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Flashcards in UWorld- Endo/Biochem Deck (64)
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what is the most common amino acid found in collagen

glycine (it is at least every third amino acid in the chain)


what's a common side effect of thiazolidinediones

fluid retention, weight gain and edema


in addition to treating beta-adrenergic effects, how else does propranolol treat hyperthyroidism

propranolol decreases peripheral conversion of T4 to T3 (mechanism unknown)


what kind of cell is most common in the pituitary vs. what kind of adenoma is most common

somatotrophs (GH secreting) are most common normally
prolactinomas are the most common pituitary tumor


what electrolyte (chem 7) differences would you expect between primary and secondary adrenal insufficiency

in primary adrenal insufficiency all 3 zones of the cortex are out ==> hyponatremia, hyperkalemia, hypochloremia and metabolic acidosis
in secondary adrenal insufficiency mineralocorticoid production is usually spared so these patients usually don't develop hyperkalemia or metabolic acidosis


through what cytokine do thiazolidinediones exert their therapeutic effect and how

thiazolidinediones (aka glitazones) bind and upregulate PPAR-gamma (an intracellular nuclear receptor) which increases adiponectin (a cytokine) levels leading to decreased insulin resistance


in what kind of thyroid cancer would you see Hurthle cells (large cells with eosinophilic cytoplasm)
what form of hypothyroidism also shows Hurthle cells

follicular thyroid carcinoma;
Hashimoto's thyroiditis


name two histologic features that differentiate papillary thyroid carcinoma from follicular thyroid carcinoma

papillary thyroid carcinoma has psammoma bodies (concentrically calcified structures) and ground glass, grooved nuclei


describe the molecular pathway by which insulin promotes glycogen synthesis

insulin bind the receptor which is a tyrosine kinase --> tyrosine kinase phosphorylates insulin receptor substrate which phosphorylates protein phosphatase--> protein phosphatase dephosphorylates and thereby activates glycogen synthase
--> upregulated glycogen synthesis


besides activating glycogen synthase, what else does protein phosphatase do (in regard to metabolic pathways)

protein phosphatase dephosphorylates and thereby inactivates F-1,6-BP, which is necessary for gluconeogensis
(so protein phosphatase inhibits gluconeogenesis)


what's an easy way to differentiate between 21-hydroxylase and 11-beta-hydroxylase deficiency

both 21-hydroxylase deficiency and 11-beta-hydroxylase deficiency cause female virilization, but in 21-hydroxylase there is hypotension and hyperkalemia due to absent mineralocorticoids;
where is 11-beta-hydroxylase there is hypertension (and low renin) since 11-deoxycorticosterone is increased and has mineralocorticoid activity


what are three classic findings for glucagonoma

diabetes mellitus, necrolytic erythema and anemia


jejunal ulcers should make you think of what tumor



what are the 3 ways that PTH increases serum calcium

1. increases bone resorption through osteoclast activity
2. increases gut absorption of calcium via activation of vitamin D
3. increases Ca2+ reabsorption in the DCT


in patients with fructose intolerance what enzyme can allow for some fructose to still be metabolized for glycogen synthesis

hexokinase converts fructose to F-6-P, which can then be converted to glucose for glycogen synthesis or F-1,6-BP for glycolysis


fatigue, weight loss with normal or increased food intake, polyuria, and polydipsia in a young physically active individual suggests what disease and what would you do to test for it

type 1 DM;
test with fasting blood glucose


describe sensors that lead to ADH secretion

osmoreceptors in the hypothalamus and baroreceptors in the carotids and atria


how can you distinguish between central DI and nephrogenic DI

on water restriction test administer DDAVP and observe whether the urine becomes even more concentrated;
if it does= central DI
if nothing changes=nephrogenic DI (unresponsive receptors to ADH)


delayed puberty plus anosmia is suggestive of what disease?
what is the etiology?

Kallman syndrome;
caused by mutation of KAL-1 gene or FGFR-1 gene leading to failure of GnRH secreting neurons to migrate from the olfactory placode to the hypothalamus


A female patient has amenorrhea due to prolactinoma. What complication or sequelae of a microprolactinoma (less than 10mm in size) would she have to worry about if she opted not to treat

osteoporosis due to downregulation of GnRH which leads to decreased FSH and LH and thereby decreased estrogen, which is important for bone density


how does the hypothalamus regulate prolactin secretion

dopamine, secreted from the hypothalamus acts on D2 receptors in the lactotrophs to downregulate prolactin secretion


what is tachyphylaxis

tachyphylaxis (aka rapid drug tolerance) is decreased response to a drug after repeated administration


what is permissive effect (with regards to drug interactions)

when one molecule has a permissive effect on another drug it allows that other drug to reach its full potential
(e.g. NE, when administered with cortisol has a greater effect on vasoconstriction than NE administered alone; note that cortisol by itself has no vasopressive actions)


in the TCA cycle which steps produce NADH?
which produce FADH2?
which produce GTP?

-NADH is generated by the 3 reactions catalyzed by isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase and malate dehydrogenase
-FADH2 is produced by rxn catalyzed by succinate dehydrogenase (succinate to fumarate)
-GTP is produced by rxn of succinyl-CoA to succinate (catalyzed by succinate thiokinase aka succinyl-CoA synthetase)


explain how pyruvate is converted to PEP in gluconeogenesis

1. pyruvate is first converted to oxaloacetate by pyruvate carboxylase
2. oxaloacetate is converted to PEP by PEP carboxykinase
(note: oxaloacetate cannot cross the mitochondrial membrane so it must either first be converted to PEP from within the mitochondria and then transported or must be transported as malate or aspartate to cytosol where cytosolic PEPCK can catalyze the rxn)


what are neurophysins

carriers of ADH and oxytocin that carry them from hypothalamus to posterior pituitary


what do acarbose and miglitol inhibit and where on the cell is it located

acarbose and miglitol treat T2DM by inhibiting alpha-glucosidase (a disaccharidase)


what is the medication of choice for treatment of gestational diabetes mellitus



why are non-selective beta blockers contraindicated in diabetes patients?
what kind of beta blocker could you use and why?

in response to hypoglycemia, the body releases Epi and NE to stimulate glucose production and decrease peripheral glucose use;
non-selective beta blockers block the adrenergic effects of Epi and NE, masking and exacerbating hypoglycemia


what embryologic process causes lingual thyroid

failure of the thyroid gland to migrate properly ==> sublingual thyroid that must be surgically removed to avoid asphyxiation