Lecture 10.1: Acute Kidney Injury Flashcards

1
Q

What is AKI long-form?

A

Acute Kidney Injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the Categories of AKIs? (3)

A
  • Pre-Renal
  • Renal
  • Post-Renal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens to Urea & Creatinine in AKI?

A

Increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When do AKIs occur (generally)?

A
  • Usually a complication of serious illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the definition of an AKI? (at least one of 3 criteria)

A
  • Increase in Serum Creatinine by 26.5 μmol/l within 48
    hours
  • Increase in Serum Creatinine to ≥ 1.5x baseline, known
    /presumed to have occurred within the prior 7 days
  • Urine volume < 0.5 ml/kg/h for 6 hours (oliguria less
    than 400ml per day)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Risk Factors for AKI

A
  • Polypharmacy
  • Elderly
  • Multiple Co-Morbidities
  • Diabetes
  • Heart Failure
  • Liver Cirrhosis
  • Dehydration
  • Infection/Sepsis
  • CKD
  • Renal Stones
  • BPH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Classification of AKI (KDIGOL): Stage 1

A
  • Serum Creatinine: 1.5–1.9 times baseline
    OR ≥0.3 mg/dl ( ≥26.5 mmol/l) increase
  • Urine Output: <0.5 ml/kg/h for 6–12 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Classification of AKI (KDIGOL): Stage 2

A
  • Serum Creatinine: 2.0–2.9 times baseline
  • Urine Output: <0.5 ml/kg/h for ≥12 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Classification of AKI (KDIGOL): Stage 3

A
  • Serum Creatinine: 3.0 times baseline OR
    Increase in serum creatinine to ≥4.0 mg/dl
    ( ≥353.6 mmol/l)
  • Urine Output: <0.3 ml/kg/h for ≥24 hours
    OR Anuria for ≥12 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Rifle and Akin AKI Classification

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of Pre-Renal AKI (6)

A
  • CHF
  • Liver Failure
  • NSAIDs
  • ARBs
  • ACE Inhibitors
  • Cyclosporine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do CHF and Liver Failure cause AKI? (3)

A
  • Hypovolemia
  • Decreased Cardiac Output
  • Decreased Effective Circulating Volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do NSAIDs, ARBs, ACE Inhibitors & Cyclosporine cause AKI? (1)

A

Impaired Renal Autoregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of Renal/Intrinsic AKI (6)

A
  • Ischaemia
  • Sepsis
  • Nephrotoxins
  • Vasculitis
  • TTP/HUS (Thrombotic Thrombocytopenic
    Purpura, Hemolytic Uremic Syndrome)
  • Malignant Hypertension
  • Acute Glomerulonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do Ischaemia, Sepsis & Nephrotoxins cause AKI? (1)

A

Tubular Damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do Vasculitis, TTP/HUS & Malignant Hypertension cause AKI? (1)

A

Vascular Damage

17
Q

Types of Post-Renal AKI (2)

A
  • Bilateral Ureteropelvic Obstruction
  • Bladder Outlet Obstruction
18
Q

Nephrotic Syndrome

A
  • Nephrotic syndrome is a condition
    involving the loss of significant volumes of
    protein via the kidneys (proteinuria) which
    results in hypoalbuminaemia
  • Massive proteinuria (≥3.5 g/day) * Hypoalbuminaemia (serum albumin ≤30
    g/L)
19
Q

Nephritic Syndrome

A
  • Haematuria
  • Mild to Moderate Proteinuria (typically less
    than 3.5g/L/day)
  • Hypertension
  • Oliguria
  • Red Cell Casts in the Urine
20
Q

Nephrotic Syndrome Mechanism

A
  • Injury to Podocytes
  • Scarring
  • Deposition of matrix or other elements
21
Q

Nephritic Syndrome Mechanism

A
  • Inflammation
  • Reactive Cell Proliferation
  • Breaks in GBM (Glomerular Basement
    Membrane)
  • Crescent Formation
22
Q

What are some other Nephrotoxins? (3)

A
  • Aminoglycosides Diuretics (gentamicin,
    amikacin)
  • Bacterial endotoxins e.g. E.coli
  • IV contrast (sometimes)
23
Q

What happens in Tumour Lysis Syndrome?

A
  • Cancer cells die rapidly → hyperuricaemia → Hyperphsophataemia
24
Q

What are the Effects of Hyperuricaemia? (5)

A
  • Precipitation in the renal tubules
  • Renal Vasoconstriction
  • Impaired Autoregulation
  • Decreased Renal Blood Flow
  • Inflammation
25
Q

What are the Effects of Hyperphsophataemia?

A
  • Calcium phosphate deposits in renal
    tubules
  • Seizures/Muscle Cramps
26
Q

Luminal Causes of Post-Renal AKI (3)

A
  • Renal Stones
  • Blood Clots
  • Sloughed Tissue
27
Q

Mural Causes of Post-Renal AKI (2)

A
  • Strictures due to infection or post
    TURP/TURBT
  • Cancer
28
Q

Extrinsic Compression Causes of Post-Renal AKI (4)

A
  • Benign Prostatic Hyperplasia
  • Cancer
  • Pregnancy
  • Retroperitoneal Fibrosis
29
Q

Signs and Symptoms of AKI (8)

A
  • Nausea
  • Lethargy
  • Decreased Urine Output
  • Haematuria
  • Dysuria
  • Fluid Overload (Oedema, Orthopnoea)
  • Electrolyte Abnormalities
  • Acid-Base Disturbance