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S2.6 Renal > Glomerular Disease > Flashcards

Glomerular Disease Flashcards

1
Q

What is glomerulonephritis?

A

Disease of glomerulus
- inflammatory or non-inflammatory

Can be primary (only glomerulus affected) or secondary to a wider condition e.g. SLE)

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2
Q

What are the general causes of glomerulonephritis?

A

Autoimmune
Infection
Malignancy
Drugs

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3
Q

What are the two different classes of glomerulonephritis, and what are some examples of each type?

A

Proliferative

  • post-infective (diffuse)
  • mesangial IgA disease (focal)
  • crescentic nephritis (focal necrotising)
  • membrano-proliferative nephritis
  • diabetic nephropathy

Non-proliferative

  • minimal change disease
  • focal segmental glomerulonephritis
  • membranous nepropathy
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4
Q

What are the two general forms of glomerulonephritis presentation, and with which types of the disease do they correlate? Which type can present with both?

A

Proliferative generally presents with nephritic state

Non-proliferative generally with nephrotic syndrome

Membrano-proliferative can present as combined nephrotic/nephritic

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5
Q

What is the commonest type of glomerulonephritis?

A

IgA nephropathy in general

Membranous is commonest nephrotic syndrome cause

Minimal change commonest in children

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6
Q

What are the 4 common symptoms/signs presenting in glomerulonephritis?

A

Haematuria
Heavy proteinuria (nephrotic syndrome)
Slowly increasing proteinuria
Acute renal failure

Hypertension also common co-morbidity

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7
Q

What is the common presentation of IgA nephropathy?

A

Microscopic haematuria
Proteinuria
Nephritic, sometimes nephrotic

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8
Q

What features may suggest minimal change disease

A

Sudden onset of oedema

Complete loss of proteinuria with steroids

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9
Q

How does focal segmental glomerulosclerosis generally present?

A

Nephrotic syndrome
Distinct patterns of sclerosis
Generally steroid resistant
High chance of end-stage kidney disease

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10
Q

What are the features of nephritic state?

A

Active urine sediment - haematuria, dysmorphic RBCs, cellular casts

Hypertension
Renal impairment

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11
Q

What are the features of nephrotic syndrome?

A

Oedema
Proteinuria >3.5g/day
Hypoalbuminaemia
Hyperlipidaemia

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12
Q

What are the 4 main pathological types of glomerulonephritis? (By Paul Brown’s standards)

A

IgA nephropathy
Membranous glomerulonephritis
Diabetic nephropathy
Crescentic glomerulonephritis

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13
Q

What investigations might be performed in suspected glomerulonephritis?

A 
Renal biopsy is key
Dipstick
Urine culture
USS
Usual bloods e.g. serum albumin, creatinine (eGFR)

Specific serological markers

  • anti-GBM antibodies in serum/kidney = anti-GBM disease (type of crescentic)
  • anti phospholipase A2 receptor antibody positive in 70% of idiopathic causes of membranous nephropathy
  • ANCA serum test (Wegener’s/microscopic polyarteritis)
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14
Q

What are some other causes of haematuria (not glomerulonephritis)?

A

UTI
Urinary tract stone
Urinary tract tumour

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15
Q

How is glomerulonephritis differentiated as diffuse/focal and global/segmental?

A 
Diffuse = >50% of glomeruli affected
Focal = <50%
Global = the entire of the affected glomeruli are affected
Segmental = only part of each affected glomerulus is affected
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16
Q

How is post-infective nephropathy treated?

A

Possible antibiotics
Loop diuretics (e.g. furosemide)
Vasodilators (amlodipine) for hypertension

17
Q

How is IgA nephropathy treated?

A

Hypertension treatments - ACEi/ARB
Immunosuppressants - cortisol
Consider statins

18
Q

How is crescentic nephropathy treated?

A

Immunosuppression - corticosteroids, plasma exchange, cytotoxic (cyclophosphamide), rituximab, complement inhibitors

Anti-GBM - aggressive immunosuppression

19
Q

What are the general measures of treatment in nephrotic syndrome?

A

Treat oedema - salt/fluid restriction and loop diuretics
Treat hypertension - RAAS blockade
Reduce thrombosis risk - warfarin/heparin
Reduce infection risk - pneumococcal vaccine
Treat lipidaemia - statins

20
Q

How is minimal-change disease treated?

A

General measures if required
Prednisolone
Slowly taper once remission achieved
Treat initial relapse with prednisolone, further relapses with cyclophosphamide, cyclosporin, tacrolimus, mycophenolate mofetil, rituximab

21
Q

How is focal segmental glomerulosclerosis treated?

A

General measures
Steroids
Alternatives - cyclosporin, cyclophosphamide, rituximab

22
Q

How is (non-proliferative) membranous nephropathy treated?

A

General measures for 6 months
Immunosuppression if symptomatic nephrotic syndrome/rising proteinuria/deteriorating renal function
Cyclophosphamide and steroids (alternating) for 6 months
Cyclosporin, rituximab

23
Q

Why does IgA deposition cause proliferation?

A

Mesangium, NOT filter membrane, clogged with IgA

IgA irritates mesangial cells, causes them to proliferate and produce more matrix

24
Q

What are the pathological features of membranous glomerulonephritis, why does this cause nephrotic syndrome?

A

Thickened glomerular basement membrane
Spikes of new basement membrane matrix material underneath podocytes
Deposit of IgG within thickened membrane
Basal lamina spike (matrix which tries to surround and remove IgG deposit)

IgG deposits itself from plasma to between basal lamina and podocyte buy cannot go further and is not filtered into urine - too big
But IgG activates complement (C3), which punches holes in filter

Leaky filter now allows albumin to be filtered into urine > nephrotic syndrome

25
Q

What is the pathology behind diabetic nephropathy?

A

Increased mesangial matrix (which compresses capillaries) - due to glycated molecules (collagen becomes protease resistant)
Thickened capillary wall which is leaking albumin
Small compressed capillary lumen
Adhesions to Bowman’s capsule are glomerulus’ attempt to stop massive leakage of albumin into urine
Thickened, narrowed arterioles reduce blood flow to glomerulus

Nodules of mesangial matrix = Kimmelsteil-Wilson lesion
- gross excess of mesangial matrix forming nodules

26
Q

What are the pathological features of crescentic glomerulonephritis?

A

Cellular proliferation and influx of macrophages (= crescent) around crushed glomerular tuft, within Bowman’s space

Different causes

  • Granulomatosis with polyangiitis (also known as Wegener’s granulomatosis)
  • Microscopic polyarteritis (A disease like Wegener’s) (serum test for ANCA - not deposited in kidneys)
  • Anti-glomerular basement membrane (GBM) disease

S2.6 Renal (8 decks)

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