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C. Year 3 MLA Urology > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
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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2
Q

Which of the following is NOT part of the definition of AKI?

1 - rise in creatinine of 26umol/l <48h
2 - rise in urea of 50mmol/l <48h
3 - rise in creatinine of 1.5 above baseline <7 days
4 - urine output <0.5ml/kg/h >6 hours

A

2 - rise in urea of 50mmol/l <48h

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3
Q

What % of all hospital admissions have AKI?

1 - 2%
2 - 20%
3 - 40%
4 - 70%

A

2 - 20%

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4
Q

AKI stage 3 can be dangerous. What is the in-hospital mortality of stage 3 AKI?

1 - 10%
2 - 15%
3 - 30%
4 - >50%

A

3 - 30%

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5
Q

There are lots of risk factors for developing AKI. Which of the following are risk factors?

1 - Chronic kidney disease
2 - Heart failure
3 - Diabetes
4 - Liver disease
5 - Older age (above 65 years)
6 - Cognitive impairment
7 - Nephrotoxic medications such as 8 - NSAIDS and ACE inhibitors
9 - Use of a contrast medium such as 10 - during CT scans
11 - all of the above

A

11 - all of the above

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6
Q

Acute kidney injury can be defined as an abrupt decline in eGFR that causes what?

1 - fluid imbalance
2 - electrolyte imbalance
3 - azotemia
4 - all of the above

A
  • azotemia = raised nitrogen containing compounds in the blood (urea and creatinine)
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7
Q

The 2 key nitrogen containing compounds in the blood are urea and creatinine. Where does urea come from?

1 - lipolysis
2 - gluconeogenesis
3 - amino acid metabolism
4 - all of the above

A

3 - amino acid metabolism

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8
Q

Urea is a waste product produced from amino acid metabolism. Is all urea excreted from the body?

A
  • no
  • 50-70% of urea is reabsorbed in the collecting ducts
  • important to ensure H2O is reabsorbed from interstitium into the blood and not lost in the urine
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9
Q

Which of the following is a key function of the nephrons?

1 - filtration
2 - secretion
3 - reabsorption
4 - excretion
5 - all of the above

A

5 - all of the above

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10
Q

Creatinine is the waste product of creatine phosphate, which is produced from creatine to enable muscle contraction. Once creatinine is formed, what happens to it?

1 - diffuse into the circulation
2 - travels to the kidneys
3 - filtered into the filtrate and excreted in the urine
4 - all of the above

A

4 - all of the above

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11
Q

Which 2 markers are often used to diagnose AKI?

1 - creatinine
2 - albumin
3 - coagulation factors
4 - urea

A

1 - creatinine
4 - urea

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12
Q

Is creatinine a good early indicator of AKI?

A
  • no
  • good marker of AKI, but is very slow to respond
  • ALWAYS CONSIDER AKI IN PATIENTS WITH MODEST CREATININE RISE
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13
Q

When trying to diagnose and stage AKI we can use creatinine levels in the plasma and urine output. Which of the following is correct for plasma concentrations of creatinine for stage 1 AKI?

1 - 1.5-1.9 above baseline OR >0.3mg/dl (>26.5 umol/L)
2 - >3 time baseline OR >4mg/dl (353.6 umol/l)
3 - 2.0-2.9 above baseline
4 - all of the above

A

1 - 1.5-1.9 above baseline OR >0.3mg/dl (>26.5 umol/L)

  • always compare against baseline where possible
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14
Q

When trying to diagnose and stage AKI we can use creatinine levels in the plasma and urine output. Which of the following is diagnostic of stage 1 AKI when using output?

1 - <0.5 ml/kg/h for >12 hours
2 - <0.5ml/kg/h for 6-12 hours
3 - <0.3ml/kg/h for >24 hours OR anuria for >12 hours
4 - all of the above

A

2 - <0.5ml/kg/h for 6-12 hours

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15
Q

When trying to diagnose and stage AKI we can use creatinine levels in the plasma and urine output. Which of the following is correct for plasma concentrations of creatinine for stage 2 AKI?

1 - 1.5-1.9 above baseline OR >0.3mg/dl (>26.5 umol/L)
2 - >3 time baseline OR >4mg/dl (353.6 umol/l)
3 - 2.0-2.9 above baseline
4 - all of the above

A

3 - 2.0-2.9 above baseline

  • always compare against baseline where possible
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16
Q

When trying to diagnose and stage AKI we can use creatinine levels in the plasma and urine output. Which of the following is diagnostic of stage 2 AKI when using output?

1 - <0.5 ml/kg/h for >12 hours
2 - <0.5ml/kg/h for 6-12 hours
3 - <0.3ml/kg/h for >24 hours OR anuria for >12 hours
4 - all of the above

A

1 - <0.5 ml/kg/h for >12 hours

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17
Q

When trying to diagnose and stage AKI we can use creatinine levels in the plasma and urine output. Which of the following is correct for plasma concentrations of creatinine for stage 3 AKI?

1 - 1.5-1.9 above baseline OR >0.3mg/dl (>26.5 umol/L)
2 - >3 time baseline OR >4mg/dl (353.6 umol/l)
3 - 2.0-2.9 above baseline
4 - all of the above

A

2 - >3 time baseline OR >4mg/dl (353.6 umol/l)

  • also includes initiation of creatinine clearance therapy
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18
Q

When trying to diagnose and stage AKI we can use creatinine levels in the plasma and urine output. Which of the following is diagnostic of stage 3 AKI when using output?

1 - <0.5 ml/kg/h for >12 hours
2 - <0.5ml/kg/h for 6-12 hours
3 - <0.3ml/kg/h for >24 hours OR anuria for >12 hours
4 - all of the above

A

3 - <0.3ml/kg/h for >24 hours OR anuria for >12 hours

  • anuria = no urine output
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19
Q

AKI can be due to a pre-renal, intra-renal or post renal. What is the cause of pre-renal AKI?

1 - hypoperfusion
2 - disease of the kidneys
3 - outflow obstruction
4 - all of the above

A

1 - hypoperfusion

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20
Q

Pre-renal AKI is caused by hypoperfusion. Which of the following is NOT a cause of pre-renal AKI?

1 - hypovolaemia
2 - acute glomerulonephritis
3 - decreased cardiac output
4 - decreased effective circulating volume
5 - impaired renal auto regulation

A

2 - acute glomerulonephritis
- this is an intrinsic cause of AKI

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21
Q

Hypovolaemia can cause AKI as there is less fluid in the blood vessels, causing low BP and reducing renal perfusion. Which of the following is typically NOT a cause of hypovolaemia?

1 - cardiac failure
2 - acute haemorrhage
3 - diarrhoea and vomiting
4 - all of the above

A

1 - cardiac failure

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22
Q

A decreased effective circulating volume, which is essentially hypervolaemia. Here fluid leaks into the interstitium and out of the blood vessels, resulting in hypoperfusion of the kidneys. Which of the following is typically NOT a cause of decreased effective circulating volume?

1 - hypoalbuminemia
2 - liver failure (hepatorenal syndrome)
3 - diarrhoea and vomiting
4 - chronic heart failure (cardiorenal syndrome)

A

3 - diarrhoea and vomiting
- this can cause AKI, but is due to loss of overall fluid so is hypovolaemic

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23
Q

A decrease in cardiac output can lead to a reduction in blood flow and their cause hypoperfusion of the kidneys and cause AKI. Which of the following is NOT a cause of decreased cardiac output?

1 - MI
2 - PE
3 - valvular disease
4 - heart failure

A

4 - heart failure
- can cause a reduced cardiac output, but this is due to a decreased effective circulating volume, which is essentially hypervolaemia

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24
Q

Specific medications can cause AKI. Which of the following is NOT typically one of these medications?

1 - loop diuretics
2 - NSAIDs
3 - ACE / ARB-I
4 - cyclosporin

A

1 - loop diuretics

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25
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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26
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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27
Q

Post-renal AKI can be cause by all of the following, EXCEPT:

1 - bladder outflow obstruction
2 - renal calculi
3 - acute glomerulonephritis
4 - bilateral ureteropelvic obstruction

A

3 - acute glomerulonephritis

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28
Q

Bladder outflow obstruction can lead to post renal AKI. Which of the following can cause bladder outflow obstruction?

1 - benign prostate enlargement
2 - abdominal cancer
3 - prostate cancer
4 - all of the above

A

4 - all of the above

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29
Q

Intra-renal AKI can be grouped into 3 basic categories:

  • acute glomerulonephritis
  • tubular damage
  • vascular

Ischaemia, sepsis and nephrotoxins can cause which 2 of the 3 categories?

A
  • acute glomerulonephritis
  • tubular damage
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30
Q

Intra-renal AKI can be grouped into 3 basic categories:

  • acute glomerulonephritis
  • tubular damage
  • vascular

Vasculitis, malignant hypoertension, Thrombotic Thrombocytopenia Purpura and hemolytic uremic syndrome can also cause which of these categories?

A
  • vascular
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31
Q

What % of all AKI does intra-renal disease account for?

1 - 1%
2 - 10%
3 - 40%
4 - 80%

A

2 - 10%
- this is what everyone focuses on, but it is not as common as other causes

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32
Q

When doing a urine dipstick, which of the following would show the highest levels of protein and blood, but no real change in WBC in the urine?

1 - glomerularnephritis
2 - infection/ Interstitial nephritis
3 - rhabdomyolysis/ obstruction
4 - pre-renal, malignancy, Acute tubular necrosis

A

1 - glomerularnephritis

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33
Q

When doing a urine dipstick, which of the following would show the highest levels of WBC in the urine?

1 - glomerularnephritis
2 - infection/ Interstitial nephritis
3 - rhabdomyolysis/ obstruction
4 - pre-renal, malignancy, Acute tubular necrosis

A

2 - infection/ Interstitial nephritis

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34
Q

When doing a urine dipstick, which of the following would show high blood, but no protein or WBC in the urine?

1 - glomerularnephritis
2 - infection/ Interstitial nephritis
3 - rhabdomyolysis/ obstruction
4 - pre-renal, malignancy, Acute tubular necrosis

A

3 - rhabdomyolysis/ obstruction

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35
Q

When doing a urine dipstick, which of the following would show no real changes in blood, protein or WBC in the urine?

1 - glomerularnephritis
2 - infection/ Interstitial nephritis
3 - rhabdomyolysis/ obstruction
4 - pre-renal, malignancy, Acute tubular necrosis

A

4 - pre-renal, malignancy, Acute tubular necrosis

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36
Q

There are a myriad of complications caused by AKI. Which one of these occurs?

1 - hypercalcaemia
2 - hyperkalaemia
3 - hypernatraemia
4 - hyperphosphatemia

A

2 - hyperkalaemia
- kidney typically filters out K+, so if they are not working K+ is retained

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37
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

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38
Q

Hyperkalaemia is a complication of AKI. Hyperkalaemia needs to be treated URGENTLY if >6.5mmol/L and/or if there are ECG changes. Which of the following is NOT typically a common ECG change?

1 - flat T waves
2 - increased PR interval
3 - small/absent P wave
4 - widened QRS complex

A

1 - flat T waves
- typically causes t tented T waves

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39
Q

Which of the following are complications caused by AKI?

1 - hyperkalaemia
2 - fluid overload, pulmonary oedema and heart failure
3 - metabolic acidosis (MA)
4 - uraemia
5 - all of the above

A

5 - all of the above

  • MA = acid / base balance is incorrect as less HCO3- produced
  • uraemia = can lead to encephalopathy, confusion and pericarditis
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40
Q

Some patients with AKI may require Dialysis or Haemofiltration (pressure and diffusion are combined to remove fluids called convection). Which of the following is NOT an indication for Dialysis or Haemofiltration in AKI?

1 - Refractory Hyperkalaemia (K+ > 7 mmol/L despite multiple treatments)
2 - Metabolic Alkalosis (pH > 7.5 and bicarbonate >12)
3 - Metabolic Acidosis (pH < 7.2, bicarbonate < 12)
4 - Pulmonary oedema, persistent anuria (no urine) despite adequate fluid resuscitation
5 - Uraemia (>30mmol/l)
Uraemic Pericarditis (rare in AKI)
Uraemic Encephalopathy

A

2 - Metabolic Alkalosis (pH > 7.5 and bicarbonate >12)
- causes acidosis due to increased K+
- there is also less HCO3- as kidneys are not making this

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41
Q

Nephritic syndrome, also called Glomerulonephritis is a group of disorders that are caused by antigen-antibody complexes (AAC) (type III hypersensitivity) inside the glomerulus. This in turn causes what to happen?

1 - AACs infiltrate glomerula and block capillaries
2 - WBCs are recruited causing inflammation
3 - inflammation damages the glomerulus basement membrane, causing podocytes to speak out
4 - blood and protein can leak into urine
5 - all of the above

A

5 - all of the above

42
Q

Nephritic sybdrome is a group of disorders that are caused by antigen-antibody complexes (AAC) (type III hypersensitivity) inside the glomerulus, leading to inflammation and damage to the golmerula, glomerulus basement membrane (epithelial cells). What of the following does NOT typically then leak out into the urine?

1 - RBCs causing Heamaturia (RBC casts)
2 - WBCs from tissue injury
3 - protein (mild proteinuria <3.5g/day)
4 - K+ and Na+

A

4 - K+ and Na+

43
Q

Nephritic syndrome is a group of disorders that are caused by antigen-antibody complexes (AAC) (type III hypersensitivity) inside the glomerulus, leading to inflammation and damage to the glomerula, glomerulus basement membrane (epithelial cells). The glomerula is unable to filter as much filtrate meaning what is reduced?

1 - increased urea in urine
2 - increased creatinine in urine
3 - oliguria
4 - all of the above

A

3 - oliguria
- urine output
- stage 1 AKI = <0.5ml/kg/h for 6-12h

44
Q

Nephritic syndrome is a group of disorders that are caused by antigen-antibody complexes (AAC) (type III hypersensitivity) inside the glomerulus, leading to inflammation and damage to the glomerula, glomerulus basement membrane (epithelial cells). The glomerula is unable to filter as much filtrate causing oliguria (reduced urine output). What can this then cause due to low filtration?

1 - hypotension
2 - increased cardiac output
3 - hypertension
4 - hyperalbuminaemia

A

3 - hypertension
- low filtration means BP is high due to electrolytes not getting filtered and retaining water

45
Q

Which of the following can cause Glomerulonephritis (Nephritic Syndrome)?

1 - Vasculitis
2 - Anti-glomerular basement membrane antibody disease (GMB)
3 - IgA nephropathy
4 - Henoch Schonlein purpura
5 - Lupus
6 - Bacterial infections (strep or staph) bacteria or infective endocarditis
7 - Toxins or medicines
8 Viral infections such as HIV, Hepatitis B and C viruses
9 - Cryoglobulinaemia (abnormal immunoglobulins)
10 - all of the above

A

10 - all of the above

46
Q

Vasculitis is an autoimmune inflammatory condition where immune cells mistake antigens on the endothelium for foreign antigens called molecular mimicry which can lead to . 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

47
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

48
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)

49
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
50
Q

Which of the following are important differentials to consider in a patient with a non-blanching rash?

1 - meningeal septicemia
2 - leukaemia
3 - idiopathic thrombocytopenic purpura
4 - haemolytic uraemic syndrome
5 - all of the above

A

5 - all of the above

51
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
52
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
53
Q

How can Henoch Schonlein purpura be treated?

1 - analgesia
2 - rest
3 - hydration
4 - all of the above

A

4 - all of the above

  • steroid may be effective if patients have severe GIT or renal involvement
  • typically self limiting in weeks, but can cause renal failure
54
Q

Acute tubular necrosis is a form of intra-renal disease that can cause AKI. Is this commonly caused by a pre-renal or post-renal cause?

A
  • pre-renal
  • necrosis is due to prolonged pre-renal hypoperfusion
55
Q

Interstitial Nephritis is an inflammation of the interstitial tissue surrounding the renal tubules. What can this be caused by?

1 - antibiotics
2 - NSAIDs
3 - PPIs
4 - infections
5 - autoimmune conditions such as sarcoidosis
6 - all of the above

A

6 - all of the above
- commonly associated with eosinophils and neutrophils

56
Q

Treating AKI quickly is important. Which of the following would prompt an early referral to the renal team?

1 - raised creatinine
2 - raised urea
3 - pulmonary oedema
4 - hyperkalaemia

A

3 - pulmonary oedema
- indication for dialysis so need input from the renal team

57
Q

Treating AKI quickly is important. If the patient is hypovolaemic, what fluid bolus should patients be given?

1 - 250ml colloids over 30 minutes
2 - 500ml colloids over 15 minutes
3 - 250ml crystalloids over 30 minutes
4 - 500ml crystalloids over 15 minutes

A

4 - 500ml crystalloids over 15 minutes
- re-asses fluid state BUT stop when patient is euvolaemic or 2L has been given

  • typically this is 0.9% saline NaCl
  • LOOK FOR RAISED K+
58
Q

In a patient with AKI they should be monitored every 4 hours. All of the following EXCEPT which one should also be performed?

1 - lactate if suggestion of sepsis
2 - urea until creatinine falls
3 - daily K+ until creatinine falls
4 - daily creatinine
5 - daily fluid intake using catheter if indicated

A

2 - urea until creatinine falls

59
Q

When investigation the causes of AKI we should perform which of the following?

1 - urine dipstick (pre catheter)
2 - ultrasound (within 24h)
3 - assess liver function (hepatorenal)
4 - platelet count (if low perform blood film)
5 - auto-antibodies for intra-renal disease
6 - all of the above

A

6 - all of the above

  • auto-antibodies for intra-renal disease = ANA, ANCA, anti-GBM
  • ANA = anti nuclear antibodies = SLE
  • ANCA = Antineutrophilic cytoplasmic antibodies = Vasculitis
  • anti-GBM = Anti-glomerular basement membrane diseases = Good Pasteurs syndrome
60
Q

Pulmonary-renal syndrome (PRS) is used to describe the combination of glomerulonephritis and pulmonary haemorrhage as a manifestation of a multisystem autoimmune disease. PRS can then be subdivided into 2 categories based on what?

1 - CRP levels
2 - ESR levels
3 - haematuria
4 - anti-neutrophilic cytoplasmic antibodies (ANCAs)

A

4 - anti-neutrophilic cytoplasmic antibodies (ANCAs)

  • PRS is very dangerous as patients can deteriorate in <48h
61
Q

Pulmonary-renal syndrome (PRS) is used to describe the combination of glomerulonephritis and pulmonary haemorrhage as a manifestation of a multisystem autoimmune disease. PRS can then be subdivided into 2 categories based on the presence of anti-neutrophilic cytoplasmic antibodies (ANCAs). Which of the following would NOT ANCA positive?

1 - Granulomatosis with polyangiitis
2 - Microscopic polyangiitis
3 - Systemic Lupus Erythematous
4 - Churg strauss syndrome
5 - Drug associated

A

3 - Systemic Lupus Erythematous

62
Q

Pulmonary-renal syndrome (PRS) is used to describe the combination of glomerulonephritis and pulmonary haemorrhage as a manifestation of a multisystem autoimmune disease. PRS can then be subdivided into 2 categories based on the presence of anti-neutrophilic cytoplasmic antibodies (ANCAs). Which of the following would NOT be ANCA positive?

1 - granulomatosis with polyangiitis
2 - henoch-schonlein purpura
3 - systemic Lupus Erythematous
4 - cryoglobulinaemia
5 - IgA neuropathy
6 - goodpasteurs syndrome

A

1 - granulomatosis with polyangiitis
- form of small vessel vasculitis that will be ANCA positive

63
Q

Patients with vasculitis can develop renal manifestations. What % of patients with vasculitis present with renal involvement?

1 - 2%
2 - 20%
3 - 45%
4 - 80%

A

2 - 20%
- BUT if untreated 80% of patients with vasculitis will develop glomerulonephritis

64
Q

20% of patients with vasculitis present with renal manifestations, and if left untreated 80% will develop glomerulonephritis. Which of the blood vessels is mainly affected?

1 - large vessels
2 - medium vessels
3 - small vessels
4 - all are affected

A

3 - small vessels

65
Q

20% of patients with vasculitis present with renal manifestations, and if left untreated 80% will develop glomerulonephritis (GN). Is this always symptomatic?

A
  • no
  • includes a range from normal eGFR to AKI to rapid progressing glomerulonephritis with need for dialysis
  • can also see Pauci-immune crescentic GN
66
Q

20% of patients with vasculitis present with renal manifestations, and if left untreated 80% will develop glomerulonephritis (GN). How can these patients be diagnosed effectively?

1 - presence of anti-neutrophilic cytoplasmic antibody (ANCA)
2 - renal biopsy (Pauci-immune crescentic GN) histology
3 - imaging (CT sinuses, HRCT, CT brain)
4 - bronchoscopy, Lung function tests, nerve conduction studies
5 - all of the above

A

5 - all of the above

  • typically patient presents as someone who just isn’t getting better, but other multi-systemic features that don’t align
67
Q

20% of patients with vasculitis present with renal manifestations, and if left untreated 80% will develop glomerulonephritis (GN). Which 2 of the following is important to rule out when thinking of a diagnosis of GN in a patient with vasculitis?

1 - CHF
2 - pulmonary hypertension
3 - TB
4 - infective endocarditis

A

3 - TB
4 - infective endocarditis

  • essentially identify the cause of infection and treat
  • then see if symptoms persist
68
Q

20% of patients with vasculitis present with renal manifestations, and if left untreated 80% will develop glomerulonephritis (GN). The 1st line treatment is induction immunosuppression. Which 2 of the following treatment options are used for 3 months to induce remission as part of the induction immunosuppression?

1 - high dose of steroids
2 - cyclophosphamide
3 - azathioprine
4 - mycophenolate mofetil

A

1 - high dose of steroids
2 - cyclophosphamide

69
Q

20% of patients with vasculitis present with renal manifestations, and if left untreated 80% will develop glomerulonephritis (GN). Following induction immunosuppression with 3 months of high dose steroids and cyclophosphamide. Which 2 of the following treatment options are used in maintenance, due to the high risk of relapse?

1 - methotrexate
2 - opioids
3 - azathioprine
4 - mycophenolate Mofetil

A

3 - azathioprine
4 - mycophenolate Mofetil

  • retuximan should be considered if patient continues to relapse (depletes B and plasma cells)
  • plasma exchange can be considered if creatinine is >500
70
Q

What is the mortality rate in 1 year if patients with vasculitis and glomerulonephritis (GN) if left untreated?

1 - 100%
2 - 50%
3 - 25%
4 - 5%

A

1 - 100%

  • even in treated patients, the main cause of mortality is infection due to the immunosuppression
71
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
72
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
73
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

74
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

75
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

76
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

77
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)

78
Q

How is good pastures syndrome (GPS) typically treated?

1 - IV methyprednisolone
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
79
Q

AKI through infection with sepsis is common. What is the mortality of patients with AKI and sepsis?

1 - 7%
2 - 37%
3 - 47%
4 - 70%

A

4 - 70%

80
Q

Does sepsis typically cause vasoconstriction or vasodilation?

A
  • vasodilation
  • typically results in fluid moving into the interstitial space and patients having oedema
81
Q

In patients who develop sepsis, they typically have a drop in blood pressure as fluid moves into the interstitial space. What can this lead to in the lungs?

1 - pulmonary hypertension
2 - pulmonary hypertension
3 - pulmonary oedema causing tissue hypoxia
4 - all of the above

A

3 - pulmonary oedema causing tissue hypoxia

  • the hypoxia is systemic and not just in the lungs
  • leads to respiratory distress syndrome and multi-organ dysfunction syndrome
  • 80-90% mortality in multi-organ failure due to sepsis
82
Q

Glomerular disease can be caused following an infection, which is typically caused by antigen-antibody complexes becoming lodged in the glomerulus causing Post Infectious Glomerulonephritis. What is one of the most common organisms to cause this?

1 - Post-streptococcal glomerulonephritis
2 - Post staphylococcus aureus glomerulonephritis
3 - Post Methicillin-resistant Staphylococcus aureus glomerulonephritis
4 - Post hepatitis B glomerulonephritis

A

1 - Post-streptococcal glomerulonephritis

  • typically occurs 5-7 days post infection
83
Q

Which of the following vital infections can cause Glomerulonephritis?

1 - hepatitis B
2 - hepatitis C
3 - human-immunodeficiency virus
4 - all of the above

A

4 - all of the above

84
Q

Kidney cancer due to Myeloma or Lymphoma or from paraneoplastic effects can cause a glomerular pathology due to infiltration of the glomerulus. Does this typically present as a nephrotic or nephritic syndrome?

A
  • nephrotic syndrome
85
Q

Do kidney cancers or the treatment for kidney cancers cause more of a glomerular pathology?

A
  • cancer treatments
  • chemotherapy for example
86
Q

Which of the following is NOT caused by leukaemia and/or lymphoma?

1 - Minimal changedisease
2 - Membraneousnephropathy​
3 - Amyloidosis
4 - Mesangiocapillary
glomerulonephriti​
5 - Cryoglobulinaemia​

A

3 - Amyloidosis
- causes my myeloma

87
Q

Which of the following is NOT caused by myeloma?

1 - Minimal changedisease
2 - Amyloidosis,​
3 - Cryoglobulinaemia,​
4 - Lightchaindeposition disease​

A

1 - Minimal changedisease
- typically caused by lymphomas or leukaemia

88
Q

Which of the following is NOT caused by carcinoma?

1 - Membraneousnephropathy,​
2 - Mesangiocapillary
glomerulonephriti​​
3 - Haemolytic Uraemic Syndrome (HUS)​
4 - Cryoglobulinaemia

A

4 - Cryoglobulinaemia

89
Q

A 62 yr old has a 4 week history of night sweats and malaise is given antibiotics by GP for cellulitis. Two weeks later he presents with nausea, lethargy and weight loss. He has been taking prn aspirin + paracetamol for joint pains. He appears cachectic but has lower limb oedema and a pinprick red rash over his ankles.
- BP is 168/94
- Creatinine is 634 (baseline 122)
- GFR 8 ml/min (baseline 67ml/min)

Which of the following will help determine cause of AKI?

1 - Venous bloodgas, Urea &Haemoglobin
2 - Electrolytes, PTH & Urine output
3 - Medicines history, Urine dipstick and Ultrasound KUB

A

3 - Medicines history, Urine dipstick and Ultrasound KUB

  • Pre-renal is most common cause of AKI
90
Q

A 62 yr old has a 4 week history of night sweats and malaise is given antibiotics by GP for cellulitis. Two weeks later he presents with nausea, lethargy and weight loss. He has been taking prn aspirin + paracetamol for joint pains. He appears cachectic but has lower limb oedema and a pinprick red rash over his ankles.
- BP is 168/94
- Creatinine is 634 (baseline 122)
- GFR 8 ml/min (baseline 67ml/min)

Which of the following causes of AKI is most likely to respond to a fluid bolus?

1 - Glomerulonephritis
2 - Acute TubularNecrosis
3 - Sepsis

A

3 - Sepsis

91
Q

A 62 yr old has a 4 week history of night sweats and malaise is given antibiotics by GP for cellulitis. Two weeks later he presents with nausea, lethargy and weight loss. He has been taking prn aspirin + paracetamol for joint pains. He appears cachectic but has lower limb oedema and a pinprick red rash over his ankles.
- BP is 168/94
- Creatinine is 634 (baseline 122)
- GFR 8 ml/min (baseline 67ml/min)

The patients urine dipstick has 3+ blood and 3+ protein. Which additional test would you consider?

1 - PSA
2 - Urine cytology and mc&s
3 - ANCA & GBM antibody

A

3 - ANCA & GBM antibody

  • could be Goodpasture’s Syndrome
  • could be vasculitis
92
Q

The same patient from the above questions has:
- BP is 168/94
- Creatinine is 634 (baseline 122)
- GFR 8 ml/min (baseline 67ml/min)

The patient has bloods taken:

  • Sodium 139 mmol/L (NR 133-146)
  • Potassium 6.7 mmol/L (NR 3.5-5.3)
  • Chloride 116 mmol/L (NR 95-108)
  • Bicarbonate 9 mmol/L (NR 22-29)
  • Urea 42 mmol/L (NR 2.5-7.8)
  • Creatinine 634 µmol/L (NR 64-104)

Which of the abnormal blood result should be treated first?

1 - high K+
2 - low HCO3-
3 - high Cl-
4 - high creatinine

A

1 - high K+
- 1st = calcium gluconate is used to stabilie heart
- 2nd is insulin with dextrose and salbutamol as this drive K+ inside cells
- 3rd is HCO3- either IV or oral to address acidosis

93
Q

The same patient from the above questions has:
- BP is 168/94
- Creatinine is 634 (baseline 122)
- GFR 8 ml/min (baseline 67ml/min)

The patient has bloods taken:

  • Sodium 139 mmol/L (NR 133-146)
  • Potassium 6.7 mmol/L (NR 3.5-5.3)
  • Chloride 116 mmol/L (NR 95-108)
  • Bicarbonate 9 mmol/L (NR 22-29)
  • Urea 42 mmol/L (NR 2.5-7.8)
  • Creatinine 634 µmol/L (NR 64-104)

The patient has a VBG: pH of 7.14. What should be calculated to further assess this?

1 - Urine pH
2 - Anion Gap
3 - Urine and serum osmolalities

A

3 - Urine and serum osmolalities

Anion gap:
- (Na+ add K+) - (HCO3- add Cl-)
- here the anion gap would be:
- (139 + 6.7) - (9 + 116) = 20.7 (3-11)

MUDPILES CAT can be used to remember the causes of anion gap metabolic acidosis

94
Q

Acidosis in kidney failure occurs due to?

1 - Inability toexcrete acidload intubules
2 - Accumulationofunmeasuredanions
3 - Both 1 and 2

A

3 - Both 1 and 2

95
Q

The same patient from the above questions has:
- BP is 168/94
- Creatinine is 634 (baseline 122)
- GFR 8 ml/min (baseline 67ml/min)

The patient has bloods taken:

  • Sodium 139 mmol/L (NR 133-146)
  • Potassium 6.7 mmol/L (NR 3.5-5.3)
  • Chloride 116 mmol/L (NR 95-108)
  • Bicarbonate 9 mmol/L (NR 22-29)
  • Urea 42 mmol/L (NR 2.5-7.8)
  • Creatinine 634 µmol/L (NR 64-104)

The patient has a VBG: pH of 7.14 and a high anion gap (20.7 (3-11 is normal) due to metabolic acidosis. How would you treat the acid-base disorder?

1 - BIPAP (non invasive ventilation)
2 - Intravenous fluids
3 - Bicarbonate replacement
4 - Diuretics

A

3 - Bicarbonate replacement

96
Q

The same patient from the above questions has:
- BP is 168/94
- Creatinine is 634 (baseline 122)
- GFR 8 ml/min (baseline 67ml/min)

The patient has bloods taken:

  • Sodium 139 mmol/L (NR 133-146)
  • Potassium 6.7 mmol/L (NR 3.5-5.3)
  • Chloride 116 mmol/L (NR 95-108)
  • Bicarbonate 9 mmol/L (NR 22-29)
  • Urea 42 mmol/L (NR 2.5-7.8)
  • Creatinine 634 µmol/L (NR 64-104)

In this patient which medication is best to lower the patients BP?

1 - ACE inhibitor or ARB
2 - Calcium Channel blocker
3 - Diuretic
4 - Beta blocker

A

2 - Calcium Channel blocker

97
Q

The same patient from the above questions has:
- BP is 168/94
- Creatinine is 634 (baseline 122)
- GFR 8 ml/min (baseline 67ml/min)

The patient has bloods taken:

  • Sodium 139 mmol/L (NR 133-146)
  • Potassium 6.7 mmol/L (NR 3.5-5.3)
  • Chloride 116 mmol/L (NR 95-108)
  • Bicarbonate 9 mmol/L (NR 22-29)
  • Urea 42 mmol/L (NR 2.5-7.8)
  • Creatinine 634 µmol/L (NR 64-104)

On Day 3, patient has a witnessed tonic-clonic seizure. His creatinine has risen by 80 each day. What is most likely cause of his seizure?

1 - Hypertension
2 - Uraemia
3 - Dehydration

A

2 - Uraemia

98
Q

A 68 yr F type 2 diabetic on Metformin with no retinopathy had an MI 6 months ago. She presents with increasing breathlessness and has bi-basal creps, leg oedema and an acute on chronic kidney decline. GFR was 35ml/min for 6 years but over 6 months has declined to 17ml/min. Bloods are taken:

Haemoglobin 85 g/L (NR 110-150)
Sodium 128 mmol/L (NR 133-146)
Potassium 6.2 (NR 3.5-5.3)
Bicarbonate 12 (NR 22-28)
Chloride 116 (NR 95-108)
Albumin 28 (NR 35-40)
ALP 189 (NR 30-130)
Corrected calcium 1.9 (NR 2.2- 2.6)
Phosphate 2.87 (NR 0.8-1.5)
PTH 218 pmol/L (NR 1.6-7.8)
Urine Dip: trace prot & trace blood

What is the likely cause of her recent kidney decline?

1 - Diabetic nephropathy
2 - Cardio-renal syndrome
3 - Metformin
4 - Nephrotic syndrome

A

2 - Cardio-renal syndrome

99
Q

A 68 yr F type 2 diabetic on Metformin with no retinopathy had an MI 6 months ago. She presents with increasing breathlessness and has bi-basal creps, leg oedema and an acute on chronic kidney decline. GFR was 35ml/min for 6 years but over 6 months has declined to 17ml/min. Bloods are taken:

Haemoglobin 85 g/L (NR 110-150)
Sodium 128 mmol/L (NR 133-146)
Potassium 6.2 (NR 3.5-5.3)
Bicarbonate 12 (NR 22-28)
Chloride 116 (NR 95-108)
Albumin 28 (NR 35-40)
ALP 189 (NR 30-130)
Corrected calcium 1.9 (NR 2.2- 2.6)
Phosphate 2.87 (NR 0.8-1.5)
PTH 218 pmol/L (NR 1.6-7.8)
Urine Dip: trace prot & trace blood

Why is she breathless?

1 - Acidosis
2 - PulmonaryOedema
3 - Anaemia
4 - all of the above

A

4 - all of the above

100
Q

A 68 yr F type 2 diabetic on Metformin with no retinopathy had an MI 6 months ago. She presents with increasing breathlessness and has bi-basal creps, leg oedema and an acute on chronic kidney decline. GFR was 35ml/min for 6 years but over 6 months has declined to 17ml/min. Bloods are taken:

Haemoglobin 85 g/L (NR 110-150)
Sodium 128 mmol/L (NR 133-146)
Potassium 6.2 (NR 3.5-5.3)
Bicarbonate 12 (NR 22-28)
Chloride 116 (NR 95-108)
Albumin 28 (NR 35-40)
ALP 189 (NR 30-130)
Corrected calcium 1.9 (NR 2.2- 2.6)
Phosphate 2.87 (NR 0.8-1.5)
PTH 218 pmol/L (NR 1.6-7.8)
Urine Dip: trace prot & trace blood

What initial treatment is recommended for her fluid overload?

1 - Spironolactone
2 - Loop diuretic
3 - Blood transfusion
4 - Dialysis

A

2 - Loop diuretic
- do not give spirolactone as K+ is already high and this is potassium sparing
- not sick enough for options 3 and 4

C. Year 3 MLA Urology (3 decks)

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