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Goljan Renal Path 2

BUN:Cr ~ 10:1 with oliguria and renal tubular casts acute tubular necrosis
Why does acute tubular necrosis have such a bad diagnosis? FAST. ischemic cause destroys GBM -> loss of polarity -> detachment -> necrosis. can't regenerate renal tubular cell w/o BM -> RF. Death usually during initial oliguric phase.
What parts of nephron is most susceptible to ischemia? straight portion of proximal tubule and thick ascending limb (medullary part). Affects Na/K/Cl co-transport
Nephrotoxic drugs...what are they and where do they affect? prognosis? gentamicin (aminoglycocides), dye from IV pyelograms; damages proximal tubule. prognosis good because they don't damage BM.
How do you separate pyelonephritis from low UTIs? acute pyelonephritis is infection of kidney proper and has fever with flank pain (CVA tenderness) and WBC casts
what is the mechanism of all UTIs ascending infection from introitus of urethra.
scarred kidney with blunted calyces (beneath scarring) chronic pyelonephritis
fever with rash, oliguria, eosinophiluria after starting drug acute drug-induced interstitial nephritis (methicillin)
what kinds of hypersensitivity are associated with acute drug-induced interstitial nephritis? combination of type I and type IV hypersensitivities
empty space on IV pyelogram analgesic nephropathy from acetaminophen and aspirin combo therapy long-term
what is the mechanism of analgesic nephropathy? acetaminophen --> produces free radicals that damage tubular cells of medulla aspirin blocks PGE2 so Angiotensin II is unopposed and peritubular capillaries have decreased blood flow causing ischemia in renal papillaries
causes of renal papillary necrosis aspirin/acetaminophen long-term, diabetes, sickle-cell disease, acute pyelonephritis (from abscess formation)
BUN/Cr >10 for more than 3 months. what is the diagnosis? Chronic renal failure
results of chronic renal failure anemia, anion-gap metabolic acidosis, osteoporosis, osteomalacia, secondary hyperparathyroidism
uncontrolled essential hypertension (over ten years) causes what? nephrosclerosis --> hyaline arteriolosclerosis (cobblestone appearance of kidney)
person with uncontrolled HTN, wakes up with bad HA, dizzy, blurred vision, BP 240/140, papilledema and flamed hemorrhages, hard and soft exudates, BUN/Cr 80/8. what is diagnosis? malignant hypertension (shows petechia visible on surface of kidney)
Treatment of malignant hypertension? IV nitroprusside
pale, depressed-looking lesions on gross examination of kidney. what do you see on LM? pale infarction --> coagulation necrosis
causes of pale infarcts in kidneys in a patient with irregular irregular pulse? A-fib, causes thromboemboli
little white dots and microabscesses on gross exam of kidneys probably caused by what? pyelonephritis
hydronephrosis and increased pressure have what affect on renal cortex and medulla? compression atrophy
staghorn calculi, alkaline urine and smells of ammonia, what is the cause? urease (+) bacteria: proteus, klebsiella, staph
most common cause of compression atrophy? stone
what is the composition of staghorn calculi magnesium ammonium phosphate
mass in kidney adult what is it? renal adenocarcinoma
mass in kidney in kid with hypertension? wilm's tumor
cause of renal adenocarcinoma? derived from proximal tubule; most common cause is smoking
what are results of renal adenocarcinoma? produce ectopic EPO, PTH-like peptide, and like to invade renal vein
why hypertension in kid with Wilm's tumor? the tumor makes renin
findings in Wilm's tumor? embryonic kidney structures; aniridia and hemi-hypertrophy of an extremity --> sign that Wilm's tumor has genetic basis
genetic abnormality in Wilm's tumor? WT-1 tumor-suppressor gene on chrom 11. AD
most common organism in cystitis? E. coli
Created by: Asclepius



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