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22 Cards in this Set

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characteristics of Nephritic syndrome
hematuria
HTN
Renal insuff
Proteinuria (above 3.5 g/day=nephrotic)

immune deposits = nephritic
UA results for nephritic (in general)
proteinuria

"Active Urine Sediment"
-RBC cast
-dysmorphic hematuria
three mechanisms for glomerulonephritis
Immune complex deposits
-IgA nephropathy
-acute/diffuse proliferative
-lupus nephritis
-rapidly progressing GN

Anti-GBM (in situ imm complex)
-anti GBM GN
-Goodpastures

ANCA
-ANCA GN
-Wegeners
-microscopic polyangiitis
-Churg strauss
LM results for nephritis
hypercellular
mesangial
complex

focal/diffuse
segmental/global

crescentic

BM changes
IM results for GNitis
granular- type III (IgA, etc)
linear- type II (anti GBM)
negative- ANCA (type IV)
asymptomatic hematuria
Thin BM dz
Airports Syndrome

IgA nephropathy
hematuria
LM normal
IMFL normal
EM thin BM
type IV coll dist normal
BFH-benign familial hematuria
"thin BM dz"


excellent prognosis- no RF
hematuria
assoc w/deafness, retinal, cornea changes
males
type IV collagen abnormal
foam cells in interstitium
basket weave BM
Alports syndrome

chronic HTN or RF
mesangial immune deposits
cresents can dvp
IMFL "punctate"
EM big, dark deposits in mesangials
IgA nephropathy

viral infections may initiate or exacerbations
Henoch-Schonlein Purpura
IgA nephropathy + vasculitis
hypocomplementemia
neutrophils
IMFL granular C3 on cell wall
IMFL "starry sky"
EM buffalo humps
Acute Diffuse Proliferative GN (Post strep)

may have pos ASO
(subepithelial humps)
LM cellular- nonspecific
IMFL "full house" staining
especially C1q (classical)
EM varies
SLE GN

Ab's against nuclear Ag's
most aggressive lesions in SLE GN
segmental
activity index in SLE GN
can treat high
chronicity index in SLE GN
get transplant if high
crescent formation
RPGN- hallmark
-ANCA & anti GBM

(also possible in IgA nephropathy)

-proliferation of epis lining BC
-stain for fibrin
-get GBM breaks
mechanisms for RPGN
rapidly progressing glomerulonephritis

-anti GBM (linear IMFL)
-ANCA (neg IMFL)
-circulating immune complex (granular IMFL)
(least common cause)
EM: crescentic GN w/ruptured capillary walls
fibrinoid necrosis
IMFL: linear IgG
anti GBM GN
-type II is attack on type IV collagen
-if lungs involved = Goodpasture's
-young men or old females (white)

-anti GBM antibodies
anti GBM antibodies
anti GBM GN or Goodpasture's

in situ complex formation

young white male or old white female
EM: crescentic GN
necrosis
IMFL: negative
ANCA GN

medical emergency
diseases assoc'd w/ ANCA GN
microscopic polyangiitis (no gran or asthma, yes vasc)
Wegener's (lung granulomas, vasculitis)
Churg-Strauss (eos & asthma)

ANCA GN (no vasculitis, gran or asthma)
pathogenesis of ANCA
Ab's to neuts, degranulate, damage endothelium

P-ANCA
-perinuclear
-myeloperoxidase

C-ANCA
-cytoplasmic
-PR3 (proteinase)