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GIR Test 2 > B5.039 - Pathology of Glomerular Disease COPY > Flashcards

B5.039 - Pathology of Glomerular Disease COPY Flashcards

1
Q
A

HTN intimal thickening

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2
Q
A

FSGS

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3
Q

systemic diseases that can cause nephrotic syndrome

A

DM

amyloidosis, MIDD

SLE

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4
Q
A

response to sytemic IFN

collapsing Glomerulopathy

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5
Q
A

FSGS

foot process effacement

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6
Q

what is familial mediterranean fever

A

pyrin mutation, chronic inflammatory disease causing amyloidosis (AA protein)

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7
Q

what is nephrotic syndrome

A

proteinuria >3.5 gm/day

hypoalbuminemia

edema

hyperlipidema

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8
Q

what is TMA

A

microvascular disease associated with microangiopathic hemolytic anemia and thrombocytopenia

disease characterized by non inflammatory injurt to small vessels, associated with fibrinoid necrosis, thrombosis, intima/subintimal edema, RBC extravasation and fragmentation

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9
Q

what is TTP

A

syndrome characterized by hemolytic anemia, thrombocytopenia, uremia, fever, mental status changes

comes from altered levels of activities of a metalloproteinase ADAMTS13 which normally cleaves vWF preventing formation of ultra large multimers

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10
Q

pathology of accelerated HTN

A

vessels show features of TMA, intimal edema. mural fibrinoid necrosis, RBC extravasation and fragmentation, thrombosis

TMA especially prominent in arteries

TMA changes with proliferation superimposed on chronic changes can create exaggerated layered appearance (onion skinning)

glomeruli - capillary thrombi, endothelial swelling, necrosis

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11
Q

decribe minimal change presentation

A

podocyte effacement leading to nephrotic syndrome, responsive to steroids usually

proteinuria usually albumin

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12
Q

diseases that primarily affect glomerluli that cause nephrotic syndrome

A

membranous glomerulopathy

minimal change disease

FSGS

IgAN, MPGN…

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13
Q
A

interstitial fibrosis in diabetic nephropathy

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14
Q
A

membranous glomerulopathy

note the little holes where the immune complexes are and the spiky reactive BM formation

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15
Q

morphologic classification of FSGS pathology

A

collapsing glomerulopathy - HIV, poorer prognosis

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16
Q

nephritis

A

hematuria, mild mid proteinuria, HTN, increased sCr, active urine sediment

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17
Q
A

massively swollen proximal tubule

membranous glomerulopathy

dots of protein resorption droplets, trying to absorb all the protein

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18
Q
A

amyloidosis

note waxy apperance of thickened GBM

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19
Q

what is HUS

A

syndrome characterized by hemolytic anemia, thrombocytopenia, uremia

associated with Shiga toxin or shiga like toxin

70% are EHEC (O157:H7) conatminated food most common

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20
Q

pneumonic for remembering risk factors for FSGS

A

Risk factors associated with FSGS can be remembered with the mnemonic MOSAIC*:

Minority (African American or Hispanic)
Obesity
Sickle cell disease
AIDS (HIV) / APOLI1 gene
IV drug abuse (heroin) and Interferon treatment
Chronic kidney disease (secondary to congenital absence or surgical removal)

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21
Q

clinical risk of membranous glomerulopathy

A

renal vein thrombosis, if you see a super full vein then think of that

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22
Q

etiologies of TMA

A

HUS

aHUS

Autoimmune

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23
Q

symptoms of accelerated HTN

A

visual disturbances, headache,stroke, dyspnea

hematuria, proteinuria, coombs negative hemolytic anemia, thrombocytopenia

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24
Q

what pathology is associated with garland, lei pattern stain for IgG and C3

A

membranous glomerulopathy

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25
Q

clinical presentation of amyloidosis

A

proteinuria, nephrotic syndrome, cardiac involvement (arrhythmia, HF), fatigue, weight loss, peripheral neuropathy, hepatomegaly

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26
Q

pathology of amyloidosis

A

diffuse expansion of mesangium/capillary loop basement membranes by waxy deposits

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27
Q

pathology of FSGS

A

segmental solidification of capillary tufts

PAS and silver +

intracapillary foam cells and swollen podocytes

biopsy might be falsley negative

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28
Q

accelerated HTN can give you what

A

TMA

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29
Q

compare and contrast minimal change, FSGS and membranous glomerulopathy epidemiology

A

minimal change mostly in kids

FSGS mostly adults

membranous glomerulopathy mostly adults

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30
Q

describe EM and IF for membranous glomerulopathy

A

IgG and C3 staining in garland or lei pattern

EM - subepithelial and/or intramembranous electron dense deposits with GBM projections

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31
Q

causes of HTN

A

most are essential aka unknown

some secondary to renal artery stenosis, kindey issues, aldosteronism

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32
Q

HUS epidemiology

A

usually children, summer, prodromal bloody diarrhea occasionaly UTI

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33
Q

clinical scenario of membranous glomerulopathy

A

proteinuria, nephrotic syndrome

most common in adult males, early 50s onset

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34
Q
A

wrinkling of GBM, a sign of chronic ischemia seen in chronic HTN

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35
Q
A

thickened tubular basement membranes

diabetic nephropathy

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36
Q
A

course granular deposits of IgG classic for membranous glomerulopathy

37
Q
A

diabetic nephropathy

38
Q
A

collapsing glomerulopathy (FSGS) HIV associated

39
Q
A

congo red stain with apple green birefringence a charcteristic of amyloid deposition

40
Q
A

chronic HTN glomerulosclerosis

41
Q

accelerated HTN

A

malignant, organ damage

42
Q
A

collapsing glomerulopathy

HIV associated

43
Q

what can slow progression of diabetic nephropathy

A

glycemic control and HTN control

44
Q
A

membranous glomerulopathy

little holes, reactive BM spikes

45
Q

diabetic nephropathy histo findings

A

glomeruli - GBM thickening, diffuse mesangial expansion, kimmelstiel wilson nodules, hyalin insudative lesions

vasculature - arteriosclerosis, afferent & efferent

tubulointerstitium - interstitial fibrosis and tubular atrophy, thickened tbm, inflammation

46
Q
A

artery shows intimal thickening due to edema from acute HTN

47
Q

renal disease risk factors for death

A

DM

48
Q

pathogenesis of amyloidosis

A

glomerular/vascular deposition of amyloid (abnormal protein with beta pleated sheet structure) detected by congo red stain usually containing clonal immunoglobulin light chain lambda

49
Q

most amyloidosis is caused by what

A

AL Ig light chain usually associaed with myeloma (CRAB)

50
Q

histo of benign HTN kidney disease

A

arteriosclerosis-fibrous intimal thickening

afferent arteriolar hyalinosis

interstitial fibrosis and tubular atrophy

glomeruli have wrinkling early on then glomerulosclerosis

51
Q

AA amyloidosis

A

associated with chronic inflammatory state

RA

inflammatory bowel disease

Familial mediterranean fever

52
Q

diabetic nephropathy pathophysiology

A

hyperfiltration and hyperperfusion (increased glomerular capillary pressure)

mitochondrial defect resulting in increased ROS

AGE products alter GBM and matrix biochem

53
Q

risk factors for developing diabetic nephropathy

A

smoking, low GFR, duration of disease

microalbuminuria

54
Q

causes of secondary membranous GN

A

drugs - penicillamine, NSAID, gold

Infx - HBV, HCV, syphilis

neoplasm - lung, colon

autoimmune - class V SLE, thyroiditis

55
Q
A

chronic HTN

solidified glomeruli

56
Q
A

membranous glomerulopathy

note the little circles, thats the antibody/Ag deposition (immune complexes done pick up stain)

57
Q
A

hyalinosis of HTN insudate in small arteriole

58
Q

pathology of membranous glomerulopathy

A

diffuse global thickening of GBM, GBM spikes when capillaries cut in cross section; holes or vacuoles when cute tangentially

segmental glomerulosclerosis

59
Q
A

amyloid doesnt stain dark these types of stains

note mesangial expansion

60
Q
A

subepithelial deposits, membranous glomerulopathy

61
Q

how does nephrotic syndrome occur

A

abnormalities in the glomerular filtration layer

62
Q

describe hypertensive kidney disease

A

25% of ESRD

elevated - 120-29/80

stage 1 - 130-39 or 80-89

stage 2 >140 or >90

63
Q

pathophys of HTN kidney disease

A

hemodynamic changes

medial/intimal thickening of vessels, endothelial injury

afferent arteriolar hyalinosis

64
Q
A

onion skin vessel from TMA due to malingnant HTN

65
Q

chronic HTN

A

benign

mostly asymptomatic

in kidney characterized by microalbuminuria, decline in eGFR

can cause nephrotic syndrome

66
Q
A

minimal change

podocyte effacement

67
Q

pathophys of accelerated HTN

A

injury to microvasculatrue

stimulatino of RAA

endothelial injury and dysfunction

thrombotic microangiopathy

68
Q
A

Edematous intima, fibrinoid material in intima

acute HTN

69
Q

9th leading cause of death in US

A

kidney disease

70
Q

minimal change disease epidemiology

A

most common cause of nephrotic syndrome in kids

may have transient decline in GFR

71
Q
A

HTN

intimal thickening

72
Q

EM and IF of FSGS

A

IF - non specific trapping

EM - foot process effacement

73
Q
A

Diabetic nephropathy

severe mesangial expansion

74
Q

collapsing glomerulopathy

A

classically associated with HIV

collapsed glomeruli, tubular microcysts, tubular reticular inclusions

75
Q

what causes ESRD in US

A

DM - 38%

HTN - 24%

Glomerulonephritis - 15%

76
Q
A

thick glomerular basement membrane

diabtetic nephropathy

77
Q

syndrome of diabetic nephropathy

A

persistent albuminuria >300 mg/d

declining GFR

HTN

78
Q

light, IF and EM of minimal change

A

only EM shows something, diffuse foot process effacement

79
Q
A

diabetic nephropathy

K - W nodule

80
Q
A

FSGS

81
Q

pathophys of membranous glomerulopathy

A

in situ immune complex formation

organ specific autoimmune disorder

autoantibody directed againts PLA2R on podocytes

Ag/Ab complexes shed from podocyt to subepithelial GBM

82
Q
A

amyloidosis AL type lambda

83
Q
A

amyloidosis looks like a ball of hair

84
Q

labs/clinicl features of membranous glomerulopathy

A

microscopic hematuria

serum complement normal

natural hx variable, 1/3 sponaneouslt remit

85
Q
A

TMA

could be due to any of the causes

intimal expanded, intimal edema, fibrin

86
Q

aHUS pathophys and symptoms

A

abherant activation of the alternative complement pathway

mutation in factor H a main driver

or acquired

autoantibody to factor H (which inactivates C3 convertase)

uremia, thrombocytopenia, hemoltyic anemia

87
Q
A

membranous glomerulopathy

note the really thick basement membrane, normal cellularity

88
Q

classification of FSGS

A

primary - idiopathic

viral - HIV, parvo

drugs - heroin, IFN alpha, lithium

maladaptive structue/fxn response

89
Q
A

TMA

glomerular capillaries large and distended by thrombi

GIR Test 2 (17 decks)

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