Renal Flashcards
(50 cards)
phosphate proximal tubule reabsorption is increased by Na+/phosphate cotransporter and not PTH because
PTH decreases it by inhibiting active transport mechanisms in the proximal tubule. PTH increases reabsorption of Ca2+ and PO43- in the gut via vitamin D
kidney stones and urine that produces a deep purple color with nitroprusside cyanide test is cystinuria and not hypophosphatemic rickets because
cyanide converts cystine to cysteine and a purple color is formed when nitroprusside binds to cysteine.
electron dense subepithelial humps
poststreptococcal glomerulonephritis
urine dipstick that show positivity for luekocyte esterase but not reactivity to nitrite contains Enterococcus faecalis and not proteus mirabilus because
enterobacter sp. (gram neg enteric rods: e coli, klebsiella, and proteus) are nitrite positive.
a 65 yr old man with oligura, edema, hemoptysis, and glomerular crescents has Anti-glomerular dz and not lupus nephritis because
lupus nephritis is common in women at childbearing age.
A tumor that has islands of stromal or epithelial cell and glomerular ortubular structures that does not cross the midline is a Wilms tumor and not neuroblastoma becuase
neuroblastomas can cross the midline and Wilm’s tumor (kidney) do not.
normal glomeruli and interstitium with coagulative necrosis of distal portion of renal pyramids is most likely caused by DM and not milliary TB because (location and necrosis type)
papillary necrosis is most commonly caused by DM, acute pyelonephritis, chronic penacetin (derivative of acetaminophen) use, and sickle cell anemia. miliary TB causes whitish seedlike nodules on renal cortex and has caseting granulomas.
given maximal urine osmolarity, plasma sodium, plasma potassium, plasma osmolarity, and minimum solute output; maximal urine osmolarity and minimum solute output is used to calculate the urine volume of a woman deprived of water for 24 hrs?
obligatory urine volume= solute load(amount)/maximal urine osmolarity (concentration-amt/vol)=urine volume
this is also equal to minimum water intake.
correcting hyponatremia too quickly leads to basis pontis damage and not cerebellar penduncles because
compensation for hyponatremia is extrusion of solutes from intracellular stores. over correction can lead to central pontine myelinolysis or osmotic demylination syndrome. the cerebellar penduncles are not vulnerable to rapid overcorrection
development of kidney
ureteric bus aka metanephric duct is diverticulum of mesonephric duct. grows to metanephric mass which becomes exceretory units of kidney. metanephros in turn induces metanephric duct to divide into calyces and CCTs of definitive kidney.
hyperplastic arteriolitits
aka onion skinning of renal arterioles suggests malignant hypertension
acetazolamide decreases NH4+ excretion and not K+ excretion because
it blocks carbonic anahydrase which causes intracellular conversion of CO2 and H2O to H2CO3 which automatically dissociates to HCO3- and H+. without it no H+ is formed and it can’t be excreted with NH3.
blocking ADH receptors will cause a decrease in urine osmolarity but no change in electrolyte excretion because
ADH works only to reabsorb water in the CCT, it doesn’t effect the PCT where most of the ion are reabsorbed. pt will become hypervolemic and hyperosmotic.
unchanged urine output after ADH administration, in the setting of hypernatremia can be caused type 2 DM and not hypoaldosteronism because
hypoaldsteronism will cause hyponatremia not hypernatremia. also DM leads to hyperglycemia leading to oversaturation of glucose reabsorption channels and increased ultrafiltrate oncotic pressure. ADH can no longer passively reabsorb water in CCT. instead RAS reabsorbs salt in an effort to maintain plasma vol.
pseudomonas cause hot tub folliculitis not pneumonia in AIDS pt because
it causes UTIs, hot-tub folliculitis and infections in burn and CF pts. pneuomnia in AIDS is caused by histoplasm capsulatum, proteus, and ureaplasma (no cell wall related to mycoplasma)
the early DCT and not the CCT has the lowest fluid osmolarity because
ADH can increase the CCT osmolarity to 1200-1400mOsm/L. the TAL and DCT are diluting segments
pt with HTN, DM, and osteoarthritis and signs of acute interstitial nephritis is mostly due to ibuprofen and not metoprolol because
ibuprofen (NSAIDS) can lead to AIN. typical presentation-acute renal failure, fever, maculopapular rash, esinophilla
give allopurinol and not acetylsalicyclic acid befoe starting chemo on a pt because
it is acitivated by xanthine oxidase and then in turn inhibits xanthing oxidase to decrease purine metabolism and decrease uric acid formation and uric kidney stones. acetylsalicylic acid is asprin at low doses can decrease uric acid secreton and cause hyperuricemia whereas at high doses it causes decrease in ureic tubullar reabsorption can cause uricosuria
the most common effect of cyclosporine (IL-1/IL-2 production inhbitor=less macs and T cells) is
nephrotoxcity. most likely due to renal vasconstriction caused by reduction in thromboxane, and reduced PGs,
what % of salt is excreted by kidney? what % by sweat and feces
95%; 5%
Wilms tumor has embryonic glomerular structures and not abudant clear cells becuase
clear cells are associated with renal cell carcinoma
thiazides increase Ca2+ serum levels and not carbonic anhydrase inhibitors because
thiazides inhbit NaCl reabsorption in DCT causing Ca2+ reabsobtion. mech not clear, maybe decreased Na in DCT causes increase Na/Ca channel acitivation in basolateral side
pt with neurogenic bladder due to paraylsis should be treated with tolterodine and not prazosin beauase
tolterodine is a compeptive muscarinic receptor antagonist that blocks hyperactivation on these receptors in bladder. prazosin is an alpha blocker and would prevent symapathetic stimulation of external sphincter making the problem worse.
captopril is an agent that can cause renal dysfunction and increased Cr and not ciprofloxacin because
captopril is an ACE inhibitor which blocks ANGII constriction of efferent arteriole to maintain GFR. ciprofloxacin has no effect on the things that can lead to prerenal azotemia (decreasd CO, decreased renal blood flow, and change in vascular resistance)
