Glomerulonephritis Flashcards

1
Q

damage to what cells can lead to vasculitis

A

mesangium

endothelial cells

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2
Q

damage to podocyte leads to what

A

non-proliferative lesions and protein in urine

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3
Q

damage to endothelium leads to what

A

proliferative lesions and red cells in urine

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4
Q

presentation of GN

A
haematuria 
AKI/CKD
HTN
Nephtotic or nephritic syndrome 
proteinuria
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5
Q

presentation of nephrotic syndrome

A
proteinuria >3g 
hypoalbuminaemia 
fluid retention and oedema 
hypercholesterolaemia 
renal vein thrombosis 
pulmonary emboli 
volume depletion 
vitamin D deficiency 
subclinical hypothyroidism
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6
Q

presentation of nephritic syndrome

A
AKI
oliguria 
oedema/fluid retention 
HTN
active urinary sediment
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7
Q

classification of proteinuria

A

microalbuminuria
asymptomatic proteinuria
heacy proteinuria -3g
nephrotic syndrome >3g

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8
Q

non-immunosuppressive management GN

A
antihypertensives <130/80
ACEI/ARB
diuretics 
statins 
anticoag/aspirin/antiplatelet 
fish oil
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9
Q

immunosuppressive management GN

A
pred
azathioprine 
cyclophosphamide 
cyclosporin
mycophenolate 
plasmapharesis 
IV Ig
Monoclonal Ab
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10
Q

general management of nephrotic syndrome

A
fluid and salt restriction 
ACEI/ARB
antiagulate 
IV albumin if volume depletion 
diuresis
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11
Q

what is complete remission from nephrotic syndrome regarded as

A

<300mg protein/day

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12
Q

what is partial remission from nephrotic syndrome regarded as

A

<3g/day protein

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13
Q

what is minimal change GN, who is it more common in, how is it managed

A

injury to podocyte and effacement of foot process
children
respond to steroids

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14
Q

what is FSGS and what causes it

A

focal segmental glomerulosclerosis

HIV, heroin, obesity, reflux nephropathy

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15
Q

how is FSGS managed

A

steroids, some have chronic disease

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16
Q

what is membranous GN, what causes it, how does it appear on biopsy

A

injury to podocyte

heb B, lupus, gold, penicillamine

17
Q

management of membraneous glomerulonephritis

A

steroids, alkylating agents, b cell monoclonal Ab

18
Q

what Ab is present in membranous GN

A

anti-PLA2r-Ab

19
Q

most common GN

A

IgA nephropathy

20
Q

presentation of IgA nephropathy

A

asympatomatic haematuria
macroscopic haematuria after infection due to rising IgA
can cause HSP

21
Q

how many with IgA nephropathy progress to ESRF

A

25% in 10-30y

22
Q

describe the pathophysiology of membranoproliferative GN

A

thickening of capillary wall and proliferation of mesangial cells
immune complex deposition and complement activation due to infection or myeloma

23
Q

what is RPGN

A

rapidly progessive GN
rapid deterioration of renal function over days/weeks
active urine sediment

24
Q

common causes of RPGN

A

GPA, MPA
goodpastures
IgA HSP

25
Q

what antibody is found in Goodpastures

A

anti-GBM

26
Q

management of RPGN

A

pred
cyclophosphamide/mycophenolate/azathioprine
plasmapharesis

27
Q

describe the formation of an immune crescent

A

neutrophils bind to Ab leading to capillary being torn open and inflammatory cells entering bowmans capsule
glomerulus becomes crushed and dies