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Glomerular- Pathology Flashcards

1
Q

This is the term where is increased nitrogenous compounds in the blood (BUN and creatinine).

A

Azotemia

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2
Q

What happens to the GFR in azotemia?

A

it ↓

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3
Q

What causes prerenal aztoemia?

A

hypoperfusion of the kidneys (↓ blood flow)

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4
Q

True or False: there is parenchymal damage in prerenal azotemia,

A

FALSE. there is impairment of renal fxn but no parenchymal damage.

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5
Q

What causes postrenal azotemia?

A

a blockage past the kidney

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6
Q

This is the term when azotemia is associated with a bunch of other signs and Sx, like failure of renal exretory fxn, metabolic and endocrine alterations, and 2o involvement of other systems.

A

Uremia

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7
Q

This is the rapid and frequently reverible deteroration of renal fxn dominated by oliguria or anuria and a recent onset of azotemia.

A

Acute Renal Failure (ARF)

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8
Q

What are the 4 stages of chronic renal fialure?

A
  1. Diminished renal reserve
  2. Renal insufficiency
    3, chronic renal failure
  3. end-stage renal disease
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9
Q

In the diminshed renal reserve stage of chronic renal failure, how much is hte GFR reduced as compared to normal?

A

50% of normal

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10
Q

In the renal insufficiency stage of chronic renal failure, what is the GFR % of normal?

A

GFR 20-50% of normal

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11
Q

In the renal insufficiency stage of chronic renal failure, what are the other Sx in addition to azotemia??

A

anemia, HTN, polyuria and nocturia

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12
Q

In the chronic renal failure stage, the GFR is < 20%, and kidney fxn really sucks, causing what Sx?

A

Edema, metabolic acidosis, hyperkalemia, and overt uremia

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13
Q

What % of GFR is at the end-stage renal disease of chronic renal failure?

A

< 5%

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14
Q

This is the glomerular syndrome where there is an acute onset of hematuria, azotemia, mild/moderate proteinuria, oliguria, edema, and HTN.

A

Nephritic syndrome

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15
Q

This is the glomerular syndrome where there is acute nephritis, proteinuria, and acute renal failure.

A

Rapidly progressing glomerulonephritis (RPGN)

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16
Q

This is the glomerular syndrome where there is heavy proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, lipiduria, and severe edema.

A

Nephrotic syndrome

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17
Q

What are the 2 components of the glomerular basement membrane?

A

type IV collagen and glycoproteins

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18
Q

These are cells that are similiar to vascular smooth muscle cells and pericytes and lie between the capillaries and support the entire glomerular tuft.

A

Mesangial cells

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19
Q

What is the fxn of mesangial cells?

A

They’re mesenchymal in origin, contractile, phagocytotic, proliferative, and secrete biologically active mediators.

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20
Q

Hypercellularity in the glomerularnephropathies causes cellular proliferation and leukocyte infiltration, leading to what formation in the glomerulus?

A

crescents

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21
Q

Crescents from hypercellualrity is from the leakage of what component into the urinary space?

A

fibrin

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22
Q

In glomerulonephropathies, the deposition of amorphous, electron-dense material and increased synthesis of the GBM’s proteins causes what?

A

GBM thickening

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23
Q

What mechanisms underlie most glomerulonephropathy?

A

immune mechnaisms

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24
Q

If immune complexes are deposited in the glomeruli, what do they look like on immunflourescence (IF)?

A

Granular

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25
Q

If antibodies are directed against antigens in the GBM, what does it look like on IF?

A

Diffuse linear pattern

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26
Q

Which syndrome gives a diffus linear parrtern of immune complexes on IF?

A

Goodpasture syndrome

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27
Q

When circulating immune complexes get deposited and cause glomerulonephritis, there is leukocyte infiltration and proliferation of what 2 cells?

A

Mesangial and endothelial cells.

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28
Q

What are the 2 major histologic characteristics of progressive renal damage?

A 
Focal Segmental Glomerulosclerosis (FSGS)
Tubulointerstitial fibrosis (TIF)
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29
Q

Is FSGS a nephritic or nephrotic syndrome?

A

Nephrotic syndrome

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30
Q

Is the protein content in urine higher or lower than 3.5g/day in nephrotic syndrome?

A

> 3.5 g/day

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31
Q

In FSGS, where to proteins accumulate when there is endothelila and epithelial are injures causing the increased glomerular permeability to proteins?

A

Accumulation in mesangial matrix

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32
Q

What happens to the foot processes in FSGS?

A

They undergo effacement (thinning)

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33
Q

In FSGS, the accumulation of proteins in the mesangium of the glomerulus caues what change of the remaining glomeruli?

A

Compensatory hyperplasia

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34
Q

The compensatory hyperplasia then causes what change in FSGS?

A

segmental glomerulosclerosis

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35
Q

Though FSGS is usually idiopathic, what are the 3 high yield assocaitions with its etiology?

A

HIV, heroin use, and sickle cell disease

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36
Q

True or False: in FSGS, there is immune complex deposition causing a granular appearence on IF.

A

FALSE

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37
Q

True or False: FSGS patients do not respond to steroid treatment.

A

True.

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38
Q

In TIF, what causes direct injury to and activation of tubular cells?

A

Proteinuria

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39
Q

The proteinuria damage in TIF cuases activation of what mediators to cause the interstitial fibrosis?

A

cytokines, chemokines, and GFs

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40
Q

This syndrome is characterized by the inflammation of the glomeruli, and involves hematuria*, red cell casts in urine, azotemia, oliguria, and mild/moderate HTN.

A

Nephritic syndrome

PHAROH

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41
Q

This nephritic syndrome occurs 1-4 weeks after a streptococcal infection.

A

Poststreptococcal Glomerulonephritis (PSGN)

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42
Q

Which patients are at most risk for PSGN?

A

Kids 6-10 (adults can get it too)

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43
Q

Which protein on the strep bug causes the cross linking to self Ag’s?

A

M protein

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44
Q

True or False: all nephritic syndromes involve immune-complex deposition.

A

true

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45
Q

There are enlarged, hypercellular glomeruli in PSGN because of the the diffuse infiltration of what cells?

A

Leukocytes

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46
Q

What are seen in the subepithelium in PSGN as a result of Ag-Ab complex depostion?

A

Subepithelial humps

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47
Q

True or False: treatment for PSGN is usually supportive.

48
Q

True or False: kids rarely progress to RF in PSGN

49
Q

What syndrome can adults progress to in PSGN?

A

Rapid Progressive Glomerulonephritis (RPGN)

50
Q

True or False: Postinfectious (nonstrep) GN causes pretty much the same characteristics as PSGN.

51
Q

This is the nephritic syndrome that progresses to renal failrue in weeks-months.

52
Q

What are in the bowmans space in RPGN?

53
Q

What are the 2 components of the crescents in RPGN?

A

Fibrin and macrophages (inflammatory debris)

54
Q

You find a young male with a linear IF pattern complaining of hemoptysis and hematuria. What is the Dx?

A

Goodpastures syndrome

55
Q

Why is Goodpastures the only RPGN to cause a linear IF?

A

because Ab’s are directed against the collagen in the glomerular and alveolar BM.

56
Q

Which 2 diseases give a Granular IF pattern in RPGN?

A

PSGN

Diffuse proliferative Glomerulonephritis (DPGN)

57
Q

DPGN are subendothelial deposits and is the msot common cause of renal disease in which patients?

58
Q

What test do u do next if you get a negative IF (pauci-immune) for RPGN?

59
Q

A patient who presents with RPGN, hemoptysis, and sinusitis problems will show which ANCA pattern?

A

c-ANCA

Wegeners

60
Q

A patient with granulomatous inflammation, eosinophilia, and asthma will show which ANCA pattern?

A

p-ANCA

Churg-Strauss

61
Q

This is the syndrome from derangement in glomerular capillary walls resulting in proteinuria (>3.5 g/day), hypoalbulinemia, edema, and hyperlipidemia and lipiduria.

A

Nephrotic syndrome

nephrOtic with ↑ prOteins makes u look like an O

62
Q

This is a common cause of nephrotic syndrome in adults and is a form of chronic immune complex-mediated disease.

A

Membranous nephropathy

63
Q

Though membranous nephropathy is mostly idiopathic, what are some high yield associations

A

HBV and HCV
Solid tumors
SLE***
Drugs (NSAIDS or penicillamine)

64
Q

What causes the glomeruli to become leaky (and thus prOteinuria) in membranous nephropathy?

A

immune-complexes against a renal autoantigen and resultant inflammation

65
Q

In membranous nephropathy, there are subepithelial immune deposits which appear with what pattern on EM?

A

Spike and dome

66
Q

What shows up on IF for membranous nephropathy?

A

grnaular deposits along the GBM

67
Q

This is the most common nephrOtic syndrome in kids ages 2-6.

A

Minimal change disease

68
Q

What usually precedes minimal change disease?

A

A respiratory tract infection and prophylactic immunizaiton

69
Q

True or False: there is immune-complex deposition in minimal change disease.

A

False. there are no immune complexes

70
Q

what is the hihg yield association with minimal change disease in adults?

A

Hodkins lymphoma

71
Q

Which mediators damage the visceral epithelial cells causing proteinuria in minimal change disease?

72
Q

What happens to the foot processes in minimal change disease?

A

Effacement

73
Q

True or False: in minimal change disease, there is selective proteinuria with usually no HTN or hematuria.

A

true

minimal change ya hearrrr

74
Q

What is a good treatment for minimal change disease?

75
Q

What happens in the PCT in minimal change?

A

They get fatty (lipoid nephrosis)

76
Q

In FSGS, the entrapment of proteins and increased ECM deposition cause which change?

A

Healinosis and sclerosis

77
Q

HIV-infected individuals are likely to develop which form of FSGS?

A

Severe collapsing FSGS

78
Q

This is the nephrotic syndrome where there are alteration in the GBM, proliferation of glomerular cells, and leukocyte infiltration.

A

Membranoproliferative Glomerulonephritis (MPGN)

79
Q

True or False: there are immune complex deposits in MPGN.

80
Q

Where are the deposits in type I MPGN?

A

subendothelium

81
Q

What are the appearance of the immune deposits on H&E for MPGN?

A

Tram-track appearance

82
Q

What are the 2 infectious associations with type I MPGN?

A

HBV and HCV

83
Q

Where are the immune deposits in type II MPGN?

A

within the basement membrane

84
Q

What do the patients with type II MPGN have that stabilizes C3 convertase –> overactivation of complement?

A

C3 nephritic factor

85
Q

Which form of MPGN can arise from chronic immune complex disordrs, A1AT deficiency, malignant disease, or hereditary deficiencies?

A

Secondary MPGN

86
Q

This is the nephritic syndrome where there is prominent IgA deposits in the mesangial regions.

A

IgA nephropathy (berger syndrome)

87
Q

There is increased IgA in the serum in Berger syndrome usually following which infections?

A

Mucus infections

88
Q

Who typically gets Berger syndorme?

A

older children and young adults

89
Q

What is the most common presentation of Bergers syndrome post infection?

A

gross hematuria

90
Q

This is the nephritic syndrome from an inherited defect (X-linked) in type IV collagen causing thinning and splitting of the GBM.

A

Alport syndrome

91
Q

What are the 3 main Sx to Alport syndrome?

A

hematuria, deafness, eye disorders

92
Q

This is the syndrome that is characterized by diffuse thinning of the GBM and asymptomatic hematuria that kinda looks like Alport syndrome.

A

Benign familial hematuria

93
Q

What Sx in benign familial hematuria differentiate it from Alport syndrome?

A

There is NO hearing loss/vision problems/family Hx

94
Q

What is the gross morphology of the kidneys in chronic renal failure (CRF)?

A

symmetrically contracted kidneys

thinned cortex

95
Q

What happens to the glomeruli in CRF?

A

obliteration of the glomeruli that turn into acellular collagen masses (like scarring)

96
Q

CRF patients with arterial intimal thickening, focal calcification, deposition of calcium oxalate crystals, cysts, and cancer are receiving what?

97
Q

What is the Tx for CRF?

A

Transplant or dialysis

98
Q

These are purpuric skin lesions on the extremities with GI and renal Sx.

A

Henoch-Schonlein Purpura (HSP)

99
Q

What is deposited in the mesangium causing mesangial proliferation and/or endocapillary to crescentric glomerulonephritis in HSP?

100
Q

This is the constion where there is immune complex nephritis from complexes of baterial Ag and Ab, causing crescents, FSGN, and DPGN.

A

Bacterial Endocarditis-Associated Glomerulonephritis

101
Q

What happens in diabetes to cause hyaline arteriolosclerosis?

A

Nonenzymatic glycosylation of GBM

102
Q

Which arteriole is more affected in diabetes to cause ↑ GFR?

A

Efferent arteriole

103
Q

Which drugs help the diabetes associated nephrotic syndrome?

104
Q

These are the things formed by diabetes from sclerosis of the mesangium,

A

Kimmelsteil-Wilson nodules

105
Q

In systemic amyloidosis, there are amyloid deposits in the mesangium leading to what characteristics under polarized light?

A

Apple-green birefringence

106
Q

Clean-up: What are the nephrotic syndromes?

A 
Minimal Change
FSGS
Membranous nephropathy
MPGN
Diabetes
Amyloidosis
107
Q

Clean-up: what are the 2 nephrotic syndrome that have effacement of foot processes?

A

Minimal change + FSGS

108
Q

Clean-up: What 2 nephrotic syndromes have immune complex deposition?

A

Membranous + MPGN

109
Q

Clean-up: What 2 nephrotic syndromes are systemic in origin?

A

Diabetes + amyloidosis

110
Q

Clean-up: Which disease responds to steroids: minimal change or FSGS?

A

Minimal change

111
Q

Clean-up: Which NEPHRIOTIC syndrome is assocaited with SLE?

A

Membraneous nephropathy

112
Q

Clean-up: Which NEPHRITIC syndrome is assoacited with SLE?

113
Q

Clean-up: What are the nephritic syndromes?

A

PSGN, Alport, IgA neuropathy, RPGN

“PAIR”

114
Q

Clean-up: What are the Sx to nephritic syndromes?

A

PHAROH

Proteinuria under 3.5, Hematiuria, Azotemia, RBC casts, oliguria, and HTN

115
Q

Clean-up: In the nephrotic syndromes, which disease causes deposits in the Subendothelium?

A

Type I MPGN

116
Q

Clean-up: In the nephrotic syndromes, which disease causes deposits in the BM?

A

Type II MPGN

117
Q

Clean-up: In the nephrotic syndromes, which disease causes deposits in the Subepithelium?

A

Membranous nephropathy

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