Glomerular nephritis Flashcards

1
Q

Define nephritis

A

A generic term that means inflammation of the Kidneys

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2
Q

What is nephritic syndrome

A

A group of symptoms indicating that inflammation has caused damage to the kidneys.

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3
Q

What are the symptoms of Nephritic syndrome

A

Haematuria
Oliguria
Proteinuria (mild/moderate <3.5g/l/day)
Fluid Retention

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4
Q

What can be found in the active urine sediment in nephritic syndrome

A

Haematuria
Dysmophic RBC
Cellular casts

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5
Q

What are cellular casts

A

Urinary casts are tiny tube-shaped particles that can be found when urine is examined under the microscope during a test called urinalysis.

Urinary casts may be made up of white blood cells, red blood cells, kidney cells, or substances such as protein or fat. The content of a cast can help tell your health care provider whether your kidney is healthy or abnormal.

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6
Q

What is the main feature of someone in the nephritic state

A

Haematuria

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7
Q

What is the pathophysiology of a nephritic syndrome

A

Neutrophils attack the basement membrane of glomerulus and podocyte processes. The triple flltration barrier is disrupted causing spillage

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8
Q

What is nephrotic syndrome

A

Nephrotic syndrome is a condition involving the loss of significant volumes of protein via the kidneys (proteinuria) which results in hypoalbuminaemia.

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9
Q

What are the group of symptoms the nephrotic state

A
Peripheral oedema
Proteinuria (frothy urine)
Serum Albumin low (hypoalbuminuria)
Hypercholesterolaemia 
Fatigue 
Poor appetite
Recurrent infections
Venous/arterial thrombosis
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10
Q

What is the most noticeable feature of nephrotic syndrome

A

The proteinuria

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11
Q

How high does the protein content in the urine need to be to call it proteinuria

A

> 3.5g in 24 hrs

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12
Q

How low does the albumin content of the blood need to be to call it hypoalbuminuria

A

<35g per litre

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13
Q

Is there more oedema in nephritic or nephrotic syndrome

A

Nephrotic

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14
Q

Why do you get oedema in the nephrotic state

A

Reduced oncotic pressure

excessive sodium

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15
Q

What is the pathophysiology of nephrotic state

A

The podocytes shrink making them come apart and spill. Also get some thickening of the basement membrane.

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16
Q

How would you treat oedema in nephrotic syndrome

A

Salt/fluid restriction and loop diuretics

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17
Q

How would you treat hypertension in nephrotic syndrome

A

Renin-angiotensin-aldosterone blockade

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18
Q

How would you reduce risk of thrombosis in nephrotic syndrome

A

Heparin/warfarin

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19
Q

How would you reduce risk of infection in nephrotic syndrome

A

Pneumaccocal vaccine

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20
Q

How would you treat dyslipidaemia in nephrotic syndrome

A

Statins

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21
Q

What medications can cause nephrotic syndrome

A

NSAIDS
Penicilline
Interferon
Captopril

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22
Q

What is glomerular nephritis

A

Inflammation of or around the glomerulus

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23
Q

What are the sub-types of glomerulonephritis

A

Proliferative

Non-Proliferative

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24
Q

What is characteristic of proliferative glomerulonephritis

A

Lots of cells in the the glomeruli , including infiltrating leukocytes

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25
Q

What is charecteristic of non-proliferative glomerulonephritis

A

Glomeruli looks normal or has areas of scarring. There are normal numbers of cells present

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26
Q

If the non-proliferative glomerulonephritis is diffuse what does that means

A

> 50% of glomeruli affected

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27
Q

If the non-proliferative glomerulonephritis is focal what does that means

A

<50% glomeruli affected

28
Q

If the non-proliferative glomerulonephritis is global what does that means

A

All of glomerulus affected

29
Q

If the non-proliferative glomerulonephritis is segemental what does that means

A

Part of glomerulus is affected

30
Q

What are the Proliferative glomerulonephritises

A

IgA nephropathy
Post streptococcal glomerulonephritis
Crescentic Glomerulonephritis
Membranoproliferative Glomerulonephritis

31
Q

What does IgA nephropathy show on histology

A

IgA deposits and glomerular Mesangial proliferation

32
Q

What is the presentation of IgA nephropathy

A

Microscopic haematuria
Microscopic proetinuria
Nephritic syndrome

33
Q

What age in IgA nephropathy most common

A

In 20s

34
Q

What sex is IgA nephropathy more common

A

Males

35
Q

Is IgA nephropathy common?

A

Yes - its the most common cause of primary glomerulonephritis.

36
Q

What is the age range for post infectious glomerulonephritis

A

Under 30 years old

37
Q

What infection is post infectious glomerulonephritis common after

A

Lancefield group A streptococci

38
Q

What syndrome for post infectious glomerulonephritis develop

A

Nephritic

39
Q

What is the prognosis like for post infectious glomerulonephritis

A

Usually get a full recovery

40
Q

What can cause crescentic glomerulonephritis

A

Anti-neutrophil cytoplasmic antibody (anca) associated
Anti-glomerular basement membrane
Others

41
Q

what are the subtypes of Anti-neutrophil cytoplasmic antibody (anca) associated

A

Microscopic polyangiitis
Granulomatosis with polyangitits
Eosinophilic granulomatosis with polyangitis.

42
Q

What is Granulomatosis with polyangitits

A

Granulomatosis with polyangiitis (GPA) is a rare condition where the blood vessels become inflamed. It mainly affects the ears, nose, sinuses, kidneys and lungs. Anyone can get it, including children, but it’s most common in adults and older people

43
Q

What is Good pastures syndrome

A

Anti-glomerular basement membrane nephritis with lung haemorrhage.

44
Q

What happens in Anti-glomerular basement membrane disease

A

Antibodies attack the basement membrane in the lungs and kidneys leading to bleeding from the lungs, glomerulonephritis and kidney failure.

45
Q

What % of crescentic GN is v caused by Anti-glomerular basement membrane

A

10-20%

46
Q

What is treatment for Anti-glomerular basement membrane disease

A

Aggressive immunosuppression
Steroids
Plasma exchange and cyclophosphamide.

47
Q

What are the non-proliferative glomerulonephritis

A

Minimal change disease
Focal and Segmental glomerulonephritis
Membranous nephropathy

48
Q

What age group is minimal change disease common

A

Children

49
Q

What is presenting symptoms of minimal change disease

A

Sudden onset of Oedema

50
Q

Histologically what is observed in minimal change disease

A

Not much seen on light microscopy
No immunodeposits
Podocytes are shrunken with smaller processes that are less interdigitated.

51
Q

What is treatment for minimal change disease

A

Prednisolone (1mg/kg) for up to 16 weeks

52
Q

What do you treat an intial relapse with in minimal change disease

A

Prednisolone

53
Q

What do you treat an 2nd and subsequent relapse with in minimal change disease

A

Cyclophosphamide
Cyclosporin
Tacrolimus
Rituximab

54
Q

What is the prognosis for minimal change disease

A

Favourable, despite the relapsing nature of the condition.

55
Q

What is focal/segmental glomerulonephritis

A

A syndrome describing a sclerosis of the kidney presenting with Nephrotic syndrome

56
Q

How do you treat focal/segmental glomerulonephritis

A

Steroids (but they dont usually work)

Cyclosporin, Cyclophosphamide, Rituximab

57
Q

What is the main cause of membranous nephropathy

A

Usually ideopathic

58
Q

Is membranous nephropathy common?

A

Its the most common nephrotic syndrome in adults

59
Q

How do you identify membranous nephropathy

A

Serological markers:

Anti phospholipase A2 receptor (PLA2r) - +ve in 70% cases
Thrombospondin type 1 domain in 2%

60
Q

What are less common causes of membranous nephropathy

A

Malignancies
SLE
Rheumatoid arthritis
Drugs: NSAID, Gold, Penicillamine

61
Q

What is treatment for membranous nephropathy

A

General measures…? for 6 monthes

immunosupression

62
Q

Wheh should you use immunosuppresion in membranous nephropathy

A

If symptomatic nephrotic syndrome with rising proteinuria or deteriorating renal function

63
Q

What is the prognosis of membranous nephropathy

A

Resolves spontaeously in 1/3
Good if treated patients whose proteinuria resolves
25% are on dialysis in 10 years

64
Q

How does reduced oncotic pressure in nephrotic syndrome cause oedema

A

Hypoalbuminemia reduces the capillary oncotic pressure and the imbalance of Starling’s forces leads to interstitial leakage of fluid and decreased circulating volume. The under-fill theory proposes that the decreased circulating volume leads to renal hypoperfusion and activation of the renin-angiotensin-aldosterone system (RAAS) Stimulation causes avid sodium and water reabsorption

65
Q

Why do you get excessive sodium retention in nephrotic syndrome

A

Excessive sodium retention occurs in some individuals with nephrotic syndrome in the absence of activation of the renin-angiotensin-aldosterone system, suggesting an intrinsic defect in sodium excretion by the kidney.