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Block 34 metabolic -Ellen > Acute Kidney injury PT1 > Flashcards

Acute Kidney injury PT1 Flashcards

1
Q

2 measures of a rapid decline in renal function

A
  • rise in serum creatinine

- decrease in urine output

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2
Q

laboratory findings for increase in creatinine

A

> 26.5 micromol/L witin 48 hours

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3
Q

increase in creatinine above baseline for AKI

A

> 1.5x within 7 days

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4
Q

decrease in urine for AKI

A

<0.5 ml/kg/h for 6 hours

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5
Q

3 types of AKI

A

pre-renal
renal
post-renal

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6
Q

Urea: creatinine ratio for normal and post renal AKI

A

40-100 : 1

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7
Q

Urea: creatinine ratio for pre-renal AKI

A

> 100: 1

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8
Q

Urea: creatinine ratio for intrinsic renal damage

A

<40: 1

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9
Q

what do pre-renal AKIs cause in the body

A

Azotemia

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10
Q

3 characteristics in prerenal failure

A

low urine Na
high urine osmolarity
high BUN:cr ratio

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11
Q

causes of prerenal failure (5)

A
  • renal artery stenosis
  • NSAID
  • systemic hypotension
  • hepatorenal syndrome
  • hypercalcaemia
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12
Q

genetic condition that can cause renal artery stenosis

A

fibromusclular dysplasia

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13
Q

diagnostic key for renal artery stenosis

A

uncontrolled hypertension refractory to treatment

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14
Q

treatment of renal artery stenosis

A

angioplasty and treat LDL with statins

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15
Q

danger of ACEi with bilateral RAS

A

can lead to a very low GFR

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16
Q

when can NSAIDs cause prerenal failure

A

in patients with pre-existing renal disease

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17
Q

what do NSAIDs block

A

prostaglandins

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18
Q

what do prostaglandins do and therefore NSAIDs stop

A

dilation of the afferent arteriole

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19
Q

what absorption co-exists with Na reabsorption

A

urea reabsorption -therefore RAAS activation causes high BUN levels

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20
Q

more commonly what type of AKI do NSAIDs cause

A

intrarenal

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21
Q

hypoadrenalism means

A

low cortisol and aldosterone

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22
Q

low cortisol and aldosterone from addison’s means the nephron can’t______

A

reabsorb Na and water leading to hypotension and hypoatremia

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23
Q

symptoms of Addisons

A 
salt craving 
weakness
abdo pain 
syncope 
higher pigmentation 
uremia
24
Q

lab results for Addison’s (5)

A 
hypotension 
hyponatremia 
hyperkalaemia 
elevated BUN:cr ratio 
acidosis
25
Q

treatment of Addison’s

A

cortisol replacement -hydrocortisone or prednisolone

mineralocorticoid replacement -fludrocortisone

26
Q

hepatorenal syndrome=

A

idiopathic prerenal failure with pre-existing liver disease

27
Q

symptoms of hepatorenal syndrome

A

jaundice
pruritis
asterixis
uremia

28
Q

most common cause of intrinsic AKI

A

acute tubular necrosis

29
Q

what happens to the epithelial cells in acute tubular necrosis

A

When epithelial cells become damaged, they slough off, accumulate and aggregate together in the renal tubule forming an obstruction→ high pressure behind obstruction reducing GFR

30
Q

cells most affected by ischaemia in acute tubular necrosis

A

PCT and TAL

31
Q

4 types of insult to the epithelial cells in Acute tubular necrosis

A

ischaemic
toxic
drugs
contrast induced

32
Q

2 toxic causes of acute tubular necrosis

A

rhambdomylosis

heme

33
Q

rhambdomylosis=

A

muscle injury

34
Q

damaged muscle causes

A

-fluid sequestration in the damaged muscle induces volume depletion, activation of the sympathetic nervous system, ADH secretion and RAS activation all of which favor vasoconstriction and renal salt and water preservation

35
Q

what can myoglobin from muscle injury do

A

myoglobin can cause direct tubular obstruction

36
Q

2 drugs causing acute tubular necrosis

A

aminoglycosides

amphotericin B

37
Q

what does contrast do to the tubules (2)

A
  • causes vasoconstriction in nephrons

- can cause direct tubular toxicity and ischaemia

38
Q

a form of inter-renal AKI caused by infiltration of neutrophils and eosinophils into the interstitium inducing inflammation

A

acute interstitial nephritis

39
Q

presentation of acute interstitial nephritis

A

eosinophils
fever
rash

40
Q

main cause of acute interstitial nephritis=

A

drug allergies

41
Q

common drug allergies causing acute interstitial nephritis (4)

A

Beta lactams
PPIs
NSAIDs
diuretics

42
Q

what type of reaction is acute interstitial nephritis

A

hypersensitivity reaction

43
Q

treatment of acute interstitial nephritis

A

cessation of inflammatory inducing medications

44
Q

if the hypersensitivity reaction of acute interstitial nephritis continues what is it called

A

renal papillary necrosis

45
Q

less common cause of acute interstitial nephritis

A

pyelonephritis

46
Q

pathology of pyelonephritis causing acute interstitial nephritis

A

chemokines and cytokines secreted by offending pathogens leads to inflammatory cell infiltration and direct damage to the interstitium

47
Q

glomerular cause of intra-renal AKI

A

glomerulonephritis (inflammation of the glomerulus)

48
Q

possible negative consequence of glomerulonephritis

A

membranous nephropathy -widespread thickening of the glomerular basement membrane

49
Q

findings of glomerulonephritis (5)

A
  • decreased GFR
  • oliguria
  • oedema
  • hypertension
  • azotemia
50
Q

what is often the cause of glomerulonephritis

A

antigen-antibody complex in the glomerulus

51
Q

what causes post-renal AKI

A

obstruction of the flow of urine

52
Q

causes of post-renal obstruction

A
  • BPH
  • intra-abdominal tumour
  • renal calculi
  • kidney stone
  • inflammation: stricture
  • post-urethral valves
  • infection: TB, schistosomiasis
53
Q

what does the obstruction cause

A

back flow of urine causing increased pressure in the tubules reducing the pressure gradient reducing GFR .

54
Q

what can high pressure in the tubules due to absorption

A

encourages reabsorption of Na, water and urea

55
Q

what is the long term effect of high pressure in tubules from obstruction

A

causes the tubular epithelial cells to die impairing reabsorption and secretion

56
Q

lab results of post renal AKI

A

azotemia
oliguria
increase BUN;cr ratio

57
Q

what does the obstruction need to be to cause AKI

A

bilateral

Block 34 metabolic -Ellen (8 decks)

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