Endo 1 Flashcards
In a male with only one descended testicle, how does this affect his hormone levels?
Normally, Inhibin B suppresses FSH secretion to regulate testosterone secretion by Leydig cells. A male w/ only one descended testicle will have dec. testosterone from Leydig cells (due to inc. temp on testis), so will have inc. FSH and dec. inhibin B.
*These patients need to be assessed for an inc. risk in cancer.
What happens if you administer glucose in a thiamine (B1) deficient patient w/ chronic alcoholism?
> Giving glucose in a B1 deficient alcoholic patient will rapidly deplete the B1 that’s left – neuronal injury in highly metabolic brain areas – Wernicke encephalopathy.
Ethanol metab consumes NAD+ (inc. NADH/NAD+ ratio) – inhibits all pathways needing NAD+ – Inc. NADH blocks glycolysis, TCA cycle – exacerbates condition cuz the B1-dependent enzymes also need NAD+ (TLCFN dehydrogenases)
What happens in 5-alpha-reductase deficiency type 2?
5-alpha-reductase is found in genitals (testosterone –> DHT).
In deficiency, male will have normal internal genitalia but external genitalia don’t develop (Male Pseudohermaphroditism) – ambiguous genitalia (small phallus, hypospadias).
How should insulin therapy be administered in a diabetic patient?
Normal pancreatic insulin is biphasic, so insulin therapy should mimic this physiology (mealtime bolus, basal secretion for steady-state b/w meals).
*Regular insulin isn’t recommended for mealtime bolus – use Rapid-acting insulin analogs (Lispro, Apart, Glulisine).
Why would a female anorexic patient develop amenorrhea?
Functional Hypothalamic Amenorrhea: Dec. leptin due to dec. adipose tissue – inhibits GnRH – dec. LH/FSH – dec. Estrogen (ovaries) – amenorrhea.
*Also due to excessive wt loss, strenuous exercise, chronic illness
Glucocorticoids effect on liver protein synthesis and peripheral protein synthesis?
> In liver, overall protein synthesis and gluconeogenesis would increase.
Peripherally, glucocorticoids antagonize insulin in skeletal muscle/adipose – proteolysis, lipolysis – substrates for gluconeogenesis and glycogenesis in liver.
Copper reduction test vs. Urine dipstick
> Copper reduction test: Nonspecifically tests for presence of reducing sugar (fructose, galactose).
Urine dipstick: uses glucose oxidase to detect urinary glucose only
How can insulin resistance be induced by TNF-a (or by catecholamines, glucocorticoids, glucagon)?
TNF-a can activate serine kinases.
TNF-a induces phosphorylation of serine/threonine residues of insulin receptor and IRS-1 – insulin resistance (by inhibition of tyrosine phosphorylation)
Sheehan syndrome
[Px]
Ischemic necrosis of pituitary ff. postpartum bleeding.
Pituitary enlarges during pregnancy (estrogen-induced hyperplasia of lactotrophs), but blood supply doesn’t proportionally increase – vulnerable to peripartum hemorrhage (hypotension).
Why does DKA show an increased triglyceride breakdown in adipose tissue?
Since there’s no uptake of glucose, and therefore no glucose to produce energy from, Hormone-sensitive Lipase in adipose metabolizes TGL into FFA + glycerol – glycerol transported to liver.
In the liver, Glycerol Kinase converts glycerol into glycerol-3-phosphate – converted to DHAP – ATP (glycolysis), glucose (gluconeogenesis).
In hyperaldosteronism, there is HTN (inc. blood volume), hypokalemia, metabolic alkalosis, and suppressed renin. Why, then, doesn’t Primary Hyperaldosteronism have significant fluid volume expansion?
With ALDOSTERONE ESCAPE, there is inc. renal blood flow, inc. GFR, inc. ANP (response to inc. blood volume) – dec. Na reabsorption; dilated afferent arterioles, constricted efferent arterioles – diuresis – limits edema, limits hypernatremia.
(Ex. Conn syndrome: Primary hyperaldosteronism due to aldosterone-producing adenoma)
What is the role of Fructose-2,6-bisphosphate and how is it regulated?
F2,6BP controls balance b/w Glycolysis and Gluconegenesis – activates PFK-1, inhibits Fructose-1,6-bisphosphatase.
>Fasting: glucagon activates F-2,6-bisphosphatase: converts F2,6BP into F6P – gluconeogenesis.
>Fed: Insulin activates PFK-2: converts F6P into F2,6BP – inc. activation of PFK-1 – converts to F1,6BP – liver glycolysis.
What are the cell types that can accumulate sorbitol w/o needing insulin for glucose transport, and why is this important in diabetics?
Lens, peripheral nerves, blood vessels, kidneys.
These tissues are prone to osmotic cellular injury w/ accumulation of sorbitol – significant in diabetic patients who develop cataracts, peripheral neuropathy, kidney injury
What is the effect of bile acid resins (cholestyramine) on circulating VLDL and LDL?
Bile acid resins prevent reabsorption of bile acids and thus divert hepatic cholesterol into making bile acid as opposed to more VLDL/LDL. So there is a dec. in VLDL and LDL.
What are the different ways to treat prostate cancer? (3)
Prostate cancer is testosterone-dependent.
>A GnRH agonist (Leuprolide) under continuous release may suppress LH secretion from Leydig cells.
>Testosterone receptor inhibitors (Flutamide, Spironolactone) are for primary tumor and metastases.
>5-alpha-reductase inhibitors (Finasteride) is used to treat BPH.
