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STEP I 2014 > Renal > Flashcards

Flashcards in Renal Deck (50):

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)


desptie increasing MAP RPF and GFR are kept constant by a. art constriction and e art dilation and not a. art dilation and e. art constriction because

a. art dilation and e. art constriction would cause and increase in RBF and GFR.

the a art constrict and to increase resistance and maintain constant GFR and RBF. decreased renin production due to high BP causes dilation of e. art


acute renal failure results in metabolic acidosis and not alkalosis because

in states of volume depletion the kidney (if normal) will absorb Na and waste K+ and H+. However in the state of renal failure the kidney is unable to maintain blood volume and thus Na+ will be reabsorbed and H+ and K+ can no longer be secreted resulting in metabolic acidosis. Note: the pt may still have elevated serum Na+ due to decreased plasma volume.


pt with recent gasteroenteritis, dark urine, with normal renal function, C3 levels is likely to have mesangial IgA deposits and not crescent formation on histology because

Berger's disease can present after a URI or acute gastroenteritis. RPGN would have decreased C3 levels as the crescents are formed from fibrin, plasma proteins (C3b), glomerular parietal cells, monocytes, and macrophages.


thickening of walls of glomerular capillaries

"tram tracking" in membranoproliferative glomerular nephritis. MPGN


nephrotic syndrome results in an increase in LDL and not HDL because

increased protein production in liver, abnormal lipid particle transport, and decreased lipid catabolism results in increases LDL, cholesterol, and triglyceride levels. HDL levels decrease.


pt with polyuria and polydpsia and dilute urine despite overnight water restriction has nephrogenic DI and not DM because

with DM pt are able to concentrate their urine


Goodpasture's disease can lead to damage of lens of eye and not fascia because

the anti-GBM are directed against type VI collagen which is present in the lungs, kidneys, and lens of the eye


type I collagen

bone, skin, tendon, dentin, fascia


type II collagen

cartilage (hyaline cartilage), vitreous body of eye, and nucleus pulposus of intervertebral disks


type X collagen

epiphyseal plates


type III

skin, blood vessels, uterus, fetal tissue and granulation tissue


newborn with clear fluid in umbilicus, pH 6.0, specific gravity 1.020, no leuks, no RBS, and no hemoglobin passes through the median umbilical ligament and not the medial umbilical ligament because

the fluid described is urine and the embryonic structure is the allantooic duct (urachus). normally the urachus obliterates and forms the median not medial umbilical ligament (from upper bladder to umbilicus). the medial umbilical ligmament is the adult derivative of the umbilical artery.
folds are parietal peritoneum that covers the ligaments.


lateral umbilical fold

fold parietal peritoneum that covers inferior epigastirc artery and vein on inferior surface of anterior abdominal wall


renal failure diet

control protein and phosphorus in pts diet, limit sodium and fluid intake. low protein and high carbs and moderate fat intake


increasing net hydrostatic pressure (capillary pressure-pressure in Bowman's space) and increasing plasma protein oncotic pressure is due to to constriction of e. arteriole and not dilation of afferent arteriole because

increasing net hydrostatic pressure would result from dilated afferent and constricted efferent. however the plasma protein oncotic pressure is an indication of filtration fraction (GFR/RBF). increasing oncotic pressure indicates an increased FF (more fluid is filtered while protein gets left behind). thus the RBF must have decreased which is due to efferent constriction. afferent dilation would have no effect on FF.


plasma osmolarity
total body osmoles

(total body osmoles-urine osmoles)/ (total body water-urine volume)
=initial plasma osmolarity*TBW


volume of fluid in a compartment

=amt of sustance given/concentration of substance in compartment
think volume of distribution=amt drug in body/plasma drug concentration.


Group A Strep and not strep. pneumo can cause glomerularnephritis because

strep pneumo causes MOPS (meningitis, otitis media, pneumo, a sinusitis)
GAS cause-pharyngitis which can lead to rheumatic fever or glomerulonephritis.


2 yr old body with gonadal dysgenesis most likely has Wilm's tumor vs other kidney tumors because

WAGR syndrome-wilm's tumor, anirida (absense of iris-colored portion of eye), genital abnormalties, and mental retardation


ovoid hyailne masses with amorphous PAS-positive material in the periphery of the glomerulus

Kimmelsteil-Wilson nodules


pt with DM2 and urinary incontinence should be given oxybutynin and not bethanechol because

bethanechol a muscarinic agonist would make her condition worse. oxybutynin and tolterondine are the the preferred anticholinergics to treat this condition.


most stones develop and can cause?

renal pelvis; renal colic if small or acute pyelonephrtis if large


pt with ADPKD is a increased risk for subarachnoid hemorrhage and not portal hypertension because

ADPKD is associated with berry aneurysms and hepatic cysts. ARPKD is associated with splenomegaly and liver fibrosis which can lead to portal hypertension.


sodium reabsorption=

amt filtered-amount excreted in urine
amt filtered=Plasma concentration*GFR
amt excreted=urine concentration*urine flow rate


sodium reabsorption=

amt filtered-amount excreted in urine
amt filtered=Plasma concentration*GFR
amt excreted=urine concentration*urine flow rate


pt with minimal change disease is suffering from lymphokine production by T cells and not immune complex deposition because

immune complex deposition is associated with type III hypersensitivity (post=strep, henoch-schonlein pupura, SLE) whereas minimal change is associated with Hodgkin's (non neoplastic T cells express cytokines) and T-cell lymphoma,