Glomerulonephritis Flashcards

1
Q

what are the consequences of inflammation of the glomeruli and nephrons

A

damage to glomerulus- restricts blood flow leading to incr BP. damage to filtration mechanism- blood and protein to enter urine,. loss of usual filtration capacity- AKI

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2
Q

what do patients present with

A

specific syndromes- nephrotic and nephritic syndromes

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3
Q

what happens to the bp in nephrotic

A

mild incr

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4
Q

what happens to the urine in nephrotic

A

proteinuria >3.5g/day

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5
Q

what happens to the GFR in nephrotic

A

mild decr

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6
Q

what happens to the bp in nephritic

A

severe incr

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7
Q

what happens to the urine in nephritic

A

haematuria (mild-macro)

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8
Q

what happens to the GFR in nephritic

A

moderate to severe decr

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9
Q

what bloods need to be done

A

FBC, U&E, LFT, ESR, CRP, immunoglobulins, electrophoresis, complement, autoantibodies, blood culture, ASOT, HBsAg, anti HCV

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10
Q

what autoantibodies are checked for

A

ANA, ANCA, anti-dsDNA, anti-GBM

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11
Q

what is tested in the urine

A

RBC casts, MC&S, Bence Jones protein, ACR

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12
Q

what imaging is performed

A

CXR, renal ultrasound

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13
Q

what type of test will give the most information

A

renal biopsy

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14
Q

what are the specific types of GN

A

IgA nephropathy, Henoch-Schlonlein purpura, SLE, anti-glomerular basement membrane disease, post-streptococcal GN, rapidly progressive GN

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15
Q

what is the commonest GN in developed world

A

IgA nephropathy

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16
Q

IgA nephropathy- presentation

A

macro or microscopic haematuria, occasionally nephritic syndrome. typical patient- young male, recovery rapid between attacks

17
Q

what is increased in IgA nephropathy

A

IgA- forms immune complexes and deposits in mesangial cells

18
Q

IgA nephropathy- treat

A

bp control with ACEi. with nephritic presentation- immunosuppression

19
Q

prognosis IgA nephropathy

A

worse if incr bp, male, proteinuria, renal failure at presentation

20
Q

what is Henoch-Schlonlein purpura

A

a systemic variant of IgA nephropathy causing small vessel vasculitis

21
Q

features of Henoch-Schlonlein purpura

A

purpuric rash on extensor surfaces typically legs, polyarthritis, abdo pain, nephritis

22
Q

treatment Henoch-Schlonlein purpura

A

bp control ACEi

23
Q

what fraction of SLE patients will have renal disease

A

1/3 with vascular, glomerular and tubulointerstitial damage

24
Q

what are the classes split into in SLE

A

I-iv: increasing in severity. v- membranous

25
Q

what is Anti-glomerular basement membrane disease also known as

A

Goodpastures disease

26
Q

Anti-glomerular basement membrane disease- what is it caused by

A

auto antibodies to type IV collagen which is an essential component of the GBM

27
Q

where else is type IV collagen found and thus is also affected in Anti-glomerular basement membrane disease

A

in the lung so pulmonary haemorrhage can occur

28
Q

Anti-glomerular basement membrane disease presentation

A

haematuria/ nephritic syndrome, AKI may occur within days

29
Q

Anti-glomerular basement membrane disease treatment

A

plasma exchange, steroids, cytotoxics. prognosis poor if dialysis dependent

30
Q

Post streptococcal GN

A

after sore throat or skin infection.

31
Q

what happens in Post streptococcal GN

A

strep antigen deposited on glomerulus causes host reaction and immune complex formation

32
Q

Post streptococcal GN presentation

A

usually nephritic syndrome

33
Q

Post streptococcal GN treatment

A

supportive

34
Q

what is the most aggressive GN

A

rapidly progressive GN

35
Q

rapidly progressive GN what can these be classified into

A

immune complex disease- post infectious; Pauci- immune disease- granulomatosis with polyangiitis; anti-GBM disease

36
Q

rapidly progressive GN clinical presentation

A

AKI +- systemic features. commonest cause of death in ANCA +ve patients- pulmonary hemorrhage

37
Q

treatment rapidly progressive GN

A

immunosuppression with high dose steroids IV, cyclophosphamide and plasma exchange.

38
Q

rapidly progressive GN prognosis

A

5 year survival 80%