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MHD II Test 4 > Renal Pathology I > Flashcards

Renal Pathology I Flashcards

1
Q

Kidney Gross

  1. weight
  2. size
  3. 2 main parts
A
  1. 150 gm each
  2. 12 x 6 cm
  3. cortex, medulla
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2
Q
  1. Which part of the kidney gets more perfusion?
  2. Walk through the path an artery takes
  3. What does this mean?
A
  1. cortex receives 90%
  2. artery flows through glomerulus, then to the medulla
  3. vessels which feed the tubules are post-glomerulus; damage to glomerulus –> poor perfusion of tubules
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3
Q

What is the role of each in the Glomerulus?

  1. endothelium
  2. mesangium
  3. podocytes
  4. What is in the basement membrane?
A
  1. have openings, filtration
  2. holds several capillaries in place; contractile, may be phagocytic, proliferation
  3. 2 layers of visceral epithleium that anchor cells and act as filtration of finer materials
  4. lamina rara interna and externa; lamina densa
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4
Q

Glomerular Filtration barrier

  1. What is it permeable to?
  2. How does it block other things?
A
  1. water and small solutes
  2. proteins: size barrier (collagen type IV and laminin), charge dependent restriction (negatively charged lamina externa and interna by heparin sulfate)
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5
Q
  1. What is the main way that glomerular injury occurs?
  2. 2 types
  3. Describe
A
  1. Immune complexes

2. either circulating or in-situ

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6
Q

3 Phases of Immune Complex Disease

A
  1. formation of Ag-Ab complexes
  2. deposition of Ag-Ab complexes and leukocyte recruitment/activation
  3. inflammatory reaction at the site of deposition
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7
Q

Formation of Immune complexes in circulation?

  1. does it always = disease?
  2. What factors affect whether or not it causes disease? (4)
  3. Why does this occur in the kidneys?
A
  1. no
  2. size of ICs
  3. functional status of mononuclear phagocytic system
  4. charge of complex, valency (antigen), avidity (Ab), affinity of the Ag to tissues, immune complex 3D structure, hemodynamics
  5. increase in vascular permeability –> immune complex binding to inflammatory cells
  6. easier to be trapped in kidneys due to lots of capillaries
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8
Q
  1. What happens when there is an antibody excess?
  2. When there is a slight antigen excess?
  3. When there is phagocytic system overload/dysfunction?
A
  1. large ICs, rapidly phagocytized
  2. small/intermediate ICs, bind less avidly to phagocytic cells and circulate longer- most pathogenic
  3. persistence of IC in circulation –> tissue deposition
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9
Q

How charge affects IC localization

  1. overall charge
  2. sub-epithelial charge
  3. sub-endothelial charge
  4. mesangial charge
  5. What happens to large IC?
A
  1. integrity of barrier is important, negative
  2. highly cationic
  3. highly anionic
  4. neutral
  5. not nephritogenic (usually), cleared by mononuclear phagocyte system
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10
Q

Antibodies directed to proximal zones

  1. location
  2. inflammatory?
  3. symptom?
A
  1. endothelium, sub-endothelium
  2. yes
  3. infiltration of leukocytes –> structural injury –> hematuria
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11
Q

Antibodies directed to distal zones

  1. location
  2. inflammatory?
  3. symptom?
A
  1. epithelium, sub-epithelium
  2. mostly no
  3. alters podocytes –> proteinuria
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12
Q

Circulating IC Glomerulonephritis

  1. Define
  2. Are Ab specific to glomerulus?
  3. What are the Ags?
  4. How is damage caused?
A
  1. trapping of circulating Ag-Ab complexes within glomeruli bc of physico-chemical properties and hemodynamic factors peculiar to glomerulus
  2. NO immunological specificity for glomerular constituents
  3. exogenous (infectious) or endogenous (autoimmunity)
  4. by eliciting inflammatory rxn at site of deposition
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13
Q

IC Deposition

  1. Histo
  2. Pathomechanism
  3. Clinical Syndrome
A
  1. leukocyte infiltration, mesangial and endothelial proliferation, structural damage to capillary wall, “swiss cheese”-large holes
  2. circulating ICs –> deposition +inflammation + endocapillary proliferation
  3. Nephritic syndrome- hematuria, mild proteinuria, renal failure, edema, HTN (fluid retention)
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14
Q

In-situ immune complex deposition

  1. Define
  2. 2 types
  3. Histo
  4. Stain for IgG
  5. What does this cause?
  6. What is this call clinically?
A
  1. Abs with immunological specificity for glomerular constituents
  2. fixed (intrinsic): within glomerular basement membrane and epithelial cells
  3. planted (intrinsic or extrinsic)
  4. parietal epithelial cells proliferate and form a crescent
  5. linear stain
  6. damage along the entire length of GBM w/ gross hematuria, crescents and, rapidly progressing renal failure
  7. rapidly progressing glomerulonephritis (RPGN)
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15
Q

Anti-GBM induced GM

  1. What happens to podocytes on EM?
  2. What else can be seen on EM?
  3. Why is there no cellular reaction?
A
  1. become effaced (fuse together)
  2. glomerular capillary has electron dense deposits under epithelial cells = sub-epithelial immune complex deposits
  3. binding occurs on the urinary side of the GBM, activation of complement and cytokine factors is modified bc the site of the deposit is remote from the activators that are normally present in circulation
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16
Q

Anti-GBM induced GM

  1. Inflammation?
  2. What happens to filtration integrity?
  3. Pathomechanism
  4. Clinical syndrome
  5. Pathology
A
  1. no inflammatory response
  2. sub-epithelial ICs impact filtration integrity of epithelial cells and GBM; creates a gauze-like or fine mesh effect –> proteinuria;
    larger particles are retained, so there is NO hematuria
  3. in-situ IC deposition
  4. Nephrotic syndrome
  5. Membranous glomerulonephritis AKA “nephropathy”
17
Q

Mediators of Glomerular injury

  1. cells
  2. soluble mediators
  3. Genetic defects can affect what (2)?
A
  1. neutrophils, monocytes, macrophages, resident glomerular cells, T lymphocytes, NK cells, platelets
  2. complement, eicosanoids, NO, angiotensin, endothelin, cytokines, chemokines, coagulation system
  3. immune response, structure
18
Q

Epithelial cell injury causes (5)

A
  1. toxins (experimental models)
  2. cytokines (permeability factor)
  3. podocyte injury (podocytopathies)
  4. reversible vs irreversible
  5. nephrotic syndrome
19
Q

Epithelial Cell Injury

  1. Pathomechanism
  2. Pattern of injury
  3. Clinical Syndrome
  4. What happens when the change is reversible?
  5. Irreversible?
A
  1. podocyte injury, NO immune complexes
  2. podocyte foot process effacement, detachment vacuolization, retraction, loss of slit diaphragm, non-inflammatory
  3. Nephrotic syndrome
  4. minimal change disease
  5. focal and segmental glomerular sclerosis
20
Q

Nephritic Syndrome

  1. main symptom
  2. what is serum sickness?
  3. What is Masugi?
A
  1. hematuria
  2. postinfectious glomerulonephritis
  3. severe nephrotic syndrome with GROSS hematuria and rapidly progressing renal failure- RPGN anti GBM
21
Q

Nephrotic syndrome

  1. main symptom
  2. What is Heymann?
  3. What happens in podocyte injury?
A
  1. proteinuria
  2. membranous glomerulonephritis
  3. minimal change disease (reversible), FSGS (irreversible)

MHD II Test 4 (4 decks)

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