Quizlet Endo

Endocrinology USMLE Step 1 Study online at quizlet.com/_d28uu 1.

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are there increased or decreased amino acids in the circulation with increased insulin?

decreased (increased uptake)

by what type of cells are carcinoid tumors caused by? where are they usually located?

neuroendocrine cells; GI

even though there is hyperkalemia in DKA there is a depleted intracellular potassium. explain.

though there is a hyperkalemia due to transcellular shift from acidosis, there really is an intracellular depletion because of the osmotic diuresis pulling potassium out (like sodium)

from what aa are catecholamines made?

tyrosine

from what cells is a medullary thyroid carcinoma?

parafollicular C cells

from what precursor is melanotropin made from? what else does this precursor make?

POMC; ACTH

from where do the islets arise from? and where in the pancreas are the islets most abundant?

pancreatic buds; in the tail of the pancreas

from where is calcitonin released? what is its function?

parafollicular (C) cells of the thyroid; oppose action of PTH- decrease bone resorption of calcium (ie cause a decrease in serum calcium)

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from where is CRH hypothalamus; ACTH release from released? what does adenohypophysis it result in? from where is dopamine released? what does it result in? in what kind of receptors?

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hypothalamus; prolactin release inhibition in adenohypophysis; D2

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from where is GHRH hypothalamus; Gh release from released? what does adenohypophysis it result in? from where is GnRH released? and does it result in?

hypothalamus; FSH and LH release

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from where is parathyroid released? exactly what type of cells?

chief cells in parathyroid gland

from where is prolactin released? what effect does it have on the hypothalamus?

adenohypophysis; increases dopamine synthesis and secretion from the hypothalamaus (negative feedback!) and decreased GnRH from hypothalamus

from where is somatostatin released? what does it result in?

hypothalamus; inhibition of Gh and TSH from adenohypophysis

from where is TRH released? what does it result in?

hypothalamus; TSH and prolactin release from adenohypophysis

how can you tell if a patient is suffering from hyperthyroidism due to exogenous thyroid ?

decreased uptake

how does a toxic multinodular goiter become nontoxic?

hyperplasia causes gland involution

how does coma and death occur in DKA

d/t dehydration from diuresis and acidosis

how does hypercalcemia cause nephrogenic diabetes insipidus?

blocks NaCl reabsorption in the thick ascending limb disrupting counter current exchange and causing inability for aquaporin to do its thing

how does obesity exacerbate insulin resistance?

because increased adipose tissue also downregulates insulin receptors

how does the body respond to the increased volume in SIADH? what does this cause? how should you correct this?

decreases aldosterone; causes even more hyponatremia and seizures!; slowly (cerebellar pontine myelinosis)

how do you diagnose a pituitary tumor of somatotrophs?

increased serum IGF-1 (produced by liver, release activated by GH), and failure to suppress serum GH following oral glucose tolerance test

how do you diagnose diabetes insipidus? and then how do you differentiate between the two types?

with water deprivation test, the urine doesnt increase in osmolality; desmopressin

how do you differentiate acute thyroiditis from subacute?

acute (usually S. aureus) will have lymphadenoapathy

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how do you differentiate a patient with cretinism from one with pituitary dwarfism?

both short stature, but cretin is increased in weight, pituitary is decreased in weight

how do you differentiate between exogenous and endogenous insulin?

exogenous wont have increased serum c peptide levels

How do you differentiate between malignancy of thryoid nodules? Give two ways.

nonneoplastic/neoplastic: hot/cold and multiple nodules/single mass

how do you differentiate between the endogenous causes of cushings? what should happen in a healthy individual?

dexamethasone suppression test which is a synthetic ACTH which should result in decreased levels of cortisol after a low dose

how do you distinguish primary from secondary addisons? why? what is a secondary form due to?

in secondary there will be no skin hyperpigmentation and no hyperkalemia or met acidosis or hypotension because aldosterone is controlled by RAAS not ACTH; deficiency in ACTH production

how do you treat a pituitary adenoma of somatotrophs?

octreotide

how do you treat hyperaldosteronism?

either surgical removal of the aldosterone secreting tumor or spironolactone (an aldosterone antagonist that is a potassium sparing diuretic)

how is T4 converted to T3? how are they different?

by 5' iodinase; T3 binds with more affinity to receptors

how is zollinger ellison syndrome treated?

octreotide, proton pump inhibitors

if vit D cares about bone health why does it activate bone resorption?

because bone has reserve of ca and phosphate and it is releasing it from that reserve for bone mineralization (in other places)

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in 17 alpha hydroxylase deficiency, how does an XY present? XX?

XY: pseduohermaphroditism (because no DHT there is female external genitalia and because of MIF presence there is no internal reprostructures); XX: "sexual infantilism": externally phenotypic female with normal internal sex organs but no secondary sexual characteristics

in a adrenal adenoma or carcinoma, what happens to the rest of the adrenal gland?

atrophies d/t decreased ACTH

in what causes of cushings do you see amennorhea, hirsutism and acne?

when there is increased ACTH (not iatrogenic or Adrenal adenoma) and thus increased androgen:estrogen ratio

in what form is iodine taken up from the blood into follicular cells of the thyroid?

I-

in what form is Vit D when it is ingested from plants? when it is converted from 7 dehydrocholesterol in the skin? what is the active form?

Vit D2; Vit D3 (cholecalciferol) ; Vit D (Calcitriol)

in what type of DM is DKA seen? why not the other type?

type I, because there is enough insulin to prevent ketoacidosis

in which congenital bilateral adrenal hyperplasia do you see hypertension? hypotension?

17 alpha hydroxylase def and 11 beta hydroxylase deficiency; 21 hydroxylase def.

in which congenital bilateral adrenal hyperplasia do you see increased renin? decreased?

21 hydroxylase def; 17 alpha hydroxylase and 11 beta hydroxylase def

in which congenital 17 alpha hydroxylase deficiency; bilateral adrenal 21 hydroxylase and 11beta hyperplasia do you see hydroxylase deficiencies male pseudohermaphrotidism? female pseudohermaphrotidism? is insulins effect an overall anabolic or catabolic effect? give examples.

anabolic; increased glycogen and protein and triglyceride synthesis and storage

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of what cells are a pheochromocytoma derived from? and where do these cells come from?

chromaffin cells; neural crest

other than decreasing sympathetic activation, what else do beta blockers do in thyrotoxicosis?

decrease T4 to T3 conversion in the periphery

other than hypoparathyroidism, what are other causes of hypocalcemia?

hypovitaminosis D, acute pancreatitis because FA in fat necrosis bind calcium

other than increased lateral bone growth,what else does acromegaly present with?

large tongue with deep furrows, big hands and feet, deep voice, coarse facial features, hypertension (sodium retention), hyperglycemia, insulin resistance due to hyperglycemia (increased gluconeogenesis)

other than increased phosphate in the urine, what else is found in the urine with PTH?

increased cAMP because decreasing phosphate reabsorption in the PT results in release of cAMP

other than increasing bone resorption, how does PTH result in increased calcium?

by increasing calcitriol production by increasing 1 alpha hydroxylase and by increasing calcium reabsorption at the DCT

other than inuslin resistance, what else contributes to insulin resistance in DM II?

inability to secrete enough insulin in response to corresponding glucose levels

other than MEN I, what is it known as known as?

Wermers

other than renin level, how do you distinguish between primary and secondary hyperaldosteronism?

edema- in primary there is no edema because of escape pathway of sodium; in secondary there is edema (that is what caused it in the first place! pull of IV volume out)

other than the neoplasias what else does MENI present with?

kidney stones and stomach ulcers (parathyroid and gastrinoma)

other than TRH what else increases prolactin release?

estrogen (from OCPs and pregnancy)

T/F ADH V1 receptor uses cAMP

False- uses IP3, V2 uses cAMP

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T/F all MEN disorders have AR inheritance

false- AD

T/F all thyroid hormone in the blood is active

false- only free hormone (both T3 and T4)

T/F a pituitary adenoma results false- rest of pituitary in hyperpituitarism becomes hypopituitary T/F beta blockers help decrease O2 consumption in thyritoxicosis

FALSE.

T/F both hashimotos and de Quervains thyroiditis can be preceded by hyperthyroid periods

true

T/F DM II has an HLA association- DR3 and 4

false DM I does

T/F DM II has a weak polygenic genetic predisposition

false- strong

T/F DM II has low beta islet cell number

not always

T/F DM I tends to present more abruptly while DM II manifestations tend to present more chronicly

true

T/F dopamine is tonically inhibited by dopamine

true

T/F follicular thyroid carcinoma has intact capsule around it

false- that is an adenoma

T/F gastrin secreting tumors are found in the pancreas

not all- also duodenum

T/F GI carcinoid tumors have have 5-HT as a marker

not all do- only those that have metastasized outside the GI (because liver metabolizes it)

T/F glucocorticoids are used in croup and COPD

True

T/F glucose is freely filtered through bowmans capsule

true

T/F GnRH uses cAMP

false- GHRH (GnRH uses IP3)

T/F Graves presents with diffuse, symmetrical tender goiter

false- nontender

T/F Hashimotos thyroiditis is usually preceded by a flulike viral illness and is self limited

false- that is deQuervains Subacute thyroiditis

T/F hashimotos thyroidits patients have a enlarged tender thyroid

False- enlarged but not tender

T/F hyperreflexia is a sign of hypocalcemia

true

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T/F hyperthyroidism can cause exopthalmos

false- graves causes this by activating fibroblasts to deposit connective tissue behind eyes

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T/F in addisons disease the adrenal medulla is spared

true

T/F in circulation cortisol is free

false- bound to corticosteroid binding globulin (CBG)

T/F Insulin is necessary always in DM I

yes

T/F it is more common to see the symptoms of polyuria, polydipsea, thirst and weight loss in DM I

true

T/F like the brain, RBCs depend on glucose and use ketones during starvation

false only the brain does this, RBCs cant use ketones

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T/F maternal thyroid can cross placenta

true! keeps baby euthyroid (brain maturation!)

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T/F most neuroblastomas are benign

false- malignant :(

T/F most thyroid hormone is in the T3 form

false! most is in T4 form and isnt converted to T3 until in periphery

T/f muscle cramps are a sign of hypercalcemia

false; opposite

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T/F only T4 is found on TBG

false TBG binds both

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T/F only vit D2 has to be hydroxylated to 1,25 (OH)2 in the liver and kidney

false- both D3 and D2 have to be activated

T/F papillary thyroid carcinoma has bad prognosis

false

T/F peptic ulcers and diabetes are sequellae of cushings

true

T/F phosphate regulates PTH secretion.

FALSE.

T/F PPAR gamma decreases insulin sensitivity

false! increases

T/F prolactin stimulates milk release from the breasts

false- oxytocin stimulates the contraction the myoepithelial cells, prolactin stimulates milk release

T/F Reidels thyroiditis is a form of hypothyroidism

true

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T/F T3 is pure catabolic

false- bone growth, CNS maturity (esp fetally!), gluconeogenesis

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T/F T3 is purely anabolic

false- glycogenolysis, lipolysis

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T/F TBG binds all T3/T4 in the blood

false- binds MOST- only free hormone is active

T/F tetany is a sign of hypocalcemia

true

T/F the chromaffin cells of the adrenal cortex are are considered preganglionic

false- postganglionic and ganglionic sympathetic

T/F the neurohypophysis receives less blood from the hypophysial portal system than adenohypophysis

true

T/F there is insulin sensitivity in cushings

false- insulin resistance (acanthosis nigricans!)

T/F Thyroid cancer patients usually present hypothyroid

false- euthyroid

T/F toxic multinodular goiter is dependent on TSH activation

false

T/F TRH uses cAMP

false- TSH (TRH uses IP3)

T/F you see tetany in hypoalbunemia

false- free ionized Calcium is the same

T/F you see tetany in resp or met alkalosis

true- free ionized calcium has decreased

what activates phosphate reabsorption from the intestine how?

low serum phosphate concentrations increase 1 alpha hydroxylase activity and get increased absorption of calcium and phosphate from the intestine

what antithyroid drugs block peroxidase?

propylthiouracil and methimazole

what are examples of lateral bone growth? linear bone growth?

jaw, hands, feet, frontal bossing (enlarged hat size); everything (epiphyses have not fused yet)

what are four causes of a central diabetes insipidus?

pituitary tumor, trauma, surgery, histiocytosis X

what are four causes of hypoparathyroidism?

hypomagnesia, DiGeorge syndrome, autoimmune destruction, accidental surgical excision

what are four causes of nephrogenic diabetes insipidus?

lithium, demecyclocine, hypercalcemia, hereditary

what are four symptoms facial flushing, diarrhea, right seen in carcinoid sided heart defects, asthamtic syndrome? wheezing

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what are Kimmelstiel Wilson Nodules?

mesangial proliferations in response to endothelial damage in glomerular basement membranes

what are neurophysins?

carrier proteins in the posterior pituitary that carry the ADH and oxytocin hormones in circulation

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hypervitaminosis D, granulamotous diseases (especially sarcoidosis), malignancies (paraneoplastic), increased bone resorption (multiple myeloma or bone mets or primary bone cancer), thiazides

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when kidney has perception of low IV volume and renin activatedchronic renal artery stenosis, CHF, chronic renal failure, cirrhosis, nephrotic syndrome; high!

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what are other causes of hypercalcemia (other than hyperparathyroid)?

what are secondary causes of hyperaldosteronism? what is the renin level? what are the 4 B's of T3?

1) bone growth 2) brain maturation 3) b1 4) increased BR

what are the 5 P's of a pheo? what else can you see in a pheo?

perspiration, paroxysmal, palpitations, pallor, pain (headache), pressure (elevated); illeus (catecholamines) and anxiety

what are the acute manifestation of diabetes mellitus? what is the serious one you see more in Type I? how about in Type II?

polyuria, polydipsia, weight loss, polyphagia; DKA (type 1); hyperosmolar coma (type II)

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what are the cardio bradycardia, dyspnea on exertion; and resp changes seen chest pain, palpitations, arrythmias in hypo/hyper (a. fib) thyroidism? what are the causes of adrenal atrophy in addisons disease? what is the mcc?

destruction by disease (autoimmune, milary TH, mets) or atrophy; autoimmune destruction

what are the characteristics of steroids? what are the implications?

lipophillic and insoluble in plasma, need to circulate bound to specific binding globulins which increase their solubility

what are the clinical findings in a cretin? (5 P's)

protruding umbilicus, protuberant tongue, pale, pot bellied, puffy faced, short

what are the clinical findings in a prolactinoma?

galactorrhea, amennorhea, infertility, low libido

what are the clinical findings in deQuervains thyroiditis?

hypothyroid, diffuse tender thyroidmegaly, jaw pain, increased ESR, think inflammation!

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what are the clinical findings that are unique in Graves? why do they occur?

pretibial myxdema and opthalmopathy (proptosis and EOM swelling) d/t mimicry in fibroblasts results in connective tissue deposition

what are the endocrine pancreas cell types and what do they produce? how are they organized?

alpha (glucagon), beta (insulin), and somatostatin; into islets of langerhans which are collections of these cells- with beta central (INsulin INside) and alpha cells peripheral and somatostatin cells interspersed

what are the fates of androstenedione and where do these changes occur?

in the adrenal cortex androstenedione is turned into testosterone and in the periphery androstenedione is turned into estrone

what are the fates of testosterone in the periphery?

via 5alpha reductase to DHT; via aromatase to estradiol

what are the findings in cushings syndrome?

hypertension, truncal obesity, moon facies, buffalo hump, hyperglycemia, osteoporosis, amennorhea, and immune suppression, muscle weakness, orthostatic hypotension

what are the findings hypokalemia, met alkalosis, in hypertension hyperaldosteronism? what are the findings of Reidels thyroiditis?

fibrotic singular hard goiter

what are the four body parts that are most affected in chronic DM?

eyes, kidneys, blood vessels, nerves

what are the glitazones and thiazolidinediones? what do they do and how?

TZDs, bind PPAR gamma a transcription factor that increase insulin sensitivity

what are the immune findings in addisons?

neutrophilia, eosinophilia, lymphocytosis

what are the immune findings in cushings? why muscle weakness?

neutropenia, eosinopenia, lymphopenia; increased proteolysis

what are the infectious complications of DKA?

mucor and rhizopus

what are the lab findings in cushings?

increased free cortisol in urine, hypokalemia and metabolic alkalosis (cortisol at high concentrations can act as a mineralicorticoid), hyperglycemia

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what are the lab values of Ca, PTH, Alk phos, phosphate in secondary parathyroidism?

PTH= high, Ca= low, alk phos= high, phosphate= low

what are the lab values of PTH, Ca, Phosphate, alk phos in hyperparathyroidism? what can you find in the urine?

PTH= high, Ca= high, phosphate= low, alk phos= high; cAMP

what are the levels of Ca and PTH in tertiary parathyroidism?

PTH= really high, Ca= high

what are the main findings in Albrights hereditary osteodystrophy? what are the levels of PTH, Ca, and phosphate?

short stature, short 4th and 5th digits, hypocalcemia, mental retardation , met calcification of basal ganglia; PTH= normal to high, Ca= low, phosphate= high

what are the main findings in hypoparathyroidism?

hyperphosphatemia (metastatic calcification in basal ganglia), hypocalcemia= tetany, Trousseau sign (occlusion of brachial artery with bp cuff causes carpal spasm), Chvostek sign

what are the manifestation of hyperinsulinemia due to insulin resistance in the prediabetic metabolic syndrome? (hints what does it do to: LDL? HDL? blood pressure and why? your endothelial cells?)

increased LDL (due to increased triglyceride synthesis), decreased HDL, causes hypertension because insulin causes sodium retention, CAD (insulin causes damage to the endothelial cells)

what are the manifestations of nonenzymatic glycosylation of large vessels in DM? what are the complications of these manifestations?

microvascular damage and macrovascular damage; retinopathy, glaucoma and nephropathy; and CAD, peripheral vascular occlusion disease and gangrene

what are the manifestations of the neuropathy seen in DM?

gastric paresis, bladder impotence, orthostatic hypotension

what are the manifestations of the retinopathy in DM ?

cotton wool spots from exudates, hemorrhage, microaneurysms and vessel proliferation

what are the metabolic findings in addisons?

hypoglycemia

what are the radiologic findings in osteitis fibrosa cystica? what is the main symptom?

salt and pepper appearance of bone and subperiosteal bone resorption

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what are the signs and symptoms of DKA? what are the lab values (glucose, acid/base, ketone, leukocytes, potassium)?

kussmaul breathing, nausea/vomitting, abdominal pain, psychosis/delirium, dehydration, fruity breath odor; hyperglycemia, acidosis, decreased bicarb, increased blood ketone levels (more betahydroxybutyrate), hyperkalemia

what are the signs of hypocalcemia?

hyperreflexia, tetany, muscle cramps, tingling, chvostek sign and trousseau sign

what are the symptoms of hypokalemia?

tetany and muscle weakness

what are the T3 functions?

bone growth (synergism with GH), CNS maturation (perinatally esp), increases beta 1 receptors on heart (CO, HR and SV all increased), increased BMR via increased Na+/K+ ATPase activity which increases O2 consumption, RR, and body temperature and increased glycogenolysis, gluconeogenesis and lipolysis

what are the three enzyme deficiencies that cause congenital bilateral adrenal hyperplasias? which is the most common? what product requires all three of these enzymes? what is two common symptoms among all three and what causes these two symptoms?

17 alpha hydroxylase, 21 hydroxylase, 11 beta hydroxylase; 21 hydroxylase deficiency; glucocorticoids; enlargement of adrenal glands due to an increase in ACTH because of low cortisol levels and hyperpigmentation because MSH (melatonin stimulating hormone) is made from the same precursor as ACTH is (POMC)

what are the three layers of the adrenal cortex? (in order from outside to inside) which is the biggest?

Zona Glomerulosa, Zona Fasciculata, Zona Reticularis; Zona Fasciulata

what are the three main symptoms of diabetes insipidus?

polyuria, polydipsia, inability to concentrate urine

what are the three main symptoms of SIADH?

urine osmolality > serum osmolality; hyponatremia (dilutional effect from hypotonic gain of water); excessive water retention

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what are the three results of no insulin, glucagon excess and increased epinephrine in DKA? (hint-what does it do to fat? protein? glucose uptake)?

increased fat lipolysis to make increased plasma FFA and ketoacids, proteinlysis leads to increase aa and nitrogen in urine, hyperglycemia and osmotic diuresis

what are the three tests in DM?

fasting serum glucose, HbA1C, glucose tolerance test

what are the two components of the pituitary? what are there embryological derivatives? which makes the majority of the pituitary?

adenohypophysis and neurohypophysis; oral ectoderm (rathkes pouch) and neuroectoderm; adenohypophysis

what are the two main causes of the chronic manifestations in diabetes mellitus?

nonenzymatic glycosylation and osmotic damage

what are the two targets of osmotic damage in DM ?

nerves and eyes

what are the two unique features seen in a child with neuroblastoma?

abdominal mass and HTN

what are the urine findings in diabetes insipidus? plasma osmolarity?

specific gravity is less than 1.006; serum osmolality is greater than 290

what are the values of Ca, phosphate and PTH in hypoparathyroidism?

Ca= low, phosphate= high, PTH= low

what are three causes of adrenal hemorrhage?

neisseria meningitidis septicemia, DIC, endotoxic shock

what are three features of a glucagonoma?

DM, necrolytic erythema, anemia

what are thyroid hormones?

iodine containing hormones that control the body's metabolic rate

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what are two causes of metastatic calcification? where does it usually occur?

hyperphospatemia and hypercalcemia; in the CNS (basal ganglia) and eyes

what are two main symptoms of a pituitary adenoma? why?

headache and no peripheral vision; mass effect increases ICP and bilateral hemianopia d/t pituitary pushing on optic chiasm

what are TZDs used for?

used in Type II DM

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what autonomic is the adrenal medulla innervated by? what are the NT? what are the receptors called? what kind of receptors are they?

sympathetic; Ach; nicotinic (N); Na+/K ligand gated channels

what autonomic receptors use cAMP as their signalling pathway?

B1, B2, D1, H2, V2

what blocks Iodine uptake from the blood into follicular cells?

anions: perchlorate and pertechnetate

what can be found in the plasma of pheo patients? urine?

increased catecholamine levels; breakdown product of norepinephrine: VMA

what can happen to a newborn in 21 hydroxylase deficiency?

saltwasting can cause hypovolemic shock

what can you find in the urine with neuroblastoma?

HMA and VMA

what causes calcitonin secretion?

increased serum Ca2+

what causes the inuslin resistance in diabetes mellitus type II?

insulin its self downregulates its own receptors

what causes the microvascular damage in DM- more specifically what is the response to the nonenzymatic glycosylation of microvessels?

diffuse thickening of the basement membraneincreased type IV collagen and mesangial deposits (KW nodules)

what causes the osmotic damage seen in DM?

glucose gets turned into sorbital by aldolase reductase which is osmotically active and causes osmotic damage

what causes the tricuspid regurg collagen dep in valves and PS in carcinoid syndrome? what causes zollinger ellison syndrome?

gastrinoma either in duodenum or pancreas

what cells in the adenohypohysis are basophils? all of these cells produce hormones with what common subunit? what is the exception?

B-FLAT: basophils- FSH, LH, ACTH, TSH; alpha; ACTH

what cells only have aldolase reductase?

Schwann cells, lens, retina and kidneys

what controls phosphate homeostasis? how?

calcitriol; increasing absorption from intestines and increased bone resorption

what controls uterine hemorrhage?

oxytocin

what decreases TRH?

negative feedback by free T3

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what do catecholamines do to insulin?

alpha receptors increase insulin

what does an adrenal adenoma or carcinoma result in? what is the gross adrenal look like? what is the ACTH level? dexamethasone suppression test response?

cushings syndrome; nodular adrenal hyperplasia; ACTH low; increased cortisol after low and high dose

what does bone resorption mean? and what hormones cause it?

it means that osteoclasts are releasing calcium and phosphate from the bone to be resorbed by the blood; PTH

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what does calcium renal stones cause?

polyuria and renal failure

what does decreased glucose uptake in DKA result in?

hyperglycemia, glucosuria and osmotic diuresis which pulls electrolytes out

what does Ectopic ACTH cause? what are common releasers of ectopic ACTH? what is the level of ACTH? what is the response with dexamethasone test?

Cushings syndrome; small cell lung cancer, bronchial carcinoids; increased ACTH; high cortisol haver both high and low doses of dexamethasone

what does excess GH cause in an adult? in a child?

acromegaly; gigantism

what does excess GH do to blood pressure?

sodium retention occur with both increased GH and insluin

what does hypomagnesia result in?

hypocalcemia! (via decreased PTH)

what does increased lipolysis in DKA result in?

increased plasma FFA and ketoacidosis

what does increased protein metabolism in DKA result in? how does this add to dehydration?

increased aa and nitrogen in the urine which pulls out more water

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what does oposclonus myoclonus jerks, chaotic myoclonus, a common eye movements paraneoplastic syndrome seen in patients with neuroblastoma, present with? what does the adenohypophysis secrete?

FSH, LH, prolactin, GH, ACTH, TSH, melanotropin

what does vit D deficiency cause?

rickets in children and osteomalacia in adults

what do pheochromocytomas secrete?

epinephrine, norepinephrine, dopamine

what drug can cause SIADH?

cyclophosphamide

what drugs can be used in a prolactinoma? give an example.

dopamine agonists; bromocriptine

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what drugs cause decreased Mg2+ (and thus decreased PTH)? what pathology state cause decreased Mg2+?

aminoglycosides, alcohol, diuretics; diarrhea

what effect do antipsychotics and OCPs have on prolactin secretion?

dopamine antagonists and estrogens stimulate prolactin secretion

what effect does alkalosis have on total and free Ca? why?

met or resp alkalosis causes an increased amount of negative charges on albumin which then takes free ionized Ca to neutralize those charges- total free Ca is normal, but ionized albumin has decreased causing an increase in PTH

what effect does calcium have on the stomach? what does hypercalcium result in because of this?

stimulates gastrin release; PUD

what effect does cortisol have on blood pressure? how?

maintains blood pressure; upregulates alpha 1 receptors

what effect does cortisol have on immune function? how?

decreases IL 2 production and decreases release of histamine and serotonin

what effect does cortisol have on inflammation? how?

its antiinflammatory by inhibiting phospholipase A2

what effect does cortisol have on metabolismspecifically glucose metabolism? fat? protein? insulin?

increases gluconeogenesis, lipolysis and proteolysis; decreases insulin concentration

what effect does cortisol have on REM? awakeness?

decreases; increases

what effect does cortisol on bone formation? how?

decreases bone formation by decreasing type I collagen formation

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what effect does hepatic failure have on TBG? free thyroid hormone? total thyroid hormone?

decreases; normal; decreases

what effect does hypoalbunemia have on total and free Ca? why?

because 40% of calcium is bound to albumin in blood, hypoalbuminemia will result in decreased bound albumin (and thus total Ca) but the same amount of free ionized Calcium so PTH is not activated- it cause the pathological state of normal PTH with low total serum Ca

what effect does hypothyroidism have on prolactin? gonadism?

increased prolactin and thus hypogonadism

what effect does increased estrogen (pregnancy) have on TBG? free thyroid hormone? total thyroid hormone?

increases, normal, increases

what effect does insulin have on alpha cells?

inhibits glucagon release

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what effect does insulin have on fructose 2,6 bisphosphate? how?

increases it by phosphorylating phosphofructokinase 2

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what effect does insulin have on potassium?

increases cellular uptake of potassium

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what effect does insulin have on sodium in the kidneys?

causes Na+ retention

what effect does magnesium have on PTH? why?

hypomagnesia causes hypoparathyroidism because magnesia is cAMP cofactor for PTH receptor

what effect does PTH have on bones? how exactly?

increases bone resorption by indirectly activating osteoclasts through increasing production of M-CSF and RANK-L on osteoblasts

what effect does PTH have on phosphate how?

decreases serum phosphate and increases urine phosphate by decreases kidney reabsorption at the PT

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what effect does somatostatin on TSH?

decreases its release

what effect does both activate and inhibit sympathetic activation insulin secretion; Beta and have on beta cells? through alpha respectively what receptors? what effect does TNF alpha have on insulin? how? what is the result on insulin senstivity?

inhibits its secretion by inducing the serine kinase of beta receptor rather than the tyrosine; results in increased insulin resistance

what effect do glucocorticoids and glucagon have on insulin secretion? how?

inhibit its secretion by inducing threonine phosphorylation instead of tyrosine; results in increased insulin resistance

what else is MEN 2A known as?

sipples syndrome

what endocrine hormones use cAMP as apart of their signaling pathway?

FLAT CHAMP goes to cAMP: FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2), MSH, PTH, calcitonin, GHRH, glucagon

what enzyme deactivates Vit D? what is this new inactive form?

24 hydroxylase in kidney; 24,25 (OH)2

what gene is associated with which MEN disorders

ret gene; MEN 2A and MEN 2B

what happens to all three products of the adrenal cortex with 17 alpha hydroxylase deficiency?

decreased sex hormones, decreased cortisol, increased aldosterone

what happens to all three products of the adrenal cortex with deficiency of 11 beta hydroxylase?

decreased aldosterone, increased 11-deoxycortisol, decreased glucocorticoids, increased sex hormones

what happens to all three products of the adrenal cortex with deficiency of 11B hydroxylase?

decreased aldosterone, decreased cortisol, increased sex hormones

what happens to reflexes and the GI system in hypo and hyperthyroidism?

relfexes go down and constipation in hypo; reflexes go up and diarrhea in hyper

what helps you distinguish between hypercalcemia due to a parathyroid adenoma or due to a different malignancy?

PTH levels

what HLA is Hashimotos associated with?

HLA- DR5

what hormones have a common alpha subunit? what differentiates them and how?

TSH, LH, FSH, hCG; a beta unit which determines the hormones specificity

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what increases PTH decreased free serum Ca; secretion? decreases decreased free Mg2+ its secretion?

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what increases the irradiation as a child risk of developing papillary carcinoma? what induces secretion of corticosteroids?

chronic stress

what infections are diabetics predisposed to?

UTIs, external otitis media, candida vulvavaginitis

what is 5 HT?

serotonin

what is a cause of hypothyroidism in children?

cretinism

what is addisons disease? what are the clinical symptoms? what is the most common cause? what are other causes?

primary chronic adrenal insufficiency; deficiency of aldosterone and cortisol causing hypotension, salt cravings, hyperkalemia, normal anion gap met acidosis, skin hyperpigmentation, fasting hypoglycemia, and lymphocytosis

what is a hurthle cell?

metaplastic epithelial cell with eosinophilic granular cytoplasm

what is an acute cause of adrenocortical deficiency? what causes the deficiency?

waterhouse friderichsen syndrome; adrenal hemorrhagic infarction d/t adrenal vessels blockage

what is an example of GLP 1 analog? what is the result?

exenatide; increase insulin and decrease glucagon release

what is a precipitator of Graves?

stress (pregnancy for ex)

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what is a tumor marker of medullary thyroid carcinoma? what else does it cause?

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what is a primary aldosterone secreting tumor; conns cause of syndrome; low hyperaldosteronism? what is it called? what is the renin level? what is a toxic multinodular goiter?

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its focal areas of hyperfunctioning follicle hyperplasia that are TSH independent d/t a mutation in TSH receptor

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calcitonin; hypocalcemia 270.

what is desmopressin used to treat?

central diabetes insipidus

what is IGF2? what is it important for? in what type of tumors is it produced in and what is the result?

insulin like growth factor 2; fetal development; mesenchymal tumors; hypoglycemia

what is IGF a receptor for?

Growth hormone!

what is nonenzymatic glycosylation? what does it lead to?

when hyperglucosemia causes glycosylation of aa in endothelial proteins leading to vessel permeability and atherogenesis

what is osteitis fibrous cystica? what is the histology you see for it? what is the pathogenesis?

bone lesions (usually in jaw and skull) associated with hyperparathyroidism; cystic brown (hemorrhagic) lesions; osteoporosis due to continual bone resorption and osteoclast activity

what is pseudohypoparathyroidism? what is another name for it? what is its mode of inheritance?

kidney unresponsiveness to PTH (or decreased 1 alpha hydroxylase activity); Albrights hereditary osteodystrophy; AD

what is renal osteodystrophy? what is it usually due to?

bone lesions in secondary (or tertiary) hyperparathyroidism due to increased levels of parathyroid from hypovitaminosis D due to renal failure

what is T3? T4?

DIT + MIT; MIT + MIT

what is tertiary hyperparathyroidism? what is it usually due to?

autonomous secretion of PTH (even after Ca has been repleted); usually due to secondary hyperparathryoidism from chronic renal disease

what is the breakdown produce of dopamine? norepinephrine? epinephrine?

HVA, VMA, metanephrine

what is the breakdown product you have find in the urine of a patient with neuroblastoma?

HVA

what is the cause of death in thyrotoxicosis?

arrhythmias (a. fib)

what is the cause of endemic endemic goiter! cretinism? what is the cause (geographical area with no of sporadic cretinism? iodine); defect in T4 formation or development failure in thyroid formation

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what is the cause of toxic multinodular goiter? what is the cause of nontoxic goiter?

mutation causes TSH independent hyperfunctioning follicular patches; iodine deficiency causes TSH dependent hyperplasia (but not hyperthyroid like toxic goiter)

what is the chvostek sign and what is a sign of?

tapping on the 7th cranial nerve causes twitching of facial muscles; hypocalcemia

what is the clinical use of glucocorticoids?

inflammation, eyes, allergies, fetal lung maturation, croup

what is the difference between GnRH and GHRH?

GnRH stimulates release of FSH and LH; GHRH stimulates release of GH

what is the direct precursor to the last step in cortisol synthesis and what enzyme is involved in this last step? what type of steroid is the precursor?

11 deoxycortisol; 11 beta hydroxylase; mineralcorticoid

what is the effect of a prolactinoma on males?

not only galactorrhea but also infertility d/t decreased GnRH

what is the embryonal origin of the adrenal cortex?

mesoderm

what is the embryonal origin of the adrenal medulla? what are the cells of the adrenal medulla called?

neural crest; chromaffin cells

what is the final step in vit D activation? what three things regulate this last step? what downregulates?

1 alpha hydroxylase in the kidney; decreased phosphate, increased PTH, and decreased free calcium; vit D feedback!

what is the first step in adrenal steroid synthesis? what enzyme is involved in this step? what activates this enzyme? deactivates it?

production of pregnelone from cholesterol via desmolase; ACTH and ketoconazole

what is the function of prolactin?

stimulates milk production in the best, inhibits ovulation and spermatogenesis

what is the glucose uptake transporter in brain and RBCs?

GLUT 1

what is the histology in a parathyroid adenoma?

sheet of chief cells

what is the histology in DM I? DM II?

islet leukocytic infiltrate; islet amyloid deposit

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what is the histology seen in a hashimotos patient?

hurthle cells, lymphocytic infiltrate (mononuclear) with germinal centers and fibrosis

what is the histology seen in follicular thyroid carcinoma? what is the prognosis?

uniform follicles; good

what is the histology seen in Graves?

follicular hyperplasia turning into papillary infolding

what is the histology seen in medullary carcinoma?

sheets of parafollicular C cells in an amyloid stroma

what is the histology seen in Subacute thyroiditis (de Quervains)?

granulomatous formation with multinucleate giant cells

what is the hypotension in addisons from?

hyponatremic volume contraction

what is the Jod Basedow phenomenon?

thyrotoxicosis in someone who was previously iodine def goiter who become iodine replete

what is the left adrenal gland vein drainage? right adrenal gland vein drainage? to what veins is this system similar to?

left adrenal vein--> left renal vein-> IVC; right adrenal vein--> IVC; gonadal veins

what is the main clinical presentation and why? how does an XY present? XX?

though decreased aldosterone there is increased 11deoxcortisol and results in hypertension, hypokalemia, metabolic alkalosis; XY: precocious puberty; XX: pseudohermaphrotidism

what is the main clinical presentation? how does an XY present? XX?

hypotension, metabolic acidosis, hyperkalemia, hypoglycemia, increased renin and volume depletion; XY: precocious puberty; XX: virilization (female pseudohermaphrotidism)

what is the main clinical presentation in 17 alpha hydroxylase deficiency?

hypertension, hypokalemia, metabolic alkalosis, decreased renin, hypoglycemia

what is the main symptom seen in zollinger ellison syndrome?

recurrent ulcers

what is the mcc of cushings? what levels of ACTH correspond? what is it called?

iatrogenic (exogenous); low; Cushings SYNDROME

what is the mcc of hyperparathyroidism?

parathyroid adenoma

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what is the mcc of hyperthyroidism?

Graves' dx

what is the mcc of hypothyroidism?

Hashimotos thyroiditis

what is the mcc of hyperparathyroidism nonmalignant hypercalcemia? what is the mcc of secondary hyperparathyroidism? what is another cause?

chronic renal disease, hypovitaminosis D

what is the mechanism of glucocoritcoids in inflammation?

block phospholipase A2 so that no leukotrienes or prostaglandins are formed

what is the most common cause of painful thyroid? hint: it is also hypothyroid

subacute deQuervains thyroiditis

what is the most common endocrine neoplasm and thyroid cancer?

papilloma carcinoma

what is the most common pituitary adenoma?

prolactinoma

what is the most common pituitary adenoma? what kind of cells are these?

prolactinoma; acidophils

what is the most common tumor of the adrenal medulla in adults?

phechromocytoma

what is the most common tumor of the adrenal medulla in adults? children?

phemochromoctyoma; neuroblastoma

what is the most common tumor of the adrenal medulla in children? of what kind of cells is this tumor?

neuroblastoma; post ganglionic sympathetic neurons

what is the number one cause of SIADH? what are two other pathological causes?

ectopic (from small cell lung cancer for example), lung disease (TB), CNS disorders/head trauma

what is the number one endogenous cause of Cushings? what is the ACTH level? what is the dexamethasone suppression test response?

Cushings DISEASE- ACTH from pituitary adenoma; high; increased cortisol with low dose and decreased coritsol after a high dose

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what is the overall goal of Vit D? what are the two specfic functions of vit D?

bone health- provide Ca and phosphate to ECF for bone mineralization; increase absorption of calcium and phosphate (intestine and kidney) and increase bone resorption to release Ca and phosphate

what is the pathogenesis of Graves?

type II hypersensitivity autoAbs (activating) to TSH receptor

what is the pathogenesis of hashimotos?

type II and type IV autoimmune hypersensitivity disorders (antibodies to thyroid and as well cytotoxic T cell destruction)

what is the pathology seen in microvascular disease in DM type II? macrovascular?

arteriosclerosis; atherosclerosis

what is the peroxisome proliferator activator receptor gamma? what is the result? what drugs activate this?

PPAR gamma is a nuclear receptor that is a transcription factor and alters gene transcription to iNCREASES insulin sensitivity; TZDs

what is the primary defect in DM I? DM II?

viral or immune destruction of beta cells; insulin resistance

what is the proinsulin hormone made of? what happens when proinsulin gets cut into insulin?

alpha and beta chain connected by disulfide bonds and a c peptide chain; c peptide gets cut off

what is the regulatory control of the adrenal medulla? what is secreted in response?

preganglionic sympathetic fibers; catecholamines (epi, NE)

what is the regulatory control of the zona fasciculata? and what does it produce in response?

ACTH from ant pit (CRH from Hypothalamus); corticosteroids

what is the regulatory control of the zona reticularis? and what does it produce in response?

ACTH (ant pit) and CRH (Hypothalamus); sex androgens

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what is the regulatory control of zona glomerulosa? and what does it produce in response?

renin-angiontensin (Ang II); Aldosterone

what is the renin level in primary Addisons? secondary addisons?

renin high; normal

what is the result on females in decreased SHBG (sex hormone binding globulin)?

hirsutism from more free testosterone

what is the result on males in increase SHBG (sex hormone binding globulin)?

gynecomastia from lower free testosterone

what is the rule of 1/3s in carcinoid syndrome?

1/3 mets, 1/3 multiple, 1/3 present with 2nd malignancy

what is the source of thyroid hormone?

follicular cells in the thyroid

what is the T3 and iodine uptake in someone with hypo/hyper thyroidism?

decreased; increased

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what is the therapeutic acute hypercalcemia use of calcitonin? what is the three main symptoms seen in primary hyperparathyroidism?

stones bones and groans: PTH causes bone resorption and lesions, hypercalcemia causes calcific stones, hypercalcemia also causes constipation

what is the toxicity of demeclocycline?

photosensitivity, bone and teeth abnormalities, nephrogenic DI

what is the toxicity of GLP 1 analogs?

nausea, vomitting, pancreatitis

what is the toxicity of glucocorticoids? how about if the drug is stopped after chronic use?

cushings syndrome; addisons

what is the toxicity of TZDs?

weight gain, edema, hepatotoxicity, CV toxicity (CHF precipitated by excess fluid)

what is the treatment for carcinoid syndrome?

octreotide

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what is the treatment adequate water intake, intranasal for diabetes insipidus? desmopressin (ADH analogue); central? nephrogenic? diuretics: HCTZ, indomethacin, amiloride

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what is the treatment for DKA?

fluids, insulin, potassium

what is the treatment for SIADH?

demeclocycline OR decrease water intake

what is the treatment of a pheo?

phenoxybenzamine (irrerversible alpha blocker) before surgery; metyrosine

what is the trousseau sign and what is a sign of?

carpopedal spasm; hypocalcemia

what is three histologic features in papillary carcinoma thyroid

orphan annie (ground glass nuclei), nuclear membrane grooves gives the impression of intranuclear inclusions, and psammoma bodies

What is thyrotoxicosis? what is it a serious complication of?

stress induced catecholamine surge; hyperthyroid states (like Grave) which cause increased catecholamine receptors

what is used to induce fetal lung maturation?

glucocorticoids

what is used to stimulate labor? what else can it stimulate?

oxytocin by stimulating uterine contractions; milke let down

what is used to treat acromegaly, carcinoid, gastrinoma and glucagonoma?

octreotide

what is used to treat GH deficiency? what else can it treat?

GH; turners syndrome

what is used to treat SIADH? of what drug family is this a member of?

demecylcocine; tetracyclines

what kind of metabolic acidosis is seen in DKA?

anion gap

what marker can be found in urine of carcinoid syndrome?

5-HIAA

what nerves are apart of the neuropathy seen in DM?

motor, sensory and autonomic (all)

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what oncogene is associated with rapid neuroblastoma progression?

N-myc

what oncogene is upregulated in neuroblastoma? what does the gene transcribe?

N myc; a transcription factor

what other cells hormones are secreted from the endocrine pancreas (other than insulin, glucagon, somatostatin)?

gastrin (gastrinoma!), VIP (vipoma!) from pancreatic polypeptide (pp) secreting cells

what other complications of DKA are there (think brain, heart)?

cerebral edema, cardiac arrythmias, heart failure

what other hormones are secreted unopposedly in diabetes mellitus? what does this do to the hyperglycemia?

epinephrine and GH; increase hyperglycemia

what pathologic state causes high PTH and high Ca? what is the mcc of this?

primary hyperparathyroidism; parathyroid adenoma

what pathologic state causes low Ca and high PTH? what is the most common cause of this?

secondary hyperparathyroidism; chronic renal failure

what pathologic state causes low PTH and high Ca? what are two things that cause this?

PTH independent hypercalcemia; malignancy induced, excess calcium ingestion

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what pathologic state causes normal serum Ca but high PTH?

resp/met alkalosis

what pathologic state results in low PTH and low Ca? what causes this state?

hypoparathyroidism; DiGeorge, autoimmune destruction, surgical excision, hypomagnesia

what pathologic state results in normal PTH and low serum Ca?

hypoalbuminemia

what percentage of pheochromocytomas are malignant? bilateral? extraadrenal? calcify? in kids? familial?

10, 10, 10, 10, 10, 10

what percentage of serum Ca++ is bound to albumin? in what form is the rest?

40%; free ionized or complexed with anion (phosphate)

what precipitates DKA? what two combining factors does this result in?

NO insulin and catecholamine stress (infection) that requires increased insulin

what regulates release of ACTH from the adenohypophysis? what controls this hormone?

CRH from the hypothalamus; increased cortisol levels decrease CRH release (and vice versa)

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what specifically is wrong with reflexes in someone with hypothyroidism?

slowed reflex recovery

what steroids are produces androstenedione; 17 alpha in the zona reticularis? what hydroxylase; 17 ketosteroids enzymes beyond desmolase are required to produce them? what is excreted in the urine with production of these? what stimulatees follicular cells? what else?

TSH; TSI (thyroid immunoglobulin in Graves)

what three neoplasias are associated with MEN 2A?

parathyroid, medullary carcinoma of the thyroid, pheo

what three neoplasias are associated with MEN 2B?

pheo, medullary carcinoma of the thyroid, oral/intestinal ganglioneuromatosis (assoc with marfanoid habitus)

what three neoplasias are associated with MEN I?

parathyroid, pancreas, and pituitary

what three steps in the peroxidase enzyme involved in in thyroid hormone synthesis? where do these steps occur?

oxidation (I- --> I2), organification (Iodide added to thyroglobulin), and coupling (of MIT and DIT); follicular cell, lumen, lumen

what thyroid cancer has a very poor prognosis? what is the patient population?

anaplastic, undifferentiated; elderly

what thyroid carcinoma is medullary carcinoma associated with MEN 2A and MEN 2B what two actions does the PTH have on the kidney?

increasing DCT reabsorption of calcium and increasing 1 alpha hydroxylase activity

what two drugs can be used as thyroxine replacement? what is the clinical use? toxicity?

levothyroxine and triiodothyrine; for hypothyroidism and myxdema; thyrotoxicosis

what two features are seen in the stomach in zollinger ellison syndrome?

acid hypersecretion and increase rugal thickening

what two neuropeptides do the neurohypophysis secrete? where are these neuropeptides made? where do the cells in the neurophyophysis come from?

vasopressin (ADH) and oxytocin; in the neurons in the supraoptic and paraventricular nuclei (NEUROpeptides); they are the cell bodies of neurons in the hypothalamus (one and the same!)

what two organs are the target of micro vascular disease in diabetes mellitus?

eyes and kidneys

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what two types of damage result from microvascular damage in the eyes due to DM?

retinopathy and glaucoma

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what type of antibodies can be seen in Hashimotos?

antimircosomal and antithyroglobulin

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what type of cells make up the majority of the adenohyophysis and where are they located?

somatotrophs; centrally

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what type of drugs can cause a shrinkage of prolactinomas? give two examples.

dopamine agonists; bromocriptine and cabergoline

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what type of drugs is beclamethasone?

glucorticoid

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what type of drugs is dexamethasone?

glucorticoid

what type of drugs is hydrocortisone? prednisone?

glucocorticoid

what type of drugs is triamcinolone?

glucocorticoid

what type of hypertension does a pheochromocytoma result in? neuroblastoma?

episodic hypertension; diastolic hypertension

what type of hypertension do you see in hypercalcemia? why?

diastolic because calcium in circulation results in increased contraction of smooth muscle arterioles

what type of hypertension do you see in hypo/ hyper thyroidism? why?

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diastolic due to water and sodium retention; systolic due to increased beta 1 receptors

what type of episodic and paraoxysmal hypertension is unique in pheochromocytoma? what type of myxdema do you see in hypo/hyper thyroidism?

facial and periorbital; pretibial (if Graves)

what type of receptor is the insulin receptor?

a tyrosine kinase receptor that is tetrameric (2alpha and 2Beta)with the intracellular 2 Beta part with tyrosine kinase activity

what type of skin do you see in hypo and hyper thyroidism? hair?

dry, cool skin and coarse hair in hypo; moist, warm skin and fine hair in hyper

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what type of steroid is aldosterone? 11 deoxycortisol? testosterone and estrogen? cortisol?

mineralicorticoid; mineralicorticoid; androgen; androgen; glucocorticoid

what type of symporter is used to uptake Iodine?

sodium potassium

what type of temperature intolerance is seen in hypothyroidism? hyperthyroidism? why?

cold intolerance (decreased BMR and so decreased body temp); heat intolerance (increased BMR so increased body temp)

what would be the main symptom of an insulinoma?

hypoglycemia

what would be the main symptom of a VIPoma? where would it be located?

diarrhea, hypotension, metabolic acidosis, hypokalemia

what would be the symptoms of a somatostatinoma? where would it most likely arise from?

gallbladder stones (inhibition of CCK!), achlorydia (inhibition of gastrin!) steatorrhea and constipation; from the pancreas

when does GH increase in normal situations?

stress, exercise, HYPOGLYCEMIA

when is prolactin increased?

pregnancy and brestfeeding

where are binding liver; estrogen globulins for steroids made? what activates their production? where are glucocorticoids produced? what enzymes beyond desmolase are required to produced them?

zona fasciculata; 17 alpha hydroxylase, 21 hydroxylase and 11beta hydroxylase

where are PTH receptors?

bone, kidney (PCT and DCT and on 1 alpha hydroxylase)

where else can a neuroblastoma occur other than in the adrenal medulla?

all along sympathetic chain

where is aldosterone produced? beyond desmolase what enzymes are required to produce aldosterone?

in the zona glomerulosa; 21 hydroxylase and 11B hydroxylase

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where is insulin made? and in response to what is it released?

beta cells; ATP from insulin independent glucose entrance into beta cells (GLUT 2) closes K+ channels and results in depolarization which opens Ca+ channels and increased intracellular Ca causes exocytosis of insulin

where is TG (thyroglobulin) stored?

lumen

which autonomic receptors use Gq?

Alpha 1, M1, M3, H1, V1

which cells dont require insulin for uptake?

brain, RBCs, liver, kidney, cornea, intestine (pancreas)

which cells in the adenohypophysis are acidophils?

prolactin and Growth hormone producing cells

which endocrine hormones use cGMP?

ANP, NO (EDRF)- think vasodilators

which endocrine hormones use IP3?

GOAT: GnRH, Oxytocin, ADH (V1 receptor), TRH

which form of hypothyroidism can present like cancer?

Reidels (due to fibrotic hard mass)

which receptors are receptor associated tyrosine kinases (JAK/STAT pathway)?

GH, prolactin and IL2

which receptors are tyrosine kinase receptors?

insulin, IGF, FGF, PDGF (think growth factors)

which steroid receptors are cytosolic?

Vit d, Estrogen, Testosterone, Cortisol, Aldosterone, Progesterone (VET CAP)

which steroid receptors are nuclear?

T3/T4

which thyroid cancer is associated with hashimotos?

lymphoma

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which tissues are adipose tissue and skeletal tissue; insulin dependent GLUT 4 on getting glucose? through what channel does the glucose enter?

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which tissues use the GLUT 2 receptor?

B islet cells, small intestine, kidney, liver

why does hyperkalemia result in DKA?

because of hydrogen shift into cells and potassium out (to help with acidosis)

why does because lower extracellular calcium hypocalcemia cause levels depolarizes the membranes tetany? making them easier to get to AP by decreasing the threshold poteential and causes contraction why does increased T3 increase the body temp

increased BMR via Na+/K+ ATPase

why does insulin resistance occur in excess GH?

because GH causes gluconeogenesis and the hyperglycemia causes insulin intolerance (same as DM)

why does PTH increase calcium but decrease phosphate?

because PTH is the master of calcium- all it wants to do increase free serum calcium and bone resorption causes increase of both phosphate and calcium and in order to get more free calcium need to get rid of phosphate

why do steroids have slow onset of action?

because protein synthesis from the need of gene transcription to make them (their receptors are transcription factors that either are in the cytosol or nucleus)

why do you see increased sex hormones in deficiencies of 21hydroxylase and 11B hydroxylase?

because intermediates in the zona glomerulosa and fasciculata that build up can get into reticularis via progesterone intermediates

why do you see skin hyperpigmentation in primary Addisons? where can you see the hyperpigmentation?

because increased ACTH production (from lack of negative feedback) results in increased MSH also (both have POMC precursor); on the buccal mucosa and skin

why is the HR increased in T3? RR?

increased B1; increased O2 consumption

why is their hyperglycemia in cushings? why skin changes and osteoporosis? why amenorrhea, hirsuitism, acne?

d/t gluconeogenesis and decreased insulin; decreased collagen synthesis; increased androgen: estrogen ratio

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why is there a dilutional hyponatremia seen in DKA?

in DKA glucosuria induced osmotic diuresis causes a dilutional hyponatremia effect that pulls sodium out

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why is there orthostatic hypotension in cushings?

...

436.

Why might a hashimotos patient be hyperthyroid?

because initial destruction of follicular cells can cause a release of thyroid hormone

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why would nephrotic syndrome and cirrhosis result in because loss of IV protein results in loss of IV osmotic pull and loss of hyperaldosteronism? volume extravascularly with bone resorption, other than calcium and phosphate is released?

hydroxyproline

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with what disease states are pheos associated with?

VHL, NF 1, MEN 2A and MEN 2B

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with what is a parathyroid adenoma associated with?

MEN I, MEN IIA

with what neoplasias is Zollinger Ellison syndrome associated?

MEN I

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