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FEK Y2 > Glomerular Disease > Flashcards

Glomerular Disease Flashcards

1
Q

trichrome stain

A

used to demonstrate fibrosis (blue)

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2
Q

focal vs. diffuse

A

refers to distribution of glomerular lesions throughout the kidney
(less than 50% of glomeruli affected = focal)

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3
Q

segmental vs. global

A

refers to distribution of lesions w/in individual glomeruli

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4
Q

endocapillary vs. extracapillary proliferation

A

endocapillary: proliferation of mesangial, endothelial, and inflammatory cells filling up capillary lumens and involve glomerular tuft
extracapillary: profile of epithelial cells in Bowman’s capsule to fill Bowman’s space = crescentic

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5
Q

nephrotic syndrome

A

heavy proteinuria
edema
hypoalbuminemia
hyperlipidemia

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6
Q

cause of nephrotic syndrome (pathology)

A

messed up epithelial foot processes – look at GBMs!

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7
Q

big 5 causes of nephrotic syndrome

A 
minimal change disease
focal segmental glomerulosclerosis (FSGS)
membranous glomerulopathy
diabetes
amyloid
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8
Q

minimal change disease pathology

A

Light and EM: normal
EM: diffuse effacement of epithelial cell foot processes
proximal tubular epithelial cells may have protein resorption droplets

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9
Q

who gets MCD? what causes it?

A

mostly children

many cases are primary, but also can be caused by NSAIDs, lithium, lymphoid malignancies, food rxns, bee stings

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10
Q

course and tx of MCD

A

benign course

responsive to steroids

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11
Q

focal segmental glomerulosclerosis pathology

A

Light microscope: focal segmental capillary collapse and sclerosis - usually solidification of part of the glomerular tuft
IF: negative - but might have non-specific IGM staining
EM: moderately extensive effacement of foot processes

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12
Q

causes of FSGS

A 
mostly primary
secondary causes:
- virus-assoc (HIV etc)
- drug induced (heroin etc)
- familial/genetic
- adaptations to hemodynamic alterations (reduction in functioning # of nephrons; hemodynamic stress on initially normal nephrons (HTN, DM, CHF, sickle cell))
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13
Q

course and tx of FSGS

A

progressive

poor response to tx

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14
Q

membranous glomerulopathy pathology

A

Light: thickened capillary walls w/ “spikes” on silver stain
IF: diffuse, granular IgG and C3 along capillary walls
EM: numerous subepithelial deposits, with eventual incorporation into GBM

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15
Q

causes of membranous glomerulopathy

A

primary

secondary: drugs, tumors, lupus, infections

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16
Q

diabetic glomerulopathy - pathology

A

light: diffuse and nodular (Kimmelstiel-Wilson) glomerulosclerosis [+ hyaline deposition in the arterioles]
IF: linear IgG and albumin in GBMs - non-specific trapping
EM: diffuse thickening of GBMs and increase in mesangial matrix [+ effacement of epithelial foot process (secondary to proteinuria)]

17
Q

amyloidosis - pathology

A

Light: diffuse and sometimes nodular glomerulosclerosis, with + congol red
IF: pos kappa or lambda light chains
EM: aggregates of 8-12nm fibrils

18
Q

glomerular diseases presenting with nephritis

A
  1. post-infectious glomerulonephritis
  2. Membranoproliferative glomerulonephritis
  3. SLE nephropathy
19
Q

post-infectious glomerulonephritis - pathology

A

gross: “flea-bitten” kidney
Light: diffuse proliferative GN (diffuse hypercellularity w/ PMNs)
IF: prominent granular or globular C3 (and sometimes IgG), mainly sub endothelial (+/- mesangial) deposits
EM: scattered large sub epithelial humps

20
Q

sx of nephritic syndrome

A

hematuria
azotemia
variable degrees of proteinuria, edema, HTN

21
Q

cause, course of post-infectious glomerulonephritis

A

classic acute diffuse proliferative GN

cause: usually streptococcal
course: prognosis good. usually self-limited, occasionally pts develop presences –> worse outcome

22
Q

membranoproliferative glomerulonephritis - pathology

A

Light: proliferative GN, often hyperlobulated w/ duplicated “tram-track” GBMs
IF: prominent granular or globular C3 (and sometimes IgG), mainly sub endothelial +/- mesangial
EM: duplicated GBMs w/ mesangial interposition and large sub endothelial (+/- mesangial) deposits

23
Q

course and causes of membranoproliferative GN

A

course: vast majority progresses to ESRD regardless of rx
causes:
- primary
- secondary: assoc w/ hepatitis B and C

24
Q

clinical presentation of membranoproliferative GN

A

combo of nephritic and nephrotic syndrome

25
Q

SLE nephropathy - pathology

A

Light: wire-loop deposits, hyaline thrombi, fibrinoid necrosis
IF: full house pattern - stains for everything
EM: extensive mesangial +/- peripheral deposits
- usual deposits are granular, may see “fingerprint” substructure; tumuloreticular inclusions
variety of appearances - 6 classes

26
Q

3 types of crescentic glomerulonephritis

A
  1. anti-GBM disease: linear IF
    - w/ pulmonary alveolar BM involvement = good pasture’s disease
  2. Immune complex-mediated disease: granular IF (lumpy-bumpy)
  3. Pauci-immune necrotizing GN: negative IF, ANCA+; caused by Wegener’s granulomatosis, microscopic angiitis, Churg-Strauss syndrome
27
Q

3 diseases that present primarily w/ hematuria

A
  1. IgA nephropathy
  2. Alport syndrome
  3. Thin basement membrane disease
28
Q

IgA nephropathy

A

Light: most commonly mesangioproliferative GN
IF: IgA dominant deposits (+/- IgG, C3, lamba)
EM: paramesangial deposits

29
Q

Henoch-Schoenlein purpura

A

same pathology as IgA

common in children under 10 during or after URI

30
Q

Thin basement membrane disease

A

aka: benign familial hematuria
persistent or intermittent microhematuria, without progression
Light and IF: normal
EM: diffuse thinning of GBM

31
Q

Alport syndrome - sx and cause

A

aka: hereditary nephritis
sx: nephritis, nerve deafness & ocular abnormalities. more rapid progression to ESRD in males (usually x-linked)
cause: genetic defects in collagen IV chain synthesis

32
Q

Alport syndrome - pathology

A

Light: no specific features
IF: negative for Igs, complement, light chains; alterations in collagen type IV staining pattern
EM: fragmentation and splitting of GBM (“basketweave” pattern)

FEK Y2 (17 decks)

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