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endocrine physio
Question | Answer |
---|---|
What promotes secretion of insulin (nervous) | ACh |
What promotes secretion of insulin (hormones) | Cortisol, GH, glucagon, GIP, Secretin and gastrin |
What promotes secretion of insulin (food) | AA (lys, arg, leu), fatty acids, sugar |
What promotes secretion of insulin? (Drugs) | sulfonylureas |
What inhibits insulin? | decreased blood glucose, somatostatin, NE, Epi (alpha adrenergic stimulation), phenytoin, vinblastine, colchine |
What are the four overall effects of insulin on blood levels? | decreased glucose, AA, fatty acids, ketoacid, hypokalemia |
Insulin acts with ___ receptor, glucagon acts with ___ | tyrosine kinase receptor, cAMP |
In obesity receptors are ___ in starvation they are __- | decreased, increased |
Beta cells have what type of GLUT receptors? | GLUT 2 |
Describe how insulin is realsed | Glu --> glut 2 --> glycolysis --> increased ATP--> ATP closes K+ channel --> depol --> open voltage Ca channels --> insulin secretion |
How does sulfonylurea increased insulin | Blocks K+ ATPase channel --> Increased depol |
How does Epi, NE, and Glucagon work to change insulin levels? | throught cAMP --> increase Ca |
Target organs of insulin? Target organs of glucagon | Insulin =liver, adipose, muscle. Glucagon = liver, adipose |
4 actions of insulin | 1. Decrease glucose, 2. decrease AA, 3. decrease fatty acid, 3. decrease potassium |
How does insulin decrease glucose? | Increase glucose uptake (glut 2), increase glycogen formation (muscle/liver), decrease gluconeogenesis (increase f26BP --> increase PFK) |
How does insulin decrease fatty acids? | stimulates fat deposition, inhibits lipolysis (fat), inhibits ketoacid formation (less FFA degradation --> less acetyl coA) |
How does insulin decrease blood AA? | stimulates AA uptake, increases protein syntheis, inhibits protein degradation |
How does insulin decrease K? | insulin increases K uptake into cells, |
What stimulates glucagon | Decreased blood sugar, increased AA(arg), NE, E, CCK (alerts to protein meal), AcH, glucocorticoids |
AA that stimulate insulin, those that stimulate glucagaon | Insulin (arg, leu, lys), glucagon (arg) |
What inhibits glucaogn secretion? | Hyperglycemia, fatty acids, ketoacids, somatostatin, insulin |
Insulin increases/decreases 2,6 bisphosphate? | Insulin increases (Shunts it to PFK) |
4 main actions of glucagon | 1. increase glucose, 2. increase fatty acids, 3. increase ketoacids, 4. increase urea |
3 main actions of somatostatin | 1. decreased secretion of insulin/glucagon, 2. decreased gastric, duodenal, gallbladder motility, 3. decreased funtion of intestinal mucosa (decreased absorption and secretion) |
Adrenal cortex ____, Medulla ____ | Mesoderm, neural crest cells |
Somatotropin release-inhibiting hormone comes from ___- and actions are ____ | SRIF (somatostatin): hypothalamus, inhibits GH, TSH |
FSH actions, LH actions | Stmiulates growth of ovarian follicles, estrogen secretion, promotes sperm maturation, Stimulates ovulation, formation of CL, synthesis of estrogen and progesterone (ovary). Stimulates synthesis and secretion of testosterone. |
T4, T3 actions | Bone maturatoin, O2 consumption (Na/K ATPase), increased BMR (increased protein, fat, carboyhydrate use, maturation of nervous system |
Estradiol | Grwoth and development of reproductive organs, follicular phase of menstrual cycle |
Aldosterone actions | Increased Na reabsorption, increased renal K secretion, increased renal H secretion |
hCG actions | Increased estrogen and progesterone synthesis in CL of pregnancy |
hPL | Same actions as growth hormone and prolactin during pregnancy |
Adrenal cortex ____, Medulla ____ | Mesoderm, neural crest cells |
Somatotropin release-inhibiting hormone comes from ___- and actions are ____ | SRIF (somatostatin): hypothalamus, inhibits GH, TSH |
FSH actions, LH actions | Stmiulates growth of ovarian follicles, estrogen secretion, promotes sperm maturation, Stimulates ovulation, formation of CL, synthesis of estrogen and progesterone (ovary). Stimulates synthesis and secretion of testosterone. |
T4, T3 actions | Bone maturatoin, O2 consumption (Na/K ATPase), increased BMR (increased protein, fat, carboyhydrate use, maturation of nervous system |
Estradiol | Grwoth and development of reproductive organs, follicular phase of menstrual cycle |
Aldosterone actions | Increased Na reabsorption, increased renal K secretion, increased renal H secretion, increased BP |
hCG actions | Increased estrogen and progesterone synthesis in CL of pregnancy |
hPL | Same actions as growth hormone and prolactin during pregnancy |
What controls prolactin synthesis | TRH stimultaes, dopamine inhibits |
What stimulates dopamine? what medical agent is similar to dopamine? | Prolactin, bromocriptine |
Prolactin action | inhibit GnRH; breast development, prevent obulation, spermatogenesis |
alpha subunit is common to what hormones? | TSH, LH/FSH, hCG |
Enzyme that converts cholesterol to pregnolone is stimulated by ___ and inhibited by ____ | Stimulated by ACTH, inhibited by ketoconazole |
Decreased sex hormones, decreased cortisol, increased mineralcorticoids: Hypertension/hypotension, Hyper/hypokalemia. XY:, XX | 17 alpha hydroxylase. SX: hypertension, hypokalemia. XY: pseudohermaphrodite (phenotypic famle, no internal structures). XX: lacking femal sexual characteristics (infantiilism) |
decreased cortisol, decreased mineral corticoids, increased sex hormones, increased ACTH. Hypo/Hypertension, Hypo/hyperkalemia, XY, XX | 21 hydroxylase deficiency. Sx: hypotension, hyperkalemia, increased plasma renin, volume depletion. Salt wasting can lead to hypovolemic shock in new borns. XX: virilization, XY: precocious puberty |
Decreased cortisol, decreased aldosterone and corticosterone, increased sex hormones. Sx: Hypo/hypertension, XX, XY | 11B hydroxylase. Hypertension, masculinization. Virilization. |
All congenital adrenal enzyme deficiencies have what feature? | They all have increased ACTH, are autosomal recessive, and have bilateral enlargement of adrenal glands |
Cortisol levels are highest ___, lowest ____ | High 8AM, low 12 AM |
Cortisol function | Anti-inflammatory, increased gluconeogenesis, lipolysis, proteolysis, decrease immune, maintain blood pressure, decrease bone formation |
CRH is released from what nucleus in HTHAl? | paraventricular nucleus |
ACTH is derived from ___ | POMC |
Dexamethosone cannot suppress __- but does suppress ___ | Suppress normal cortisol secretion, ACTH secreting tumors; cannot suppress adrenal cortical tumors |
What stimulates the RAA system? | decreased blood volume, decreased renal perfusion, increased renin |
Where does aldosterone act in the kidney | increased NA reabsortpion/K secretion = distal collecting duct by principal cells; increased H secretion: intercalated cells of distal collecting ducts |
Parathyroid has two types of cells: which one is pink, which one is purple | Oxyphil, chief cell |
60% of calcium is free/bound | Bound |
3 functions of parathyroid. What cells secrete PTH? What cells do PTH stimulate? | Chief cells: Increased serum Ca, Decreased serum PO4, Increased Urine PO4 (cAMP); OB, OC |
What increases PTH/inhibits PTH | decreased Ca, Increased PTH secretion. Decrease: low Mg, increase Ca, decrease PO4 |
How does PTH work on the intestine | Increases PO4 and Ca from intestine indirectly by stimulatint 1,25 D3 |
What stimulates vitamin D production | Decreased Ca, increased 1,25 (OH)2 from liver, decrease PO4 production |
PTH and Vitamin D: calcium, phosphate | PTH: increases calcium reabsorption, decreases phosphate reabsortpion, Vitamin D: increases reabsorption of calcium and phosphate. |
Unlike Osteoperosis, the ratio of mineral to osteoid in rickets is ___ | Decreased (more osteoid), not just bone loss, but dimneralization |
Labs for rickets: | Increased alkaline phosphate (increased collagen syntehsis) |
What is derived from POMC | Alpha MSH, Beta MSH, ACTH |
How is growth hromone secreted? when is it increased? decreased? | GH: pulsatile fashion; Increased: sleep, stress, puberty hormones, exercise, hypoglycemia, starvation. Decreased: somatostain, somatmedins, obesity, hyperglycemia, pregnancy |
GHRH is inhibited by __- | negative feedback |
Somatomedins are made from ___, due to ___ whereas somatotstain is made from ____ | Somatomedins = liver and created with high levels of growth horomone. somatostatin = HTHAL, delta cells |
IGF is a ___ and has ___ activity | IGF = somatomedin that has tyrosine kinase activity |
Actions of growth hormone | decreased glucose uptake (diabetogenic), increased lipolyis, increased protein syntehsis in muscle, increased lean body mass, increased production of IGF |
Actions of growth hormone via IGF | Increased protein synthesis in chondrocytes, increased linear growth, increased lean body mass, increased organ size |
Octreotide = | somatostatin analog which inhibits growth hormone |
Factors that stimulate prolactin secretions | Estrogen, breast-feeding, sleep, stress, TRH, dopamine antagonsists |
ADH is made in the ___ nuclei. It's stimulated by | supraoptic nuclei. osmolarity, pain, nausea, hypoglycemia, nicotine, opiates, antineoplastic agents |
Factors that decrease ADH secretion include | decreased serum osmolarity, ethanol, alpha agonists, ANP |
Oxytocin is made in the ___ nuclei | paraventricular nuclei |
Function of oxytocin | milk ejection,reduce postpartum bleeding, induce labor, |
What increases oxytocin secretion | suckling, oxytocin, dilation of cervix, orgasm |
What is a medullary carcinoma | abrnomal proliferation of parafollicular cells wtih amyloid stroma |
Inhibits Na/I pump | Thiocyanate, percholate |
Inhibit organification (MIT, DIT formation). | Too much iodide (Wolff Chaikoff effect) |
Mimic I2 deficiency | Deficiency of thyroid deiodinase |
What is a goiter and what can cause it? | enlargement of thyroid. Hashimoto, goitrogens, iodine deficiency, physiologic enlargment (not uncommon during puberty and pregnancy) |
TBG is ___ during pregnancy which means that __ is increased and TBG is ____ during hepatic injury, which means ___ is decreased | Increased = pregnancy which means that total serum T4 is increased (free remains the same) decreased = hepatic injury, total serum T4 is decreased (free T4 remains the same) |
Precocious puberty in boys is usually caused by | midline harmartoma |
In order to cahnge total serum T4 you must have an | Increase/decrease in FT4 |
Increased FT4, decreased FT4 | Grave's, thyroiditis; Hypothyroidism |
Increased iodine uptake maeans that there is | an increased synthesis of T4(examples: Grave's disease, toxic nodular goiter |
Decreased iodine uptake means that there is | a decreased synthesis of T4 (inactivity, thyroiditis) |
Cold nodule=, increased uptake | decreased uptake = cyst, cancer, Increased uptake = toxic nodular goiter |
Branchial cleft cyst vs. thyroglossal cyst | branchial cleft anterolateral neck, thyroglossal = cystic midline mass |
acute vs. granulomatous thyroiditis | acute= fever, tender galnd with painful cervical adenopathy, initial increased T4, decreased I. Subacute = viral infection (coxsackie), women 40-50, granulomatous with multinucleated giant cells. |
Hashimoto is associated with what HLA types; what is it, antibodies? | DR3, DR5; toxicosis --> hypothyroidism; antimicrosomal, thyroglobulin (result of gland injury) |
Types of Cushing syndrome? | Pituitary (adenoma), Adrenal, ectopic, drug related |
Which type of Cushing syndrome can be suppressed by dexamethasone? | Pituitary |
In the presence of increased cortisol, what does a normal -increased, decreased, very high ACTH mean? | Pituitary, Adrenal, Ectopic |
Primary aldosteronism is also known as ___. Secondary aldosteronism is due to ___-, ___, ___,____. Which is associated with high Renin? low renin? | Conn's syndrome. Caused by an aldosterone secreting (low renin. Renal artery stenosis, chronic renal failure, CHF, cirrhosis, nephrotic syndrome (caused by kidney perception of low intravascular volume in an overactive renin-angiotensin system. High renin |
Hyperaldosteronism produces what lab? | hypertension, hypokalemia, metabolic alkalosis |
Causes of acute adrenocortical insuffiency | abrupt withdrawl of corticosteroids, waterhouse friderichsen syndrome, anticoagulation therapy |
Waterhouse Friderichsen synrome is caused by __- | Septicemia from Neisseria meningitidis. patients develop endotoxic shock (release thromboplastin --> DIC). Bilateral adrenal hemorrhage (fibrin clots in vessels causing hemorrhagic infarction) |
Causes of chronic adrenocortical insufficiency | Addison's: TB, autoimmune, adrenogenital syndrome, metastasis (lung) |
symptoms for addison | due to deficiency of aldosterone and coritosl (adrenal atrophy): hypotension, skin hyperpigmentation. |
What causes Sheehan's syndrome? | Postpartum hypopituitarism. increased lactotrophs during pregnancy withouth blood supplye --> infarction of pituitary gland and bleeding/hypoperfusion during delivery. Sx: fatigue, anorexia, loss of pubic/axillary hair. |
Pheochromocytoma secretes ____. | secretes NE, EPi, DA in episodic waves. Causes hypertension and sever hyperglycemia. |
What products are urine of a patient with pheochromocytoma | HVA (dopamine), Norepinephrin (VMA), Epinephrine (metanephrine) metabolites. |
What diseases are associated with pheochromocytoma? | MEN 2A/B, neurofibromatosis, vHL disease |
Treatment for pheochromocytoma | alpha antagonists, phenoxybenzamine (nonselective irreversible alpha blocker) |
What are the 5 Ps of pheochromocytoma? | Pressure, pain (headache), perspiration, palpitations (tachycardia), pallor |
Neuroblastoma most commonly found in what age group. where do they occur? How are they diagnosed. how are they different than pheochromocytomas in adults. What gene are tehy associated with? What do they usually look like? | Most common tumor in adrenal medulla of children. Can occur anywhere along sympathetic chain. HVA (DA breakdown) in urine. Less likely to develop htn. N-myc oncogene amplifications. Presents with abdominal mass |
What are the neuroblastoma gene products recognized? | double minute chromosomes; related to aggressiveness of tumor |
MEN 1 ___, Men 2A ___ | MEN1 = Wermer's syndrome, MEN 2A = Sipple's syndrome |
What are the Ps for MEN 1, 2A, 2B? | Pancreas, Pituitary, Parathyroid; Pheochromocytoma, parathyroid; pheochromocytoma, |
What are the pituitary tumors associated with MEN1? Pancreatic tumors? | Pituitary: GH, prolactin; Pancreatic: Zollinger-Ellison, insulinomas, VIPomas, glucagonomas; |
MEn syndrome taht presents with kidney stones and stomach ulcers | MEN 1 |
What tumor secretes calcitonin? | medullary thyroid carcinoma |
Which MEN is associated with marfinoid habitus? Why does this happen? | MEN2b; Oral/intestinal ganglioneuromatosis |
what gene is associated with MEn? | Ret: MEN 2A 2B |
Which men is associated with medullary thyroid carcinoma? | MEN 2A/B |
Most common cause of hypopituitarism in children? | Craniopharyngioma (pituitary tumor of Rathke's pouch); located above sella turcicca |
What is associated with a craniopharyngioma? | cystic tumor with hemorrhage and calcfication, bilateral hemioanopsia, |