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Renal > AKI > Flashcards

AKI Flashcards

1
Q

How do pre-renal causes lead to an AKI?

A

renal hypo perfusion leading to ischaemic damage–>acute tubular necrosis

can be cardiogenic (low CO or myocardial ischamia), hypovolaemic (blood loss or dehydration), sepsis (due to vasodilation and 3rd space loss), drug induced e.g NSAIDs and ACEi

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2
Q

How do intra-renal causes lead to an AKI?

A

resulting from abnormalities within the kidneys i.e. glomerular, interstitial or the vessels e.g. malignant HTN, acute glomerulonephritis, acute tubular necrosis or acute pyelonephritis, DIC, vasculitis

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3
Q

How do post renal causes lead to an AKI?

A

resulting from an obstruction anywhere from the renal calyces to the outflow tract from the bladder
SNIPPIN: stone, neoplasm, inflammation (stricture), prostatic hypertrophy (BPH), posterior urethral valves, infection (TB, schisto), Neuro (post op, neuropathy)

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4
Q

what are the urine output and creatinine levels in stage 1 AKI?

A

creatinine >26umol/l (>1.5xbaseline)

urine output<0.5ml/kg/hr for 6-12 hrs

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5
Q

what are the urine output and creatinine levels in stage 2 AKI?

A

creatinine 2-2.9 Xbaseline

urine output<0.5ml/kg/hr for >12hrs

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6
Q

what are the urine output and creatinine levels in stage 3 AKI?

A

creatinine >353umol/l

urine output<0.3ml/kg/hr for 24hrs or anuria for 12hrs.

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7
Q

what is a diagnosis of an AKI based on?

A

creatinine and eGFR levels

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8
Q

management of an AKI

A

treat cause
fluid balance management
be wary of acidosis, hyperkalaemia.
drug review, stop nephrotoxic drugs

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9
Q

what investigations would you order if you suspected AKI?

A

urine dip- (haematuria and proteinuria may suggest intrinsic renal disease)
US within 2hrs- small shiny kidneys suggest CKD
Liver function tests- to rule out hepatorenal syndrome

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10
Q

What is acute kidney injury?

A

acute deterioration in renal function over hrs-days.

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11
Q

What are the 3 phases of AKI?

A

Oliguria (obstruction from dead cells and oedema)
Polyuria (tubules open but not functioning)
Recovery

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12
Q

what are the 2 main complications of AKI that can lead to death?

A

pulmonary oedema and hyperkalaemia

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13
Q

what is the key part of assessing someone with an AKI?

A

Assess their fluid status.

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14
Q

What is the classification of AKI based on?

A

GFR
or
urine output

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15
Q

what are the main aspects of AKI management?

A

identify underlying cause
resuscitate A-E and monitor fluid status
prevent and treat complications such a hyperkalaemia and pulmonary oedema

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16
Q

describe the management of hyperkalaemia?

A

10ml 10% calcium gluconate
100ml 20% glucose and 10U of act rapid insulin
salbutamol nebuliser 5mg
consider dialysis
Ion exchange resins e.g. calcium resonium 15g PO or 30mg PR

17
Q

How would you manage pulmonary oedema?

A

Sit the patient up and give high flowO2
morphine 2.5mg (+/- 10mg IV metoclopramide)
furosemide 120-250mg IV over 1hr
GTN spray +/- isosorbide mononitrate IV
If no response consider CPAP, haemofiltration/dialysis

18
Q

why can AKI lead to bleeding?

A

increase urea impairs homeostasis

19
Q

what are the indications for acute dialysis?

A 
persistent hyperkalaemia (>7mM)
refractory pulmonary oedema
symptomatic uraemia (encephalopathy, pericarditis)
severe metabolic acidosis (pH<7.2)
poisoning e.g. aspirin
20
Q

what are the risk factors for Contrast nephropathy?

A 
high contrast load
high iodine content of contrast
hypovolaemia
myeloma
age
hyperuricaemia
diabetes especially if taking Metformin
hypercalcaemia
pre-existing CKD
21
Q

What is acute tubulointerstitial nephritis?

A

an immune mediated hypersensitivity reaction to a drug or infection leading to acute kidney injury

22
Q

what are the presentations of acute tubulointerstitial nephritis?

A

systemic manifestations of hypersensitivity e.g. fever, arthralgia, rash
AKI (oliguria)
uveitis

23
Q

What would you expect to find on urine dip in a patient with acute tubulointerstitial nephritis?

A

proteinuria, haematuria, sterile pyuria (raised WCC in the absence of bacteriuria)

24
Q

what type of hypersensitivity reaction is involved in actor tubulointerstitial nephritis?

A

type 1 immune mediated ypersensitivity with raised IgE levels

25
Q

what would you expect to happen to the IgE levels and the eosinophils in acute tubulointerstital nephritis?

A

raised IgE levels

raised eosinophils

26
Q

what is the treatment for acute interstitial nephritis?

A

stop causative agent eg drug

steroids can hasten renal function recovery

27
Q

how is acute tubulointerstilal nephritis different to acute tubular necrosis?

A

acute tubulointerstilal nephritis involves inflammation of the tubules where as acute tubular necrosis involves ischaemia or toxic necrosis to the tubular cells.

28
Q

when skeletal muscles break down what does it release?

A

K, PO, urate

myoglobin and CK

29
Q

what is rhabdomyolysis?

A

muscle damage (skeletal muscle breakdown) with release of myoglobin can cause severe AKI

30
Q

what are some common causes of rhabdomyolysis?

A

crush injuries e.g. trauma, compartment syndrome, immobilisation
uncontrolled fitting
drugs e.g. statins, vibrates
overdose on barbiturates, alcohol, heroin and ecstasy

31
Q

what drugs can lead to rhabdomyolysis?

A

statins and fibrates

32
Q

how does rhabdomyolysis present?

A

muscle pain and swelling, red-brown urine

AKI occurs 10-12 hrs later

33
Q

what would you expect on a urine dipstick in rhabdomyolysis?

A

+ve Hb, -ve RBC

34
Q

describe the management of rhabdomyolysis

A

manage hyperkalaemia
IV rehydration
central venous pressure monitoring if oliguric (this would require a central line access)
Can use IV NaHCO to alkalinise urine and stabilise less toxic form of myoglobin.

Renal (8 decks)

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