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
what is Anti-glomerular basement membrane disease also known as
Goodpastures disease
26
Anti-glomerular basement membrane disease- what is it caused by
auto antibodies to type IV collagen which is an essential component of the GBM
27
where else is type IV collagen found and thus is also affected in Anti-glomerular basement membrane disease
in the lung so pulmonary haemorrhage can occur
28
Anti-glomerular basement membrane disease presentation
haematuria/ nephritic syndrome, AKI may occur within days
29
Anti-glomerular basement membrane disease treatment
plasma exchange, steroids, cytotoxics. prognosis poor if dialysis dependent
30
Post streptococcal GN
after sore throat or skin infection.
31
what happens in Post streptococcal GN
strep antigen deposited on glomerulus causes host reaction and immune complex formation
32
Post streptococcal GN presentation
usually nephritic syndrome
33
Post streptococcal GN treatment
supportive
34
what is the most aggressive GN
rapidly progressive GN
35
rapidly progressive GN what can these be classified into
immune complex disease- post infectious; Pauci- immune disease- granulomatosis with polyangiitis; anti-GBM disease
36
rapidly progressive GN clinical presentation
AKI +- systemic features. commonest cause of death in ANCA +ve patients- pulmonary hemorrhage
37
treatment rapidly progressive GN
immunosuppression with high dose steroids IV, cyclophosphamide and plasma exchange.
38
rapidly progressive GN prognosis
5 year survival 80%