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Y4: Renal > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

Rapidly progressive glomerulonephritis: rapid loss of renal function associated with formation of ___ ___ in the majority of glomeruli.

A

epithelial crescents

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2
Q

causes of rapidly progressive glomerulonephritis?

A

Anti-GBM disease (Goodpastures)
GPA (Wegener’s)
SLE, microscopic polyarteritis

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3
Q

features of rapidly progressive glomerulonephritis?

A

nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria

features specific to underlying cause: haemoptysis in anti-GBM, vasculitis rash or sinusitis with Wegener’s

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4
Q

what is anti-glomerular basement membrane (GBM) disease?

previously known as Goodpasture’s syndrome

A

rare type of small-vessel vasculitis associated with both both pulmonary haemorrhage and rapidly progressive glomerulonephritis

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5
Q

anti-glomerular basement membrane (GBM) disease

1) cause
2) associated with what gene mutation
3) features?

A

1) anti-GBM antibodies against type IV collagen
2) HLA-DR2
3) pulmonary haemorrhage, rapidly progressIive GM: rapid onset AKI, nephritis (proteinuria + haematuria)

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6
Q

anti-glomerular basement membrane (GBM) disease

1) investigations?
2) management?

A

1) renal biopsy (linear IgG deposits along BM), raised transfer factor due to pulmonary haemorrhage
2) plasmapheresis, steroids, cyclophosphamide

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7
Q

what is the main complication of anti-glomerular basement membrane? what factors increase risk of this occurring?

A

pulmonary haemorrhage

- smoking, LRTI, pulmonary oedema, inhalation of hydrocarbons, young male

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8
Q

What is granulomatosis with polyangiitis (prev Wegener’s)

A

an autoimmune condition associated with necrotising granulomatous vasculitis, affecting both upper and lower respiratory tract + kidneys

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9
Q

features of granulomatosis with polyangiitis?

A

upper RT: epistaxis, nasal crusting
lower RT: haemoptysis, dyspnoea
rapidly progressive GM
Saddle shaped nose deformity

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10
Q

Ix in GPA?

A

cANCA +ve >90% (pANCA in 25%)
CXR: cavitating lesions
Renal biopsy: epithelial crescents in Bowman’s capsule

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11
Q

Management of GPA?

A

Steroids
Cyclophosphamide (90% response)
Plasma exchange

NB: median survival is 8-9 years

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12
Q

Membranoproliferative glomerulonephritis is aka ______ glomerulonephritis. It may present how? Prognosis?

A

mesangiocapillary

nephrotic syndrome, proteinuria, haematuria

poor prognosis

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13
Q

Membranoproliferative glomerulonephritis

1) type 1 or 2 more common?
2) cause of type 1?
3) renal biopsy of type 1?

A

1) type 1 (90%)
2) cryoglobulinaemia, hepatitis C
3) ‘tram-track appearance’

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14
Q

Membranoproliferative glomerulonephritis type 2

1) cause
2) patients wwill have low circulating levels of ___
3) ___ ___ factor is found in 70%
4) renal biopsy

A

1) partial lipodystrophy (classically loss of sc tissue in their face), factor H deficiency. Caused by persistent activation of complement pathway.
2) C3
3) C3b nephritic factor
4) ‘dense deposits’

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15
Q

tetrad of nephrotic syndrome?

A

proteinuria (>3g/ day)
hypoalbuminaemia (<30g/L)
hypercholesterolaemia
Oedema

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16
Q

what type of glomerulonephritis is
1) nephritic
2) nephrotic
syndrome associated with

A

1) rapidly progressive (anti-GBM, GPA), IgA nephropathy

2) membranous, focal segmental

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17
Q

causes of nephrotic syndrome?

A 
membraneous GN
minimal change disease
focal segmental glomerulosclerosis
amyloidosis 
diabetic nephropathy
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18
Q

why is there increased risk of thrombosis in nephrotic syndrome?

A

loss of anti-thrombin III, protein C and S plus associated rise in fibrinogen levels

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19
Q

why is there increased risk of thrombosis in nephrotic syndrome?

A

loss of anti-thrombin III, protein C and S plus associated rise in fibrinogen levels

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20
Q

commonest cause of gloumerulonephritis?

A

IgA nephropathy (Berger’s disease)

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21
Q

IgA nephropathy classic presentation?

A

macroscopic haematuria in young people following an URTI

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22
Q

conditions associated with IgA nephropathy?

A

alcoholic cirrhosis
coeliac/ dermatitis herpetiformis
Henoch schonlein purpura

23
Q

IgA nephropathy

1) pathophysiology
2) histology

A

1) mesangial deposition of IgA immune complexes

2) mesangial hypercellularity, positive immunofluroscence for IgA and C3

24
Q

IgA nephropathy

Typically presents in a young ___ with recurrent episodes of ___ ___

Typically associated with a recent ____

Nephrotic range proteinuria is COMMON/ RARE

Renal failure is COMMON/ RARE

A 
males
macroscopic haematuria (IgA - mAcroscopic)

URTI

rare

rare

25
Q

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis

post-strep GN is associated with low ____ levels

main symptom in post-strep GN is ______

Interval from URTI to onset of renal problems is approximately __ __ in IgA nephropathy and __ __ in post-strep GN

A

complement

proteinuria (although haematuria can occur)

1-2d IgA
1-2w PSGN

26
Q

T/F: steroids/ immunosuppression is first line in IgA nephropathy

A

false - not shown to be useful

27
Q

IgA nephropathy

1) markers of good prognosis?
2) markers of poor prognosis?

A

1) frank haematuria
2) male, proteinuria (esp>2g/ day), smoking, hypertension, hyperlipidaemia, ACE genotype DD

25% develop ESRF

28
Q

membranous glomerulonephritis is the common type of GN in ___. It usually presents with ___ syndrome or ___

A

adults
nephrotic
proteinuria

29
Q

what is seen on electron microscopy of a renal biopsy in membranous GN?

A

thickened BM with subepithelial electron dense deposits

> ‘spike and dome’ appearance

30
Q

Management of membranous GN?

A

all patients given ACEI or ARB (reduces proteinuria and improves prognosis)

immunosuppression only if symptoms severe/ progressive (many improve spontaneously)

31
Q

prognosis rule of thirds in membranous GN?

A

1/3 spontaneous remission

1/3 remain proteinuric

1/3 develop ESRF

32
Q

T/F: if indicated, corticosteroids are the agent of choice in membranous GN

A

false- corticosteroids alone not useful

use corticosteroid + something else e.g. cyclophosphamide

33
Q

Causes of membranous GN

idiopathic: due to ____ ____ antibodies
infections e.g. …

malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia

drugs e.g. …

autoimmune disease e.g. …

A

anti-phospholipase A2

hepatitis B, malaria, syphilis

gold, penicillamine, NSAIDs

systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

34
Q

in nephrotic syndrome, inflammation of the ___, causes damage to which cells?
what is the function of these cells?

A

glomerulus

podocytes- which normally function to prevent protein loss

35
Q

T/F: haematuria is not seen in nephrotic syndrome

A

false- may be seen, depending on degree of damage to glomerulus

36
Q

why are those with nephrotic syndrome at increased risk of infection?

A

loss of immunoglobulins (which are proteins)

37
Q

why does hypercholesterolaemia occur in nephrotic syndrome?

A

loss of protein > liver works overtime to replace > increased production of albumin and cholesterol

38
Q

why is GFR decreased in nephrotic syndrome?

A

water moves out of circulating volume to interstitium > decreased venous return to heart > decreased renal blood flow

39
Q

signs and symptoms in nephrotic syndrome?

A

hypercholesterolaemia> xanthelasma, xanthomata

hypoalbuminaemia > tired, leukonychia, oedema (periorbital, ascites, peripheral, pulmonary)

proteinuria > frothy urine

40
Q

Focal segmental glomerulosclerosis (FSGS) is a cause of _____ syndrome and chronic kidney disease.

It generally presents in what age group?

T/F: renal transplant is generally curative

Renal biopsy

  • on light miscoscopy?
  • on electron microscopy?

management?

A

nephrotic

young adults

false- high rate of recurrence in renal transplants

light: focal and segmental sclerosis and hyalinosis
electron: effacement of foot processes

steroids +/- immunosuppressants

41
Q

Alport’s syndrome is usually inherited in what pattern?

It is due to a defect in the gene which codes for type IV ___ resulting in an abnormal ___ ___ ___

The disease is more severe in MALES/ FEMALES

A

x-linked dominant
collagen
glomerular BM
males

42
Q

presentation of Alport’s syndrome?

A

microscopic haematuria

progressive RF

bilateral SN deafness

lenticonus

retinitis pigmentosa

43
Q

electron micoscopy of renal biopsy in Alport’s syndrome?

A

splitting of lamina densa (‘basket weave’ appearance)

44
Q

Post-streptococcal glomerulonephritis typically occurs ___ ___ following what?

It is caused by ___ ___ deposition in the glomeruli.

Young children are most commonly affected.

A

1-2 weeks

a group A beta-haemolytic Streptococcus infection (usually S.pyogenes)

immune complex (IgG, IgM and C3)

45
Q

what type of GN produces a ‘starry sky’ appearance on immunofluorescence?

A

post-strep GN

46
Q

Nephrotic syndrome

1) classic triad
2) other features: hyper____, a hyper___ state (due to loss of __ __) and a predisposition to ____ (due to loss of ____)
3) there is also an assocation with HYPER/ HYPO calcaemia- why?

A

1) proteinuria, hypoalbuminaemia, oedema
2) hyperlipidaemia, hypercoagulable state (loss of antithrombin III), predisposition to infection (loss of IGs)
3) hypocalcaemia (vit D lost in urine)

47
Q

what is seen on urinalysis in nephritic syndrome?

A

red cell casts

48
Q

minimal change disease nearly always presents as ___ syndrome

T/F: most causes are idiopathic

Potential causes?

A

nephrotic

true

10-20% of cases have causes: drugs (NSAIDS, rifampicin), Hodgkin’s lymphoma, thymoma
Infectious mono

49
Q

features of minimal change disease?

A

nephrotic syndrome
normotension
highly selective proteinuria (intermediate sized proteins e.g. albumin and transferrin leak through)

50
Q

what is seen on renal biopsy in minimal change disease?

A

light: glomerulus normal (hence ‘MINIMAL CHANGE’)
electron: fusion of podocytes, effacement of foot processes

51
Q

minimal change disease management?

A

80% corticosteroid responsive

cyclophosphamide 2nd line

52
Q

most common nephrotic syndrome in children?

A

minimal change disease

53
Q

this is the pathophysiology of which cause of nephrotic syndrome

‘T-cells release cytokines that damage foot processes of podocytes. Leads to selective proteinuria’

A

minimal change disease

Y4: Renal (7 decks)

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