MET EOYS5 Flashcards

1
Q

Explain why a patient with cholestatic problem would have pale stools [1] and dark urine [1]

A

Pale stools: no bilirubin reaches the gastrointestinal tract
Dark urine: reflux of conjugated bilirubin into blood which is excreted in the urine

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2
Q

Paul is a 47-year-old with a long history of alcohol abuse.

Which of the following LFT results would be most likely?

Very high AST, high ALT, high GGT
Very high AST, high ALT, low GGT
High AST, very high ALT, high GGT
Low AST, high ALT, high GGT
High AST, very high ALT, low GGT

A

Paul is a 47-year-old with a long history of alcohol abuse.

Which of the following LFT results would be most likely?

Very high AST, high ALT, high GGT

The typical LFT pattern in alcoholic liver disease is high AST and ALT (with AST typically twice as high as ALT).

In the context of acute liver damage, ALT and AST are also raised, however, ALT tends to be significantly higher than AST.

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3
Q

A 43-year-old lady attends A&E at 8pm with right upper quadrant (RUQ) pain, nausea and vomiting. On examination, you note she has a BMI of 33kg/m2, yellowing of the sclera and she states the pain is worse after eating.

Given the likely diagnosis, what pattern would you expect to see on her blood tests?

High unconjugated bilirubin, low conjugated bilirubin, low haemoglobin
Normal unconjugated bilirubin, high conjugated bilirubin, normal haemoglobin
High unconjugated bilirubin, high conjugated bilirubin, normal haemoglobin
Low unconjugated bilirubin, low conjugated bilirubin, low haemoglobin
Normal unconjugated bilirubin, high conjugated bilirubin, low haemoglobin

A

A 43-year-old lady attends A&E at 8pm with right upper quadrant (RUQ) pain, nausea and vomiting. On examination, you note she has a BMI of 33kg/m2, yellowing of the sclera and she states the pain is worse after eating.

Given the likely diagnosis, what pattern would you expect to see on her blood tests?

High unconjugated bilirubin, low conjugated bilirubin, low haemoglobin
Normal unconjugated bilirubin, high conjugated bilirubin, normal haemoglobin

Gallstones are most common in middle-aged women and are associated with an increased BMI.
They typically cause pain after eating a fatty meal. Large gallstones may become stuck in the common bile duct and block the flow of bile. This can cause post-hepatic jaundice as conjugated bilirubin from the liver is not excreted and the concentration increase in the blood. Unconjugated bilirubin is usually at a normal level as the hepatocytes are not damaged. Low haemoglobin in the context of jaundice is an indicator of a pre-hepatic cause, such as haemolytic anaemia. The most likely pattern of blood results for this patient is, therefore, normal unconjugated bilirubin, high conjugated bilirubin and normal haemoglobin.

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4
Q

Excess aldosterone would lead to

Metabolic acidosis
Metabolic alkalosis
Resp. acidosis
Resp. alkaloisis

A

Metabolic alkalosis

The physiologic increase in aldosterone secretion contributes to the development of metabolic alkalosis as salt retention by the kidneys is linked to increased bicarbonate reabsorption and acid excretion

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5
Q

The level of the ratio of AST:ALT can be helpful: in diagonsis:

A ratio of AST: ALT >2 suggests which pathology? [1]
A a ratio of AST: ALT <1 suggests which pathology? [1]

A

A ratio of AST: ALT >2 suggests alcoholic liver disease
A a ratio of AST: ALT <1 suggests non-alcoholic liver disease

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6
Q

Chronic liver diesease would present with which of the following?

AST > ALT
ALT > AST
ALT = AST
Raised ALP

A

Chronic liver diesease would present with which of the following?

AST > ALT
ALT > AST
ALT = AST
Raised ALP

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7
Q

Metabolic alkalosis is usually accompanied by [hypokalemia / hyperkalemia]

A

Metabolic alkalosis is usually accompanied by hypokalemia

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8
Q

How does liver disease progress? (is similar for no. of pathologies)

A
  1. Primary Injury: liver cells are damaged.

2.This causes inflammation

  1. This causes liver cell injury / death from primary injury or inflam. response
  2. Fibrosis occurs if cell death is too advanced / regen capacity is exhausted / process has been to extensive: causes pathological scar tissue (fibrosis).
  3. Eventually fibrotic nodules are formed: this is when we classify as cirrhosis
  4. A liver can function normally with cirrhosis (& be asymptomatic) but can lead to liver failure or cancer
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9
Q

Symptoms of liver disease?

Systemic [2]
Cholestatic? [2]

A

None

Systemic:
* Weight loss
* Tiredness

Cholestatic (reduction in bile flow)
* Pruritis (itchy skin; Cholestatic liver disease increases levels of bile salt which accumulate under the skin causing itch)
* Pale stools/dark urine

Complications of underlying disease

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10
Q

Signs of Chronic Liver Disease? [5]

A

Palmar erythema
Spider naevi
(most specific)

Hair loss
Gynaecomastia (man boobs)

Leuchonychia / Clubbing
Proximal wasting
Scratch marks
Xanthelasma

Palmar erythema
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11
Q

Indicators of liver status:

Which blood tests would be useful to indicate liver function? [2]
Which blood tests would be useful to indicate stage of liver disease? [2]

A

Which blood tests would be useful to indicate liver function? [2]
* Albumin
* INR (Prothrombin Time)

Which blood tests would be useful to indicate stage of liver disease? [2]
* Platelet count (as spleen enlarges, can have consumption of platelets)
* ALT/AST

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12
Q

What could be ruled out of causing ALT > 500?
What would ALT of 500-100 indicate is the source?
What would ALT of 1500+ indicate?

A

ALT:
Alcohol doesn’t put ALT > 500
500 – 1500: autoimmune hepatitis
more than 1500: hepatitis viruses / drugs / ischaemia

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13
Q

How can you treat variceal bleeding [4]

What can you give as primary and secondary prophylaxis for variceal bleeding? [2]

A

Treatment:
Resuscitation
Terlipressin (inhibits portal hypertension with simultaneous reduction of blood circulation in portal vessels) and Antibiotics
Banding or injection sclerotherapy
TIPSS

Primary + secondary prophylaxis beta blockers
Propranolol / Carvedilol
Banding

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14
Q

How is ammonia produced in health? What happens after this?

A

NH3 is produced when glutamine converted to glutamate

In health: NH3 is converted to urea & excreted in kidney OR in reverse of reaction, back to glutamine

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15
Q

How can you stop the production of NH3 to treat encephalopathy? [2]

A

Rifaximin: reduces the production of NH3 in the gut

L-Ornithine L-arginine: stops the conversion of glutamate to glutamine

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16
Q

What scoring system do you use to assess if have decompensated liver? [1]

What score would classify a decompensated liver? [1]

A

Child-Pugh score:
over 7 points: decompensated

17
Q

What effect does low pH on the body if it is out of control acutely? [4]

A

Acutely:
* Negatively inotropic
* ‘Air hunger’: panting away
* Part of critical illness syndrome – generalised cellular dysfunction
* Affects body K+ distribution (net shift of K+ from the intracellular to the extracellular space)

18
Q

What is Henderson-Hasselbach equation in the body for pH blood plasma? [1]

A
19
Q

Which imaging modality is normally used first for assessing liver disease?

CT
Ultrasound
MRI
ERCP / MRCP

A

Which imaging modality is normally used first for assessing liver disease?

CT
Ultrasound
MRI
ERCP / MRCP

20
Q

How can you cause metabolic acodosis? [4]

A

Adding Acid to your body:
- Ingestion of acid (Aspirin)
- Generation of acid (lactic acid, ketones)
- Retention of acid (renal failure)

Loss of bicarbonate:
- Gut – eg diarrhoea, Kidneys - RTA

21
Q

What is hyperchloremic metabolic acidosis?

What is the most common cause? [1]
More rare cause? [1]

A

Normal anion gap acidosis is an acidosis that is not accompanied by an abnormally increased anion gap.

Caused by loss of HCO3- WITH a compensatory rise in Chlorine

Most common cause: diarrhoea
Also caused by: renal tubular acidosis

22
Q

What are the characteristics of compensated resp acidosis:

pH? [1]
pCO2? [1]
HCO3-? [1]

A
  • Normal pH
  • high pCO2
  • compensatory high HCO3-
23
Q

How does lactic acidosis / ketoacidosis commonly present with regards to:

  • pH
  • HCO3-
  • CO2
A

Low pH, low HCO3-, often low CO2

24
Q

What would cause normal anion gap metabolic acidosis?

A

= ‘Hyperchloraemic metabolic acidosis’
Usually due to bicarbonate loss
* Kidneys: Renal tubular acidosis
* Gut: diarrhoea

Compensatory rise in chloride to maintain electrical neutrality

25
Q

Why might HCO3- rise in Ptxs? [4]

A

As H+ is lost:
* Diarrhoea
* Diuretics
* Mineralocorticoid excess
* Vomiting/NG drainage

As H+ moves into cells: Hypokalaemia

26
Q

The best liver function test is:

a. AST/ALT

b. Alkaline phosphatase

c. Bilirubin

d. INR

A

The best liver function test is:

a. AST/ALT

b. Alkaline phosphatase

c. Bilirubin

d. INR

Of the above, only the INR is a true liver function test as it examines the capacity of the liver to synthesize clotting factors. AST and ALT are enzymes that are elevated in hepatocellular injury. Alkaline phosphatase is an enzyme that is elevated in cholestatic injury. Bilirubin is a pigment secreted by the liver that is elevated with liver dysfunction but can also be elevated with bile obstruction (even though liver function is normal).