Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1 STEP Renal pathology > Nephrotic syndrome 12/21 > Flashcards

Nephrotic syndrome 12/21 Flashcards

1
Q

pathoma. how is characterized neohrotic?

A

proteinuria > 3,5 g/d

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

pathoma. 4 points about nephrotic

A
  1. Hypoalbuminemia –> pitting edema
  2. Hypogammaglobulinemia -> infection risk
  3. hypercoagulable state -> loss of ATIII.
  4. hyperlipidemia and hypercholesterolemia - may result in fatty casts in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hypoalbuminemia –>

A

Hypoalbuminemia –> pitting edema

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

Hypogammaglobulinemia ->

A

Hypogammaglobulinemia -> infection risk

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

hypercoagulable state ->

A

Hypercoagulable state -> loss of ATIII, protein C and S.

Also, increased synthesis of fibrinogen

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

Hyperlipidemia and hypercholesterolemia –>

A

hyperlipidemia and hypercholesterolemia - may result in fatty casts in urine

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

Minimal change diseases - causes?

A

usually idopathic;
may be assoc. with hodgkin lymphoma

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

LM - normal glomeruli; IF - negative, EM - effacement of podocyte foot processes. What disease?

A

Minimal change disease.

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

Most common cause of nephrotic syndrome in children?

A

Minimal change disease.

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

minimal change disease - response to steroids?
why?

A

excellent
because damage is mediated by cytokines from T cells

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

what proteinuria in minimal change disease?

A

Selective.
Loss of albimun, but not immunoglobulin

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

LM - segmental sclerosis and hyalinosis, IF - negative (often), EM - effacement of podocyte foot processes. What disease?

A

Focal segmental glomerulosclerosis.

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

Focal glomerular sclerosis causes? 1 and 2.

A

1 - Idiopatic.

2 - HIV, heroin abuse, sickle cell disease, obesity, interferon treatment, congenital malformations.

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

What disease is associated with drugs (NSAIDs, penicillamine)?

A

Membranous nephropathy.

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

LM - diffuse capillary and GBM thickening without hypercellularity, IF - granular, EM - ,,spike and dome” appearance of subepithelial deposits. What disease?

A

Membranous nephropathy.

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

Which of nephoritc syndromes is mediated by immune complexes?

A

Membranous nephropathy and membranoproliferative GN.

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

Most common syndrome in African Americans?

A

Focal segmental glomerulosclerosis.

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

Membranous nephropathy causes? 1 and 2.

A

1 - Idiopathic. (In FA 1 is antibodies to phospholipase A2 receptors).
2 - Drugs (NSAIDs, penicillamine, gold), infections (HBV, HCV, syphilis), SLE, tumors.

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

EM - ,,spike and dome” appearance of subepithelial deposits. What disease?

A

Membranous nephropathy.

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

Diabetic glomerulonephropathy mechanism?

A

Hyperglycemia –> nonenzymatic glycosylation of the vascular basement membrane/ tissue proteins–> hyaline arteriosclerosis/mesangial expansion.

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

What is Kimmelstiel-Wilson nodules? What disease?

A

Nodular sclerosis of mesangium in diabetic glomerulonephropathy.

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

Why there is hyaline arteriosclerosis in diabetic glomerulonephropathy?

A

Nonenzymatic glycosylation of vascular basement membrane –> hyaline arteriosclerosis.

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

Which arteriole is more affected by diabetic nephropathy? What effect on glomerul?

A

Efferent arteriole. It leads to high GF pressure –> hyperfiltration –> glomerular hypertrophy and glomerulosclerosis.

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

What deposits are in IF of membranous nephropathy?

A

Granular.

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

What are disruptions of glomerular charge barrier?

A

1 - direct sclerosis of podocytes.

2 - systemic process damages podocytes, e.g. diabetes, SLE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why there is hypercoagulable state in nephrotic syndrome?

A

Due to loss of antithrombin III.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Why there is increased risk of infections in nephrotic syndrome?

A

Due to hypogammaglobulinemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is proteinuria in nephrotic syndrome? ( g/day)

A

> 3,5 g/day.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the difference in pathogenesis of nephritic and nephrotic syndromes?

A

Nephritic: neutrophil-mediated glomeruli injury.
Nephrotic: T-cell and cytokines damage podocytes to lose their negative charge.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the hallmark of neprotic syndrome?

A

Effacement of podocyte foot processes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

A child with lymphoma. What renal disease is most likely to appear?

A

Minimal change disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What disease can trigger recent infections, immunization or immune stimulus? What is it - primary or secondary reason?

A

Minimal change disease. Primary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which disease has excellent response to corticosteroids?

A

Minimal change disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What disease can provoke sicle cells disease and HIV?

A

Focal segmental glomerulosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

African american uses heroin. What renal disease most likely to appear?

A

Focal segmental glomerulosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

O patient is treated with interferon. What renal disease most likely to appear?

A

Focal segmental glomerulosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

In focal segmental glomerulosclerosis IF usually is negative, but sometimes positive. For what structures it would be positive?

A

May be positive for nonspecific focal deposits of IgM, C3, C1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which 2 diseases have poor response to corticosteroids?

A

Focal segmental glomerulosclerosis and primary membranous nephropathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What disease cause antibodies to phospholipase A2 receptors? Is it primary or secondary reason?

A

Membranous nephropathy. Primary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Which two nephrotic syndrome disease may progress to CKD?

A

Focal segmental glomerulosclerosis and membranous nephropathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What changes are seen in GBM affected by hyperglycemia?

A

GBM thickening and increased permeability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What changes of glomeruli is caused by hyperfiltration?

A

Glomerular hypertrophy and glomerular scarring (glomerulosclerosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How is stained nodular glomerularsclerosis (Kimmelstiel-Wilson)?

A

Eosinophilic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

LM - mesangial expansion, GMB thickening, nodular glomerulosclerosis. What disease?

A

Diabetic glomerulonephropathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What states leads to further progression o nephropathy in diabethic glomerulonephropathy?

A

Glomerular hypertrophy and glomerulosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is seen in LM when diabetic glomerulonephropathy?3

A

Mesangial expansion, GMB thickening, nodular glomerulosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What causes mesangial expansion in diabetic nehpropathy?

A

nonenzymatic glycolysation of tissue proteins.

47
Q

In what disease are seen lipids in PCT?

A

Minimal change disease.

48
Q

hematuria in nephrotic?

A

ABSENT

49
Q

what is response of liver in nephrotic syndrome?

A

loss of albumin -> liver responds by increasing albumin synthesis. (AS WELL AS LIPIDS –> HYPERLIPIDEMIA)

50
Q

mechanism in nephrotic. scheme.

A

glomerular injury -> inc. glomerular permeability -> proteinuri -> hypoalbuminemia -> decr. oncotic pressure. It leads to 2:
1. hypovolemia –> incr. aldosterone and ADH -> na and water retention - edema (due to retention and hypoalbuminemia directly)
2. incr. liver protein and lipid synthesis -> hyperlipidemia

51
Q

What type of hyperaldosteronism are in nephrotic?

A

secondary hyperaldosteornism

52
Q

Why liver produce lipids?

A

liver produce lipoproteins.
also, liver catabolism is impaired due to decreased lipoprotein lipase and abnormal transport of ciculating lipid particles

53
Q

factors that leads to hypercoagulability in nephrotic?

A

loss of ATIII, loss of protein C and S, increased synthesis of fibrinogen

54
Q

charge of GBM?

A

negative

55
Q

to what charge molecules membrane is impermeable, normally?

A

membrane - negative;
impermeable to proteins, that are also negative (ALBUMIN)

56
Q

in what nephrotic syndrome is selective proteinuria?

A

ONLY IN MINIMAL CHANGE.
in others - nonselective

57
Q

what morphologic changes leads to nonselective proteinuria?

A

podocyte damage and fusion -> nonselective proteinuria

58
Q

what GRG and Cr in nephrotic?

A

normal.
damaged glomeruli continue to operate at normal filtration rate, therefore renal function remains unchanged while proteins are still released into the urine

59
Q

nephrotic. loss of PLASMA proteins –>?

A

decr. plasma protein binding –> increase in free plasma drug concentration, but drug toxicity is usually not increased

60
Q

nephrotic. loss of transport proteins –> ?? 2 examples.

A

loss of thyroglobulin transport protein 0> thyroxin deficiency
loss of vit.D binding protein –> vit. D deficiency

61
Q

minimal change. glomeruli - normal, but what may be seen?

A

lipids in PCT cells.

62
Q

minimal change. population?

A

children (2-3 y/os), but may be teenagers (was the case with 15y/o girl using NSAIDS)

63
Q

minimal change. characteristic feature?

A

diffuse effacement and fusion of podocyte foot

64
Q

minimal change. two groups of causes?

A
  1. idiopathic
  2. immune dysregulation
65
Q

minimal change. why immune dysregulation?

A

due to immunologic reaction to: immunizations, upper resp. infection (eg viral upper resp. infection), atopic disorders (reaction to pollen, dust, stings), drugs (eg NSAIDS), malignancy (Hodgkin lymphoma)

66
Q

minimal change. Immune dysregulation mechanism. What cells?

A

T cells dysfunction

67
Q

minimal change. T cells dysfunction –> overproduction of what?

A

IL-13

68
Q

minimal change. how is named Il-13 (its function?)

A

glomerular permeability factor –> affected glomerular capillary wall/direct damages to podocytes -> effacement and fusion of foot processes

69
Q

minimal change. two main points in patho?

A

T-cell dysregulation -> IL13 production, which is glomerular permeability factor

70
Q

minimal change. what clinical unexpected?

A

hypertension and hematuria

note: urine - frothy (due to proteins)

71
Q

focal segmental. LM?

A

SEGMENTAL SCLEROSIS AND HYALINOSIS

72
Q

focal segmental. EM?

A

diffuse podocyte foot processe effacement similar as seen in minimal change disease

73
Q

focal segmental. IF?

A

negative. sometimes might be positive if immune deposits occur in sclerotic region (IgM, C3, C1) (NOT ALONG GBM)

74
Q

If in focal segmental IF positive, where deposits?

A

in sclerotic region

75
Q

in what 2 diseases sclerosis and hyalinosis are typical?

A

Diabetic nephropathy and focal segmental

76
Q

Diabetic nephropathy and focal segmental. What is the difference in symtoms?

A

Diabetes - autonomic neuropathy with overflow incontinence (rare, typically in chronic poorly controlled DM)
Focal segemtal - NO lower urinary symptoms

77
Q

severe obesity - what diseases?

A

focal segmental

78
Q

Diabetic nephropathy and focal segmental. due to direct and indirect podocyte injury. What are the examples?

A

direct - cytotoxic drugs
indirect - glomerular hyperfiltration

79
Q

focal segmental - population?

A

adults

80
Q

in children what diseases?

A

minimal change

81
Q

in adult hispanics and african americans?

A

focal segmental

82
Q

in adult caucasians?

A

membranous nephropathy

83
Q

membranous nephropathy. LM?

A

DIFFUSE thickening of the GBM WITHOUT an increase in glomerular cellularity (hypercellularity)

84
Q

membranous nephropathy. EM?

A

Subepithelial deposits.
Irregural, IgG + C3 complexes.
Resembles Spikes and domes - when stained with silver stain

85
Q

membranous nephropathy. IF?

A

Granular deposits (IgG +C3)

86
Q

membranous nephropathy. 2 causes group?

A
  1. primary: idiopathic - anti-phospholipase A2 receptor antibodies
  2. secondary - infections, drugs, solid tumors, SLE
87
Q

anti-phospholipase A2 receptor antibodies (Anti-PLA2R antibodies) binds what?

A

PLA2R - autoantigen in glomerular podocytes

88
Q

where is PLA2R?

A

autoantigen in glomerular podocytes

89
Q

which autoantigen is very specific for membranous nephropathy?

A

Anti-PLA2R antibodies - positive titer rule out other nephrotic syndromes. also, titers correlate with diseases activity

90
Q

membranous nephropathy. what chronic infections?

A

HBV, HCV, syphilis

91
Q

membranous nephropathy. what solid tumors?

A

eg. lung, breast, prostate, colon

92
Q

membranous nephropathy. drugs?

A

NSAIDS, penicilamine, gold

93
Q

membranous nephropathy. what autoimmune?

A

SLE

94
Q

most common cause of end-stage renal disease in USA?

A

diabetic nephropathy

95
Q

diabetic nephropathy DM1 vs DM2? onset

A

DM1 >5years takes to develop
DM2 - can bet at the time of diagnosis

96
Q

diabetic nephropathy. typical patients?

A

middle age-elderly with long history of DM

97
Q

diabetic nephropathy. What is thickened?

A

GBM

98
Q

diabetic nephropathy. what is expanded?

A

mesangium - increased mesangial matrix deposition

99
Q

diabetic nephropathy. Glomerusclerosis - what finding? name

A

Kimmelstiel-Wilson nodules

100
Q

diabetic nephropathy. what indicated IRREVERSIBLE damage?

A

Kimmelstiel-Wilson nodules

101
Q

diabetic nephropathy. mechanism of function decline>

A

Over time, expansion of the mesangium and KW nodules formation compress the glomerular capillaries –> loss of glomerular function

102
Q

where are Kimmelstiel-Wilson nodules?

A

in mesangium

103
Q

Kimmelstiel-Wilson nodules - how stain?

A

H and E - eosinophilic
PAS positive

Ovoid/spherical shaped
lammelated appearance

104
Q

diabetic neohropaty. urinalysis?

A

No red or white cells.

105
Q

diabetic neohropaty. type of proteinuria?

A

affected more eferent than afferent –> high filtration rate –> hyperfiltration injury leads to MICROALMUNINURIA –> eventually to nephrotic syndrome

106
Q

what molecule is negatively charged in GBM?

A

Heparan sulfate

107
Q

mechanism how is lost negative charge in DM?

A

progressive loss of negative charge due to heparanase expression by renal epithelial cells –> leakage of albumins and other plasma proteins.

108
Q

what are earliest morphological changes in DM nephropathy?

A

GBM thickening and mesangium expansion

109
Q

What is screened for renal damage in DM?

A

ALBUMINS - with albumin specific urine assay (regular dipstic has low sensitivity)

110
Q

Earliest manifestation of DM nephropathy?

A

ALBUMINURIA

111
Q

what reflects glycosuria?

A

poor glycemic control

112
Q

Ketones levels?

A

transient phenomenom in DM

113
Q

what are 3 stages of DM nephropathy?

A

Hyperfiltration, incipient DN, overt DN

114
Q

DN. Hyperfiltration? (2)

A

Glomerular hypertrophy and INCREASED GFR (GRAFIKAS!!!!!!)

115
Q

DN. Incipient DN? 3

A

Mesangial expansion, GBM thickening, arteriolar hyalinosis
Moderately increased albuminuria
hypertension

116
Q

DN. Overt DN?4

A

Mesangial nodule (KW), tubulointerstitial fibsosis

overt proteinuria

Nephrotic syndrome

decr. GFR

1 STEP Renal pathology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions