Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Renal > Nephrotic Syndrome 2 > Flashcards

Nephrotic Syndrome 2 Flashcards

(52 cards)

Start Studying
1
Q

What are the 2 podoctyopathies?

A

minimal change disease and focal segmental glomerulosclerosis

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

Who usually gets minimal change disease?

A

very young and very old - bimodal distribution

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

What is the most common cause of nephrotic syndrome in kids?

A

minimal change disease

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

What other clinical findings are common in minimal change disease?

A
  1. insidious onset of edema
  2. normal blood pressure
  3. usually normal renal function
  4. highly selective proteinuria - albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is thought to be the pathogenesis for minimal change disease?

A

not clear but thought to be mediated by a T cell that secretes a circulating permeability factor that causes podocyte damage

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

What is seen w/ minimal change disease for pathology?

A

effacement and detachment of foot processes

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

What is the treatment for minimal change disease?

A

oral glucocorticoids

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

Who responds well to steriods in minimal change disease?

A

kids

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

If there is a poor response to steroids what should be done?

A
  1. look for other cause (especially in children)

2. unsampled focal segmental glomerulosclerosis

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

What are some clinical findings for focal segmental glomerulosclerosis?

A
  1. high BP

2. low albumin –> proteinuria

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

How many of the pts w/ focal segmental glomerulosclerosis develop end stage kidney disease?

A

50%

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

What is Supar?

A

the circulating factor that binds to beta2 integrin and causes effacement of podocytes

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

What are some secondary causes of focal segmental glomerulosclerosis?

A
  1. familial – mutation in genes alpha-actinin-4, podosin, TRCP6, and APOL1
  2. infection - HIV or Parvo virus
  3. drugs - pamidronate, heroin, Li
  4. Loss of nephron mass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why are people of African descent susceptible to getting focal segmental glomerulosclerosis?

A

b/c 40% of them have mutations in APOL1 making them susceptible to African sleeping sickness

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

Why does hyalinosis occur in FSG?

A

accumulation of leaked plasma proteins and lipids

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

T or F. Adhesion of involved segment to Bowman Capsule does occur in FSG?

A

T

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

What are subtypes of FSG?

A
  1. collapsing
  2. cellular
  3. tip
  4. Perhiliar
  5. not otherwise specified (42%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which of the subtypes of FSG will most likely obtain remission?

A

Tip

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

What is found in the collapsing type of FSG?

A

collapsed BM and adhesions common

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

What shows up on immunofluoresence for FSG?

A

nothing really

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

What is the treatment for FSG?

Study These Flashcards
A

sterois and immunosuppressive

22
Q

what immunosuppressive drugs are used for FSG?

Study These Flashcards
A

calcinuerin inhibitors – cyclosporine and tacrolimus

23
Q

What is steroid sensitivity for FSG?

Study These Flashcards
A
  1. Steroid Sensitive - proteinuria remits w/ treatment and means good prognosis
  2. Sterois resistant - proteinuria persists and means bad prognosis
24
Q

What happens to repeated relapses of Minimal change disease in children w/ steroid responsive nephrotic syndrome?

Study These Flashcards
A

may develops into FSG secondar to repreated renal injury

25
What is the filtered cationic Ag formation of membranous nephropathy?
deposits from circulation cross endothelium and GBM and localize in the subepithelial spaces, then Abs localize and cause nephritis
26
What is the Autoimmunity model of in-situ formation of membranous nephropathy (MN)?
locally generated Ag and filtered AutoAb
27
What are examples of autoimmunity model?
1. M-type Phospholipase A2 Recepto (PLA2R) -- Primary MN | 2. Neutral endopeptidase (NEP) - target Ag in congentical MN
28
How is PLA2R involved in primary MN?
- expressed by podocytes in normal human glomeruli | - found to be co-localized w/ IgG4 in immune deposits in glomeruli of patients w/ idiopathic MN
29
What are some secondary diseases taht MN is associated w/?
1. infection - Hep B, syphilis, Malaria 2. Autoimmune - SLE 3. Drugs - Gold, penicillamine, captopril, NSAID 4. Malignancy - lung cancer, colon cancer, melanoma
30
What is the most common cause of nephrotic syndrome in Caucasian adults?
Membranous nephropathy
31
What is the epidemiology of MN?
- peaks in 4th to 6th decades | - males commonly affected
32
What happens to pts w/ MN?
1. spontaneous resolution in 30% 2. progressive renal failure in 40% 3. presistent proteinuria w/ variable renal dysfuntion in 30%
33
What are risk factors for loss of renal function in MN?
1. male 2. >10g/24 hrs of proteinuria 3. HTN 4. Azotemia 5. Tubulointerstitial fibrosis 6. glomerulosclerosis
34
What do you see on light microscopy for MN?
thickened BM w/out increased cellularity
35
What do you see w/ immunofluorescence in MN?
granular deposits of IgG and complement
36
What would you see on electron microscopy for MN?
diffusely thickened BM w/ subepithelial deposits separated by spikes of new GBM --> spike and dome pattern
37
Is there inflammation found in MN?
no -- remember it's nephrotic! complement that you see is activated at a site that is not in contact w/ circulating inflammatory cells
38
What happens if MN is secondary to another disease?
resolution of subepithelial depotis is slow w/ concomitant slow resolution of proteinuria -- up to 2 yrs
39
What is the likely mechanism for the retraction and effacement of podocyte foot processes in subepithelial deposits?
-complement dependent process mediated by MAC and intermediary chemotactic fragments are washed away into urinary space
40
What are the clinical findings w/ post-infectious glomerulonephritis? (PIGN)
- usually associated w/ recent infection - gross hematuria - HTN common - signs of fluid retention --peripheral edema, ascites - proteinuria - impaired renal function
41
What are the lab result findings for PIGN?
- low C3 and C4 - elevated anti-streptolysin O titers if preceded by throat infection - elevated anti-DNAse B titers if preceded by skin infection - positive blood culture in sepsis
42
What is seen on light microscopy for PIGN?
- diffuse endocapillary proliferation and infiltration by numerous PMNS
43
What is seen on immunofluorescence for PIGN?
diffuse grandular deposits in capillary walls and mesangium (IgG and C3)
44
What is seen on EM for PIGN?
subepithelial humps
45
What are supportive measures for PIGN?
- control HTN w/ antihypertensives and diuretics - renal replacement therapy if sever kidney dysfunction - treat infection
46
How long does it take to resolve the HTN?
a few weeks
47
How long to get normal C3 levels
6 wks
48
how long to resolve hematuria
w/in 12 months
49
Summary -- What is seen w/ the different kidney biopsies for minimal change disease?
LM- normal Immuno - normal EM - podocyte foot process fusion
50
Summary -- What is seen w/ the different kidney biopsies for focal segmental glomerulosclerosis?
- LM - scarring and adhesion to Bowman's Capsule - Immuno - normal - EM - podocyte foot process fusion
51
Summary -- What is seen w/ the different kidney biopsies for MN?
LM - diffuse thickening of glomerular BM w/ normal cellularity Immuno - fine granular w/ IgG and complement EM - subepithelial deposits
52
Summary -- What is seen w/ the different kidney biopsies for PIGN?
LM- proliferation , inflammation Immuno- granular deposition of C3 and IgG EM - subepithelial humps

Renal (33 decks)

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