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Renal Medicine > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What does the term Glomerulonephritis encompasses?

*includes 5 things

A
  • Caused by pathology in glomerulus
  • diagnosed on renal biopsy
  • causes CKD
  • can progress to kidney failure (except minimal change disease)
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2
Q

What Ix would you order for glomerulonephritis?

A
  • Bloods
    • FBC, U&E, LFT, CRP, Immunoglobulins, complement (C3,C4), autoantibodies (ANA, ANCA, andti-DSDNA, anti GBM)
  • Urinanalysis
    • MC&S
    • Bence Jones
    • A:CR/P:CR
    • RBC Cast
  • Imaging
    • CXR - pulmonary haemorrhage
    • Renal USS
  • Renal Biopsy (definitive)
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3
Q

What is Nephritic syndrome?

A

Group of sx, not diagnosis

  • Haematuria
  • Protenuria (<3.5g/24hrs)
  • Low GFR
  • Oliguria
  • HTN
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4
Q

What is Nephrotic syndrome?

A

Group of sx, not diagnosis

  • Proteinuria (>3g/day)
  • Peripheral oedema
  • Hypoalbuminamia (<30g/L)
  • Hypercholesterolaemia
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5
Q

What is interstitial nephritis?

What are the types of interstitial nephritis?

A
  • inflammation of spaces between cells and tubules
  • acute interstitial nephritis & chronic tubulointerstitial nephritis
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6
Q

What is glomerulosclerosis?

What causes golmeruosclerosis?

A
  • Pathological processes of scarring of tissue in the glomerulus
  • Any glomerulonephritis, obstructive uropathy, focal segmental glomeruloscelrosis
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7
Q

What causes nephrotic syndrome?

A
  • Primary renal disease
    • Minimal Chnage Disease (most common in children)
    • Membranous nephorpathy
    • Focal Segmental Glomerulosclerosis
    • Membranoproliferative GN
  • Secondary
    • DM
    • myeloma
    • amyloidosis
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8
Q

What causes proteinuria?

A
  • Damage to podocytes
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9
Q

How would you Mx nephrotic syndrome?

A
  1. Reduce odema
    • Fluid & salt restriction
    • Loop diuretics
    • Add thiazide if oedema persist
    • Aim 0.5-1kg/day weight loss
  2. Treat underlying cause
    • Corticosteroids - causes remission
    • Renal biopsy
  3. Reduce proteinuria
    • ACEi/ARB
  4. Treat complications
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10
Q

`What are the Cx of nephrotic syndrome?

A
  • Thromboembolism
    • Eg: Renal vein thrombosis, DVT
    • Px: anti thrombin 3 loss through filtration in kidneys
    • Tx: Warfarin, low dose LMWH
  • Infection
    • Eg: RTI, UTI, Cellulitis, CNS infection
  • Hyperlipidaemia
    • Px: hepatic synthesis due to low oncotic pressure and dec. lipid breakdown
    • Tx: Statin
  • HTN & CKD
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11
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal Change Disease

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12
Q

What is the Px Minimal Change DIsease?

A
  1. T cells release cytokines
  2. Damage foot processes of podocytes
  3. Effacement occurs
  4. Loss of charge barriers
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13
Q

What causes minimal change disease?

A
  • Idiopathic (most)
  • NSAIDs, lithium
  • Paraneoplastic
    • hodgkin’s lymphoma
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14
Q

How would you diagnose MCD?

A
  • Light microscope
    • normal
  • Electron microscope
    • effacemet (narrowing) of podocyte foot process
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15
Q

How would you treat MCD?

A
  • Prednisolone 1mg/kg - 4-16weeks
  • If relapse
    • cyclophosphamide
    • calcineurin inhibitors
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16
Q

What is the most common cause of nephrotic syndrome in adults?

A
  • Membranous nephropathy
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17
Q

What causes Membranous Nephropathy?

A
  • Primary
    • idiopathic
  • Seconary
    • malignancy: lung, breast, GI, prostate
    • infection: schistosomiasis, hepatitis b/c strep, malaria
    • immunological disease: SLE, RA, sarcoidosis, sjogren
    • drug: gold, penicillamine
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18
Q

How would you diagnose MN?

A
  • Bloods
    • Antiphospholipase A2 receptor antibody
  • Histology
    • Thickened GBM
    • IgG deposits
    • Spikes on silver stain
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19
Q

How would you tx MN?

A
  • ACEi/ARB in all
  • Corticosteroid + cyclophosphamide in high risk progression
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20
Q

When would you consider a patient having MN being high risk of progression?

A
  • porteinuria >4g
  • no response to ACEi/ARB after 6months
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21
Q
A
22
Q

What is the commonest glmerulonephritis seen on renal biopsy?

A
  • Focal segmental glomerulosclerosis
23
Q

What causes FSGS?

A
  • Idiopathic
  • Seconday
    • HIV
    • Heroin
    • Lithium
    • Lymphoma
    • scarring due to other glomerulonephritis
24
Q

What are FSGS all at risk of?

A
  • CKD and Kidney Failure
  • high proteinuria worsens prognosis
25
Q

How would you diagnose FSGS?

A
  • Histology
    • focal sclerosis
26
Q

How would you tx FSGS?

A
  • ACEi/ARB in all
  • Corticosteroid
  • Calcineurin inhibitor
  • Rituximab & palsma exchange in renal transplant
27
Q
A
28
Q

How would you mx pt with renal biopsy?

*think pre and post procedure

A
  • Pre-procedure
    • BP - follow local protocol
    • FBC - Hb>9, plt>100, clotting (pt&aptt <1.2)
    • Consent
    • Explain complication
    • Stop anticoagulants
  • Post procedure
    • Bed rest min 4hrs
    • Monitor pulse, BP, sx and urine colour
    • Macroscopic haematuria settles - can discharge
    • Start anticoagulants
29
Q

What is IgA N also known as?

A

Berger’s disease

30
Q

What is the most commonest primary glomerulonephritis in developed countries?

A
  • IgA nephorpathy
31
Q

How does IgA Nephropathy (Berger’s Disease) present?

A
  • Asymptomatic
  • non-visible haematuria
  • high BP
  • Proteinuria
  • slow progression to RF
32
Q

How would you diagnose IgA N?

A
  • Histology
    • IgA in mesangium cells
33
Q

How would you tx IgA N?

A
  • ACEi/ARB
  • Corticosteroid
  • Fish oil
34
Q

What are the examples of diseases causing nephritic syndrome?

A
  • IgA Nephropathy
  • Anti-GBM disease (goodpasture syndrome)
  • Post-streptococcal GN
  • ANCA associated vasculitis
    • Granulomatosis c polyangiitis
    • Microscopic polyangiitis
    • Eosinophilic granulomatosis c polyangiitis (churg strauss syndrome)
  • Thin basement membrane disease
  • Alport syndrome
  • Lupus Nephritis
35
Q

What is anti-GBM disease previously known as?

A
  • Goodpasture disease
36
Q

What is the presentation of anti-GBM disease?

A

Renal pathology

  • Oliguria
  • Haematuria
  • AKI

Lung pathology

  • SOB
  • Haemoptysis
  • pulmonary haemorrhage
37
Q

What does the anti-GBM antibody target?

A
  • T4 collagen found in glomerular and alveolar basement membranes
38
Q

How would you diagnose anti-GBM disease?

A
  • Blood
    • anti-gbm in circulation
39
Q

How would you tx anti-gbm disease?

A
  • Plasma exchange
  • corticosteroid
  • cyclophosphamide
40
Q

anti-GBM disease and ANCA associated vasculitis (Wegener’s granulomatosis) presents the same. How would you differentiate between the two?

A
  • anti-GBM D: have anti-GBM antibodies
  • WG: have Anti Neutrophil Cytoplasmic Antibodies (ANCA)
41
Q

How does post-streptococcal GN present?

A
  • 2 weeks after throat infection
  • 3-6 weeks after skin infection
  • haematuria
  • oedema
  • high BP
  • oliguria
42
Q

How would you diagnose and tx PSGN?

A
    • anti-strep antibodies (ASO titre)
  • low C3
  • IgG, IgM, C3 deposition on biopsy
  • Self limiting
  • ACEi/ARB, low sodium diet
  • If ESRF - RRT
43
Q
A
44
Q

What causes rapidly progressive GN?

A
  • ANCA vasculitis
  • lupus nephritis
  • anti-GBM disease
  • IgA N
  • MN
45
Q

How would you diagnose RPGN?

A
  • Histology
    • cresenteric GN
46
Q

How would you tx RPGN?

A
  • Corticosteroids
  • cyclophosphamide
  • plasma exchange - antiGBM/ANCA vasculitis
  • monoclonal antibodies - lupus nephritis
47
Q

What is Henoch-Schonlein Purpura?

A
  • Small vessel vasculitis & systemic variant of IgA N
  • IgA deposit in skin/joint/gut/kidney
48
Q

How does HSP present?

A
  • Purpuric rash on extensor surfaces
  • fitting polyarthritis
  • abdominal pain
  • nephritis
49
Q

How would you diagnose HSP?

A
  • Clinically
  • Skin
    • IgA
    • C3
  • Renal biopsy
50
Q

How would you tx HSP?

A
  • same as IgA nephropathy
51
Q
A
52
Q

How would you briefly tx Glomerulonephritis?

*Think supportive therapy, immunosuppresive therapy, invasive therapy

A
  • supportive therapy
    • Discuss with renal team
    • MDT approach
    • ACEi/ARB for proteinuria
    • BP control
    • Salt, water restriction and diuretics - if fluid overload
    • LMWH if hypoalbuminaemia
    • Statins for HCL
  • Immunosuppresive therapy
    • Oral corticosteroid, IV methylprednisolone, Cyclophosphamide, Tacrolimmus, Ciclosporin, Rituximab, MMF, Azathioprine
  • Invasive therapy
    • RRT
    • Plasma exchange for AAV, anti-GBM

Renal Medicine (11 decks)

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