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Renal YR3 > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

Presentation of nephrotic syndrome

A
  • Oedema
  • Albumin less than 30g/L
  • Urine more than 3g protein in 24hrs
  • Hypercholesterolaemia
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2
Q

Complications of nephrotic syndrome

A
  • Higher risk of infection
  • VTE
  • Progression of CKD
  • HTN
  • Hyperlipidaemia
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3
Q

Causes of nephrotic syndrome

A
  • Minimal change disease - most common GN in children
  • Focal segmental glomerulosclerosis - idiopathic or secondary to infection, malignancy, drugs etc
  • Membranous nephropathy - same as above, most common adult cause
  • Membranoproliferative glomerulonephritis (but more commonly presents as nephritic)
  • Amyloidosis/myeloma/diabetes - proteinuria but no other nephrotic features
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4
Q

Presentation of nephritic syndrome

A
  • AKI - sometimes GFR can drop drastically
  • Blood +/- protein +/- on urine dip
  • Sometimes mild/moderate oedema
  • Proteinuria less than 3/5g in 24hrs though
  • HTN
  • Haematuria visible?
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5
Q

Causes of nephritic syndrome

A
  • Post streptococcal
  • IgA nephropathy
  • Small vessel vasculitis (ANCA)
  • Anti GBM disease (Goodpastures)
  • Thin basement membrane disease
  • Alport syndrome
  • Lupus nephritis
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6
Q

Associations of post streptococcal GN

A
  • Weeks after Group A beta haemolytic streptoccal infections
  • 1-2 weeks post tonsillitis/pharyngitis
  • 3-4 weeks after impetigo/cellulitis
  • Children ages 3-12
  • Can lead to rapid progressive GN
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7
Q

Investigation features of post strep GN

A
  • Positive anti-streptococcal antibodies - anti-streptolysin O titre
  • Low serum C3
  • Biopsy shows immune complex deposition IgG, IgM, C3
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8
Q

Treatment for post strep GN

A
  • Usually self limiting
  • Supportive therapy of ACEi/ARB for proteinuria and HTN
  • Low sodium diet
  • If proceeds to ESRF –> RRT
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9
Q

Associations of IgA nephropathy

A
  • Most common idiopathic GN worldwide
  • Episodic gross haematuria during/directly after URTI, GI infections or strenous exercise
  • Affects males more than females
  • Peak incidence 20-30s
  • 25-30% progress to ESRF within 20-25yrs
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10
Q

Investigation findigns for IgA nephropathy

A
  • Asymptomatic microhaematuria
  • Intermittent visible haematuria
  • Increase serum IgA
  • Normal C3 and C4
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11
Q

Biopsy findings IgA nephropathy

A
  • Biopsy shows mesangial immune complex deposits in glomeruli
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12
Q

Treatment for IgA nephrotpathy

A

Supportive:
* ACEi/ARB for proteinuria and HTN

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13
Q

3 types of small vessel vasculitis (ANCA associated)

A
  • Granulomatosis with polyangitis (GPA)
  • Microscopic polyangitis (MPA)
  • Eosinophilic granulomatosis (Churg-Strauss syndrome)
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14
Q

Associations of GPA vasculitis

A

Pulmonary and nasopharyngeal involvement - haemoptysis and nasal ulcers/polyps
Saddle nose
Nasal crusting

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15
Q

Investigation findings for GPA vasculitis

A
  • c-ANCA (PR3)
  • Biopsy shows segmental necrotizing GN
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16
Q

Treatment for all small vessel vasculitis (ANCA associated)

A

Immunosupression

17
Q

Associations of MPA vasculitis

A

Mild respiratory symptoms

18
Q

Investigation findigns for MPA vasculitis

A
  • p-ANCA (MPO)
  • Biopsy shows segmental necrotizing GN (same as GPA)
19
Q

Associations of Churg-strauss syndrome

A
  • Asthma
  • Allergic rhinitis
  • Purpura
  • Peripheral neuropathy
20
Q

Inv findings for Churg-Strauss syndrome

A
  • p-ANCA
  • Bloods show eosinophilia
  • Biopsy shows focal segmental necrotizing GN
21
Q

Associations with Goodpastures syndrome

A

Two peaks:
* 30s - affecting male more than females
* 60s - affecting females more than males
* Antibodies against type IV collagen - react with pulmonary BM causing pulmonary haemorrhage
* Can lead to rapdly progressive GN

22
Q

Inv findings for Goodpastures

A
  • Anti GBM antibodies
  • Pulmonary infiltrates on CXR
  • Biopsy shows linear deposition of IgG along BM
23
Q

Treatment for Goodpastures

A

Plasma exchange
Immunosupression

24
Q

Associations with thin basement membrane disease

A
  • Hereditary
  • Abnormalities with Type IV collagen
  • Good prognosis
25
Q

Inv findigns for thin basement membrane disease

A
  • Peristent microscopic haematuria - possible intermittent visible
  • Biopsy shows diffuse thinning of GBM
26
Q

Treatment for thin basement membrane disease

A
  • Monitor renal function
  • Supportive treatment
27
Q

Associations with alport syndrome

A
  • X linked - affects males mostly
  • Mutation in gene coding for Type IV collagen
  • Associated with hearing loss and abnormalities of eyes
  • Often leads to ESRF
28
Q

Inv findings for Alport syndrome

A
  • Persistent microscopic haematuria with intermittent visible
  • Sensorineural hearing loss
  • Biopsy - splitting of GBM and alternating thickening and thinning
  • Genetic studies show FH
29
Q

Treatment for alport syndrome

A
  • Supportive
  • RRT
  • Renal transplant - BUT can lead to development of Goodpasture syndrome
30
Q

Associations of lupus nephritis

A
  • Complication of SLE
  • Nephritic or nephrotic
31
Q

Inv findings for lupus nephritis

A
  • ANA and anti-dsDNA +ve
  • Biopsy shows 6 different classes with different presentations and varied treatment options
32
Q

Treatment for lupus nephritis

A

Supportive therapy
Immunosupressive based on classification/presentation

33
Q

Supportive general therapy of glomerulonephritis

A
  • If suspect GN - discuss with renal team
  • MDT approach
  • ACEi/ARB control proteinuria
  • Control BP
  • Salt and water restriction if fluid overload/diuretics
  • If hypoalbuminaemic less than 20g/dL then higher risk of VTE - consider LMWH
  • Statins for hypercholesterolaemia
34
Q

Examples of immunosupressive therapy

A
  • Oral corticosteroids
  • IV pulsed methylprednisolone
  • Cyclophosphamide
  • Tacrolimus
  • Ciclosporin
  • Rituximab
  • Mycophenolate Mofetil
  • Azathioprine
35
Q

Invasive therapy for GN

A
  • RRT/haemodialysis if severe AKI or ESRF
  • Plasma exchange for ANCA associated vasculitis and anti GBM (goodpastures)
36
Q
A

Renal YR3 (11 decks)

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