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Pathology -- Nephrology > Glomerular Diseases > Flashcards

Glomerular Diseases Flashcards

1
Q

Systemic diseases that may lead on to glomerulonephritis…

A

Vascular – HTN, PAN
Metabolic – Diabetes
Hereditary – Alport, Fabry
Autoimmune – SLE

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2
Q

Five glormerular syndromes

A 
Acute Nephritis
Rapidly progressive glomerular nephritis
Nephrotic Syndrome
Chronic Renal Failure
Asymptomatic Hematuria/Proteinuria
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3
Q

Four Potential hallmarks of glomerular injury

A

No Histological Alteration
Hypercellularity
Basement Membrane Thickening
Hyalinization and Sclerosis

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4
Q

Glomerular disease marked by no histological alteration

A

Minimal Change Disease – Visceral epithelial cells are injured with loss of foot processes leading to nephrotic syndrome

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5
Q

What happens in glomerular disease processes marked by hypercellularity

A

Could be immune infiltrates
Could be mesangial, endothelial, or epithelial prolif.
If rapidly progresing – form crecents

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6
Q

What happens in glomerular disease processes marked by basement membrane thickening

A

Thickening of Capillary Walls
Deposition of Material within BM
Amorphous Electron-Dense Material (precip. proteins)
IGs, complexes, fibrin, amyloid, cryo

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7
Q

What happens in glomerular disease processes marked by hyalinization and sclerosis

A
  • Accumulation of homo., eosinoph. material precipitated from plasma proteins
  • Increased BM, Mesangial Matrix
  • Obliteration of Structural detail of Glom. tuft.
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8
Q

Important details for in situ immune complex fomation/deposition that damages the glomer.

A
  • Ab directed against intrinsic fixed antigens that are components of the BM proper (ex. Goodpasture’s)
  • Homogenous, Diffuse Linear Pattern by IF
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9
Q

Important details for glomerular damage associated with antibodies against planted antigens

A
  • Non-glomerular antigens
  • Assoc. w/ DNA, Bacterial Products, Large Aggregated Proteins, Drugs (Mostly cationic molecules)
  • Granular/Heterogenous Pattern of Ig deposit
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10
Q

Important details for glomerular damage associated with circulating immune complex nephritis

A
  • Immune complexes precipitate in glomeruli
  • SLE, HEP B, HEP C, Tumor Antigens
  • Leads to Leukocytic Infil. -> Endo./Mesangial Prolif
  • IC in mesangium or btw BM and endo (Granular Deposits)
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11
Q

Important details for glomerular damage associated with antibodies to glomerular cells

A

Mesangial, endothelial cell antigens -> Injury + Thrombosis

Can cause proteinuria

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12
Q

Important details for glomerular damage associated with cell-mediated immunity

A

Sensitized nephrogenic T cells with activated mps + lympho

Experimentally assoc. w/ crecenteric GN

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13
Q

Acute proliferative glomerulonephritis results from..

A

acute deposition, as seen in post-streptococcal glomerulonephritis.

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14
Q

Effects of acute inflammatory rxns

A

Acute nephritis w/ hematuria + RBC Casts, azotemia, oliguria, mild HTN

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15
Q

Acute renal failure is associated with ______ GN

A

Rapidly Progressive (Crecentic)

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16
Q

Three types of glomerular disease associated with nephrotic syndrome

A

Membranous GN
Minimal Change Disease
Focal Segmental GN

17
Q

Hallmark of persistent GN

A

Focal segmental glomerulosclerosis w/ proteinuria

Caused by compensatory hypertrophy of remaining glomeruli

18
Q

How does glomerular sclerosis happen?

A

Endothelial and epithelial cell injury, Increased glom. permeability to proteins, accumulation of proteins in the mesangial matrix, fibrin deposition

19
Q

Potential causes of GN –> tubulointerstitial damage

A

Chronic Ischemia, Immune Rxn to Shared Antigens, Phos. or Ammonia Retention, Proteinuria

20
Q

Important details on Minimal Change Disease

A

No changes on light micro, loss of foot processes on e-
Lipid Accumulates in the tubule cels
No Immune Deposits
Massive Selective (Albumin) Proteinuria

21
Q

Important details on membranous GN?

A

Chronic Ag-Ab mediated disease
Diffuse thickening of Glom. cap wall
Irregularly dense deposits btw BM and Epithelial Cells
Markedly thickened membrane

22
Q

Important details on focal segmental glomerulonephritis

A
  • Collapse of BM, increase in Matrix. Deposition of Hyaline masses. Lipid Droplets + Foam cells. Hyaline thickening of afferents.
  • Non-involved glomeruli either appear normal or show increased mesangial matrix.
23
Q

Disease marked as mixed nephritic and nephrotic syndrome

A

Menbranoproliferative GN

24
Q

What happens in Membranoproliferative GN

A
  • Proliferation of glom cells and leukocytic infiltration
  • Large, Hypercelllar glomeruli, prolif mesangial matrix
  • Two Types
  • Can progress rapidly to progressive GN with crescents
25
Q

Differentiate the two types of membranoproliferative

A

I – Granular Deposits of Complement

II – Deposits into the BM proper, no dense

26
Q

Which glomerulonephritis-es are mostly nephritic

A

Acute Proliferative GN
Focal Proliferative and Necrotizing GN
Rapidly Progressive (Crecenteric) GN

27
Q

Important details for Acute Proliferative GN

A 
Immune complex deosition, prolif of glomerular cells, influx of leukocytes
Granular Immune deposit
Hypercellularity
Subepithelial ED Deposits
Resolves with therapy
28
Q

Important details on focal proliferative and necrotizing GN

A

Glom prolif restricted to segs of individual glomeruli

Focal necrosis and Fibrin Deposits

29
Q

Important details for Rapidly progressive (Crecenteric) GN

A
  • Distinctive Crescents made of infiltrating leukocytes and prolif. epithelial cells in glomeruli, fibrin strand btw
  • Obliteration of Bowman’s Space
  • Three types
30
Q

Three types of Rapidly progressive (Crecenteric) GN

A

I – Idiopathic (Goodpasture’s)
II – Immune Complex Mediated
III — Pauci-Immune (Wegeners, microPAN)

31
Q

Types of GN that rarely progress to chronic GN?

A

Acute (post-streptococcal) GN, Minimal Change Disease

32
Q

Types of GN that sometimes progress to chronic GN?

A

Membranous, Membranproliferative, IgA

33
Q

Types of GN that commonly progress to chronic GN?

A

Focal sclerotic, RPGN

Pathology -- Nephrology (12 decks)

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