AKI Flashcards

(35 cards)

1
Q

causes of AKI?

A

PRERENAL: decreased blood flow
- absolute loss of fluid: diarrhoea, vomiting, blood loss, severe burns
- relative loss of fluid: CHF, distributive shock
- renal artery stenosis
INTRARENAL: damage to tubules, glomerululus or interstitium
- acute tubular necrosis
- glomerulonephritis
- acute interstitial nephritis
- rhabdomyolysis
- tumour lysis syndrome
POSTRENAL: obstruction to outflow
- blockage: kidney stones
- external compression of ureter: BPH, intra-abdominal tumours

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2
Q

what patients are at increased risk of AKI

A

history of AKI
CKD
other organ failure/ chronic disease e.g. HF, liver disease, DM
use of nephrotoxic drugs
iodinated contrast in past week
65 or over
cognitive impairment > reduced fluid intake

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3
Q

what is done for patients at risk of AKI who are undergoing an investigation requiring contrast

A

IV fluids to reduce risk

ACEIs and ARBS temporarily withheld

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4
Q

the kidneys are primarily responsible for ___ balance and maintaining ___

A

fluid

homeostasis

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5
Q

how is AKI detected?

A

decreased UO
electrolyte disturbance
fluid overload

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6
Q

symptoms of AKI?

A

oliguria (<0.5ml/kg/hr)
pulmonary and peripheral oedema
arrhythmias (changes in potassium and acid-base balance)
uraemia (pericarditis, encephalopathy)

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7
Q

what is included in ‘urea and electrolytes’

A

urea
creatinine
potassium
sodium

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8
Q

criteria for diagnosing AKI?

A

rise in creatinine of ≥26mmol/L in 48 hours

≥50% rise in serum creatinine known/ presumed in past 7 days

oliguria for >6 hours in adults (8 in children)

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9
Q

All patients with AKI should have ____ (Ix)

What patients should have renal US?

A

urinalysis

no identifiable cause/ at risk of urinary tract obstruction

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10
Q

management of AKI?

A

mainly supportive

  • careful fluid balance
  • med review
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11
Q

which medications should be stopped in AKI as they may worsen renal function?

A
NSAIDS (except aspirin at cardioprotective dose- 75mg OD)
Aminoglycosides
ACEI
ARBS
Diuretics

these are NAAAD good

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12
Q

which medications may have to be stopped in AKI due to increased risk of toxicity? (but don’t usually worsen AKI themselves)

A

metformin
lithium
digoxin

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13
Q

which of the following should be stopped in AKI and why

  • paracetamol
  • ARBs
  • diuretics
  • statins
  • aspirin 75mg OD
  • metformin
  • aminoglycosides
A

ARBS, aminoglycosides and diuretics should be stopped as they may worsen renal function

Metformin should be stopped due to increased risk of toxicity

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14
Q

T/F: loop diuretics are recommended in AKI to boost urine output

A

False

can, however, be used in those who experience significant fluid overload

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15
Q

T/F: low dose dopamine is recommended in AKI to boost renal perfusion

A

False

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16
Q

in AKI, hyperkalaemia requires prompt treatment to avoid ____

A

arrhythmias

which can be life threatening

17
Q

treatment of hyperkalaemia?

A

stabilise cardiac membrane: IV calcium gluconate

Shift in potassium from extracellular to intracellular: insulin/ dextrose infusion + neb salbutamol
Removal of potassium from body: calcium resonium, loop diuretics, dialysis

18
Q

when is renal replacement therapy e.g. haemodialysis indicated in AKI?

A

pt not responding to medical treatment of complications e.g. hyperkalaemia, pulmonary oedema, acidosis, uraemia

19
Q

what is azotemia?

A

&&&&&&&&&&&

occurs in AKI

20
Q

what is tumour lysis syndrome and what kind of AKI is it associated with?

A

cancer treatment > increased uric acid (waste product from dead cancer cells) > nephrotoxic > ATN > intrarenal AKI

21
Q

what is azotemia?

A

aka uraemia

high levels of nitrogen containing compounds in the blood (creatinine, urea)

occurs in AKI due to reduced GFR

22
Q

what cause of AKI presents with oliguria, eosinophilia, fever, rash

A

acute interstitial nephritis

23
Q

causes of acute interstitial nephritis?

A

type I or IV hypersensitivity (infiltration of immune cells (neutrophils, oesinophils)> inflammation)

typically caused by medications e.g. NSAIDs, penicillin, diuretics

24
Q

presence of “muddy brown casts” in urinalysis is pathognomonic for what underlying cause of AKI?

A

acute tubular necrosis (dead cells build up in tubules then excreted out as dead, brown cylinders)

25
cause of ATN?
ischaemia (often caused by a prerenal AKI) | nephrotoxins: aminoglycosides, heavy metals, myoglobun, radiocontrast, uric acid
26
most common cause of AKI?
ATN
27
cause of ATN?
ischaemia (often caused by a prerenal AKI) | nephrotoxins: aminoglycosides, heavy metals, myoglobun, radiocontrast, uric acid
28
T/F: acute tubular necrosis is reversible
true- usually takes 7-10 days for full recovery
29
T/F: acute tubular necrosis is reversible
true- usually takes 7-10 days for full recovery
30
pre-renal uraemia vs acute tubular necrosis 1) urine sodium 2) urine osmolality 3) response to fluid challenge 4) serum urea: creatinine ratio
``` PRU 1) low 2) high 3) good 4) increased ATN 1) high 2) low 3) poor 4) normal ``` (prerenal: kidneys hold on to sodium to preserve volume)
31
how to differentiate between acute and chronic renal failure
renal USS best (most pts have bilateral small kidneys) | Hypocalcaemia also suggests chronic- lack of vitamin D
32
exceptions to the rule that CRF patients have bilateral small kidneys?
ADPKD Diabetic nephropathy Amyloidosis HIV-associated nephropathy
33
ADPKD 1) gene mutations? 2) screening investigation for relatives? 3) management?
1) PDK1 (polycystin-1): 85% of cases. PKD2 (polycystin-2): 15% of cases. 2) abdominal USS 3) tolvaptan (if CKD 2 or 3/ rapidly progressive)
34
features of ADPKD
``` hypertension recurrent UTIs abdo pain renal stones haematuria CKD ```
35
extra-renal manifestations of ADPKD?
liver cysts (most common) berry aneurysm cardiovascular: mitral valve prolapse, mitral/tricupspid incompetence, aortic root dilation, aortic dissection