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ESA3 - Urinary System > Glomerular Pathology > Flashcards

Glomerular Pathology Flashcards

1
Q

What characterises nephrotic syndrome?

A
  • Proteinuria
  • Hypoalbumiaemia
  • Peripheral oedema
    (also hyperlipidaemia)
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2
Q

How does urine appear in a patient with nephrotic syndrome?

A

Frothy

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3
Q

Why does hypoalbuminaemia occur in a patient with nephrotic syndrome?

A

Albumin is lost in urine -> proteinuria

This is because gaps in podocytes allow proteins to leak

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4
Q

Why does a patient with nephrotic syndrome present with peripheral oedema?

A

Decreased intravascular oncotic pressure

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5
Q

Why does a patient with nephrotic syndrome present with hyperlipidaemia?

A

Liver tries to compensate for hypoalbuminaemia and increases production - the side effect is an increase in the production of lipids

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6
Q

What are the primary causes of nephrotic syndrome?

A
  • Minimal change glomerulonephritis
  • Focal segmental glomerulosclerosis
  • Membranous glomerulonephritis
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7
Q

What are some secondary causes of nephrotic syndrome?

A
  • SLE
  • Hep B and C
  • HIV
  • Diabetes
  • Malignancy
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8
Q

What kind of syndrome does minimal change glomerulonephritis lead to?

A

Nephrotic syndrome

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9
Q

How does minimal change glomerulonephritis appear under a microscope?

A

Under light microscope - normal

Under electron microscope - loss of foot processes on podocytes - widening of filtration slits

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10
Q

What do most patients with minimal change glomerulonephritis respond well to?

A

Steroids

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11
Q

What is the pathogenesis of minimal change glomerulonephritis?

A

Unknown circulating factor causing damage to podocytes

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12
Q

What is focal segmental glomerulosclerosis and what does it lead to?

A

Nephrotic syndrome

Like the adult version of minimal change

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13
Q

What is the commonest cause of primary nephrotic syndrome in adults?

A

Membranous glomerulonephritis

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14
Q

What is one difference between membranous glomerulonephritis and focal segmental glomerulosclerosis?

A

FSGM - no immune complexes deposited

MGN - immune complexes are deposited

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15
Q

What characterises nephritic syndrome?

A
  • Haematuria
  • Oligouria
  • Red cell casts (distinguishing feature)
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16
Q

What is the most common cause of primary nephritic syndrome?

A

Berger’s disease (IgA nephropathy)

17
Q

What are some causes of nephritic syndrome?

A
  • Post streptococcal glomerulonephritis
  • IgA nephropathy
  • Goodpasture’s syndrome
  • SLE
  • Hepatitis
  • Systemic vasculitis
18
Q

What is goodpasture’s syndrome?

A

An autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs and kidney failure

19
Q

In what syndrome are red cell casts present?

A

Nephritic

20
Q

What is Alport syndrome?

A

A genetic disease characterised by progressive chronic kidney disease with symptoms of haematuria, sensorineural deafness and ocular abnormalities

21
Q

How is Alport syndrome inherited?

A

X linked recessive

22
Q

What is the cause of Alport syndrome?

A

Mutation in the gene that codes for a5 chain of type IV collagen

23
Q

What class of drugs are known to slow the progression of renal disease?

A

ACE inhibitors

24
Q

What are the 3 layers of the glomerulus?

A

Endothelium, basement membrane (type IV collagen) and epithelial podocytes

25
Q

What is the name of the spaces between the foot processes of podocytes?

A

Filtration slits

26
Q

What is the commonest cause of end stage renal disease?

A

Diabetic nephropathy

27
Q

Why isn’t diabetic nephropathy seen in children?

A

It does not develop until a patient has had diabetes

(either type 1 or type 2) for around 8-15 years.

28
Q

What is the earliest change seen in diabetic nephropathy?

A

Hyperfiltration and an increase in GFR

29
Q

What histological changes are seen in diabetic nephropathy?

A

Glomerular BM thickening, mesangial expansion and glomerular sclerosis

30
Q

What is diabetic nephropathy characterised by?

A
  • Proteinuria
  • A gradual decline in GFR
  • Hypertension
31
Q

Why does a thickened GBM allow more bigger molecules to get through?

A

Thickened GBM increases pore size, also high intraglomerular pressure increases chance of more bigger molecules getting through

32
Q

What are the nodules seen in diabetic nephropathy called?

A

Kimmelstiel-wilson nodules

33
Q

What is the first clinical sign of diabetic nephropathy?

A

Microalbuminuria

34
Q

Why does GFR fall in the later stages of diabetic nephropathy?

A

Mesangial expansion/sclerosis -> reduced surface area for filtration

Overt proteinuria

35
Q

How long do most patients with diabetic nephropathy take to reach end stage kidney disease?

A

3-7 years

36
Q

What are the risk factors for diabetic nephropathy?

A
  • Genetics
  • Race (causasians have a lower risk)
  • Hypertension
  • Hyperglycaemia
  • High level of hyperfiltration
  • Older age
  • Smoking
37
Q

How can you prevent diabetic nephropathy?

A

Tight glycaemic and BP control

38
Q

What effect does angII have on glomerularly permeability to proteins?

A

Increases permeability

39
Q

What histological changes are seen in hypertensive nephrosclerosis?

A
  • Vascular changes tor renal arteries and arterioles
  • Fibroelastic intimal thickening - narrowing of lumen
  • Hyalinosis of afferent arteriolar walls

ESA3 - Urinary System (16 decks)

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