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Renal > 05.05 - Glomerular Structure, Injury (Nichols, Handorf) - Based on word doc > Flashcards

05.05 - Glomerular Structure, Injury (Nichols, Handorf) - Based on word doc Flashcards

1
Q

Hyaline Sclerosis in HTN vs DM

A

In HTN, just afferent arteriole; In DM, both

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1
Q

Anti-GBM disease is associated with

A

Smoking, being male

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1
Q

Location of In situ immune complex formation and deposition

A

Subepithelial

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1
Q

What does Trichrome stain highlight

A

Collagen

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2
Q

Treatment of Anti-GBM Ab disease

A

Removing them with Plasmapharesis

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2
Q

IgA Nephropathy is due to

A

Production of Abnormal IgA that self-aggregates and binds IgG –> immune complex formation –> Mesangial cell activation –> Complement-mediated injurious inflammation

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2
Q

What stain highlights the GBM

A

Jones silver stain

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2
Q

What is becoming the most common type of Crescentic Glomerulonephritis

A

Pauci-immune

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3
Q

3 most common types of glomerular disease

A

(1) HTN, (2) Diabetic, (3) Immune-mediated

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3
Q

Most common cause of glomerular disease

A

Hypertension

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3
Q

Platelet mechanisms of glomerular injury in immune-mediated disease

A

Release AA metabolites

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3
Q

In situ immune complex formation with Ab’s against podocyte cell membrane antigens causes great majority of

A

Membranous Glomerulonephritis

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4
Q

Calcium binding properties

A

Features of Entactin

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4
Q

What does Global Glomerular Disease refer to

A

Involves all of a single glomerulus

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5
Q

Feedback loop with hypertensive kidney disease

A

Glomerular Disease causes HTN, and HTN causes glomerular disease

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5
Q

What happens to GBM in DM

A

Glycosylated plasma proteins get trapped –> GBM gets thickened

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5
Q

What does Diffuse Mesangial Sclerosis mean

A

Sclerosis of all the mesangium in one glomerulus

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6
Q

What causes Crescentic Glomerulonephritis

A

Leakage of Plasma Proteins into urinary space (particularly when mixed with Ab’s, Immune Complexes, Inflammatory Cytokines, Inflammaotry cells, and ROS)

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6
Q

Location of immune complex deposition in Post-Strep Glomerulonephritis

A

Subepithelial

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8
Q

Important Concept: ____ is a major mechanisms of glomerular injury

A

Antibody deposition

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9
Q

Mutations in what result in congenital nephrotic syndromes?

A

Nephrin and Podocin

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10
Q

Urine in Malignant HTN

A

Marked Proteinuria, Microscopic Hematuria

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11
Q

Features of Perlecan

A

Strong negative charge - prevents Albumin from entering

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12
Q

Crescent Glomerulonephritis is associated with

A

Rapid Progression of Disease

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12
Q

What activates the Complement pathway in IgA Nephropathy

A

Mesangial cells are activated in response to binding and phagocytosing immune complexes –> Proliferate and increase production of ECM proteins and cytokines

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13
Q

Features of Laminin

A

Binds to other components

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14
Q

Features of Entactin

A

Calcium binding properties

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14
Q

Form of Glomerulonephritis w/ localization of immune complexes in the mesangium

A

IgA Nephropathy

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14
Q

Subepithelial Humps

A

Pattern of immune complex deposits in Post-Strep Glomerulonephritis EM

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15
Q

Leukocyte mechanisms of glomerular injury and malfunction

A

Leakage of lysosomal proteases and ROS, Production of AA metabolites that reduce GFR

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17
Q

What is the Non-Collagenous Domain

A

Non-helical globular domain

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19
Q

Infectious diseases involve what parts of nephron

A

Tubules and Interstitium far more often than glomeruli

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20
Q

What are Thrombotic Microangiopathies

A

Loss of normal endothelial function needed to prevent thrombosis

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20
Q

Result of Foot Process Effacement

A

Retraction and loss of SPD; Detachment from GBM and degradation of GBM –> Plasma protein linkage

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20
Q

What mediates the accelerated aging in DM

A

Advanced Glycation end-products (AGE)

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21
Q

What is Arterio-Nephro-Sclerosis

A

(1) Narrowing of lumen from plasma leakage; (2) Gradual ischemic atrophy of glomerulus; (3) End result is global sclerosis of glomeruli

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23
Q

In whom is malignant HTN more common

A

Black males around 40

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24
Q

What tends to have a Linear pattern on immunofluorescence and be invisible on EM

A

Anti-GBM Ab deposition

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26
Q

2 diseases associated leading to Arterionephrosclerosis

27
Q

Wire Loops

A

Extensive confluent subendothelial deposits thickening the capillary walls

29
Q

Nephrin and its associated protein are crucial to

A

Maintaining selective permeability of glomerular filtration barrier

31
Q

Gross appearance of kidney in malignant HTN

A

Flea-Bitten

31
Q

Crescent-shaped area of inflammation w/ proliferation of parietal epithelial cells

A

Crescentic Glomerulonephritis

32
Q

2 diseases associated with ApoL1 mutation

A

Arterionephrosclerosis, Focal Segmental Glomerulosclerosis

33
Q

Strong negative charge - prevents Albumin from entering

A

Features of Perlecan

35
Q

What happens to arterioles in Malignant HTN

A

Fibrinoid Necrosis of Arterioles

36
Q

What is Crescentic Glomerulonephritis

A

Crescent-shaped area of inflammation w/ proliferation of parietal epithelial cells

37
Q

Diseases caused by Ab’s against epitope in the NC1 domain of alpha3 chain cause

A

Glomerulonephritis w/ Hematuria

38
Q

Effects if DM on nephron

A

Mesangial cell hypertrophy and hyperplasia; Diffuse mesangial matrix production; Podocyte injury and apoptosis; Thickening of tubular BM’s

39
Q

Most common glomerular disease

A

Vascular, Hypertensive Nephropathy

40
Q

What causes the damage in IgA Nephropathy

A

Complement activation generates the injurious inflammation

42
Q

In whom is end-stage renal disease due to HTN more common

A

8x more common in blacks

43
Q

What can cause Crescentic Glomerulonephritis

A

Leakage of plasma proteins into urinary space (particularly when mixed with Ab’s, Immune Complexes, Inflammatory Cells, and ROS)

44
Q

Renal neoplasms arise from

A

Tubular Epithelium

46
Q

Result of injury to glomerular capillary endothelium

A

Loss of normal endothelial function needed to prevent thrombosis

47
Q

Pattern of immune complex deposition in immunofluorescence

A

Clumps, granular pattern

48
Q

Goodpasture Syndrome

A

Glomerulonephritis w Hematuria, along w/ Pulmonary Hemorrhage and Hemoptysis

48
Q

What does PAS stain highlight

A

Cellular cytoplasmic inclusions

50
Q

Effect of supra-normal glomerular capillary pressure on glomerulus

A

GBM thickening, Mesangial Hypertrophy and Hyperplasia, Mesangial Matrix production

52
Q

When proliferating parietal epithelial cells and infiltrating macrophages and inflammatory exudate and leaked plasma create a visible crescent of inflammation around glomerular tuft of cpaillaries

A

Crescentic Glomerulonephritis

54
Q

Slit Pore Diaphragm proteins that serve to bind adjacent pediceles

A

Cadherin, FAT

56
Q

Glomerular diseases that involve the capillary endothelium or subendotheial portion of glomeruli tend to cause

57
Q

Site of Ab deposition in SLE

A

Subendothelial

58
Q

Compensation for nephron loss requires

A

Increased filtration per glomerulus and increased glomerular transcapillary pressure

59
Q

In conditions causing severe loss of protein thru slit pore diaphragms, EM frequently shows

A

Fusion of Foot Processes = Effacement

61
Q

Ab against NC1 domain + Ab’s against lung basement membrane

A

Goodpasture Syndrome

62
Q

Second most common glomerular disease

63
Q

Mesenchymal cells w/ phagocytic and contractile properites

A

Mesangial Cells

64
Q

With what is C-ANCA associated

A

Granulomatosis with Polyangiitis

65
Q

Vascular clotting disorders such as HUS, TTP, and DIC involve what part of nephron

A

Glomerulus

65
Q

Anti-GBM Ab deposition tends to have what pattern

A

Linear pattern on immunofluorescence and be invisible on EM

67
Q

End result of many glomerular diseases

A

Fibrous replacement of glomerulus = Glomerulosclerosis

69
Q

What is hypothesized to happen in Post-Strep Glomerulonephritis

A

Antigens and Ab’s arrive in glomerulus separately and form complexes in situ

70
Q

Features of Fibronectin

A

Connection and adhesion of components

71
Q

Extensive confluent subendothelial deposits thickening the capillary walls

A

Wire Loops

72
Q

Connection and adhesion of components

A

Fibronectin

73
Q

Glomerular diseases that involve which side of glomerulus are worse

A

Capillary side

75
Q

What causes the great majority of Membranous Glomerulonephritis

A

In situ immune complex formation with Ab’s against podocyte cell membrane antigens

76
Q

Glomerular diseases that involve only the podocytes, slit diaphragm, or subepithelial portion of the glomeruli tend to cause

A

Proteinuria

78
Q

Presentation of Malignant HTN

A

Symptoms of increased intracranial pressure: Headache, Scotomas, Vomitting

80
Q

What happens to surviving nephrons after nephron loss

A

Hypertrophy, with hyperplasia of glomerular and tubular cells, longer tubules

81
Q

Hyperplastic Arteriosclerosis + Arterial Fibrinoid Necrosis

A

Malignant HTN

82
Q

What causes Flea-Bitten Kidney

A

Small arteries/arterioles damaged by malignant HTN rupture all over kidney

83
Q

Toxic diseases tend to involve what part of nephron

A

Tubules more than Glomeruli

85
Q

(1) Narrowing of lumen from plasma leakage; (2) Gradual ischemic atrophy of glomerulus; (3) End result is global sclerosis of glomeruli

A

What is Arterio-Nephro-Sclerosis

86
Q

Glomerulonephritis w Hematuria, along w/ Pulmonary Hemorrhage and Hemoptysis

A

Goodpasture Syndrome

87
Q

Histopathologic correlate of the clinical syndrome of rapidly progressive glomerulonephritis

A

Crescentic Glomerulonephritis

88
Q

What does Segmental Glomerular Disease mean

A

Involves only part of glomerulus

89
Q

Membranous glomerulopathy is characterized by

A

Increased glomerular basement membrane, w/out an increase in cells

90
Q

What percent of glomerular disease in children is primary? In adults?

91
Q

With what is P-ANCA associated

A

Microscopic Polyangiitis, Churg-Strauss

92
Q

Cell binding of basement membrane is mediated mostly by

93
Q

Slit Pore Diaphragm proteins that play role in filtration

A

Nephrin, Podocin

94
Q

Effect of AA metabolites on glomerulus

A

Reduce GFR

95
Q

AI diseases highly favor what part of nephron

Renal (31 decks)

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