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Renal 2 > Path - Glomerular Structure and Mechanisms of Disease > Flashcards

Path - Glomerular Structure and Mechanisms of Disease Flashcards

1
Q

3 layers of Glomerulus?

A

Capillary to urinary space

  1. Fenestrated endothelium
  2. Glomerular basement membrane
  3. Pedicels (foot processes) on epithelium
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2
Q

Men or women have thicker glomerular basement membrane?

A

Men

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3
Q

glomerular basement membrane (GBM) disease more common in men?

A

Anti-GBM disease

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4
Q

What % of capillary surface may correspond with fenestrations?

A

Up to 50%

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5
Q

Relationship between podocytes and foot processes (pedicels)?

A

Each adjacent pedicel belongs to a single podocyte. Therefore, there is an extensive network covering capillaries

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6
Q

3 layers of the basement membrane?

A

Endothelium (capillary space) to epithelium (urinary space)

  1. Lamina lucida (rara)
  2. Lamina densa
  3. Lamina rara externa
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7
Q

Thickest layer of GBM?

A

Lamina densa (double the thickness of lamina rara)

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8
Q

Minimal space between 2 pedicels = ?

A

Filtration slit

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9
Q

Slit pore diaphragm = ?

A

thin structure bridging the space between two pedicels

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10
Q

4 main slit pore diaphragm proteins?

A

Cadherin, FAT, Nephrin, Podocin

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11
Q

2 slit pore diaphragm proteins involved with binding adjacent pedicels?

A

Cadherin, FAT

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12
Q

2 main slit pore diaphragm proteins involved with filtration?

A

Nephrin, Podocin

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13
Q

Major component of the glomerular basement membrane?

A

Type IV collagen

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14
Q

4 major components of glomerular basement membrane?

A

(PELT) = Perlecan, Entactin, Laminin, & type IV collagen

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15
Q

Significant component of perlecan and function of this component?

A

Perlecan contains heparan sulfate, producing the main negative charge of the GBM. This negative charge prevents albumin (also negatively charged) from permeating through GBM.

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16
Q

Entactin binds what ion?

A

Calcium

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17
Q

Laminin is formed of how many different chains?

A

3

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18
Q

How many different alpha chains form Type IV collagen family? How many chains needed to form a collagen molecule? Conclusion based on these numbers?

A

6 numbered alpha chains. 3 needed to form a collagen molecule. Therefore, there is significant variability in the composition of individual molecules and basement membranes.

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19
Q

What is a “non-collagenous” domain?

A

Most of the alpha chains of type IV collagen are in the characteristic helical conformation; however, “non-collagenous” domain = non-helical globular domain

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20
Q

antibodies attack what in Goodpasture syndrome?

A

antibodies attack NC1 (non-collagenous 1) domain of the alpha3 chain of Type IV collagen, causing glomerulonephritis with hematuria AND pulmonary hemorrhage with hemoptysis.

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21
Q

2 main clinical findings leading to Goodpasture syndrome?

A
  1. Glomerulonephritis with hematuria
  2. Pulmonary hemorrhage with hemoptysis

Need both clinical findings to be considered Goodpasture syndrome

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22
Q

3 main functions of mesangial cells?

A
  1. Structural support to glomerulus
  2. Phagocytic properties
  3. Contractile properties
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23
Q

Describe phagocytic properties of mesangial cells?

A

Mesangial cells within the mesangial matrix will trap antibodies and Antigen-antibody complexes and eventually phagocytose them.

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24
Q

3 most common mechanisms of glomerular disease?

A
  1. Immune-mediated
  2. Metabolic
  3. Hemodynamic
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25
Q

Immune mediated glomerular disease are caused by?

A
  1. antibodies, 2. immune complexes
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26
Q

Immune complexes involved in glomerular diseases can be present in what 2 forms?

A

Can be 1) deposited from the circulation or 2)form in situ

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27
Q

In situ antibodies (related to immune complexes of glomerular diseases) can be against what 2 types of antigens?

A

Can be against 1) intrinsic (fixed) antigens in the glomerulus or 2) “planted” antigens originally found in the bloodstream

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28
Q

Mechanism of “planted” antigens

A

Antigens and antibodies are floating in circulation. Antigen gets to glomerulus 1st, then antibody gets there and recognizes “planted” antigen

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29
Q

Describe immune complexes in lupus nephritis?

A

Large circulating immune complexes will pass through fenestrations of endothelium and get stuck in subendothelial location of GBM.

30
Q

Immune complex of Lupus nephritis/SLE

A

Immune complexes deposited in CLUMPS and have a GRANULAR PATTERN

31
Q

Goodpasture syndrome antibody feature?

A

Circulating antibodies against the GBM deposit in a subendothelial location ALL ALONG the GBM

32
Q

Pattern of antibody deposition in Goodpasture syndrome?

A

Linear pattern all along the GBM

33
Q

anti-GBM disease = ?

A

Considered half of good pasture syndrome, only involving the kidney

34
Q

Treatment against anti-GBM antibodies? Why is this method of treatment effective?

A

Plasmapheresis. B/c the anti-GBM antibodies circulate before they are deposited within the glomerulus

35
Q

Membranous nephropathy antibody feature?

A

Circulating antibodies against antigens in the cell membrane of podocytes deposit OUTSIDE the GBM and injure podocytes

36
Q

Post-streptococcal glomerulonephritis = immune complex disease against ?

A

Primarily against streptococcal pyogenic exotoxin B

37
Q

Immune complex deposition of post streptococcal glomerulonephritis = ?

A

SUBEPITHELIAL “HUMPS” with granular deposits (more granular than lupus granular deposits)

38
Q

What metabolic disease causes glomerular injury?

A

Diabetes

39
Q

Diabetes causes what to occur in proteins?

A

Non-enzymatic glycosolation of proteins

40
Q

Which type of proteins are affected in diabetes (circulating or intrinsic to GBM)

A

Both. Glycosolation of both circulating proteins and intrinsic proteins of GBM can occur

41
Q

In Diabetes, what happens to plasma and intrinsic proteins following glycosolation?

A

These proteins will get trapped in GBM, stimulating production of new GBM proteins.

42
Q

What pathologic process is being shown here? Early or later stages?

A

Later stages in diabetes. After production of new GBM proteins (following glycosolation of plasma/intrinsic proteins), the GBM will eventually thicken, as shown in the picture. Advanced glycation end products (AGE) are produced (discussed on different notecard)

43
Q

What are advanced glycation end products (AGE)?

A

In diabetes, some glycosylated proteins are further metabolized, forming AGE. These accelerate the effects that diabetes has on other organs = bad news.

44
Q

List the 4 factors involved in progression to diabetic nephropathy? By what mechanism?

A

1) Advanced oxidation protein products [AOPP], 2) Renin-Angiotensin system, 3) TGF-beta, & 4) advanced glycation end products (AGEs) activate NADPH oxidase, producing ROS, causing mesangial matrix production, podocyte injury, apoptosis, and proteinuria. All these = diabetic nephropathy.

45
Q

Hydrostatic pressure in glomerular capillary vs other capillaries?

A

Higher in glomerular capillary (50 mm Hg) vs usual 35 mmHg in other capillaries

46
Q

Bowman’s space pressure vs other capillary pressure?

A

Lower, roughly half (18 mm Hg) vs normal capillaries (35 mm Hg)

47
Q

Increased hyrostatic pressure causes what 3 pathologic processes of glomerulus?

A
  1. Stimulates GBM thickening
  2. Mesangial cell hypertrophy and hyperplasia
  3. Increased mesangial matrix production
48
Q

HTN causes hyaline sclerosis of (afferent/efferent) arterioles?

A

Afferent arterioles. gradually narrows the lumen causing gradual ischemic atrophy of the glomerulus

49
Q

End stage hypertensive nephropathy = ?

A

Arterionephrosclerosis

50
Q

Arterionephrosclerosis more common in blacks or whites?

A

8x more common in blacks.

51
Q

African sleeping sickness due to what bug?

A

Trypanosoma brucei rhodesiense

52
Q

What mutation confers resistance to Trypanosomes in Africans? MOA?

A

Mutation in the gene for apolipoprotein L1, forming variant apolipoprotein L1. This variant doesnt bind trypanosomal protein, confering resistance to trypansosomes.

53
Q

Malignant HTN classifed as what BP?

A

>200/120 mmHg

54
Q

Scotomas = what? = feature of what?

A

Scotoma - “spots before the eyes”, feature of malignant HTN

55
Q

2 common pathologic results of malignant HTN?

A
  1. Fibrinoid necrosis
  2. Hyperplastic arteriosclerosis
56
Q

What is the pathophysiology of a “flea bitten kidney” ?

A

Malignant HTN damages small arteries and arterioles all over the kidney, giving it a “flea bitten” appearance

57
Q

What is considered to be a medical emergency in terms of glomerular diseases?

A

MALIGNANT HTN

58
Q

Kidney biopsies require what 3 types of microscopy?

A
  1. Light microscopy
  2. Immunofluorescence
  3. Electron microscopy
59
Q

Glomerular disease terminology. “involving all or most of the glomeruli” = ?

A

Diffuse

60
Q

Glomerular disease terminology, “involving some but not most of the glomeruli” = ?

A

Focal

61
Q

Glomerular disease terminology. “involving the whole glomerulus” = ?

A

Global = how much of 1 glomerulus

62
Q

Glomerular disease terminology. “involving only part of the glomerulus” = ?

A

Segmental

63
Q

Proliferative, Membranous, or Membranoproliferative? Definition of answer?

A

Proliferative. Increased # of cells (proliferative native cells, but also infiltrating inflammatory cells)

64
Q

Proliferative, Membranous, or Membranoproliferative? Definition of answer?

A

Membranoproliferative = combination of membranous and proliferative (hence the name).

65
Q

Proliferative, Membranous, or Membranoproliferative? Definition of answer?

A

Membraneous, increased GBM without increased # cells

66
Q

3 features of crescentic glomerulonephritis?

A
  1. Involves bowmans space
  2. Proliferating epithelial cells
  3. infiltrating macrophages
67
Q

What is considered to be the largest subset of crescentic glomerulonephritis?

A

“pauci-immune” crescentic glomerulonephritis

68
Q

P-ANCA is associated with what 2 pathologies?

A

Microscopic polyangiitis, Churg-Strauss syndrome

69
Q

C-ANCA (antiproteinase 3) associated with what pathology?

A

Wegener’s (granulomatous with polyangiitis)

70
Q

fibrous scar replacing glomerulus = ?

A

glomerulosclerosis

71
Q

fibrous scar replacing part of glomerulus = ?

A

Segmental glomerulosclerosis

72
Q

Which is considered worse, acute necrotizing crescentic glomerulonephritis or focal segmental glomerulosclerosis? Why?

A

Acute necrotizing crescentic glomerulonephritis. If it involves bowman’s space (as in crescentic) it means that disease has spread past the bloodstream into urinary space = bad news bears

Renal 2 (11 decks)

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