Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Renal Path MC > Renal 4 > Flashcards

Renal 4 Flashcards

(88 cards)

Start Studying
1
Q

characterizes diabetes kidney problems (early on)

A

glomerulosclerosis (hyaline deposits)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

3 syndromes associated with glomerulosclerosis in diabetes

A

non-nephrotic proteinuria, nephrotic syndrome, CRF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

changes other than glomerulosclerosis that is associated with diabetes

A

afferent/efferent arteriolar sclerosis, papillary necrosis (increased infection), tubular lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

responsible for thickening of BM in diabetes

A

increased collagen IV and fibronectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

hallmark of diabetic nephropathy; what is stain for matrix deposits?

A

nodular glomerulosclerosis (Kimmelstiel-Wilson disease); PAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

clinical features of diabetic nephropathy

A

microalbuminemia, overt proteinuria, progressive loss GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

most common type of GN worldwide

A

IgA nephropathy (Berger’s disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

vasculitis from IgA deposition -> purpuric skin lesions, renal disease also

A

Henoch-Schnolein purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

renal manifestations of HSP

A

hematuria, proteinuria, nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is defective in Alport syndrome?

A

type IV collagen synthesis -> defective BM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

this causes hyalinosis and sclerosis in FSGN

A

entrapment plasma proteins with increased ECM deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

hyaline thickening of what in FSGS?

A

afferent arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

glomerular disease characterized by nonselctive proteinuria, hematuria, reduced GFR, HTN -> no response to corticosteroids, no immune complexes

A

focal segmental glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

condition in which you see sub-epithelial spikes

A

membranous GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

irregular dense deposits that occur in membranous GN with loss of foot processes

A

sub-epithelial spikes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

seen on immunofluorescence of membranous GN

A

granular deposits containing Ig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

these are present in granular deposits of membranous GN

A

Ig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

where are granular deposits located in membranous GN

A

between BM and epithelium (sub-epithelial spikes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ab to these structures is responsible for idiopathic membranous GN

A

podocyte membrane antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

causes of membranous GN

A

Ab podocyte membrane antigens, SLE, hep B, drugs, malignant tumors, diabetes/thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

this occurs in mixed nephrotic and nephritic disease (membranoproliferative GN)

A

thickened BM, increased mesangial cells and matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

varying degrees of membranoproliferative GN

A

asymptomatic hematuria, nephrotic syndrome w/ hematuria, decreased GFR/azotemia and HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

morphology of major changes seen in membranoproliferative GN

A

BM alterations, proliferation glomerular cells, leukocyte infiltration, proliferating mesangial cells and increased matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is present in granular deposits in Type I of membranoproliferative GN

A

complement w/ or w/o Ig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
where are granular deposits seen in type 1 membranoproliferative GN
subendothelial
26
this renal disease causes "tram tracking" and sub endothelial deposits
type I MPGN
27
mesangial cells interspersed between old and new BM (as result of reduplication of membranes)
tram-tracking
28
morphology of type II MPGN
dense deposition w/in BM proper, complement (NOT in deposits), no IgG
29
this glomerular disease causes profound hypocomplementemia (activation of classic and alternative pathway)
MPGN
30
major cause of MPGN
SLE
31
causes of MPGN
idiopathic, chronic immune complex disorder, SLE, hepatitis, HIV, malignant disease, hereditary complement deficiency
32
glomerular diseases that are primarily nephritic
acute proliferative GN, focal proliferative and necrotizing GN, RPGN
33
nephritic disease characterized by mesangial infiltration of cells and deposition of protein
acute proliferative GN
34
morphology of acute proliferative GN
immune complex deposition, proliferation glomerular cells, influx leukocytes, granular deposits Ig/complement
35
this causes hypercellularity of acute proliferative GN
leukocyte infiltration, proliferation endothelial and mesangial cells
36
most common cause of acute proliferative GN
post-strep GN
37
signs/symptoms of acute proliferative GN
red cell casts, mild proteinuria, periorbital edema, moderate HTN, oliguria
38
condition with sub epithelial humps
acute proliferative GN
39
kind of deposits present in acute proliferative GN
subepithelial humps
40
onset of post-strep GN in adults
sudden HTN, edema, elevated BUN
41
can cause focal proliferative and necrotizing GN
SLE, Henoch-Schonlein purpura, Goodpasture's, IgA nephropathy
42
these make up crescent that fills Bowman's space in rapidly progressive GN
infiltrating leukocytes and proliferating epithelial cells
43
morphology of RPGN
obliteration Bowman's space, fibrinogen/fibrin strands/scaffold, ruptures of BM, infiltrating leukocytes, proliferating epithelial cells
44
antibodies in micro-polyarteritis nodosa (can cause type 3 RPGN)
p-ANCA
45
most common type of RPGN in 40+ age group
type 3 (pauci immune...micro-PAN or Wegener's)
46
most common type of RPGN in 10-40 age group
type 2 (immune complex)
47
these glomerular diseases commonly progress to chronic GN
focal sclerotic and RPGN
48
morphology of chronic GN
contracted/scarred kidneys, hyaline obliteration glomeruli, afferent arterial sclerosis, tubule atrophy, interstitial fibrosis, lymphocyte infiltration
49
immunofluorescence of Goodpasture's
linear deposits Ig and complement
50
manifestation of renal Goodpasture's; lung manifestation
proliferating GN; necrotizing hemorrhagic interstitial pneumonitis
51
Ab against this in Goodpasture's disease
non-collagenous part BM collagen type IV
52
environmental exposures that act as co-factors in Goodpastures' disease
hydrocarbon solvents, virus infection, smoking
53
this is treatment for Goodpastures -> removes circulating Ab and inflammatory cytokines
plasma exchange
54
GN associated with URT infections/manifestations
Wegeners
55
associated findings with focal lesions of Wegener's
hematuria and proteinuria
56
treatment for Wegener's
immunosuppressive meds
57
2 forms of Wegener's renal disease
focal necrotizing GN OR diffuse necrosis, proliferation, and crescent formation
58
SLE Ab associated with renal disease
anti-DSS
59
signs/symptoms of combination of nephrotic/nephritic most commonly seen in SLE
recurrent hematuria, acute nephritis, CRF, HTN
60
3 kinds of renal lesions seen in SLE
focal, diffuse proliferative, or diffuse membranous GN
61
key pathologic features of renal SLE
mesangial and endocapillary proliferation, membranous change -> membranous GN or MPGN I (sub endothelial deposits Ig and complement)
62
morphology of glomerular membrane change in diabetes
BM thickening, decreased heparan sulfate (loss negative charge), non enzymatic glycosylation proteins
63
3 main components of pathogenesis of renal involvement in diabetes
thickened/leaky BM, increased mesangial matrix, progressive GS (hemodynamic abnormalities)
64
result of sclerosis (as seen in diabetic nephropathy)
decreased GFR, increased glomerular filtration area, increased glomerular capillary pressure, glomerular hypertrophy
65
nephropathy in which mesangial area expands to fill entire glomerulus, ovoid/spherical hyaline masses in periphery of glomerulus, matrix deposits continuous w/ hyaline thickening of arterioles
diabetes
66
late lesions of diabetic nephropathy
ischemic tubular atrophy, interstitial fibrosis, contraction of kidney, papillary necrosis with increased pyelonephritis
67
these can slow progression of diabetic nephropathy
ACE inhibitors
68
characteristic of Henoch-Schonlein purport and IgA nephropathy
mesangial IgA deposits
69
precedes IgA nephropathy/Berger'd disease in children/young adults
respiratory, GI infection, lower urinary infection
70
associated conditions with IgA nephropathy/Berger's disease -> increased IgA synthesis
mucosal infections, celiac disease
71
morphology of IgA nephropathy/Berger's disease
mesangial hypercellularity, increased mesangial matrix with IgA and C3
72
where are purpura located in HSP? what causes them?
extensor surface arms/legs, buttocks; necrotizing vasculitis
73
signs/symptoms of Henoch-Schonlein purport (after infection...mostly 3-8 y.o)
purpuric skin lesions, GI pain/vomiting/bleeding, non migrating arthralgia, hematuria/proteinuria/nephrotic syndrome
74
Alport syndrome renal manifestations
glomerular segmental proliferation or sclerosis, hematuria (varying progression to end stage renal disease)
75
this is defect in hereditary nephritis/thin membrane disease
collagen
76
glomerular disease with subepithelial spikes
membranous
77
glomerular disease with subepithelial humps
immune complexes (acute proliferative, post-strep)
78
glomerular disease with sub endothelial deposits
SLE, MP type I
79
glomerular disease with sub endothelial deposits w/ duplication of the membrane (tram tracking)
MP type II
80
glomerular disease with effacement of podocyte foot processes
minimal change disease/lipoid nephrosis
81
glomerular disease with areas of thickened and thinned basement membrane
Alport's disease
82
conditions with increased mesangial matrix
diabetes, IgA nephropathy
83
Ab present in MPGN type II
C3NeF Ab to C3 convertase
84
stain for crescentic disease
fibrinogen
85
condition with ANA antibody
SLE
86
condition with c-ANCA antibody
Wegener's
87
Ab present in post-streptococcal GN
anti-streptolysin O
88
hepatitis B surface antigen associated with this glomerular disease
membranous GN

Renal Path MC (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions