Glomerulonephritis Flashcards

1
Q

a disease of the renal parenchyma is a disease of the…

A

kidney itself

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2
Q

most common cause of end stage renal failure?

A

diabetes

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3
Q

2nd most common cause of end stage renal failure?

A

chronic glomerulonephritis

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4
Q

define GN

A

immune-mediated disease of the kidneys affecting the glomeruli

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5
Q

what immune cells drives the immunological disease in GN?

A

antibodies

T cells

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6
Q

describe the role of immune complexes in GN?

A

antibody binds to antigen and deposits in the kidney

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7
Q

what lines the outside of the glomerulus?

A

bowmans capsule

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8
Q

what does the bowmans’ space contain?

A

the tubular fluid

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9
Q

podocytes are present in the glomerulus T or F

A

T

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10
Q

why do you get leakage of substances in GN?

A

there is a disruption to the glomerular capillary wall

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11
Q

what would be found on urinalysis of GN?

A

haematuria

proteinuria (due to wall damage)

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12
Q

damage to podocytes leads to what kind of lesion?

A

non-proliferative

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13
Q

damage to endothelial and mesangial cells lead to what kind of lesion?

A

proliferative

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14
Q

a proliferative lesion will lead to ___ on urinalysis

A

haematuria

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15
Q

a non-proliferative lesion will lead to ___ on urinalysis

A

proteinuria

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16
Q

what happens to podocytes when they are damaged?

A

undergo atrophy

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17
Q

normal creatinine along with blood and protein in urine indicates damage to what kind of glomerular cell?

A

mesangium

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18
Q

consequence of endothelial cell damage in the glomerulus?

A

vasculitis

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19
Q

name the 3 types of cell in the glomerulus?

A

endothelial
mesangial
podocyte

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20
Q

what would be found on urine microscopy of GN?

A

dysmorphic RBCs
granular casts
lipiduria

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21
Q

what kind of urine cast does GN present with?

A

granular

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22
Q

how is the level of proteinuria quantified in GN?

A

urine:creatinine ratio

24hr urine test

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23
Q

painless macroscopic haematuria suggests…

A

infection - immune cells are at work

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24
Q

30 to __ mg of protein in the blood is classed as microalbuminuria

A

300

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25
Q

how many grams of protein per day in urine equate to nephrotic syndrome?

A

> 3g

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26
Q

how can you tell the lesion is in the glomerulus from looking at RBCs?

A

if they are dysmorphic they are from the glomerulus

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27
Q

how much urine is passed per hr in nephritic syndrome?

A

<30ml per hr

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28
Q

why do you get hypertension in nephritic syndrome?

A

retaining fluid by not peeing

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29
Q

pt presents with acute renal failure, oliguria, oedema and HT….

A

nephritic syndrome

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30
Q

why do you get oedema in nephrotic syndrome?

A

lost so much albumin you lose your oncotic pressure so fluid leaks into the subcut tissues

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31
Q

what glomerular cells does nephritic syndrome affect and what process would this therefore cause?

A

endothelial cells; proliferative

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32
Q

pt presents with high proteinuria, oedema, hypercholestererolaemia and normal renal function tests…

A

nephrotic syndrome

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33
Q

why can you get thrombosis and PEs as complications of nephrotic syndrome?

A

liver makes clotting factors and are putting lots of pressure on it

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34
Q

what glomerular cells does nephrotic syndrome affect and what process would this cause?

A

podocytes, non-proliferative

35
Q

if the glomerulus isnt affected, what would not be present in the urine?

A

RBCs

albumin

36
Q

primary cause of GN?

A

idiopathic

37
Q

secondary causes of GN?

A
infection
drugs
malignancy
vasculitis
lupus
38
Q

how should GN be investigated?

A
  1. renal biopsy (use light microscopy/immunofluorescence/electron microscope)
39
Q

if a glomerular lesion is described as “focal what does this mean?

A

<50% of the glomeruli are affected

40
Q

if a glomerular lesion is described as “diffuse” what does this mean?

A

> 50% of the glomeruli are affected

41
Q

if a glomerular lesion is described as global what does this mean?

A

all of the glomerulus is affected

42
Q

if a glomerular lesion is described as segmental what does this mean?

A

part of the glomerulus is affected

43
Q

main aims of treatment for GN?

A

reduce proteinuria
stop nephrotic syndrome
preserve renal function

44
Q

4 non immunosuppresive drugs involved in the Tx of GN?

A

antihypertensives
ACEi
diuretic
statin

45
Q

target BP for non-proteinuria GN patients?

A

<130/80

46
Q

target BP for proteinuria GN patients?

A

<120/80

47
Q

why is immunosuppression the mainstay of GN Tx?

A

an immune process is the cause of it

48
Q

what drugs are used for immunosuppression in GN

A

prednisolone PO
azathioprine
cyclophosphamide
calcineurin inhibitors

49
Q

what treatment is good for vasculitis as a result of endothelial cell damage?

A

plasmapharesis

50
Q

why are calcineurin inhibitors used?

A

it activates T cells so drugs can stop this

51
Q

what should you give if a patient with nephrotic syndrome is volume deplete?

A

IV albumin

52
Q

Tx of nephrotic patients?

A
diuretics
salt restriction
fluid restriction
ACEi
IV albumin (only if vol deplete)
53
Q

when is a nephrotic patient said to be in remission?

A

when their proteinuria is <300mg/day

54
Q

risks of immunosuppressing a nephrotic patient?

A

infection (already more prone)

55
Q

a GN that is normal on microscopy will be in what category of GN?

A

minimal change nephropathy

56
Q

name the 5 types of primary GN?

A
minimal change
FSGS
membranous
membranoproliferative
IgA nephropathy
57
Q

commonest cause of nephrotic syndrome in children?

A

minimal change nephropathy

58
Q

what does renal biopsy look like in minimal change nephropathy?

A

normal

59
Q

Tx of minimal change nephropathy?

A
  1. oral steroid

2. cyclophosphamide

60
Q

commonest cause of nephrotic syndrome in adults WORLDWIDE?

A

focal segmental glomerulosclerosis (FSGS)

61
Q

secondary causes of FSGS?

A

HIV
heroin use
obesity
reflux nephropathy

62
Q

is primary or secondary FSGS more common?

A

primary ++

63
Q

appearance of FSGS on renal biopsy?

A

get focal sclerosis- minimal antibody/complement deposition

64
Q

most common cause of nephrotic syndrome in the UK in adults?

A

membranous nephropathy

65
Q

appearance of membranous nephropathy on renal biopsy? what immune cells cause this?

A

subepithelial immune complex deposition in the basement membrane

66
Q

are you more likely to progress to ESRF in 10 yrs if you have FSGS or membranous nephropathy?

A

FSGS

67
Q

Tx of membranous nephropathy?

A

steroids
b cell monoclonal Ab
alkylating agents eg cyclophosphamide

68
Q

what type of antibody is present in most cases of membranous nephropathy?

A

anti PLA2r antibody

69
Q

what stain is used to see thickened basement membranes? what condition would this be good for?

A

silver stain; membranous nephropathy

70
Q

commonest type of GN in the world?

A

IgA nephropathy

71
Q

patient with macroscopic haematuria after a resp/gi infection…

A

IgA nephropathy

72
Q

IgA nephropathy is associated with what derm condition?

A

henoch schonlein purpura

73
Q

what types of cells are affected in IgA nephropathy?

A

mesangial

74
Q

signs of IgA nephropathy?

A

micro/macro haematuria with AKI or CKD

have henoch schonlein purpura

75
Q

Tx of IgA nephropathy?

A

BP control
ACEi
fish oil

76
Q

immunofluorescence of IgA nephropathy would show…

A

IgA immune complex deposits in the mesangium

77
Q

what stain should be used to look for cell proliferation and expansion

A

H + E stain

78
Q

what does RPGN stand for when discussing neuropathy?

A

rapidly progressive glomerulonephritis

79
Q

pathophysiology of ANCA vasculitis?

A

plasma cell makes ANCA
binds to neutrophil
makes proteolytic enzymes
burst through the blood vessel wall

80
Q

characteristic appearance of RPGN on biopsy?

A

glomerular crescents present

81
Q

RPGN causes slow deterioration of renal function T or F

A

F, causes rapid deterioration

82
Q

how can you tell apart a normal glomerulus from an abnormal one just by appearance?

A

normal should have white parts in it

83
Q

what is goodpasture’s syndrome?

A

“pulmonary-renal syndrome”

84
Q

Tx of RPGN?

A

rapid immunosuppression - steroids, cyclophosphamide

dialysis if needed