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Y4: Renal > AKI > Flashcards

AKI Flashcards

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
Q

cause of ATN?

A

ischaemia (often caused by a prerenal AKI)

nephrotoxins: aminoglycosides, heavy metals, myoglobun, radiocontrast, uric acid

26
Q

most common cause of AKI?

A

ATN

27
Q

cause of ATN?

A

ischaemia (often caused by a prerenal AKI)

nephrotoxins: aminoglycosides, heavy metals, myoglobun, radiocontrast, uric acid

28
Q

T/F: acute tubular necrosis is reversible

A

true- usually takes 7-10 days for full recovery

29
Q

T/F: acute tubular necrosis is reversible

A

true- usually takes 7-10 days for full recovery

30
Q

pre-renal uraemia vs acute tubular necrosis

1) urine sodium
2) urine osmolality
3) response to fluid challenge
4) serum urea: creatinine ratio

A 
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
Q

how to differentiate between acute and chronic renal failure

A

renal USS best (most pts have bilateral small kidneys)

Hypocalcaemia also suggests chronic- lack of vitamin D

32
Q

exceptions to the rule that CRF patients have bilateral small kidneys?

A

ADPKD
Diabetic nephropathy
Amyloidosis
HIV-associated nephropathy

33
Q

ADPKD

1) gene mutations?
2) screening investigation for relatives?
3) management?

A

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
Q

features of ADPKD

A 
hypertension
recurrent UTIs 
abdo pain
renal stones
haematuria
CKD
35
Q

extra-renal manifestations of ADPKD?

A

liver cysts (most common)
berry aneurysm
cardiovascular: mitral valve prolapse, mitral/tricupspid incompetence, aortic root dilation, aortic dissection

Y4: Renal (7 decks)

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