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Renal/Resp > Glomerular Disease 1 > Flashcards

Glomerular Disease 1 Flashcards

1
Q

how does glomerular disease present?

A

Hematuria (quality)

Loss of GFR (temporal change)

Proteinuria (quantity)

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2
Q

factors of nephrotic syndrome

A

Proteinuria >3.5 g/day

Hypoalbuminemia

Edema

Hyperlipidemia (increased hepatic production)

Lipiduria

Hypercaogulabiltiy (loss of anticoag C and S)

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3
Q

nephrtitis

A

mild proteinuria

**Hematuria **(RBCs, RBC casts, dysmorphic RBCs)

HTN

Edema

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4
Q

causes of acute glomerulonephritis

A

IgA nephropathy

Post-infectious GN

Anti-GMB disease / good pastures

small vessel vasculitis

lupus nephritis

membranproliferative GN

(I poop good, small, little, marbels)

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5
Q

most common Gn

A

IgA nephropahty

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6
Q

most prominent feature IgA nephropathy

A

hematuria (50-60% episodic, 30% persistent, 10% acute Gn or nerphtoic syndrome)

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7
Q

presentation IgA nephropathy

A

Dysuria

Loin Pain

Hematuria

co-present w/ URI (synpharrngitic hematuria)

pos HTN

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8
Q

Histology IgA nephopathy

A

LM - messangianl hypercellularity, scelorosis+necrosis with crescents

IF: **Msangial IgA deposition **

EM- mesangional paramesangial elctron dense deposits

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9
Q

treatment IgA nephropathy

A

fish oil may slow

ACE

corticosteroids or other immunosuppresants

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10
Q

presentation Henoch-Schonlein Purpura

A

skin non blanching pupura on legs+buttucks

transient arthraligias

GI (hematochezia)

kidney - hematuria, proteinuria

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11
Q

infection presentation post infectious GN

A

7-14 days post pahryngitis, 14-28 post skin infection (esp A beta hemolytic strep)

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12
Q

clinical presentatiion Post strep GN

A

sudden onset HTN

azotemia

oliguria

edema

tea-colored urine

**Labs: **low C3 comp, ASO elevated, RBC casts in urine, proteinuria

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13
Q

histo post strep GN

A

LM - enlarged hypercell. glomeruli

diffuse mesangial+endocapilary proliferation with PMNs

crescents

**IF **granular capillary wall, mesangial IgG and C3

EM: Mesangial and large subepithelial humb-like deposits

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14
Q

causes of rapidly progressive GN

description

A

classic nephritic syndrome with rapid progression to renal failure

anti GBM / Goodpastures

ANCA asssociated GN (Pauci Immune)

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15
Q

histo rapidily progressive GN

A

crescentic

early segmental necrosis early

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16
Q

cause of Anti GBM / goodpastures

A

circulating anti GBM antibody (antigen is a3chain of type IV collagen)

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17
Q

posible presentation of Anti-GBM ./ goodpastures

A

Males>femailes

pulmonary renal syndome: hemoptysis, pulmonary infiltrates, glomerulonephritis

18
Q

diagnosis/ treatment anti-GBM / goodpastures

A

antiGBM in blood

Linear IgG and C3 on kidney biospy IF

plasmapheresis, prednisone, cytoxan

19
Q

crescenteric GN with little deposition of immune reactants

A

Pauci-immune

20
Q

pauci - immune GN possibly associated with

A

ANCA vasculititis

21
Q

differentiation

microscopic polyangiitis

wegner’s granulomatosis

churg straus

A

**microscopic polyangiitis: **no granulomatous inflam, no asthma

wegner’s granulomatosis: necrtizing granulomatous inflam, no asthma

**churg strauss: **necrotizing granulomatous inflam, asthma, eosinophilia

22
Q

renal biopsy wegenrs

A

cresenteric GN without immune deposits

23
Q

treatment for all causes of nephrotic syndrome

A

ACE/ARBs to lower pressure+reduce proteinuria

Statins reduce lipids

diuretics+salt restriction to improve edema

24
Q

most common cause of nephrotic syndrome in children

A

minimal change disease

25
Q

adult associations minimal change disease

A

NSAIDs

neoplasms esp Hodgkins Lymphoma

Syphilis, HIV

26
Q

histo Minimal change disease

A

LM: glmeruli intersitium and tubules normal

IF negative or mesangial IgM

EM: podocyte foot process effacement (fusion)

27
Q

treatment minimal change disease

A

corticosteroids (adults take longer, more remission)

28
Q

most common cause of nephrotic syndrome in cuacasian adults

A

membranous nephropathy

29
Q

secondary causes membranous nephrpathy

A

infection (HBV)

Connective tissue disease (SLE)

Neoplasms: carcinoma of lung, colon, stomach or breast, Non hodkin’s lymphoma

Drugs

30
Q

presentation membranous nephropathy

A

heavy proteinuria and nephrotic syndrome

HTN and azotemia later

renal vein thrombosis in 20%

31
Q

histo membranous nephropathy

A

LM: diffuse thickening of GBM, GBM spikes on silver stain

IF: granular GBM deposits of IgG

EM: subepithelial depsoits

32
Q

membranous nephropathy outcome

A

1/3 spontaneous remission

1/3 partial remissions + stable

1/3 slow progressive loss of renal function

33
Q

treatment Membranous neropathy

A

ok prognosis : ACE or ARB

poor prognosis : steroids or other immunosuprresion

34
Q

most common casue of nephrotic syndrome in African americans

A

focal segmental glomerulosclerosis

35
Q

presentation focal segmental glomerulosclerosis

A

HTN

Hematuria

end stage renal disease in 5 years

primary = acute onset nephrotic syndrome

secondary: slow renal insufficiency+ proteinuria

36
Q

cauases secondary FSGS

A

Drugs - NSAIDs, heroin

infections HIV

obesity

past glomerular injury

loss of renal mass

37
Q

histology focal segmental glomerular sclerosis

A

LM: glomerular scloeriss with capilalry colapse, hyaline and lipid deposits in bowman’s capsule

IF: negative or IgM and c3 in mesangium or in segmental scars

EM: podocyte foot process effacemen,t segmental sclerosis

38
Q

treatment FSGS

A

ACE, corticosteroids,

39
Q

presentation membranoproliferative glomerulonephrtiis

A

proteinuria+hematuria

HTN

low C3 complement

variable (nephrotic/asympotomatic preteinuria+hematuria/acute GN)

40
Q

secondary causss PRGN

A

connective tissue disease (SLE)

Cryoglobulinemia

Infection: **Hep C, **Hep B, endocarditis, abscesses

neoplasm

41
Q

histo MPGN

A

LM: hypercellular glomeruli, endocapillary prlif, lobular apparing glomeruli

IF: granular C3 depotsits

EM: subendothelial deposits

Renal/Resp (43 decks)

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