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Z Year3 Urology > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What are the 2 types of glomerulonephritis?

A
  1. Nonproliferative (cells do not multiply): nephrotic

2. Proliferative (cells multiple): nephritic

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2
Q

What are features of nephrotic syndrome?

A
  1. Massive proteinuria (>3.5g/d) – foamy urine
  2. Hypoalbuminaemia (<25g/L)
  3. Oedema (peripheries, eyes)
  4. Hyperlipidaemia + lipiduria – fatty casts on microscopy
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3
Q

What are features of nephritic syndrome?

A
  1. Haematuria - red cell casts (dmage is enough to let RBC through)
  2. Proteinuria (1-3.5g/d)
  3. Oedema
  4. Progressive renal impairment
  5. HTN
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4
Q

How do you remember nephrotic syndrome?

A
  • Protein COAL
    1. Proteinuria
    2. Cholesterol up
    3. Oedema
    4. Albumin down
    5. Lipids up
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5
Q

How do you remember nephritic syndrome?

A
  • Protein HOB
    1. Proteinuria
    2. Haematuria
    3. Oedema
    4. Blood pressure up
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6
Q

What are the primary causes of nephrotic syndrome?

A
  1. Minimal changes disease
  2. Membranous GN
  3. FSGS
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7
Q

What are the secondary causes of nephrotic syndrome?

A
  1. Diabetic nephropathy

2. Amyloid nephropathy

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8
Q

What is minimal changes disease?

A

most common form of nephrotic syndrome in children

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9
Q

What is the cause of minimal changes disease?

A
  1. Idiopathic

2. often triggered by immunological insult

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10
Q

What are minimal changes disease associated with?

A

non-hodgkins lymphoma

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11
Q

What are symptoms of minimal changes disease?

A
  1. FULLY NEPHROTIC PICTURE

2. facial or generalized oedema

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12
Q

What are two investigations for minimal changes disease?

A
  1. Light microscopy

2. Electron microscopy

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13
Q

What would light microscopy show on minimal changes disease?

A

minimal histological changes on biopsy (only reserved to patients not responding to treatment/ frequent relapses)

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14
Q

What would electron microscopy show on minimal changes disease?

A
  1. Podocyte effacement

2. Negative immunofluorescence (no IC deposition)

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15
Q

What is the management for minimal changes disease?

A

corticosteroids (complete recovery)

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16
Q

What is the epid for membranous GN?

A

commonest form of nephrotic syndrome in adults

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17
Q

What is the aetiology for membranous GN?

A

SUBEPITHELIAL Deposition of immune complexes on BM

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18
Q

What are RF for membranous GN?

A
  1. autoimmune disease
  2. hep B/C
  3. syphilis
  4. malignancy
  5. certain medications (NSAIDs, gold, lithium)
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19
Q

What are symptoms for membranous GN?

A
  1. Often asymptomatic
  2. Oedema
  3. Xanthelasma
  4. foamy urine
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20
Q

How do you diagnosis membranous GN?

A

Diagnosis by exclusion, renal biopsy for definite diagnosis

  1. Light microscopy
  2. Electron microscopy
  3. Immunofluroscence
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21
Q

What do you see for light microscopy in membranous GN?

A

BM thickening

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22
Q

What do you see for electron microscopy in membranous GN?

A

spike & dome appearance (glomerular matrix on top of IC deposits); podocyte effacement

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23
Q

What would imunofluresnece show in membranous GN?

A

granular immunofluorescence; IgG4 antibodies against phospholipase A2 receptors

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24
Q

What is the management for membranous gN?

A
  1. LOW RESPONSE TO STEROIDS
  2. Conservative management (low salt low protein diet)
  3. Symptomatic management: corticosteroids + cytotoxic/immunosup therapy
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25
Q

What is FSGS?

A

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

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26
Q

What is the aetiology of FSGS?

A

Injury to podocytes

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27
Q

What are RF for FSGS?

A
  1. HIV
  2. heroin abuse
  3. congenital malformations
  4. INF treatment
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28
Q

What are symptoms for FSGS?

A

Asymptomatic or nephrotic syndrome

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29
Q

What investigations are done for FSGS?

A
  1. Renal biopsy

2. Electron miscrospy

30
Q

What does Renal Biopsy show in FSGS?

A

focal segmental areas of mesangial collapse and sclerosis

31
Q

What does electron microscopy show in FSGS?

A

effacement of foot processes of podocytes

32
Q

What is the management of FSGS?

A

corticosteroids, symptomatic management

33
Q

What is the aeitology of diabetic nephropathy?

A

Kidney damage caused by type I or type II diabetes

34
Q

What is the patho of diabetic nephropathy?

A
  1. Excess glucose in urine
  2. So Glycation of proteins
  3. Then BM thickening of efferent arteriole
  4. So high pressure state
  5. Then Matrix deposition & mesangial expansion
  6. Forms Kimmelstiel-Wilson nodules + Glomerular damage
35
Q

What are symptoms for diabetic nephropathy?

A

mostly asymptomatic

36
Q

What is needed for diagnosis of diabetic nephropathy?

A
  1. Microalbuminuria

2. Light microscopy

37
Q

What can be seen on light microscopy for diabetic nephropathy?

A
  1. Mesangial expansion
  2. GBM thicjening
  3. Kimmelstiel-Wilson nodules
38
Q

What is the management of diabetic nephropathy?

A
  1. Diabetic control

2. ACEi/ARBs (lower pressure in glomerulus)

39
Q

What is amyloid nephropathy caused by?

A

secondary to amyloidosis

40
Q

What is the patho of amyloid nephropathy?

A

Abnormal amyloid protein deposits leads to Tissue damage (if in kidneys: nodular glomerulosclerosis)

41
Q

What investigation is used for amyloid nephropathy?

A

Biopsy showing nodular glomerulosclerosis

42
Q

What stain and result is used to diagnose amyloid nephropathy?

A

Congo red stain + polarizing light leads to apple green birefringence

43
Q

What are the 2 causes for nephritic syndrome?

A
  1. MPGN

2. RPGN/Crescenteric GN

44
Q

What is MPGN?

A

MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

45
Q

What is the aetiology of MPGN?

A
  1. Subendothelial Immune deposits
  2. lead to Inflammation
  3. amking structural damage of glomerulus
46
Q

What are the two types of MOGN?

A
  1. Type 1: immune complex deposits

2. Type 2: Complement deposits

47
Q

What is Type 1 MPGN caused by?

A

resulting from chronic infection, i.e.: hep B or C – complexes

48
Q

What is Type 2 MPGN caused by?

A

inappropriate activation of alternative complement pathway aka. C3 breakdown

49
Q

What are symptoms for MPGN?

A

Mixed picture

Both nephritic and nephrotic like haematuria and high protein

50
Q

What investigation is done and what does it show for MPGN?

A 
Light microscopy showing BM
double contour (Tram tracking)
51
Q

What is the management of MPGN?

A

steroids

52
Q

What is RPGN?

A

RAPIDLY PROLIFERATIVE GLOMERULONEPHRITIS

53
Q

What is the aetiology of RPGN?

A

Proliferation of cells in the Bowman’s space leads to Crescent shape

54
Q

What investigations are done for RPGN?

A
  1. BIOPSY
  2. light microcopy
  3. electron microscopy
  4. immunofluorescence
55
Q

What is the management of RPGN?

A
  1. Anticoagulants might be used to reduce fibrin buildup in crescent formation
  2. Plasmapheresis is usually used in combination with immunosuppressants (i.e.: corticosteroids)
56
Q

What are the 3 types of FPGN?

A

TYPE 1: Goodpasture syndrome
TYPE 2: Immune-complex mediated
TYPE 3: Pauci-immune

57
Q

What is the patho of good pastures syndrome?

A

Anti-glomerular membrane (GBM) antibodies trigger a TII hypersensitivity reaction

58
Q

What are symptoms of goodpasture syndrome?

A
  1. Damage to BM in lungs (initial presentation: haemoptysis, SOB)
  2. and kidneys (nephritic syndrome)
59
Q

How do you investigate goodpastures syndrome?

A
  1. Light microscopy: Crescent

2. Immunofluorescence: Linear deposition

60
Q

What are the types of immune complex mediated FPGN nephritic syndrome?

A
  1. Poststreptococcal GN
  2. SLE
  3. IgA nephropahy/ Berger’s disease
  4. Henoch-Schonlein purpura
61
Q

What is Poststreptococcal GN?

A
  1. Several weeks after group A beta-hemolytic streptococcus infection (6w after impetigo; 1-2w post throat infection)
  2. IC formation and subepithelial depositions
  3. Sx: fever, smokey urine
62
Q

What is invesitgations and management for poststrep GN?

A
  1. Dx: Antibodies anti strep (Anti-sptreptolysin O antibody)

2. Mx: supportive

63
Q

What is SLE?

A

Diffuse (all nephrons in both kidneys) or focal (some nephrons in one kidney)
Nuclear antigen + Anti-nuclear antibodies = IC deposits trigger Type III hypersensitivity reaction

64
Q

What is IgA nephropahy/ Berger’s disease?

A
  1. 1-2 days post-GI/resp infections: Formation of IgA ICs which deposit in mesangium
  2. Sx: Episodic macroscopic haematuria
65
Q

What investigations and results are done for IgA nephropahy/ Berger’s disease?

A
  1. Mesangial proliferation on LM
  2. EM & Immunofluorescence showing
  3. IC deposition in mensagium
66
Q

What is Henoch-Schonlein purpura?

A
  1. IgA vasculitis: IgA deposition in small
    vessels
  2. Sx: Ig A nephropathy + Arthralgia + purpura
67
Q

What is the aetiology of Type 2 Pauci-Immune nephritic syndrome FPGN?

A

no immune deposits, associated with anti-neutrophilic cytoplasmic antibodies (ANCA)

68
Q

What investigations are done for Pacui-immune?

A

Immnofluorescence is negative (no immune deposits); +ve ANCA

69
Q

What is cANCA pauci-immune?

A
  1. Wegener’s granulomatosis

2. Associated symptoms: Saddle nose shape, sinusitis

70
Q

What is pANCAs pauci-immune?

A
  1. Microscopic polyangiitis (Associated symptoms: purpuric rash)
  2. Churg Strauss (Associated symptoms: granulomatous inflammation, asthma and eosinophilia)

Z Year3 Urology (18 decks)

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