergency - can lead to cardiovascular collapse. etiology: loss of sodium and water = decrease in circulating volume, hyperkalemia has cardiac implications. cause is usually sudden withdrawal of exogenous glucocorticosteroids - must taper them off. Tx: stabilize F&E, Na+ replacement, dextrose, steroid replacement

cushing’s disease and cushing’s syndrome are both…

overactivity of the adrenal gland. have similar manifestations but different etiologies. tx: surgical removal of tumor, radiation, medications. Labs: high ACTH = secondary etiology/disease, low ACTH = primary etiology/syndrome, 24 urine test to measure cortisol

cushing’s disease

secondary etiology, pituitary tumor producing and releasing too much ACTH

cushing’s syndrome

primary etiology, excess production of cortisol by the adrenal gland, or also could be iatrogenic due to exogenous glucocorticosteroids

cushing’s manifestations

weight gain, abnormal fat distribution (eggs on legs), moon face, buffalo hump, central obesity, hyperglycemia, muscle wasting, fluid retention, fragile skin, impaired wound healing, immunosuppressed = increased risk for infection, impaired prostaglandin synthesis = bleeding GI ulcers, osteoporosis, GI upset and bleeding, hirsutism

Conn’s syndrome

only affects zone glomerulosa - hyperaldosteronism. Excess Na and water retention and K loss → fluid volume overload, HTN, hyperkalemia. Tx: stabilize BP, F&E, remove overactive cells of cortex

growth hormone

produced and released by anterior pituitary when hypothalamus sends GHRH. only primary (pituitary issue) and secondary (hypothalamus issue) etiologies

growth hormone deficiency

rare, most commonly a genetic deficiency of GH or GHRH, can also be due to trauma, radiation, tumors. Sx: proportional small stature in children - not same thing as dwarfism. Dx: growth charts and GH levels. Tx: recombinant DNA GH injections

growth hormone excess

gigantism: excess in children, affects length of long bones

acromegaly: excess in adults, affects face, hands, feet, internal organs

Tx: growth hormone antagonists, surgery of tumor

marfan syndrome

genetic disorder that causes weak connective tissue, tall, disproportional elongated limbs, prone to having spinal issues, scoliosis. No elevation in GH. Most concerned for aortic dissection.