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A. MLA Map Acute and Emergency > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

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1
Q

Acute kidney injury (AKI) describes a a rapid reduction in renal function following an insult to the kidneys. What % of all hospital admissions have AKI?

1 - 1-2%
2 - 15-20%
3 - 30-40%
4 - 70-80%

A

2 - 15-20%

Carries a 30% mortality in hospital

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2
Q

What is the key marker that determines if a patient has an acute kidney injury?

1 - urea
2 - hematuria
3 - creatinine
4 - Na+

A

3 - creatinine

Creatinine and urea filtered by the kidneys comes from amino acid metabolism

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3
Q

Accoridng to NICE guidelines, which of the following are diagnostic of acute kidney injury can be made using all of the following, EXCEPT which one?

1 - rise in creatinine of more than 25 micromol/L in 48 hours
2 - <0.5ml/kg/hour urine output >6 hours
3 - reduction in eGFR function by >50%
4 - rise in creatinine by 50% in 7 days

A

3 - reduction in eGFR function by >50%

  • eGFR is not typically a good measure of AKI

Staging of AKI is seen in the image

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4
Q

Which 2 of the following is an AKI most likley to occur in?

1 - older patients
2 - infected patients
3 - post-surgery
4 - female gender

A

2 - infected patients
3 - post-surgery

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5
Q

Which of the following are risk factors for developing AKI?

1 - Older age >65 years
2 - Sepsis
3 - Chronic kidney disease
4 - Heart failure
5 - Diabetes
6 - Liver disease
7 - Cognitive impairment (reduced fluid intake)
8 - Radiocontrast agents (e.g., used during CT scans)
9 - all of the above

A

9 - all of the above

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6
Q

All of the following medications can increase the risk of an AKI, EXCEPT which one?

1 - Ibuprofen
2 - Ramipril or Losartan
3 - Warfarin
4 - Gentamicin
5 - Indapamide

A

3 - Warfarin

  • NSAIDs
  • Diuretics
  • ACE-I and ARB-II
  • Diuretics

Some drugs in these classes are better than others though

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7
Q

How can NSAIDs cause AKI?

1 - induce vasoconstriction of efferent arterioles
2 - inhibit prostaglandin, inducing vasoconstriction of afferent arterioles
3 - increase prostaglandin and therefore increase eGFR
4 - all of the above

A

2 - inhibit prostaglandin, inducing vasoconstriction of afferent arterioles
- vasoconstriction causes hypoperfusion of kidneys

  • prostaglandin induce vasodilation of afferent arterioles to maintain eGFR
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8
Q

How can ACE and ARB-I cause AKI?

1 - induce vasoconstriction of efferent arterioles
2 - inhibit prostaglandin, inducing vasoconstriction of afferent arterioles
3 - increase prostaglandin and therefore increase eGFR
4 - induce vasodilation of efferent arterioles

A

4 - induce vasodilation of efferent arterioles
- reduces blood flow and eGFR due to hypoperfusion

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9
Q

Are ACE inhibitors nephrotoxic?

A
  • No
  • Should be stopped in AKI due to reducing the filtration pressure
  • ACE inhibitors have a protective effect on the kidneys long-term and can protect the kidneys, but in AKI they should NOT be used
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10
Q

Acute kidney injury (AKI) can be categorised as:

  • pre-renal
  • renal
  • post renal

Which of these categories is the most common?

A
  • pre-renal
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11
Q

Acute kidney injury (AKI) can be categorised as:

  • pre-renal
  • renal
  • post renal

Which of the following is NOT a pre-renal cause of AKI?

1 - Dehydration
2 - Renal calculi
3 - Shock (sepsis, anaphylaxis, acute blood loss)
4 - Heart failure

A

2 - Renal calculi
This is a post-renal issue

Pre-renal causes are typically due to hypoperfusion if the kidneys

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12
Q

Acute kidney injury is defined as an abrupt decline in kidney function. Which blood vessels supplies the kidneys?

1 - abdominal artery
2 - renal artery
3 - superior mesenteric artery
4 - inferior mesenteric artery

A

2 - renal artery
- branch from abdominal aorta
- renal vein drains the kidneys

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13
Q

Acute kidney injury (AKI) can be categorised as:

  • pre-renal
  • renal
  • post renal

Renal causes of AKI are intrinsic to the kidneys and accounts for 10% of all AKIs. Which of the following is NOT a renal cause of AKI?

1 - Acute tubular necrosis (ATN)
2 - Glomerulonephritis
3 - Acute interstitial nephritis (AIN)
4 - Shock (e.g., sepsis or acute blood loss)
5 - Haemolytic uraemic syndrome
6 - Rhabdomyolysis

A

4 - Shock (e.g., sepsis or acute blood loss)

Nephron = whole unit
Tubules = part of the nephron that filter
Glomerulus = network of small blood vessels that filters waste into the tubules

  • ATN = ischaemia due to pre-renal, or toxins, drugs, contrast, rhabdomyolysis
  • AIN = Typically drug-induced, but can also be infections or autoimmune diseases

Glomerular: Rapidly progressive glomerulonephritis or other glomerulopathies

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14
Q

All of the following can cause intra-renal AKI, but which is most common?

1 - Acute tubular necrosis (ATN)
2 - Glomerulonephritis
3 - Acute interstitial nephritis (AIN)
4 - Haemolytic uraemic syndrome
5 - Rhabdomyolysis

A

1 - Acute tubular necrosis (ATN)

Relates to damage and death of the epithelial cells of the collecting tubules of the nephrons.

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15
Q

Acute tubular necrosis (ATN) is the most common cause of intra-renal AKI. All of the following can cause ATN, EXCEPT which one?

1 - ibuprofen
2 - gentamicin
3 - secondary ischaemia (pre-renal)
4 - renal calculi
5 - radiology contrasts

A

4 - renal calculi

Secondary ischaemia (pre-renal):
- hypoperfusion/shock
- sepsis
- dehydration

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16
Q

Acute tubular necrosis (ATN) is the most common cause of intra-renal AKI. Is ATN reversible?

A
  • Yes

Typically takes 7-21 days for epithelial cells to regenerate

Look for Muddy brown casts on urinalysis

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17
Q

Nephrotic and nephritic syndrome are both intra-renal kidney conditions that affect the glomeruli.

  • Nephrotic syndrome = loss/reduced function of podocyte and foot processes and/or basement membrane
  • Nephritic syndrome = immune complexes become deposited in glomerular capillaries causing immune response against capillaires

Which of these syndromes presents with the following?

  • proteinuria >3.5g/day
  • systemic oedema due to lost intravascular protein (mainly albumin)
  • frothy urine
  • hyperlipidaemia (liver attempts to compensate)
  • antithrombin 3 lost in urine (prevents excessive clotting) so patients have hypercoaguable state
A
  • NephrOtic syndrome
    Think O in nephrOtic = Open podocytes

Loss of antithrombin III increases risk of thromboembolism in the renal vein that can cause a blood clot travelling to the lungs

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18
Q

Nephrotic and nephritic syndrome are both intra-renal kidney conditions that affect the glomeruli.

  • Nephrotic syndrome = loss/reduced function of podocyte and foot processes
  • Nephritic syndrome = immune complexes become deposited in glomerular capillaries causing immune response against capillaires

Which of these syndromes presents with the following?

  • proteinuria <3.5g/day
  • haematuria and RBC casts may cause cola coloured urine
  • pyuria (WBCs) in the urine
  • mild oedema
  • hypertension with low eGFR
  • oliguria as glomerulus is damaged and cannot filter urine
A
  • Nephritic syndrome
    Also called Glomerulonephritis

This is a cause of intra-renal AKI called Acute interstitial nephritis

Antigen-antibody complexes (AAC) (type III hypersensitivity) inside the glomerulus capillaries cause:

  • AACs infiltrate glomerula and block capillaries
  • WBCs are recruited causing inflammation
  • inflammation damages the glomerulus basement membrane, causing podocytes to spread out
  • blood and protein can leak into urine
19
Q

In patients with AKI due to Acute interstitial nephritis (AIN), which of the following may also be present in addition to the AKI?

1 - Rash
2 - Fever
3 - Flank pain
4 - Eosinophilia (high levels)
5 - all of the above

A

5 - all of the above

Steroids can be useful when treating AIN

20
Q

Post-renal causes of AKI involve obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy. Obstruction can be caused by which of the following?

1 - Kidney stones
2 - Tumours
3 - Strictures of the ureters or urethra
4 - Benign prostatic hyperplasia
5 - Neurogenic bladder
6 - all of the above

A

6 - all of the above

21
Q

When trying to diagnose the AKI, all of the following can be performed, but which is typically 1st line?

1 - Blood samples
2 - Urinalysis
3 - Imaging
4 - Autoimmune profiling

A

2 - Urinalysis

  • Leucocytes and nitrites suggest infection
  • Protein and blood suggest acute nephritis (but can be positive in infection)
  • Glucose suggests diabetes

Microscopy, culture and sensitivity MC&S may be needed if any evidence of UTI on the urine dipstick

22
Q

If acute glomerularnephritis is suspected, which of the following should be calculated?

1 - urea : creatiine ratio
2 - protein : creatinine ratio
3 - blood : creatinine ratio
4 - glucose : creatinine ratio

A

2 - protein : creatinine ratio

23
Q

U&Es is important to measure in a patient with AKI. Which of the following derangement is most common in AKI?

1 - hyperkalemia and hyponatremia
2 - hypokalemia and hyponatremia
3 - hypercalcaemia and hyponatremia
4 - hypomagnesium and hyponatremia

A

1 - hyperkalemia and hyponatremia

Typically kidneys retain Na+ and excrete K+ to maintain body fluid balance

24
Q

What is the 1st line imaging for AKI?

1 - ultrasound
2 - MRI
3 - CT
4 - X-ray

A

1 - ultrasound

Mainly used in post-renal

25
Q

Which of the following approaches should be used in an attempt to reduce AKI?

1 - Avoiding/stop nephrotoxic medications
2 - adequate fluid intake oral and IV
3 - Additional fluids before and after radiocontrast agents
4 - all of the above

A

4 - all of the above

26
Q

All of the following are effective in various causes of AKI (main cause needs to be identified), EXCEPT which one?

1 - IV fluids for dehydration and hypovolaemia
2 - administer ACE inhibitors to protect kidney function
3 - Stop/adjust medications that may accumulate with reduced renal function (e.g., metformin and opiates)
4 - Relieve the obstruction in a post-renal AKI
5 - Dialysis may be required in severe cases

A

2 - administer ACE inhibitors to protect kidney function

Good long term
Must be stopped in AKI

27
Q

Which of the following is NOT a common complication of AKI?

1 - Fluid overload, heart failure and pulmonary oedema
2 - Hyperkalaemia
3 - Metabolic alkalosis
4 - Uraemia (high urea), which can lead to encephalopathy and pericarditis

A

3 - Metabolic alkalosis

Commonly causes metabolic acidosis due to less HCO3- being produced

28
Q

Hyperkalaemia is a complication of AKI. At what concentration does this need to be treated URGENTLY?

1 - >3.5mmol/L
2 - >4.5mmol/L
3 - >5.5mmol/L
4 - >6.5mmol/L

A

4 - >6.5mmol/L
- OR if ECG changes are present

29
Q

Vasculitis is an autoimmune inflammatory condition where immune cells mistake antigens on the endothelium for foreign antigens called molecular mimicry. Which of the following vasculitis conditions matches the following:

  • IgA antiibodies involved
  • skin, kidneys and GIT involved
  • purpuric rash in legs and bum of children
  • inflammation in vasculature due to IgA antibodies

1 - IgA nephropathy
2 - Henoch Schonlein purpura
3 - Lupus
4 - Leukaemia

A

2 - Henoch Schonlein purpura

IgA nephropathy affects just the kidneys and occurs 1-3 days post infection

30
Q

Henoch Schonlein purpura is a form of vasculitis affecting the skin, kidneys and GIT. IgA antibodies enter affected tissues in blood vessels and lead to inflammation. This affects children of what age?

1 - newborns
2 - children <5
3 - children <10
4 - children <15

A

3 - children <10
- typically occurs following gastroenteritis or upper airway infection

31
Q

Which of the following is NOT one of the 4 classic signs in Henoch Schonlein purpura, a form of vasculitis affecting the skin, kidneys and GIT?

1 - purpura (100% of children)
2 - pericarditis (60% of children)
3 - joint pain (75%
4 - abdominal pain (50% of children)
5 - kidney impairment ((50% of children)

A

2 - pericarditis (60% of children)

32
Q

Purpura, which occurs in 100% of children is a classic sign in Henoch Schonlein purpura. Is this rash blanching or non-blanching?

A
  • non-blanching
  • it says red when you apply pressure
  • purpura is blood from small blood vessels
  • palpable on the skin
33
Q

Henoch Schonlein purpura is a form of vasculitis affecting the skin, kidneys and GIT. IgA antibodies enter affected tissues in blood vessels and lead to inflammation. Does this cause nephritis or nephrotic syndrome?

A
  • nephritis syndrome
  • causes haematuria and proteinuria
  • BUT if patient has ++ protein, they have developed nephrotic syndrome
34
Q

Henoch Schonlein purpura is a form of vasculitis affecting the skin, kidneys and GIT. IgA antibodies enter affected tissues in blood vessels and lead to inflammation. How are these patients diagnosed?

1 - FBC and blood film
2 - renal profile
3 - serum albumin
4 - CRP and blood culture (sepsis)
5 - urine dipstick (proteinuria, ACR)
6 - BP
7 - all of the above

A

7 - all of the above

  • FBC and blood film = rules out sepsis, leukaemia and thrombocytopenic
  • serum albumin = rule out nephrotic syndrome
35
Q

What is another condition that can cause pulmonary-renal syndrome?

1 - TB
2 - Good Pastures Syndrome
3 - SLE
4 - Infective endocarditis

A

2 - Good Pastures Syndrome
- autoimmune inflammatory condition affecting the lungs and kidneys

  • causes haemoptysis in lungs and haematuria in the kidneys
  • typically triggered by infection or agent
36
Q

Good pastures syndrome (GPS) is able to cause pulmonary-renal syndrome. What is the trigger for GPS?

1 - IgE from mast cells is released and binds to type IV collagen
2 - IgG/IgM antibodies bind to type IV collagen
3 - antibody-immune complexes forms on type IV collagen
4 - cytotoxic T cells target and begin to degrade type IV collagen

A

2 - IgG/IgM antibodies bind to type IV collagen
- type 2 hypersensitivity that triggers the complement pathway

  • type IV collagen is present in abundance in the basement membranes of the glomerulus and alveolar basement membranes
37
Q

In good pastures syndrome (GPS), which can causes pulmonary-renal syndrome, the Fab region of the antibody binds to type IV collagen. The Fc portion then binds with what to trigger the complement pathway?

1 - C1
2 - C2
3 - C3
4 - C4

A

1 - C1
- complement pathway is then activated

38
Q

In good pastures syndrome (GPS), which can causes pulmonary-renal syndrome, once the complement pathway is activated, C3a, 4a and 5a act as chemotactic agents and attract which cell?

1 - basophils
2 - cytotoxic T cells
3 - B cells
4 - neutrophils

A

4 - neutrophils

39
Q

In good pastures syndrome (GPS), which can causes pulmonary-renal syndrome, once the complement pathway is activated, C3a, 4a and 5a act as chemotactic agents and attract neutrophils. What do the neutrophils then release that damages the collagen and therefore the basement membranes?

1 - peroxidase
2 - myeloperoxidase
3 - proteinase-3
4 - all of the above

A

4 - all of the above
- all cause free oxygen radicals that form and damage the basement membranes

40
Q

Which of the following is NOT a common symptom in good pastures syndrome (GPS)?

1 - dysponea/cough
2 - glomerularnephritis
3 - proteinuria >3.5g
4 - haemoptysis

A

3 - proteinuria >3.5g

41
Q

Which of the following antibody can be screened for to diagnose good pastures syndrome (GPS)?

1 - anti-glomerular basement (GBM)
2 - anti-neutrophil cytoplasmic antibodies (ANCA)
3 - cytoplasmic-ANCA
4 - proteinase 3-ANCA

A

1 - anti-glomerular basement (GBM)

42
Q

How is good pastures syndrome (GPS) typically treated?

1 - high dose of steroids
2 - cyclophosphamide
3 - plasmapheresis
4 - all of the above

A

4 - all of the above

  • typically does not relapse and is a 1 hit wonder

Steroid is methylprednisolone, if this fails then use cyclophosphamide

43
Q

Calculate AKI stage. Patient is 50kg and has 240ml urine output in 24h. What stage AKI are they?

1 - stage 1
2 - stage 2
3 - stage 3

A

3 - stage 3

Minimum in UK = 0.5 ml/kg/h
- (50kg x 0.5 = 25ml/h) x 24 = 600ml

Here calculation is:
- (240/24 = 10ml/h) / 50kg = 0.2ml/h

A. MLA Map Acute and Emergency (42 decks)

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