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pathology 2 > renal disease classification > Flashcards

renal disease classification Flashcards

1
Q

most common cause of chronic Renal failure requiring dialysis/renal transplantation

A
  • diabetes
  • glomerulonephritis
  • hypertension
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2
Q

clinical presentation of renal disease

A
  • acute renal failure
  • chronic renal failure
  • nephritic syndrome - rapidly progressive glomerulonephritis
  • nephrotic syndrome
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3
Q

acute renal failure presentation

A
  • azotaemia/uraemia
  • usually accompanied by oliguria/anuria
  • may completely resolve or progress to chronic renal syndrome
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4
Q

azotaemia

A

rise in serum urea and creatinine

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5
Q

serum creatinine is a marker of

A

renal function

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6
Q

uraemia

A

azotaemia becoming symptomatic

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7
Q

oligourea

A

drop in urine volume

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8
Q

anuria

A

failure to urinate completely

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9
Q

chronic renal failure presentation

A

gradual rise in serum urea/creatinine
symptoms and signs of renal dysfunction
eventual progressioon to end stage renal failure eGFR <5%
requiring dialysis/transplantation

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10
Q

clinical manifestations of renal dysfunction

A 
lethargy 
anorexia 
SOB 
peripheral neuropathy 
oedema
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11
Q

pre renal cause of renal failure

A

anything impairing renal perfusion

  • drop n blood volume
  • cardiac shock
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12
Q

renal causes of renal failure

A

disease intrinsic to the kidney

  • glomerulonephritis
  • acute tubular necrosis
  • scute interstitial nephritis
  • tumour lysis syndrome
  • drug induced nephrotoxicity
  • contrast-induced nephropathy
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13
Q

post renal causes of renal failure

A

anything obstructing urine outflow

  • stones
  • stricture due to radiotherapy or trauma
  • due to aa tumour growing in the retroperitoneum
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14
Q

nephritic syndrome

A
  • azotaemia/uraemia
  • oliguria
  • haematuria - often macroscopic - mild to moderate proteinuria
  • hypertension
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15
Q

nephritic syndrome usually due to

A

glomerularnephritis

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16
Q

rapidly progressive glomerulonephritis

A

RPGN

  • subset of nephritic syndrome
  • rise in serum level creatinine/urea is rapid and severe
  • usually due to crescentic glomerulonephritis
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17
Q

RPGN is a subset of

A

nephritic syndrome

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18
Q

nephrotic syndrome

A
  • proteinuria
  • hypoalbuminaemia
  • peripheral oedema
  • hyperlipidaemia
  • lipduria
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19
Q

mechanisms of nephrotic syndrome

A

increased glomerular capillary permeability - leaky
low serum protein - leaks into urine
reduced serum oncotic pressure
increased hepatic lipid synthesis - liver attempts to compensate

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20
Q

oncotic pressure

A

the ability of the vascular system to maintain fluid within the vascular system

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21
Q

pitting oedema

A

pressing down on the skin leaves an imprint

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22
Q

Dendant oedema

A

accumulates in areas under gravitational force

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23
Q

pathogenesis of glomerular nephritis

A

2 main pathogeneses

  • immune complexes
  • structural abnormalities - usually in podocytes, podcytopathy
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24
Q

immune complex pathogenesis of glomerulonephritis

A

proteins become trapped
immune complexes in thee mesangium - masangial cells proliferate causing mesangial hypercellularity and mesangial matrix expansion
immune complexes in sub endothelial space - between the endothelium and glomerular basement membrane, glomerulus proliferates endothelial cells, endothelial proliferation
immune complexes in the epimembranous/subepithelial space - glomerulus produces new basement membrane called ‘spikes’

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25
Q

diagnostic core biopsy

A
  • light microscopy
  • electron microscopy
  • immunoflourescence
26
Q

immunofluorescence

A

manufactured antibodies with fluorescent signal attatched that are specific for components of immune complexes

27
Q

primary glomerulonephritis

A

no identifiable cause

idiopathic

28
Q

secondary glomerulonephritis

A
  • drug
  • infections
  • autoimmune diseases
  • malignancy
29
Q

minimal change disease

A
  • type of glomerulonephritis
  • disease of children
  • structural abnormality - podocytopathy
  • normal glomeruli under light microscopy
  • no immune complexes
30
Q

electron microscopy findings for minimal change disease

A

normal podocyte findings:
- cytoplasmic extensions - foot processes
- spaces in between called slit diaphragms - have an electrical charge which repels electrical charge in protein keeping protein in the circulation
minimal change disease finings:
- foot processes are fused which means slit diaphragms are lost causing protein to leak into urine causing nephritic syndrome

31
Q

secondary causes of minimal change disease

A
  • drugs
  • malignancy
  • vaccinations
32
Q

prognosis of minimal change disease

A
  • good in children - highly responsive to steroids

- poorer response in adults

33
Q

membranous nephropathy

A
  • usually effects adults especially Middle Ages males
  • immune complex mediates
  • nephritic syndrome/nephritic range proteinuria
34
Q

findings for membranous nephropathy

A

light microscopy
- circumferential thickening of glomerular capillary loops - thickening due to immune complexes
- glomerulus reacts by producing new basement membrane spikes alternating with subepithelial deposits
immune fluorescence
- immune complexes - IgG and C3 (evidence of complement cascade)
electron microscopy
- subepitheial deposits
- intervening basement membrane spikes

35
Q

primary membranous nephropathy

A

now known to be due to autoantibodies - protein on the podocytes

36
Q

prognosis of membranous nephropathy

A

generally indolent

may progress to chronic renal failure

37
Q

focal or diffuse glomerular nephropathy

A
  • focal affects <50% of glomeruli

- diffuse affects >50%

38
Q

segmental and global glomerular nephropathy

A

segmental affects <50% of an individual glomerulus

global affects >50%

39
Q

focal segmental glomerulosclerosis

A
  • most common cause of nephrotic syndrome in adults
    structural abnormality
  • nephrotic syndrome.nephritic range proteinuria
40
Q

findings of focal segmental glomerulosclerosis

A

focal and segmental
collapse of the capillary loops with scarring and fibrous adhesions to the bowman’s capsule
immunofluorescence
- antibodies found but not immune complex mediated, antibodies just trapped
electron microscopy
- segmental scarring
- subtotal effacement of the podocytic foot processes

41
Q

secondary causes of FSGS

A
  • any cause of nephron loss
  • HIV, sickle cell, herion abuse, obesity
  • all other types of glomerulonephritis
42
Q

prognosis of FSGS

A

some respond to steroids

remainder progress to chronic renal failure

43
Q

post infectious glomerular nephritis

A

acute proliferative/post streptococcal glomerulonephritis

  • usually children
  • 1-4 weeks post cellulitis/pharyngitis
  • immune complex mediated - planted streptococcal pyogenic exotoxin (protein on the streptococcal organism)
44
Q

findings I posy infectious glomerulonephritis

A 
diffuse proliferative 
mesangial hypercellularity
endocapillary proliferation 
neutropenic inflammation 
immunoflourescens 
- granular, mesangial and capillary loop IgG and C3 
electron microscopy 
- sup epithelial 'humps'
45
Q

cause of post infectious G

A
  • always secondary - post infectious
  • usually S progenies
  • non streptococcal causes include other bacteria, viral and parasitic organisms
46
Q

prognosis of post infectious G

A

most children recover with conservative treatment

adults may progress to chronic renal failure

47
Q

IgA nephropathy

A
  • berger’s disease
    most common cause of G
    usually young adults
    immune complex mediated
48
Q

clinical presentation of IgA nephropathy

A

microscopic haematuria/nephritic syndrome

sometimes precipitated by URTI

49
Q

findings of IgA nephropathy

A 
light microscopy 
diffuse mesangiaal matrix expansion and hypercellularity 
immunoflurescence
- granular mesangial IgA 
electron microscopy 
- mesangiaal immune complex deposits
50
Q

causes of IgA nephropathy

A
  • drugs
  • infections
  • hepatobillary, GI, rheumatological diseases and malignancy
51
Q

prognosis of IgA nephropathy

A
  • 1/3 resolve
  • 1/3 stable disease
  • 1/3 progress to secondary FSGS/CRF
52
Q

crescentic glomerulonephritis

A

pathological correlate to clinical presentation of rapidly progressive glomerulonephritis
- nephritic syndrome with rapid and severe rise in serum urea/creatinine
medical emergency - chronic renal failure within weeks to months untreated
histological pattern - not a diagnosis

53
Q

crescentic GN under the microscope

A

crescent

  • filing and occlusion of the bowman’s space by proliferation of parietal epithelial cells
  • due to rupture of capillary loops - sign of severe glomerular injury
54
Q

types of crescentic GN

A
  • type 1 - anti glomerular basement membrane disease
  • type 2 - immune complex mediated - post infectious, IgAA, mesangiocapillary GN
  • type 3 - pauci immune GN
55
Q

anti-GBM disease

A

autoantibody to a3 chain of type 4 collagen of GBM

autoantibodies may cross react with basement membrane of pulmonary alveolar ca[illaries

56
Q

findings in anti-GBM syndrome

A

crescents with necrosis
linear capillary loop IgG
angle antibodies - no immune complexes found

57
Q

lupus nephritis

A

lupus can affect the glomeruli in many ways

58
Q

pauci-immune GN

A

anti neutrophil cytoplasmic antibody associated glomerulonephritis and vasculitis
autoantibodies against cytoplasmic enzymes in neutrophils are released - toxic and damage endothelial cells
associated with systemic small vessel vasculitis

59
Q

two syndromes associated with pauci-immune GN

A

wegener’s GN - necorising graanulomaatous inflammatioon of upper and lower respiratory tract and kidney
charge-strauss syndrome - similar to WG with asthma and peripheral eosinophilia

60
Q

findings in pauci-immune GN

A

crescents and granulomatous inflammation in Wegener’s
eosinophil rich granuloma in charge- Strauss syndrome

no findings in immunoflourescence and no immune complexes in electron microscopy

pathology 2 (47 decks)

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