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

B5.039 - Pathology of Glomerular Disease Flashcards

1
Q

9th leading cause of death in US

A

kidney disease

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2
Q

what causes ESRD in US

A

DM - 38%

HTN - 24%

Glomerulonephritis - 15%

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3
Q

syndrome of diabetic nephropathy

A

persistent albuminuria >300 mg/d

declining GFR

HTN

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4
Q

renal disease risk factors for death

A

DM

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5
Q

risk factors for developing diabetic nephropathy

A

smoking, low GFR, duration of disease

microalbuminuria

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6
Q

what can slow progression of diabetic nephropathy

A

glycemic control and HTN control

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7
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

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8
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

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9
Q
A

Diabetic nephropathy

severe mesangial expansion

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10
Q
A

diabetic nephropathy

K - W nodule

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11
Q
A

diabetic nephropathy

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12
Q
A

interstitial fibrosis in diabetic nephropathy

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13
Q
A

thickened tubular basement membranes

diabetic nephropathy

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14
Q
A

thick glomerular basement membrane

diabtetic nephropathy

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15
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

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16
Q

causes of HTN

A

most are essential aka unknown

some secondary to renal artery stenosis, kindey issues, aldosteronism

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17
Q

chronic HTN

A

benign

mostly asymptomatic

in kidney characterized by microalbuminuria, decline in eGFR

can cause nephrotic syndrome

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18
Q

accelerated HTN

A

malignant, organ damage

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19
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

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20
Q
A

HTN

intimal thickening

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21
Q
A

HTN intimal thickening

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22
Q
A

hyalinosis of HTN insudate in small arteriole

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23
Q
A

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

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24
Q
A

chronic HTN

solidified glomeruli

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25
Q
A

chronic HTN glomerulosclerosis

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26
Q

pathophys of HTN kidney disease

A

hemodynamic changes

medial/intimal thickening of vessels, endothelial injury

afferent arteriolar hyalinosis

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27
Q

symptoms of accelerated HTN

A

visual disturbances, headache,stroke, dyspnea

hematuria, proteinuria, coombs negative hemolytic anemia, thrombocytopenia

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28
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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29
Q
A

artery shows intimal thickening due to edema from acute HTN

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30
Q
A

Edematous intima, fibrinoid material in intima

acute HTN

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31
Q
A

onion skin vessel from TMA due to malingnant HTN

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32
Q

pathophys of accelerated HTN

A

injury to microvasculatrue

stimulatino of RAA

endothelial injury and dysfunction

thrombotic microangiopathy

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33
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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34
Q

etiologies of TMA

A

HUS

aHUS

Autoimmune

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35
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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36
Q

HUS epidemiology

A

usually children, summer, prodromal bloody diarrhea occasionaly UTI

37
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

38
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

39
Q
A

TMA

could be due to any of the causes

intimal expanded, intimal edema, fibrin

40
Q
A

TMA

glomerular capillaries large and distended by thrombi

41
Q

accelerated HTN can give you what

42
Q

what is nephrotic syndrome

A

proteinuria >3.5 gm/day

hypoalbuminemia

edema

hyperlipidema

43
Q

nephritis

A

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

44
Q

how does nephrotic syndrome occur

A

abnormalities in the glomerular filtration layer

45
Q

systemic diseases that can cause nephrotic syndrome

A

DM

amyloidosis, MIDD

SLE

46
Q

diseases that primarily affect glomerluli that cause nephrotic syndrome

A

membranous glomerulopathy

minimal change disease

FSGS

IgAN, MPGN…

47
Q

clinical presentation of amyloidosis

A

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

48
Q

pathology of amyloidosis

A

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

49
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

50
Q

most amyloidosis is caused by what

A

AL Ig light chain usually associaed with myeloma (CRAB)

51
Q

what is familial mediterranean fever

A

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

52
Q

AA amyloidosis

A

associated with chronic inflammatory state

RA

inflammatory bowel disease

Familial mediterranean fever

53
Q
A

amyloidosis

note waxy apperance of thickened GBM

54
Q
A

amyloid doesnt stain dark these types of stains

note mesangial expansion

55
Q
A

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

56
Q
A

amyloidosis AL type lambda

57
Q
A

amyloidosis looks like a ball of hair

58
Q

compare and contrast minimal change, FSGS and membranous glomerulopathy epidemiology

A

minimal change mostly in kids

FSGS mostly adults

membranous glomerulopathy mostly adults

59
Q

clinical scenario of membranous glomerulopathy

A

proteinuria, nephrotic syndrome

most common in adult males, early 50s onset

60
Q

labs/clinicl features of membranous glomerulopathy

A

microscopic hematuria

serum complement normal

natural hx variable, 1/3 sponaneouslt remit

61
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

62
Q
A

massively swollen proximal tubule

membranous glomerulopathy

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

63
Q

clinical risk of membranous glomerulopathy

A

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

64
Q
A

membranous glomerulopathy

note the really thick basement membrane, normal cellularity

65
Q
A

membranous glomerulopathy

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

66
Q
A

membranous glomerulopathy

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

67
Q
A

membranous glomerulopathy

little holes, reactive BM spikes

68
Q

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

A

membranous glomerulopathy

69
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

70
Q
A

course granular deposits of IgG classic for membranous glomerulopathy

71
Q
A

subepithelial deposits, membranous glomerulopathy

72
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

73
Q

causes of secondary membranous GN

A

drugs - penicillamine, NSAID, gold

Infx - HBV, HCV, syphilis

neoplasm - lung, colon

autoimmune - class V SLE, thyroiditis

74
Q

minimal change disease epidemiology

A

most common cause of nephrotic syndrome in kids

may have transient decline in GFR

75
Q

decribe minimal change presentation

A

podocyte effacement leading to nephrotic syndrome, responsive to steroids usually

proteinuria usually albumin

76
Q

light, IF and EM of minimal change

A

only EM shows something, diffuse foot process effacement

77
Q
A

minimal change

podocyte effacement

78
Q

pathology of FSGS

A

segmental solidification of capillary tufts

PAS and silver +

intracapillary foam cells and swollen podocytes

biopsy might be falsley negative

79
Q

EM and IF of FSGS

A

IF - non specific trapping

EM - foot process effacement

81
Q
A

FSGS

foot process effacement

83
Q

classification of FSGS

A

primary - idiopathic

viral - HIV, parvo

drugs - heroin, IFN alpha, lithium

maladaptive structue/fxn response

84
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)

85
Q

morphologic classification of FSGS pathology

A

collapsing glomerulopathy - HIV, poorer prognosis

86
Q

collapsing glomerulopathy

A

classically associated with HIV

collapsed glomeruli, tubular microcysts, tubular reticular inclusions

87
Q
A

collapsing glomerulopathy (FSGS) HIV associated

88
Q
A

collapsing glomerulopathy

HIV associated

89
Q
A

response to sytemic IFN

collapsing Glomerulopathy

GIR Test 2 (17 decks)

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