Acute Medicine Flashcards

1
Q

Define acute kidney injury (AKI)

A

An acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output

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2
Q

AKI causes are classified into which 3 main types?

A

Pre-kidney causes (e.g. poor perfusion)

Intrinsic causes

Post-kidney causes (e.g. obstruction)

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3
Q

Give 6 examples of pre-kidney causes of AKI

A

Anything that can lead to poor perfusion such as:

Hypovolaemia

Sepsis

Overdiuresis (excessive urine production often caused by diuretic medication)

Heart failure

Renovascular diseases (e.g. bilateral renal artery stenosis patient given ACE inhibitors leading to acute tubular stenosis)

Severe liver disease (Hepatorenal syndrome which is a form of pre-renal AKI irresponsive to fluids)

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4
Q

Give 5 examples of intrinsic causes of AKI

A

Rapidly progressing glomerulonephritis (infectious and autoimmune causes)

Interstitial nephritis (Infections and medications)

Haemolytic ureamic syndrome (e.g. EHEC enterohaemorrhagic e.coli)

Scleroderma (Can lead to scleroderma renal crisis)

Embolism or thrombolism

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5
Q

Give 6 examples of post-kidney causes of AKI

A

Urinary retention

Ascending urinary infection (e.g. pyelonephritis)

Tumor

Lymphoma

Prostate hyperplasia

Retroperitoneal fibrosis

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6
Q

List 9 risk factors for AKI

A

Age: Over 65 (especially if frail)

Chronic kidney disease (CKD)

Heart failure

Liver disease

Diabetes

Dementia (or any other neurological/cognitive impairment that may result in limited access to oral fluids).

Previous AKI

Myeloproliferative disorder (e.g., multiple myeloma)

Medications (e.g. ACE or diuretics)

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7
Q

List 8 medications that can lead to AKI

A

ACE inhibitors or ARBs

NSAIDs

Diuretics (especially if recently started)

Recreational drugs

Acyclovir (Antiviral)

Methotrexate (Immunosupresant chemotherapy)

Indinavir (Used to treat AIDS/HIV)

Triameterene (Diuretic)

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8
Q

What are the main signs/symptoms of AKI? (8)

A

Mainly asymptomatic(always look at AKI risk factors for patients that present with acute illness and any factors that can lead to kidney insult e.g:

Acute illneses: Sepsis, burns, acute pancreatitis

Hypovolaemia

`Exposure to nephrotoxins (e.g. NSAIDs and aminoglycoside ABx)

Recent surgery (especially cardiovascular)

Other symtpoms:

Reduced urine output (Oliguria or anuria)

Fever, rash (e.g. insterstitial nephritis)

Haematuria (e.g. kidney stones, tumors, infection)

Palpable bladder

Lower urinary tract symptoms (e.g. urgency, frequency or hesitancy)

Symptoms of volume overload

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9
Q

List some clinical examination findings which can present themselves in patients with AKI. (7)

For each finding what is the most likely cause for the AKI?

A

Findings depends on the cause:

Skin signs:e.g. 1) Livedo reticularis, butterfly rash, digital ischaemia, palpable purpura) [Systemic vasculitis]

2) Maculopapular rash [allergic interstitial nephritis]
3) Track marks (IV drug abuse)
4) Jaundice (Liver disease)

Altered confusion [Sepsis or uraemia from the AKI]

Low BP [Postural hypotension suggestive of pre-AKI cause]

Pericardial friction rub [Indicated acute pericarditis which is a complication of severe AKI]

Abdominal bruit [renovascular disease]

Muscle tenderness [Suspect intrinsic AKI secondary to rhabdomyolysis]

Asterixis [Possible symptom of uraemia]

Palpable bladder, enlarged prostate or abdominal distention

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10
Q

What investigations should be performed to rule out AKI? (11)

What findings from these investigations is suggestive of AKI?

A

1) Basic metabolic profile: Acutely elevated creatinine, High serum pottasium, metabolic acidosis. [May show deranged LFTs if cause is due to hepatorenal syndrome].
2) Serum pottasium (hyperkalaemia)
3) FBC (anaemia, leukocytosis, thrombocytopenia [maybe sepsis for leuko and thrombo or HUS, vasculitis for anaemia])
4) C-reactive protein (Elevated in infection or vasculitis)
5) Blood culture (if sepsis is suspected)
6) Urinalysis (RBCs, WBCs, cellular casts, proteinuria, positive nitrite, and leukocyte esterase can indicate intrinsic causes)
7) Bicarbonate (low indicative of acidosis)
8) Urine culture (rule out a UTI cause)
9) Urine output monitoring (low urine output)
10) ECG (to assess hyperkalaemia)
11) CXR (may show signs of infection, fluid, cardiomegaly, or haemorrhage)

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11
Q

Which patients should always be tested for serum creatinine?

A

All acutely presenting patients with any risk factors for AKI (e.g. age,>65. suspected sepsis, medications, Phx of AKI episode).

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12
Q

What are the 2 main priorities when managing a patient with AKI?

A

Treat hypovolaemia: IV fluids

Correct electrolyte imabalances

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13
Q

What is the management plan for a partient with AKI? (4)

A

STOP AKI acronym

S: Septic screen

T: Toxins, Stop/avoid nephrotoxins (e.g., NSAIDs, aminoglycoside antibiotics, iodinated contrast agents).

O: Optimise BP (e.g. IV fluids)

P: Prevent harm by idenitfying and treating the cause of AKI

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14
Q

What treatment option should be considered in cases of severe AKI?

A

Renal replacement therapy

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15
Q

What are some of the complications of AKI? (5)

A

Hyperphosphataemia

Uraemia

Hyperkalaemia

Chronic progressive kidney disease

End-stage kindey disease

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16
Q
A