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Metabolic - Nephrology > Acute kidney injury > Flashcards

Acute kidney injury Flashcards

1
Q

Define AKI

A

An abrupt deterioration in renal function, usually over hours - days

Usually reversible

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2
Q

What are the hallmarks of AKI?

A

Falling urine output + rising creatinine and urea

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3
Q

Discuss RIFLE classification of AKI

A

Describes AKI - uniform definition

Three severity levels:

R - risk (patient is at risk of kidney damage)

I - injury (kidneys have been inured)

F - failure (kidneys have failed)

Two outcomes:

L - loss (loss of funtion)

E - end stage renal disease (end stage renal disease has developed)

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4
Q

What are the stages of AKI outlined by RIFLE?

A
  • R = stage 1 (a serum creatinine rise of >26.4micromol/L or a 1.5x increase in 48hrs)
  • I = stage 2 (a 2-3x increase in serum creatinine)
  • F = stage 3 (a >300% increase in serum creatinine equal to >354micromol/L)
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5
Q

What is normal serum creatinine?

A

Women: 53-115 umol/L (0.5-1.0mg/dL)

Men: 88-150umol/L (0.7-1.2mg/dL)

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6
Q

What level of creatinine might indicate renal

A

>1.2mg/dL / >115umol/L

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7
Q

Why do men have higher creatinine levels?

A

Higher muscle mass generally

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8
Q

What are causes for increased urea, other than altered renal function?

A
  • Corticosteroid treatment
  • Tetracycline treatment
  • GI bleed (blood enters gut, it is high in protein and leads to production of urea)
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9
Q

Outline causes of high creatinine other than renal damage

A
  • High muscle mass
  • Red meat ingestion
  • Muscle damage/ rhabdomyolysis
  • Decreased tubular secretion due to durgs such as cimetidine or trimethoprim)
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10
Q

Discuss mortality rates associated with AKI

A
  • Uncomplicated AKI 5-10%
  • AKI complicating non-renal organ failure 50-70%
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11
Q

Outline some causes of AKI

A
  • Rhabdomylolysis: crush injuries, myoglobin (nephrotoxin) released, resulting in acute tubular necrosis. Can also occur in haemolysis where haemoglobin is the nephrotoxin
  • Acute cortical necrosis: renal hypoperfusion causes blood to be diverted to the medulla of the kidney meaning the cortex is hypoperfused and irreversible glomerular damage occurs (cortical necrosis)
  • Contrast nephropathy: in patients with impaired renal function iodinated radiological contrast media can be nephrotoxic
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12
Q

What is creatinine?

A
  • Indicator of renal health
  • Breakdown product of creatine phosphtae in muscle, produced at a constant rate
  • Removed from the blood purely by the kidneys
  • High creatinine = low GFR
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13
Q

What is the most accurate way to measure GFR?

A
  • Measuring clearance of exogenous filtration markers e.g. inulin, iothalamate or iohexol

* Rarely done because it is £££ and requires strict protocol

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14
Q

What are the stages of AKI

A

Stage 1: Rise in serum creatinine >26.5mmol/L or 150-200% of baseline

Stage 2: increase of creatinine 200-300% of baseline

Stage 3: >300% increase of baseline

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15
Q

What are the disadvantages of using serum creatinine to measure GFR?

A
  • Many factors affect serum creatinine
  • Rises in serum creatinine take 12-24hrs to rise following surgery
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16
Q

Outline pre- renal causes of AKI

A
  • Reduced perfusion (hypovolemia or haemorrhage)
  • Sepsis
  • Third spacing of fluid (e.g. pancreatitis, fluids leak out into peritoneal cavity thus depleting vascular fluids)
  • Heart failure
  • Renovascular disease
  • Patients with bilateral artery stenosis that have been started on ACEi, causes ATN
17
Q

Outline renal causes of AKI

A
  • ATN
  • Glomerulonephritis
  • Interstitial nephritis
18
Q

Outline post-renal causes of AKI

A
  • Mechanical obstruction
  • Retroperitoneal fibrosis
  • Lymphoma
  • Tumour
  • Enlarged prostate
  • Stricture
  • Ascending UTI
  • Urinary retention
19
Q

What is the most common form of AKI?

A

ATN due to prolonged ischaemia

20
Q

Outline some causes of ATN

A
  • ROS
  • Compliment activation
  • Drugs
  • Endotoxins
  • Radiocontrast media

*45% of cases of AKI are caused by ATN

21
Q

History associated with pre-renal AKI

A

Haemorrhage, vomiting, diarrhoea, sweating

Hx of sepsis, burns, GI surgery or pancreatitis

Thirst, dizziness, tachycardia, oliguria, anuria

22
Q

History associated with intrinsic/ renal AKI

A

Usually ATN caused by:

  • Severe infection, nephrotoxic drugs, major surgery
  • Hx of rash, haematuria or oedema with hypertension suggestive of nephritic syndrome
  • Query recent drug use and medications
23
Q

Patients most likel to present with post-renal AKI

A
  • Men with prostate enlargement
  • Hx of malignancy
24
Q

Discuss physical examination findings of a patient with AKI

A
  • Hypo/ hypertension
  • Asterixis
  • Fluid loss? Hypotension and signs of circulatory collapse
  • Glomerular disease? Hypertension, oedema, proteinuria, microscopic haematuria
  • Presence of rash/ pettechiae? suggestive of glomerulonephritis
  • Abdominal bruit? Renovascular disease
  • Prostatic disease? Abdo distension due to full bladder
25
Q

What tests would be done if AKI was suspected?

A
  • Metabolic profile
  • FBC

Venous blood gases

  • Urinalysis and culture
  • Renal ultrasound
  • Chest x-ray (pulmonary oedema/ cardiomegaly)

Subsequent: CT/ MRI to evaluate cases of obstruction, cytoscopy if urethral stenosis suspected

*Renal biopsies rarely carried out for AKI

26
Q

How many litres of fluid are filtered by the kidney every day?

A

180L

2L of urine produced

27
Q

Electrolyte disturbance in AKI

A

Acute kidney injury (AKI) is often associated with systemic complications including volume overload; electrolyte and acid-base disturbances, particularly hyponatremia, hyperkalemia and metabolic acidosis

28
Q

Why might a patient not have a metabolic acidosis due to AKI?

A

Vomiting

29
Q

How are pre, intra and post renal AKI diagnosed?

A

Pre renal: largerly a clinical diagnosis e.g. if a patient has had a big bleed etc

Can be tricky to differentiate between pre-renal and renal esp. as pre renal can cause ATN (renal)

Renal: assess how full the bladder is

30
Q

How can we differentiate between pre-renal and renal AKI?

A

Pre-renal: RAAS is activated leading to sodium and water retention = higher urine osmolality (>500)

Intra-renal: water isnt retained as well so urine osmolality is generally lower (<500), ATN = cell casts in urine, renal tubular epithelial cells, glomerulonephritis will cause haematuria

31
Q
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32
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34
Q
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Metabolic - Nephrology (18 decks)

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