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Renal and Electrolytes > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Define AKI

A

AKI (previously known as acute renal failure) is an acute decline in GFR from baseline w/ or w/out anuria/oliguria

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2
Q

Define AKI

A

AKI (previously known as acute renal failure) is an acute decline in GFR from baseline w/ or w/out anuria/oliguria

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3
Q

Classifications of causes of AKI

A

Pre-renal azotemiaIntra renalPost renal

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4
Q

List the pre-renal causes of AKI

A

Hypoperfusion caused by:A. Systemic hypotension due to 1. Hypovolemia 2. cardiogenic shock (haemorrhage, MI, CHF)3. septic shock 4. 3rd spacing due to hypoalbuminaemia or in severe pancreatitis5. hypoaldosteronism due to Addison’s B. NSAID induced pre-renal failureC. Renal artery stenosisD. Hepatorenal syndrome

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5
Q

Define azotemia and uraemia

A

Azotemia: Increase in blood nitrogen compoundsUraemia: when azotemia leads to Sx (pericarditis, increase infection as WBC cannot degranulate, bleeding as platelets cannot stick)

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6
Q

List the intrinsic renal failure causes

A

A. Acute tubular necrosisB. Interstitial nephritisC. Glomerulonephritis

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7
Q

List the post renal causes

A

Obstruction of urinary outflow tract:Proximal to bladder:a. Retroperitoneal fibrosisb. Bilateral stones c. Bladder cancerDistal to bladder:a. BPHb. Neurogenic bladder c. Urethral strictures

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8
Q

Classifications of causes of AKI

A

a. Pre-renal: failure due to impaired renal perfusion, with an appropriate renal responseb. Intrinsic: failure due to direct injury to renal parenchymac. Post renal: failure due to obstruction of urinary outflow

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9
Q

List the post renal causes

A

Obstruction of urinary outflow tract:Proximal to bladder:a. Retroperitoneal fibrosisb. Bilateral stones c. Bladder cancerDistal to bladder:a. BPHb. Neurogenic bladder c. Urethral strictures

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10
Q

List the post renal causes

A

Obstruction of urinary outflow tract:Proximal to bladder:a. Retroperitoneal fibrosisb. Bilateral stones c. Bladder cancerDistal to bladder:a. BPHb. Neurogenic bladder c. Urethral strictures

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11
Q

Ix of AKI

A

Main tests include:1. Basic metabolic profile (high serum creatinine, high serum K, metabolic acidosis)2. Urea:Creatinine ratio3. Urinalysis: RBCs, WBCs, cellular casts, proteinuria, bacteria, positive nitirite, leukocyte esterase4. Urine sodium concentration5.Urine osmolality

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12
Q

What acronym is used to know when to dialyse a patient?

A

AEIOUA = acidosis (metabolic)E = electrolyte imabalance with ECG changes (hyperkalaemia)I = intoxication (SLIME): salicylic acid, lithium, isopropanol, Mg laxatives, ethylene glycol)I = infection (related to uraemia)O = overload of fluid that is not responsive to diureticsU = uraemia Sx (pericarditis, malfunction of platelets, increase infections)

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13
Q

What acronym is used to know when to dialyse a patient?

A

AEIOUA = acidosis (metabolic)E = electrolyte imabalance with ECG changes (hyperkalaemia)I = intoxication (SLIME): salicylic acid, lithium, isopropanol, Mg laxatives, ethylene glycol)I = infection (related to uraemia)O = overload of fluid that is not responsive to diureticsU = uraemia Sx (pericarditis, malfunction of platelets, increase infections)

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14
Q

What is renal artery stenosis usually caused by?

A

Atherosclerosis + poorly controlled HTN

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15
Q

What is renal artery stenosis (RAS) usually caused by?

A

Atherosclerosis + poorly controlled HTN

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16
Q

Ix of RAS

A

Renal artery angiogram

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17
Q

Rx of RAS

A

1st line: statins to control LDLSurgery: angioplasty

18
Q

Rx of RAS

A

1st line: statins to control LDLSurgery: angioplasty

19
Q

Why should we NEVER use ACE inhibitors in patients with bilateral RAS?

A
  • Aldosterone normally leads to constriction of the eff arteriole leading to increased P, therefore increased GFR - ACE inhibitors prevent aldosterone from constricting the efferent arteriole - Pts with BL RAS have V. V. low P and GFR already- ACE inhibitors will exacerbate this issue causing dangerously low GFR (uraemia)
20
Q

Why are ACE inhibitors normally used in renal failure?

A

ACE inhibitors dilate the eff arteriole (by opposing action of aldosterone).Therefore there is a decrease in GFR thereby reducing the load on the glomerulus= slows progression of renal disease in long termNB: exception is bilateral RAS

21
Q

List the pre-renal causes of AKI

A

Hypoperfusion caused by:A. Systemic hypotension due to 1. Hypovolemia 2. cardiogenic shock (haemorrhage, MI, CHF)3. septic shock 4. 3rd spacing due to hypoalbuminaemia or in severe pancreatitis5. hypoaldosteronism due to Addison’s B. NSAID induced pre-renal failureC. ACEI or ARBs induced AKID. Renal artery stenosisE. Hepatorenal syndrome

22
Q

What Rx should we never use in patients with bilateral RAS?

A

NEVER use ACE inhibitors or ARBs:- Aldosterone normally leads to constriction of the eff arteriole leading to increased P, therefore increased GFR - ACEI and ARBs prevent aldosterone from constricting the efferent arteriole - Pts with BL RAS have V. V. low P and GFR already- ACE inhibitors will exacerbate this issue causing dangerously low GFR (uraemia)

23
Q

Why are ACE inhibitors normally used in renal failure?

A

ACE inhibitors dilate the eff arteriole (by opposing action of aldosterone).Therefore there is a decrease in GFR thereby reducing the load on the glomerulus= slows progression of renal disease in long termNB: exception is bilateral RAS

24
Q

What is NSAID induced pre-renal failure?

A

NSAIDs can cause pre-renal failure in pts with pre-existing renal disease

25
Q

Explain how AKI can be due to ACEI and ARBs

A
  1. Several conditions depend on eff arteriole vasoconstriction to maintain adequate glomerular filtration: volume depletion, vasoconstriction caused by NSAIDs, CKD, CHF (decreased circulatory volume), bilateral RAS2. ACEI and ARBs selectively dilate the efferent arteriole, therefore reduce GFR
26
Q

What is NSAID induced pre-renal failure?

A
  1. NSAIDs can cause pre-renal failure in pts with pre-existing renal disease (diabetic nephropathy, bilateral RAS)2. PGs act on aff arteriole to dilate and therefore allow more BF and increase GFR3. NSAIDs block PG production, leading to a decrease in GFR
27
Q

Explain how AKI can be due to ACEI and ARBs

A
  1. Several conditions depend on eff arteriole vasoconstriction to maintain adequate glomerular filtration: volume depletion, vasoconstriction caused by NSAIDs, CKD, CHF (decreased circulatory volume), bilateral RAS2. ACEI and ARBs selectively dilate the efferent arteriole, therefore reduce GFR
28
Q

What is NSAID induced pre-renal failure?

A
  1. NSAIDs can cause pre-renal failure in pts with pre-existing renal disease (diabetic nephropathy, bilateral RAS)2. PGs act on aff arteriole to dilate and therefore allow more BF and increase GFR3. NSAIDs block PG production, leading to a decrease in GFRNB: NSAIDs cause more intrinsic failure due to (inflam rxn)
29
Q

Explain how AKI can be due to ACEI and ARBs

A
  1. Several conditions depend on eff arteriole vasoconstriction to maintain adequate glomerular filtration: volume depletion, vasoconstriction caused by NSAIDs, CKD, CHF (decreased circulatory volume), bilateral RAS2. ACEI and ARBs selectively dilate the efferent arteriole, therefore reduce GFR
30
Q

T/F Avoid prescribing NSAIDs with existing renal disease

A

True

31
Q

T/F Avoid prescribing NSAIDs with existing renal disease

A

True

32
Q

What is the hepatorenal syndrome?

A

= idiopathic pre-renal failure along with pre-existing liver disease

33
Q

What is the hepatorenal syndrome?

A

= idiopathic pre-renal failure along with pre-existing liver disease

34
Q

Compare Sx between urinary obstruction proximal to bladder v distal to bladder

A

Proximal: pt anuricDistal:pt difficulty in urinating despite urge

35
Q

Compare Sx between urinary obstruction proximal to bladder v distal to bladder

A

Proximal: pt anuricDistal:pt difficulty in urinating despite urge

36
Q

Dora to complete - intrinsic causes

A

d

37
Q

Dora to complete - intrinsic causes

A

d

38
Q

What is the principle behind the urea:creatinine ratio?

A
  • urea and creatinine are both waste products produced and filtered thru glomerulus at same rate- urea and creatinine are both freely filtered at the glomerulus but, - creatinine is not reabsorbed (all in urine)- whereas some of urea is reabsorbed by tubules back into blood- therefore the blood will have more urea than creatinine, creating the urea: creatinine blood serum rationormal is 40-100:1 mmol/L (i.e. 40-100 urea to 1 creatinine)
39
Q

What are the values of urea:creatinine ratio for a. Pre-renal AKIb. Normal/post renal AKIc. Intrinsic AKI

A

Pre renal: > 100:1 (as decrease in GFR leads to filtrate moving v. slowly, therefore increasing the reabsorption of urea to blood)Normal/Post renal: 40-100:1Intrinsic:

40
Q

What are the values of urea:creatinine ratio for a. Pre-renal AKIb. Normal/post renal AKIc. Intrinsic AKI

A

Pre renal: > 100:1 (as decrease in GFR leads to filtrate moving v. slowly, therefore increasing the reabsorption of urea to blood)Normal/Post renal: 40-100:1Intrinsic:

Renal and Electrolytes (4 decks)

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