Brs- Kidney And Urinary Tract Pathology

Front 1

morphology of minimal change disease?

Back 1

effacement of foot processes, otherwise kidney appears normal
lipid laden renal cortices

Front 2

morphology of focal segmental glomerulosclerosis?

Back 2

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

Front 3

morphology of membranous glomerulonephritis?

Back 3

spike and dome (BM and mesangial cells)
IgG and C3 deposition in the subepithelium
granular immunofluorescence

Front 4

morphology of diabetic nephropathy?

Back 4

2 types of morphologies possible: (BM markedly thickened in both)
diffuse glomerulosclerosis
kimmelsteil-wilson nodules (nodular glomerulosclerosis)

Front 5

morphology of renal amyloidosis?

Back 5

amyloid deposition in the subendothelium and mesangium
criss-cross fibrillary pattern

Front 6

what are the morphological features of lupus nephropathy?

Back 6

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

Front 7

morphology of post-streptococcal glomerulonephritis?

Back 7

hemorrhages on the surface of each kidney
enlarged, hypercellular, swollen, bloodless glomeruli
lumpy-bumpy immunofluorescence (IgG and C3)
subepithelial localization

Front 8

morphology of RPGN

Back 8

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

Front 9

causes of RPGN

Back 9

post-streptococcal (50%)
Goodpastrue's (10% of time)

Front 10

what is the association of RPGN with ANCA?

Back 10

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)

Front 11

morphology of renal dz seen in Goodpasture's

Back 11

linear IgG immunofluorescence

Front 12

clinical manifestations of Goodpasture's dz

Back 12

nephritic syndrome
pneumonitis with hemoptysis
RPGN crescentic dz with linear immunofluorescence

Front 13

morphology of focal glomerulonephritis

Back 13

focal and segmental involvement, with inflammatory and proliferative changes (as opposed to sclerotic changes seen in FSGS)

Front 14

cliical features of Alport syndrome

Back 14

nerve deafness
ocular d/o
lens dislocation
cataracts
renal failure by 30yo

Front 15

morphology of alport syndrome

Back 15

splitting of the lamina densa (basketweave)
IRREGULAR basement membrane thickening

Front 16

Berger dz

Back 16

IgA deposition in mesangium
very common dz

Front 17

clinical picture of Berger Dz

Back 17

benign recurrent hematuria in children, following an infection
lasts 1-2 days, has little clinical significance
can be a component of Henoch-Schnolein

Front 18

presenting feature of Berger Dz

Back 18

focal glomerulonephritis

Front 19

clinical presentation of membranoproliferative glomerulonephritis

Back 19

slow progression to chronic renal failure

Front 20

morphology of MPGN

Back 20

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

Front 21

what are the different types of MPGN

Back 21

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

Front 22

renal colic

Back 22

excruciating pain from distending ureter d/t stone

Front 23

hydronephrosis

Back 23

progressive dilation fo renal pelvis and calyces

Front 24

clinical manifestations of urinary tract infections

Back 24

increased urinary frequency
dysuria
pyuria (PMNLs in urine)
hematuria
bacteruria

Front 25

causes and manifestations of acute drug-induced interstitial nephritis

Back 25

caused by penicillin and it's derivatives or NSAIDS
immune etiology
acute interstitial inflammation

Front 26

causes of papillary necrosis

Back 26

DM (#1 cause)
aspirin or other NSAIDS, phenacetin (no longer OTC)

Front 27

morphology of renal papillary necrosis

Back 27

loss and atrophy of tubules
interstitial fibrosis
inflammation

Front 28

what is the most common cause of acute renal shutdown?>

Back 28

acute tubular necrosis

Front 29

is ATN reversible?

Back 29

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

Front 30

clinical progression of ATN

Back 30

iniating stage from inciting events
initial oliguric phase (--> hyperkalemia and cardiac complications), renal failure
recovery stage with increased urine volumes and hypokalemia

Front 31

causes of ATN

Back 31

renal ischemia from prolonged hypotension/shock, gram negative sepsis, or crush injury

mercuric chloride, gentamycin, ethylne glycol

Front 32

clinical presentation of fanconi syndrome

Back 32

impaired reabsorption at the proximal tubules
glucosuria, phosphaturia, aminoaciduria, systemic acidosis, and hypophospatemia

Front 33

hartnup dz

Back 33

impaired tubular reabsorption of tryptophan
--> pellagra manifrestations

Front 34

morphology of chronic pyelonephritis

Back 34

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

Front 35

when is thyroidization of the kidney seen?

Back 35

chronic pyelonephritis

Front 36

clinical presentation of chronic pyelonephritis

Back 36

chronic UTI and repeated bouts of inflammation
--> renal HTN and ESRD

Front 37

causes of diffuse cortical necrosis

Back 37

obstetric catastrophe
septic shock

Front 38

what is nephrocalcinosis

Back 38

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

Front 39

what is the milk alkali syndrome?

Back 39

nephrocalcinosis and renal stones from self-medicating for peptic ulcer with milk and absorbable antacids

Front 40

morphology of chronic tubular interstitial nephritis

Back 40

kidneys are small and atrophic
tubular lumens show marked dilation
infiltrate is mononuclear and there is prominent interstitial fibrosis with tubular atrophy

Front 41

clinical presentation of chronic interstitial nephritIS

Back 41

no edema
minimal proteinuria
normal or slightly elevated BP

Front 42

what is the morphologic difference between adult and juvenile onset polycycstic kidney dz

Back 42

in juvenile onset: outer surface of kidney is smooth, with no visible cysts (cysts are closed and not connected to collecting ducts)

Front 43

general features of chronic interstitial nephritis

Back 43

any dz where tubulointerstitial area is more affected than glomeruli

Front 44

how does protein affect nitrogen balance

Back 44

if high protein, then + n balance, b/c higher BUN, thus raising BUN/Cr

Front 45

what effect does rhabdo have on BUN:Cr?

Back 45

it decreases the ratio by increasing the cr

Front 46

what is nephronophthisis

Back 46

cysts in medulla that result in renal failure

Front 47

what causes acquired cystic dz of the kidney

Back 47

long-term dialysis

Front 48

morphology of acquired cystic dz of kidney

Back 48

cysts, glomerular and tubular atrophy
scarring

Front 49

what is associated with acquired cystic dz of kidney

Back 49

renal cell carcinoma risk

Front 50

characteristics of uremia

Back 50

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

Front 51

causes of prerenal azotemia

Back 51

blood loss
peripheral pooling from gram negative sepsis
systemic hypovolemia
heatstroke
bilateral RAS

Front 52

BUN:Cr in prerenal azotemia

Back 52

>15

Front 53

what are the different types of RTA

Back 53

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

Front 54

what are the benign tumors of the kidney

Back 54

adenoma
angiomyolipoma

Front 55

what is angiomyolipoma

Back 55

hamartoma consisting of fat, smooth muscle, BV
associated with tuberous sclerosis syndrome

Front 56

what are the malignant tumors of the kidney

Back 56

renal cell carcinoma
wilms tumor
transitional cell carcinoma
squamous cell carcinoma

Front 57

demographics of renal cell carcinoma

Back 57

men 50-70yo
smokers

Front 58

what is the most common type of renal cell carcinoma

Back 58

clear cell carcinoma (chrom 3 gene deletion)

Front 59

where does renal cell carcinoma originate

Back 59

renal tubules, usually at the upper pole

Front 60

mets of renal cell carcinoma

Back 60

usually hematogenous
travels through renal veins and IVC

Front 61

histology of renal cell carcinoma

Back 61

polygonal clear cells

Front 62

clinical features of renal cell carcinoma

Back 62

flank pain
hematuria
palpable mass
fever
flank pain
secondary polycythemia
ectopic production of various hormones

Front 63

what drugs/toxic exposures has been associatd with transitional cell carcinoma

Back 63

phenacetin
b-napthylamine
benzidine
aniline dyes
smoking
cyclophosphamide

Front 64

etiology of squamous cell carcinoma

Back 64

chronic inflammation
schistosoma haematobium infection
renal calculi