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

B5.039 - Pathology of Glomerular Disease COPY Flashcards

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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
clinical presentation of amyloidosis
proteinuria, nephrotic syndrome, **cardiac involvement (arrhythmia, HF)**, fatigue, weight loss, peripheral neuropathy, **hepatomegaly**
26
pathology of amyloidosis
diffuse **expansion of mesangium**/capillary loop basement membranes by **waxy deposits**
27
pathology of FSGS
segmental solidification of capillary tufts PAS and silver + **intracapillary foam cells** and swollen podocytes biopsy might be falsley negative
28
accelerated HTN can give you what
TMA
29
compare and contrast minimal change, FSGS and membranous glomerulopathy epidemiology
minimal change mostly in kids FSGS mostly adults membranous glomerulopathy mostly adults
30
describe EM and IF for membranous glomerulopathy
IgG and C3 staining in garland or lei pattern EM - subepithelial and/or intramembranous electron dense deposits with GBM projections
31
causes of HTN
most are essential aka unknown some secondary to renal artery stenosis, kindey issues, aldosteronism
32
HUS epidemiology
usually children, summer, prodromal bloody diarrhea occasionaly UTI
33
clinical scenario of membranous glomerulopathy
proteinuria, nephrotic syndrome most common in adult males, early 50s onset
34
wrinkling of GBM, a sign of chronic ischemia seen in chronic HTN
35
thickened tubular basement membranes diabetic nephropathy
36
course **granular** deposits of IgG classic for membranous glomerulopathy
37
diabetic nephropathy
38
collapsing glomerulopathy (FSGS) HIV associated
39
congo red stain with apple green birefringence a charcteristic of amyloid deposition
40
chronic HTN glomerulosclerosis
41
accelerated HTN
malignant, organ damage
42
collapsing glomerulopathy HIV associated
43
what can slow progression of diabetic nephropathy
glycemic control and HTN control
44
membranous glomerulopathy little holes, reactive BM spikes
45
diabetic nephropathy histo findings
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
artery shows intimal thickening due to edema from acute HTN
47
renal disease risk factors for death
DM
48
pathogenesis of amyloidosis
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
most amyloidosis is caused by what
AL Ig light chain usually associaed with myeloma (CRAB)
50
histo of benign HTN kidney disease
arteriosclerosis-fibrous intimal thickening afferent arteriolar hyalinosis interstitial fibrosis and tubular atrophy glomeruli have wrinkling early on then glomerulosclerosis
51
AA amyloidosis
associated with chronic inflammatory state ## Footnote **RA** **inflammatory bowel disease** **Familial mediterranean fever**
52
diabetic nephropathy pathophysiology
hyperfiltration and hyperperfusion (increased glomerular capillary pressure) mitochondrial defect resulting in increased ROS AGE products alter GBM and matrix biochem
53
risk factors for developing diabetic nephropathy
smoking, low GFR, duration of disease microalbuminuria
54
causes of secondary membranous GN
drugs - penicillamine, NSAID, gold Infx - HBV, HCV, syphilis **neoplasm - lung, colon** autoimmune - class V SLE, thyroiditis
55
chronic HTN solidified glomeruli
56
membranous glomerulopathy note the little circles, thats the antibody/Ag deposition (immune complexes done pick up stain)
57
hyalinosis of HTN insudate in small arteriole
58
pathology of membranous glomerulopathy
diffuse global thickening of GBM, GBM spikes when capillaries cut in cross section; holes or vacuoles when cute tangentially segmental glomerulosclerosis
59
amyloid doesnt stain dark these types of stains note mesangial expansion
60
subepithelial deposits, membranous glomerulopathy
61
how does nephrotic syndrome occur
abnormalities in the glomerular filtration layer
62
describe hypertensive kidney disease
25% of ESRD elevated - 120-29/80 stage 1 - 130-39 or 80-89 stage 2 \>140 or \>90
63
pathophys of HTN kidney disease
hemodynamic changes medial/intimal thickening of vessels, endothelial injury afferent arteriolar hyalinosis
64
onion skin vessel from TMA due to malingnant HTN
65
chronic HTN
benign mostly asymptomatic in kidney characterized by microalbuminuria, decline in eGFR can cause nephrotic syndrome
66
minimal change podocyte effacement
67
pathophys of accelerated HTN
injury to microvasculatrue stimulatino of RAA endothelial injury and dysfunction thrombotic microangiopathy
68
Edematous intima, fibrinoid material in intima acute HTN
69
9th leading cause of death in US
kidney disease
70
minimal change disease epidemiology
most common cause of nephrotic syndrome in kids may have transient decline in GFR
71
HTN intimal thickening
72
EM and IF of FSGS
IF - non specific trapping EM - foot process effacement
73
Diabetic nephropathy severe mesangial expansion
74
collapsing glomerulopathy
classically associated with HIV collapsed glomeruli, tubular microcysts, **tubular reticular inclusions**
75
what causes ESRD in US
DM - 38% HTN - 24% Glomerulonephritis - 15%
76
thick glomerular basement membrane diabtetic nephropathy
77
syndrome of diabetic nephropathy
persistent albuminuria \>300 mg/d declining GFR HTN
78
light, IF and EM of minimal change
only EM shows something, diffuse foot process effacement
79
diabetic nephropathy K - W nodule
80
FSGS
81
pathophys of membranous glomerulopathy
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
amyloidosis AL type lambda
83
amyloidosis looks like a ball of hair
84
labs/clinicl features of membranous glomerulopathy
microscopic hematuria serum complement normal natural hx variable, 1/3 sponaneouslt remit
85
TMA could be due to any of the causes intimal expanded, intimal edema, fibrin
86
aHUS pathophys and symptoms
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
membranous glomerulopathy note the really thick basement membrane, normal cellularity
88
classification of FSGS
primary - idiopathic viral - HIV, parvo drugs - heroin, IFN alpha, lithium maladaptive structue/fxn response
89
TMA glomerular capillaries large and distended by thrombi

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