NEPHROLOGY Flashcards

1
Q

WHAT IS GLOMERULONEPHRITIS?

A

Inflammation of nephrons and glomerulus due to an infection where the antigen-antibody complexes attack the nephrons.

> can be sudden (acute) / gradually (chronic)

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2
Q

WHAT IS NEPHRITIS?

A
LEAK OF RED BLOOD CELLS + MILD PROTEINS 
> hematuria 
> oligouria > less urine volume 
> azotemia - elevation in blood urea nitrogen + serum creatinine levels 
> arterial hypertension
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3
Q

WHAT IS NEPHROSIS?

A

> HEAVY PROTEINURIA > 3.5g/day
hypoalbuminemia
hyperlipidemia
edema

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4
Q

OUTLINE MORPHOLOGICAL PHASES OF GLOMERULAR INJURY?

A

> EXUDATIVE PHASE
PROLIFERATIVE PHASE
SCLEROTIC PHASE OF INFLAMMATORY PROCESS

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5
Q

OUTLINE INJURY MECHANISM FOR GLOMERULONEPHRITIS?

A
  1. IMMUNE COMPLEX ASSOCIATED INJURY

2. INJURY ASSOCIATED WITH ANTIBODY TO GLOMERULAR BASEMENT MEMBRANE

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6
Q

DESCRIBE IMMUNE COMPLEX ASSOCIATED INJURY TO NEPHRONS?

A

> presence of antigen-antibody complexes
circulating in blood or in situ of glomerulus
in situ complexes formed when Ab directed at glomerular Ag or foreign bodies + get trapped in glomerulus&raquo_space; SLE
Ag-Ab complexes entrapped + precipitates in glomerular basement membrane

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7
Q

DESCRIBE INJURY ASSOCIATED WITH ANTIBODY TO GLOMERULAR BASEMENT MEMBRANE

A

> Ab directed against Ag of basement membrane
Ab reacts with Ag
this is seen with immunofluroscent staining for IgG
Ab + Ag reaction > activates inflammatory mediators
inflammation > glomerular injury
godpasteurs syndrome

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8
Q

WHAT IS GODPASTEURS SYNDROME

A

> group of acute illnesses affecting lungs + kidneys
autoimmune disorder
immune system > antibodies attack lungs + kidneys
GLOMERULONEPHRITIS
PULMONARY HEMORRHAGES
ANTIGENS ATTACKING ALVEOLAR BASEMENT MEMB.

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9
Q

OUTLINE MEDIATORS OF GLOMERULAR DAMAGE?

A
1. COMPLEMENT 
> role of inflammatory process 
> activated by immune complexes 
> attract neutrophil polymorph 
> increase vascular permeability 
> membrane damage 
  1. POLYMORPHONUCLEAR LEUKOCYTES
    > attracted by C5a
    > bind to complexes by C3 + FC receptors
    > release lysosomes in response to trapped complexes
    > further increase damage to glomerular basement memb
3. CLOTTING FACTORS
> mediate glomerular damage 
> fibrin - entraps platelets due to C3 + FC receptors
> micro thrombi formation 
> degranulation 
> release of vasoactive peptides 
> increase vascular permeability
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10
Q

OUTLINE MORPHOLOGICAL DIAGNOSTICS FOR GLOMERULONEPHRITIS

A
  1. Ab tagged with fluorochrome
    - localise immuinoreactants in glomerulus
  2. Ultrastructural studies
    - position of immune complexes
    - basement membrane reactions
    - epithelial changes
  3. Renal biopsy
    - light microscopy > 20 glomeruli
    - immunofluorescence > 5 glomeruli
    - electron microscopy > 2 glomeruli
  4. Glomerular hypercellularity
  5. Podocytes
    - intracapillary > mesangium + endothelium
    - intercapillary > mesangium
    - extracapillary > bowmans capsule
  6. Thickening of glomerular capillary loops
    - deposition of immune complexes
    - increase GBM material
    - infiltrate abnormal materials - amyloid
  7. Basement membrane immune deposition
    - sub epithelial
    - intramembranous
    - sub endothelial
  8. Hyalinosis
  9. Sclerosis/ Collagenous scarring
    - irreversible damage due to chronic process
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11
Q

WHAT POST-STREPTOCOCCAL GLOMERULONEPHRITIS

A

> 10-14 days after upper respiratory infection w/ nephritic strains of beta hemolytic streptococci.

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12
Q

DESCRBINE PATHOGENISIS OF POST-STREPTOCOCCAL GN?

A
> immune complexes of strept. Ag-Ab
> circulate in blood 
> deposit in glomeruli 
OR 
> immune complexes formed in situ from bacterial Ag that are trapped in glomeruli
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13
Q

OUTLINE CLINICAL MANIFESTATIONS OF POST-STREPTOCOCCAL GN?

A
> most common in children 
> proteinuria 
> hematouria 
> hypoalbuminemia 
> edema 
> hypertension 
> renal failure 
>> leading to slow progression of chronic glomerulonephritis or rapid progression of progressive glomerulonephritis
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14
Q

DESCRIBE MICRO OF POST-STREPTOCOCCAL GN?

A

> diffuse + inflammation of glomeruli
enlarged + hypercellular glomeruli
> due to proliferation of mesengial cells + inflammatory inflitration of neutrophils + macrophages

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15
Q

DESCRIBE ELECTRON MICROSCOPY OF POST-STREPTOCOCCAL GN?

A

> inflammatory cells appear in capillaries attached to basement membrane
osmophilic dense deposits of immune complexes
> form large humps on subepithelium

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