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pathology 2 > renal disease classification 2 > Flashcards

renal disease classification 2 Flashcards

1
Q

hypertensive nephrosclerosis

A

may be benign or malignant

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2
Q

benign hypertensive nephrosclerosis

A

due to chronic hyper tension

most due to primary essential hypertension eg. usually elderly, multifactorial hypertension

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3
Q

malignant hypertensive nephrosclerosis

A

due to accelerated hypertension
causes acute end organ damage
medical emergency

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4
Q

pathogenesis of benign hypertensive nephrosclerosis

A

thickening (sclerosis) of small arteries and arterioles
ischaemic damage to glomeruli and tubules
glomeruloslcerosis - scarring

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5
Q

clinical presentation of benign hypertensive nephrosclerosis

A

asymptomatic urinary abnormalities - proteinuria

chronic renal failure

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6
Q

pathogenesis malignant hypertensive nephrosclerosis

A
  • requires urgent but controlled reduction in blood pressure
  • severe damage to small arteries and arterioles
  • ischaemic injury to glomeruli and tubules
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7
Q

presentation of malignant hypertensive nephrosclerosis

A

acute renal failure

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8
Q

renal artery stenosis

A

uncommon cause of secondary hypertension

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9
Q

pathogenesis of renal artery stenosis

A

usually unilateral critical narrowing of main renal artery
due to atheromatous disease in elderly
rarely, due to fibromuscular dysplasia in young women
ischaemic damage to glomeruli and tubules
narrowing to main renal artery reduces blood perfusing the kidney
kidney recognises reduced oxygen and secretes renin which is an enzyme catalysing conversion of angiotensin to angiotensin 1
cells in the lungs secrete Ace which converts angiotensin 1 to angiotensin 2 which is a vasoconstrictor
systemic vasoconstriction occurs increasing blood pressure
ACE inhibitor drugs required

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10
Q

kidney response to narrowing of main renal artery

A

responds to decreased perfusion by secreting renin, an enzyme catalysing conversion of angiotensin to angiotensin 1

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11
Q

angiotensin 1

A

is converted to angiotensin 2 by ACE, which is secreted by cells in the lungs

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12
Q

angiotensin 2

A

a vasoconstrictor, causes systemic vasoconstriction and rise in blood pressure

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13
Q

fibromuiscular displasia

A

patients develop thinking of all layers of the blood vessel in the renal artery
angiogram shows alnernating patterns of narrowing and dilatation like beads on a string
cause of renal artery stenosis

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14
Q

acute tubular necrosis

A

one of the most common causes of acute renal failure
tubular injury/necorisi due too either
- iachaemia
- toxins

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15
Q

acute tubuler necrosis due to ischaemia

A

reduced renal perfusion

- shock, hypevolaemia, vascular compromise (vasculitis, malignant hypertension, thrombotic microangiopathy)

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16
Q

acute tubular necrosis due to toxins

A

endogenous - myoglobin, haemoglobin, light chains

exogenous - drugs, radio contrast dyes, heavy metals

17
Q

clinical course of acute tubularr necrosis

A

initiation phase - mild oliguria with mild increase in serum creatinine
maintenance phase - sustained oliguria, rising serum creatinine with uraemia
recovery phase - massive diuresis with electrolyte disturbances

18
Q

histology of acute tubular necrosis

A

injury to the tubular epithelial cells

19
Q

tubulointerstitial nephritis

A

tubulointerstitial inflammation due to various causes

  • acute - interstitial oedema with neutrophilic/eosinophiliss infiltrate
  • chronic - lymphocytic infiltrate with tubular atrophy and interstitial fibrosis (chronic and irreversible)
20
Q

aetiology of tubulointerstitial nephritis

A
  • usually drugs - NSAIDs, PPIs, antibiotics

- others

21
Q

pathogenesis drug related tubulointerstitial nephritis

A

drug-related TIN usually idiosyncratic and not dose related

drugs act as a happen, combining with components of tubular epithelial cells to elicit immune reaction

22
Q

clinical presentation of tubulointerstitial nephritis

A

fever, peripheral eosinophilia, rash, mild proteinuria, eosinophils in urine and acute renal failure

23
Q

histology of acute TIN

A

mixed inflammation with tubulitiss and tubular injury

24
Q

histology of chronic TIN

A

chronic inflammation with tubular atrophy/interstitial fibrosis

25
Q

acute TIN vs acute pyelonephritis

A

pyelonephritis usually cause by ascending UTI not drugs
inflammation of pyelonephritis usually centred around renal calyces, pelvis and tubulointerstitial compartment instead of just tubulointerstitial compartment
pyelonephritis has tubular micro abscesses not just tubulitis
pyelonephritis treated with antibiotics, whereas TIN treated with removal of offending agent and steroids

26
Q

chronic pylonephritis

A

chronic inflammation and scarring centered on renal calyces, pelvis and tubulointerstitium
two main clinical settings
- reflux nephropathy due to congenital vesocoureteric reflux
- obstructive nephropathy due to chronic ureteric obstruction

27
Q

myeloma kidney

A
  • plasma cell myeloma - malignant clonal proliferation of plasma cells
  • bone lesions, serum paraprotein, kidney injury
28
Q

renal complications of plasma cell myeloma

A
  • cast nephropathy
  • amyloidosis
  • acute tubular necrosis (calcium, light chains, uric acid)
  • light chain deposition disease
  • renal vein thrombosis
29
Q

myeloma cast nephropathy

A

medical emergency
widespread tubular abstructiin by intraluminal light chain chants causing acute renal failure
immunoflourescence shoes kappa or lambda light chains (not both)

30
Q

amyloidosis

A

accumulation of amyloid protein - which is abnormally folded causing it to be hard to degrade
resistant to enzymatic degradation
have unusual physiochemical properties - form beta pleased sheets
can be identified on the microscope using Congo red stain, where the proteins stain salmon pink colour
deposits in glomeruli, vessels and interstitial presenting as severe proteinuria

31
Q

histology of myeloma kidney

A

large pink amorphous deposits - amyloidosis

  • salmon pink under Congo red stain
  • apple green on polarising LM stain

pathology 2 (47 decks)

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