hormone deficiency, hypersecretion Flashcards
Increased GH can cause
-prolactin like symptoms
Growth Hormone Excess
before closure of epiphesial plates- gigantism hyperglycemia, if closed acromegaly(due to tumor soft tissue growth) -widely spaced teeth, and increased slant of forehead, prognathism(growth of mandible -increased organ size –hypertrophy of organs, hypertension, compresson of nerves and diabetes.
Growth hormone deficiency
panhypopituitarism, results in dwarfism, Laron has bad receptors. if you treat with IGF you will increase their height.
pituatary stalk injury results in
diabetes insipidus, panhypopituatarism, hyperprolactinemia
hypersecretion of prolactin
Galactorrhea, decreased libido, decreased obulation and spermatogenesis by inhibiting GnRH Prolactinomas- benign tumors, compresses optic chiasm if greater than 15 cm bitemporal hemianopiea,
Prolactin deficiency results in
failure to lactate
Diabetes insipidus
Central-low levels of ADH due to CNS lesion, treated with ADH analogue and dDAVP Nephrogenic- high levels of ADH, defect is V2 receptor, Gs proteins or adenylyl cyclase
Syndrome of inappropriate ADH
oat cell in lung cuases increased ADh secerion, increased water retention and urinary concentration which will decrease the serum osmolarity
Pregnancy and estrogen increases levles of
TBG
Plummers disease
overactive lump, hyperthyroidism
Hypertyroidism causes
thyroid enlargement, overative lump, toxic multinodular goiter
symptoms of hyperthyroidism
irrtability, weight loss, amenorrhea, palpitations, increased bowel movments, heat intolerance, CHF in elderly
causes of hypothyroidism
Haschimoto’s thyroiditis, thyroidectomy, iodide deficiency, secondary, insufficient pituitary action, resistance of organs to TH
hypothyroidism in newborns
iodidedeficiency, placental transver of TSH antibodies. show respiratory problems, jaundice, poor feeding, umbilical hernia, reduction of bone development.
hypothyroidism in children
growth and mental retardation
hypothyroidsim in adults
fatigue, cold intolerance, weight gain, menstrual problems, slow deep tendon reflexes, usually slow relaxation phase, coarse dry skin, bradycardia, constipation myxedema, due to accumulation of GAGs, puffiness
Amenorrhea in hypothyroidism
decrease in T3 means increase in TRH and TSH, Increased TRH causes Increased Prolactin and decrease in GnRH- anovulatory cycle.
Hyperaldosteronism
–increased Na and water retention in plasma and potassium secretion into urine, –increased plasma volume causes hypertension –increased H+ exchanged for ICF K+ leading to alkalosis, and hypokalemia causing muscle wekanesss and arrhytmias
Primary hyperaldosteronism
Conn’s syndrome from an adrenal tumor or hyperplasia, decreased renin levels.
secondary hyperaldosteronism
increased renin levels
hyposecretion of aldosterone
hyperkalemia, decreased K excretion –metabolic acidosis, increased H+ retention Hyponatremia- decreased Na reabsorption decreased extracellular fluid and volume, shock.
21 Beta hydroxylase deficiency
lack of corticosterone/aldosterone, Cortisol and accumulation of progesterone, 17 hydroxy progesterone, and Androtenedione Hypovolemia, hyperkalemia, hypoglycemia due to cortisol, high levels of renin. Hyper androgen production.
17 alpha hydroxylase deficiency
can only synthesize corticosteroids, no cortisol or androgens. hypertension, hypervolumia, hypokalemia and increased sodium retention, low renin levels. Glucocorticoid deficiency but not as asevere because you still have corticosterone.
11 Beta Hydroxylase deficiency
same as 21 beta but you have hyper tension becasue 11deoxycorticosterone can have aldosterone like affects, increased renin, but hypoglycemia
17-20 lyase deficiency
deficiency in androgens, more severe in femalse.
pheochromocytoma
hypersecretion of medullary hormones, hyperglycemia, Hypertension, increased in basal metabolic rate and orhtostatic hypotension, going from sitting to standing will drop by 20 in systolic or 10 in diastolic.
Stress response
activates both adrenal medulla and cortex, medulla is immediate and releases catecholamines that increase HR, BP GLUCOSE, BMR, Bronchodilation. Adrenal cortex releases gulcocorticoids whihc cause protein, fat, breakdown and immune suppresion.
Diabetes Mellitus
increased glucose, FFA’s AA’s and ketone bodies which causes ketoacidosid or Diabetic KA, this will cause H+ to be exchanged for K+ and this will cause K to be secreted due to increased RAAS in kidneys, osmotic diuresis, dehydration. Type 1- destruction of beta cells, Type II- insulin resistant- don’t develop ketoacidosis- loosing weight can improve it. can get a hyperosmol coma. - treat with sulfonylurea drugs and biguanide- metformin to upregulate insulin receptors
complications of diabetes
risk of stroke, risk of heart disease, increased blood pressure, leading caue of blindness in adults, end stage renal disease, peripheral nueropathy.
Hypoglycemia
caused by failure to adjust meds in diabetic patients, exercise in diabetics, alcohol, insulinoma. sympotms are excitability, tremors, coma(Below 40), disoriented confuesd(below60)
Alkalosis affect on calcium
incrased in calcium binding and decrease in plasma calcium
acidosis affect on calcium
less calcium binding and increased plasma calcium
hypocalcemia
increases membrane exictability and causes paresthesias, hypocalcemic tetany, chvoestek’s sign twitching of facial muscles. Trousseaus sign EKG shows shortened QT interval
hypercalcemia
nephrogenic DI, polyuria, polydipsia, Peptic ulcer, due to direct stim of praieta cells, Kidtney stones, neuro symptoms, pshych symptoms EKG shows shortened QT interval.
Primary hyper PTH
usually due to parathyroid hormone, shows hyperalcemia symptoms
secondary hyperparathydroidsi
deficient in vitamin d or poor absorption of fat, inability to synthesize D3 or increased need for Calcium (pregnancy) Serum PTH are high and Ca is normal to low. serum phosphate is low but urine phosphate is high.
rickets/osteomalacia
low vit d, demineralization of bones.
Primary hypoparathyroidism
accidental removal, low Ca, and high Phosphate. - tetany below 6 mg of Ca in blood can lead to death.
Hypogonadism
non functional testes or loss of testes, prepuberty, longer less strong bones, develop femal sex organs. post puverty, increase of voice pitch, loss of bone, protein and less easy for erection.
adiposogenital syndrome
can’t Make GnRh, also affects feeding center and causes obesity and hypogandism.
Panhypopituitarism
deficiency in all pituitary hormones –occurs later in life due to infarction as in Sheehan’s syndrome due to post partum hemorrhage – in children leads to dwarfism in adults, hypothyroidism, decrease in sexual hormones, decrease in glucocoticoids
