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64 Cards in this Set
- Front
- Back
morphology of minimal change disease?
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effacement of foot processes, otherwise kidney appears normal
lipid laden renal cortices |
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morphology of focal segmental glomerulosclerosis?
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not all of the glomeruli are involved and the entire glomerular region is not necessarily involved
usually onlly the glomeruli in the medulla are involved |
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morphology of membranous glomerulonephritis?
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spike and dome (BM and mesangial cells)
IgG and C3 deposition in the subepithelium granular immunofluorescence |
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morphology of diabetic nephropathy?
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2 types of morphologies possible: (BM markedly thickened in both)
diffuse glomerulosclerosis kimmelsteil-wilson nodules (nodular glomerulosclerosis) |
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morphology of renal amyloidosis?
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amyloid deposition in the subendothelium and mesangium
criss-cross fibrillary pattern |
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what are the morphological features of lupus nephropathy?
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5 forms:
I: no clinical consequence II: hematuria with proteinuria (increase in mesangium) III: focal proliferative form (<50% of glomeruli) IV: wire-loop abnormalities, endothelial cell proliferation, subendothelial immune complex deposits V: same as diffuse membranous glomerulonephritis |
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morphology of post-streptococcal glomerulonephritis?
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hemorrhages on the surface of each kidney
enlarged, hypercellular, swollen, bloodless glomeruli lumpy-bumpy immunofluorescence (IgG and C3) subepithelial localization |
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morphology of RPGN
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50% of the time is post-streptococcal with immune complex deposition
crescents between Bowman's capsule (fibrin deposition) can also be pauci-immune type with no immune deposition or anti-glomerular BM AB |
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causes of RPGN
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post-streptococcal (50%)
Goodpastrue's (10% of time) |
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what is the association of RPGN with ANCA?
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can be associated with ANCA (type III, pauci-immune) or not associated with ANCA
if not, types I (with anti-glomerular BM AB) and type II (immune complex type) |
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morphology of renal dz seen in Goodpasture's
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linear IgG immunofluorescence
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clinical manifestations of Goodpasture's dz
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nephritic syndrome
pneumonitis with hemoptysis RPGN crescentic dz with linear immunofluorescence |
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morphology of focal glomerulonephritis
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focal and segmental involvement, with inflammatory and proliferative changes (as opposed to sclerotic changes seen in FSGS)
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cliical features of Alport syndrome
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nerve deafness
ocular d/o lens dislocation cataracts renal failure by 30yo |
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morphology of alport syndrome
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splitting of the lamina densa (basketweave)
IRREGULAR basement membrane thickening |
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Berger dz
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IgA deposition in mesangium
very common dz |
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clinical picture of Berger Dz
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benign recurrent hematuria in children, following an infection
lasts 1-2 days, has little clinical significance can be a component of Henoch-Schnolein |
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presenting feature of Berger Dz
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focal glomerulonephritis
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clinical presentation of membranoproliferative glomerulonephritis
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slow progression to chronic renal failure
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morphology of MPGN
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BM thickening and cellular proliferation
tram-track appearance of BM b/c of reduplication of glomerular BM into 2 layers from expansion of mesangial matrix into glomerular capillary loops |
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what are the different types of MPGN
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type I: tram track appearance
type II: dense deposits with C3 adjacent (NOT within); caused by IgG autoantibody to C3 convertase that stabilizes the enzyme and constitutively activates convertase |
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renal colic
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excruciating pain from distending ureter d/t stone
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hydronephrosis
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progressive dilation fo renal pelvis and calyces
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clinical manifestations of urinary tract infections
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increased urinary frequency
dysuria pyuria (PMNLs in urine) hematuria bacteruria |
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causes and manifestations of acute drug-induced interstitial nephritis
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caused by penicillin and it's derivatives or NSAIDS
immune etiology acute interstitial inflammation |
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causes of papillary necrosis
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DM (#1 cause)
aspirin or other NSAIDS, phenacetin (no longer OTC) |
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morphology of renal papillary necrosis
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loss and atrophy of tubules
interstitial fibrosis inflammation |
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what is the most common cause of acute renal shutdown?>
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acute tubular necrosis
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is ATN reversible?
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yes, just takes time for the necrotic renal tubular cells to be replaced with new healthy cells (approx 2 weeks)
complete return of renal fxn is possible if pt is maintained on dialysis while symptomatic |
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clinical progression of ATN
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iniating stage from inciting events
initial oliguric phase (--> hyperkalemia and cardiac complications), renal failure recovery stage with increased urine volumes and hypokalemia |
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causes of ATN
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renal ischemia from prolonged hypotension/shock, gram negative sepsis, or crush injury
mercuric chloride, gentamycin, ethylne glycol |
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clinical presentation of fanconi syndrome
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impaired reabsorption at the proximal tubules
glucosuria, phosphaturia, aminoaciduria, systemic acidosis, and hypophospatemia |
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hartnup dz
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impaired tubular reabsorption of tryptophan
--> pellagra manifrestations |
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morphology of chronic pyelonephritis
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deformity of renal pelvis and calyces
interstitial inflammatory infiltrate (early stages) and later with interstitial fibrosis with tubular atrophy atrophic tubules contain eosinophilic protein casts that look like thyroid follicles |
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when is thyroidization of the kidney seen?
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chronic pyelonephritis
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clinical presentation of chronic pyelonephritis
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chronic UTI and repeated bouts of inflammation
--> renal HTN and ESRD |
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causes of diffuse cortical necrosis
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obstetric catastrophe
septic shock |
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what is nephrocalcinosis
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Ca deposition in kidney parenchyma --> renal failure, caused by hypercalcemia or can be caused by hyperphosphatemia
can be a cause or an effect of renal failure |
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what is the milk alkali syndrome?
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nephrocalcinosis and renal stones from self-medicating for peptic ulcer with milk and absorbable antacids
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morphology of chronic tubular interstitial nephritis
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kidneys are small and atrophic
tubular lumens show marked dilation infiltrate is mononuclear and there is prominent interstitial fibrosis with tubular atrophy |
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clinical presentation of chronic interstitial nephritIS
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no edema
minimal proteinuria normal or slightly elevated BP |
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what is the morphologic difference between adult and juvenile onset polycycstic kidney dz
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in juvenile onset: outer surface of kidney is smooth, with no visible cysts (cysts are closed and not connected to collecting ducts)
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general features of chronic interstitial nephritis
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any dz where tubulointerstitial area is more affected than glomeruli
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how does protein affect nitrogen balance
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if high protein, then + n balance, b/c higher BUN, thus raising BUN/Cr
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what effect does rhabdo have on BUN:Cr?
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it decreases the ratio by increasing the cr
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what is nephronophthisis
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cysts in medulla that result in renal failure
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what causes acquired cystic dz of the kidney
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long-term dialysis
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morphology of acquired cystic dz of kidney
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cysts, glomerular and tubular atrophy
scarring |
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what is associated with acquired cystic dz of kidney
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renal cell carcinoma risk
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characteristics of uremia
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azotemia
acidosis (from accumulation of phosphates, sulfates, adn organic acids) hyperkalemia abnormal control of fluid volume (early inability to [] urine, then inability to dilute urine) hypocalcemia anemia hypertension anorexia n/v neuro d/o bleeding from d/o platelet fxn accumulation in skin of urochrome and other pigments fibrinous pericarditis |
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causes of prerenal azotemia
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blood loss
peripheral pooling from gram negative sepsis systemic hypovolemia heatstroke bilateral RAS |
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BUN:Cr in prerenal azotemia
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>15
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what are the different types of RTA
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type 1: distal tubular dfect (can't establish H+ gradient --> metabolic acidosis with urine pH >5.5)
type 2: proximal tubule failure to reabsorb HCO3-, urine pH >5.5 initially then <5.5 later type 4: low aldosterone --> hyperkalemia and hyperchloremia; urine pH <5.5 |
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what are the benign tumors of the kidney
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adenoma
angiomyolipoma |
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what is angiomyolipoma
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hamartoma consisting of fat, smooth muscle, BV
associated with tuberous sclerosis syndrome |
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what are the malignant tumors of the kidney
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renal cell carcinoma
wilms tumor transitional cell carcinoma squamous cell carcinoma |
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demographics of renal cell carcinoma
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men 50-70yo
smokers |
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what is the most common type of renal cell carcinoma
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clear cell carcinoma (chrom 3 gene deletion)
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where does renal cell carcinoma originate
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renal tubules, usually at the upper pole
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mets of renal cell carcinoma
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usually hematogenous
travels through renal veins and IVC |
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histology of renal cell carcinoma
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polygonal clear cells
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clinical features of renal cell carcinoma
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flank pain
hematuria palpable mass fever flank pain secondary polycythemia ectopic production of various hormones |
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what drugs/toxic exposures has been associatd with transitional cell carcinoma
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phenacetin
b-napthylamine benzidine aniline dyes smoking cyclophosphamide |
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etiology of squamous cell carcinoma
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chronic inflammation
schistosoma haematobium infection renal calculi |