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UTHSC M2016 CBD - Renal > Glomerular Structure and Mechanisms of Disease (Nichols) > Flashcards

Glomerular Structure and Mechanisms of Disease (Nichols) Flashcards

1
Q

9 places in a glomerulus that disease can be located

A

1 arterioles
2 capillaries (lumen & endothelial cells)
3 subendothelial (btwn capilary endothelial cells & GBM)
4 GBM
5 subepithelial (btwn GBM & epithelial cells)
6 in slit pore diaphragm
7 podocytes
8 bowman space and capsule
9 mesangium

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2
Q

8 most common primary glomerular diseases

A 
1 minimal change disease
2 focal segmental glomerulosclerosis
3 membranous nephropathy
4 acute post-streptococcal glomerulonephritis
5 membranoproliferative glomerulonephritis
6 IgA nephropathy (Berger disease)
7 hereditary nephritis (Alport syndrome)
8 congenital nephrotic syndrome
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3
Q

5 most common secondary glomerular diseases

A 
1 hypertensive nephropathy
2 diabetic nephropathy
3 lupus nephritis
4 amyloidosis
5 Goodpasture syndrome
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4
Q

3 most common types of glomerular disease in order of prevalence

A

1 hypertensive
2 diabetic
3 immune-mediated

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5
Q

pathophys of hypertensive glomerular disease

A

most common cause of glomerular disease
injury to endothelium -> thrombus
thrombotic microangiopathy
positive feedback loop

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6
Q

Malignant htn

A 
black males ~40
intracranial pressure, headache, scotomas, vomiting
BP >200/120 mmHg
proteinuria, microscopic hematuria
fibrinoid necrosis of arterioles
proliferation of intimal cells in small arteries
hyperplastic arteriosclerosis 
     *onion-skin appearance*
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7
Q

anti-GBM disease

A

More common in men as their GBM is thicker
associated with smoking
Tx by plasmapheresis

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8
Q

podocyte disease

A

??

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9
Q

crescentic nephritis

A

proliferative parietal epithelial cells, exudate, leaked plasma, visible crescent in BS

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10
Q

slit pore diaphragm disease

A

??

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11
Q

patterns and locations of immune complexes & diagnostic examples

A

mesangial - IgA nephropathy
subepithelial - post strep. glomerulonephritis
subendothelial - lupus

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12
Q

foot processes

A

part of pedicles - interdigitates with another

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13
Q

mesangium

A

mesanchymal cells
phagocytic
contractile
produce mesangial matrix

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14
Q

GBM

A

glomerular basement membrane

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15
Q

parlecan

A

basement membrane

highly charged w/heparan sulfate

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16
Q

entactin

A

basement membrane

Ca++ binding

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17
Q

fibronectin

A

basement membrane

high MW - binds collagen, heparan sulfate, integrins

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18
Q

laminin

A

basement membrane - binds type IV collagen, entactin, heparan sulfate, and cells

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19
Q

type IV collagen location & 2 types

A

basement membrane
alpha3, alpha4, alpha5 (IV)
alpha5, alpha5, alpha6 (IV)

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20
Q

noncollagenous domain of alpha3 (IV) chain

A

antiodies attack in Goodpasture’s

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21
Q

nephrin

A

transmembrane - major component of slit pore diaphragm. disulfide bridges

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22
Q

podocin

A

part of split pore diaphragm

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23
Q

metabolic (diabetic) nephropathy

A

hyperglycemia -> glycosylation of proteins
they get trapped in GBM, stim new GBM
GBM thickened
AGE & AOPP

24
Q

diabetic protein glycosylation

A

non-enzymatic due to high glc

25
Q

hemodynamic glomerular injury

A

pressure -> physical injury

26
Q

diffuse vs focal glomerular disease

A

diffuse - most or all glomeruli

focal - few glomeruli

27
Q

global vs segmental glomerular disease

A

global - the whole thing(s)

segmental - part of it (them)

28
Q

proliferative glomerulonephritis

A

cells grow

29
Q

membranous nephropathy

A

membrane thickening

30
Q

membranoproliferative glomerulonephritis

A

both proliferative and membrane thickening

31
Q

pauci-immune glomerulonephritis

A

no immunofluorescence
most patients have ANCA

pANCA
cANCA

32
Q

glomerulosclerosis

A

fibrous replacement of the glomerulus

33
Q

glomerular basement membrane layers

A 
lamina lucida/rara (close to endothelial cells)
lamina densa (double usual thickness)
lamina rara externa (close to epithelial cells)
34
Q

non-glomerular basement membrane layers

A 
lamina rara (close to endothelial cells)
lamina densa
35
Q

Goodpasture syndrome

A

antibodies against alpha3 (IV) non-collagenous NC domain

36
Q

antibodies to non-collagenous collagen

A

antibodies against alpha3 (IV) non-collagenous NC domain

37
Q

how is African sleeping sickness circumvented?

A

Disease is caused by Trypanosoma brucei rhodesiense

variant apoL1 doesn’t bind trypanosomal protein, which would ordinarily lyse parasites.

Mutation associated with focal segmental glomerulosclerosis

38
Q

foot process effacement

A

long segments of a capillary are covered by a single podocyte - no longer interigitating foot processes

39
Q

nephrotic syndrome

A

severe loss of protein through slit pore diaphragms - shows effacement

40
Q

FAT & cadherin function

A

binds adjacent pedicles

41
Q

nephrin

A

transmembrane
filtration role in slit-pore diaphragm
disulfide bridges

42
Q

IgA nephropathy

A

abnormal IgA - uncapped in hinge region
reduced negative charge allows filtration
binds IgA, fibronectin, CD89 (soluble IgA receptor), transferrin receptor (CD71) on mesangial cells
compliment activated 75% lectin, 25% alt.
anaphylotoxins, injury/inflammation

43
Q

immune-mediated glomerular disease

A

fixed or planted antigens
directly toxic or (more likely) elicit leukocyte damage
platelets aggregate
IL-1 release, arachidonic acid metabolytes, NO, endothelin

44
Q

large circulating immune complexes give this appearance microscopically

A

wire loops - can’t evenly distribute on basement membrane

45
Q

streptococcal antigens appearance

A

planted - formed in place

subepithelial location

46
Q

poststreptococcal eglomerulonephritis (abs against what?)

A

streptococcal exotoxin B
streptococcal GAPDH
endostroptosin

47
Q

subepithelial humps inimmunofluorescence (suggest what?)

A

post-streptococcal glomerulonephritis

48
Q

anti-GMB immunofluorescence pattern

A

linear pattern on GMB

49
Q

4 stains and their uses in glomerulonephropathy

A

Hematoxylin & eosin (routine)

Jones methenamine silver (basement membranes)

periodic acid schiff (PAS) (cellular cytoplasmic inclusions)

trichrome (collagen)

50
Q

pANCA
cANCA

(associations)

A

pANCA - microscopic polyangiitis or Churg-Strauss

cANCA - Wegener’s

51
Q

AGE

A

advanced glycolation end-products

seen in diabetic/metabolic glomerular injury

leads to ROS, podocyte injury, apoptosis

52
Q

AOPP

A

advanced oxidation protein products

seen in diabetic/metabolic glomerular injury

leads to ROS, podocyte injury, apoptosis

53
Q

flea-bitten kidney

A

small vessel ruptures over kidney (htn)

54
Q

scotomas

A

spots before eyes (htn)

55
Q

% children’s glomerular disease primary

% adults’ glomerular disease primary

A

95% children

60% adults

56
Q

onion-skin-like appearance

A

hyperplastic artherosclerosis

seen in malignant htn

UTHSC M2016 CBD - Renal (7 decks)

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