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4th year passmedicine by topic > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What are some examples of nephrotoxic drugs?

A

NSAIDs
aminoglycosides
ACE inhibitors/angiotensin II receptor antagonists
diuretics

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2
Q

The criteria for diagnosing AKI looks at what parameter(s)?

A

Rise in creatinine OR
Fall in urine output OR
Fall in eGFR in children / young adults

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3
Q

In terms of creatinine, what is the criteria for diagnosing AKI?

A

Rise in creatinine of 26µmol/L or more in 48 hours OR

>= 50% rise in creatinine over 7 days

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4
Q

In terms of fall in urine output, what is the criteria for diagnosing AKI?

A

Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children)

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5
Q

In terms of egfr, what is the criteria for diagnosing AKI?

A

> = 25% fall in eGFR in children / young adults in 7 days

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6
Q

what increases the risk of AKI?

A

Surgery: Emergency surgery, ie, risk of sepsis or hypovolaemia, Intraperitoneal surgery

CKD, ie if eGFR < 60

Age >65 years

Disease: Liver disease, Diabetes, Heart failure

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7
Q

Acute kidney injury (AKI), previously termed acute renal failure, describes what?

A

reduction in renal function following an insult to the kidneys

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8
Q

Around what % of patients admitted to hospital develop AKI?

A

15%

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9
Q

NICE estimate that inpatient mortality of AKI in the UK might typically be 25-30% or more

A

true

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10
Q

Causes of AKI are traditionally divided into?

A

prerenal, intrinsic and postrenal causes

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11
Q

What are some examples of prerenal AKI causes?

A

hypovolaemia secondary to diarrhoea/vomiting

renal artery stenosis

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12
Q

What can cause intrinsic AKI?

A

toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.

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13
Q

What are some examples of conditions that can result in intrinsic AKI?

A 
glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome
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14
Q

What are some example causes of postrenal AKI?

A

kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter

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15
Q

use of iodinated contrast agents within the past what is a risk factor for AKI?

A

week

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16
Q

Define oliguria

A

urine output less than 0.5 ml/kg/hour

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17
Q

What steps can be undertaken for patients who are at risk of AKI and who are undergoing an investigation requiring contrast?

A

IV fluids

Certain drugs such as ACE inhibitors and ARBs may also be temporarily stopped.

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18
Q

How would AKI present?

A

Many patients with early AKI may experience no symptoms. However, as renal failure progresses the following may be seen:
reduced urine output
pulmonary and peripheral oedema
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia

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19
Q

What are the features of uraemia?

A

pericarditis or encephalopathy

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20
Q

What is a common blood test that can help detect AKI? What does this include?

A 
'urea and electrolytes' or 'U&Es'. This returns a number of markers, including
sodium
potassium
urea
creatinine
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21
Q

all patients with suspected AKI should have what investigation?

A

urinalysis

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22
Q

if patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have what investigation?

A

renal ultrasound within 24 hours of assessment.

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23
Q

What are the principles of AKI management?

A

Largely supportive
Fluid balance - to ensure that the kidneys are properly perfused but not excessively to avoid fluid overload
Review medications

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24
Q

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

A
  • NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
  • Aminoglycosides
  • ACE inhibitors
  • Angiotensin II receptor antagonists
  • Diuretics
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25
Q

What medications may have to be stopped in AKI?

A

• Metformin
• Lithium
• Digoxin
May have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)

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26
Q

What medications are usually SAFE to continue in AKI?

A
  • Paracetamol
  • Warfarin
  • Statins
  • Aspirin (at a cardioprotective dose of 75mg od)
  • Clopidogrel
  • Beta-blockers
27
Q

loop diuretics are routinely reccomended to artificially boost urine output

A

FALSE
not recommend
There is however a role for loop diuretics in patients who experience significant fluid overload.

28
Q

low-dose dopamine are routinely reccomended (in an attempt to increase renal perfusion)

A

false

29
Q

Hyperkalaemia needs prompt treatment to avoid arrhythmias which may potentially be life-threatening.

A

true

30
Q

What is the role of Intravenous calcium gluconate in management of hyperkalaemia?

A

Stabilisation of the cardiac membrane

31
Q

What medications aid Short-term shift in potassium from extracellular to intracellular fluid compartment in hyperkalaemia?

A
  • Combined insulin/dextrose infusion

* Nebulised salbutamol

32
Q

What medications remove potassium from the body in hyperkalaemia?

A
  • Calcium resonium (orally or enema)
  • Loop diuretics
  • Dialysis
33
Q

When is Renal replacement therapy (e.g. haemodialysis) used in the context of AKI?

A

when a patient is not responding to medical treatment of complications

34
Q

What are the complications of AKI?

A

hyperkalaemia
pulmonary oedema
acidosis
uraemia

35
Q

DAMN mnemonic for drugs to stop in AKI -

A

diuretics, ACEi/ ARBs, metformin, NSAIDs

36
Q

Why would Metformin be held in the context of AKI?

A

can cause Lactic Acidosis so must be stopped, if egfr is 30 or less then patients cannot take metformin

37
Q

What investigation would you do if you suspected hydronephrosis?

A

US KUB

38
Q

Renal artery stenosis is caused by?

A

atherosclerosis accounts for around 90%

fibromuscular dysplasia being the most common cause of the remaining 10%.

39
Q

What are the features of renal artery stenosis?

A

hypertension
kidney disease (chronic or AKI)
‘flash pulmonary oedema’

40
Q

Acute interstitial nephritis accounts for what % of drug-induced acute kidney injury?

A

25%

41
Q

What can cause Acute interstitial nephritis?

A

drugs: the most common cause, particularly antibiotics
systemic disease: SLE, sarcoidosis, and Sjögren’s syndrome
infection: Hanta virus , staphylococci

42
Q

What specific drugs can cause Acute interstitial nephritis?

A 
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
43
Q

Describe the histology of Acute interstitial nephritis?

A

marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

44
Q

Describe the symptoms & features of Acute interstitial nephritis?

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

45
Q

What will you see in urinalysis of Acute interstitial nephritis?

A

sterile pyuria
white cell casts
Eosinophilic casts

46
Q

Tubulointerstitial nephritis with uveitis (TINU) usually occurs in which group?

A

young females.

47
Q

What are the symptoms of Tubulointerstitial nephritis with uveitis (TINU) ? What would urinalysis show?

A

fever, weight loss and painful, red eyes

Urinalysis is positive for leukocytes and protein.

48
Q

What is the most common cause of AKI?

A

Acute tubular necrosis (ATN)

49
Q

Is Acute tubular necrosis (ATN) reversible?

A

In the early stages ATN is reversible if the cause if removed.

50
Q

What are the two main causes of Acute tubular necrosis (ATN) ?

A

ischaemia: shock, sepsis
nephrotoxins: aminoglycosides, myoglobin secondary to rhabdomyolysis, radiocontrast agents, lead

51
Q

What are the features of Acute tubular necrosis (ATN) ?

A

features of AKI: raised urea, creatinine, potassium

muddy brown casts in the urine

52
Q

What are the histo-pathological featyres of Acute tubular necrosis (ATN) ?

A

tubular epithelium necrosis: loss of nuclei and detachment of tubular cells from the basement membrane
dilatation of the tubules may occur
necrotic cells obstruct the tubule lumen

53
Q

What are the 3 phases of ATN?

A

oliguric phase
polyuric phase
recovery phase

54
Q

What is tumour lysis syndrome?

A

breakdown of the tumour cells and the subsequent release of chemicals from the cell.
Associated with treatment of high-grade lymphomas and leukaemias.
It can occur in the absence of chemotherapy but is usually triggered by the introduction of combination chemotherapy.

55
Q

tumour lysis syndrome can sometimes arise from steroid treatment alone

A

true

56
Q

When should you suspect tumour lysis syndrome in AKI?

A

presence of a high phosphate and high uric acid level

57
Q

What electrolyte imbalances can tumour lysis result in?

A

high potassium and high phosphate level in the presence of a low calcium.

58
Q

Patients at high risk of TLS should be given what medications immediately prior to and during the first days of chemotherapy?

A

IV allopurinol or IV rasburicase

Patients in lower-risk groups should be given oral allopurinol during chemotherapy cycles in an attempt to avoid the condition.

59
Q

Why should Rasbicurase and allopurinol not be given together?

A

reduces the effect of rasburicase

60
Q

How does rasburicase work?

A

Rasburicase is a recombinant version of urate oxidase, an enzyme that metabolizes uric acid to allantoin. Allantoin is much more water-soluble than uric acid and is, therefore, more easily excreted by the kidneys.

61
Q

How is TLS graded?

A

Cairo-Bishop scoring system

62
Q

Describe the Cairo-Bishop scoring system

A 
Laboratory tumor lysis syndrome: abnormality in two or more of the following, occurring within three days before or seven days after chemotherapy.
uric acid > 475umol/l or 25% increase
potassium > 6 mmol/l or 25% increase
phosphate > 1.125mmol/l or 25% increase
calcium < 1.75mmol/l or 25% decrease
63
Q

What is clinical TLS?

A

laboratory tumour lysis syndrome plus one or more of the following:
increased serum creatinine (1.5 times upper limit of normal)
cardiac arrhythmia or sudden death
seizure

4th year passmedicine by topic (96 decks)

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