Alcohol Symposium: The Whole World is a Bottle

Question 1

What does a blood pH of 7.21 indicate?

Answer 1

Acidosis Normal is 7.35-7.45

Question 2

If the blood bicarbonate is low, what is the type of acidosis?

Answer 2

Metabolic

Question 3

Why might a patient be breathing out excessive CO2?

Answer 3

To compensate for the acidosis

Question 4

What might a low potassium level mean?

Answer 4

Vomiting or malnourishment (chloride may also be lost in the vomit)

Question 5

Even if the patient is vomiting, why do they stay acidotic?

Answer 5

Their acid load is much more significant than what they’re vomiting

Question 6

Why might a urea value within normal range really be high?

Answer 6

The patient has low muscle mass

Question 7

Why might the creatinine high?

Answer 7

Indicative of AKI

Question 8

How do you calculate the osmolal gap?

Answer 8

Serum osmolality - (2x Na + Urea + Glucose) = osmolal gap

Question 9

What may the osmolal gap mean?

Answer 9

“something else in the blood” e.g. ethanol

Question 10

What does the anion gap help understand?

Answer 10

The difference in the presence of anions and cation

Question 11

How is the anion gap calculated?

Answer 11

(Na+ + K+) – (HCO3- + Cl-) Normal gap = 8 to 16 mmol/L

Question 12

What does it mean if the gap is >16 mol/l?

Answer 12

There is/are (an) unmeasured anion(s) present here contributing to the acidosis.

Question 13

What blood sign would exclude DKA?

Answer 13

Normal glucose

Question 14

When does alcoholic ketoacidosis occur?

Answer 14

The day after a binge

Question 15

Which ketone is in excess in AKA?

Answer 15

Beta-Hydroxybutyrate

Question 16

How is there an increase in Beta-Hydroxybutyrate?

Answer 16

Alcohol metabolism drives the production of NADH. To breakdown NADH to NAD, acetate is converted to beta-hydroxybutyrate.

Question 17

What is the consequence of the malnutrition of chronic alcohol users?

Answer 17

They have depleted reserve. Ethanol provide calorie intake but glycogen stores will be depleted.

Question 18

What is another consequence of raised NADH levels?

Answer 18

It impairs hepatic gluconeogenesis and the metabolism of lactate - this drives hypoglycaemia and acidosis

Question 19

How do you stabilise a patient with AKA?

Answer 19

IV fluids IV thiamine (vit B1) - Pabrinex

Question 20

You have noticed that the patient has ophthalmoplegia, gait ataxia, and is confused. What do you give next?

Answer 20

(Wernicke’s) Glucose after Pabrinex

Question 21

How else might you help manage the alcohol withdrawal?

Answer 21

Symptom-triggered diazepam scoring chart

Question 22

What may Wernicke’s progress to and is it reversible?

Answer 22

Korsokoff’s and NO

Question 23

Why is thiamine so important and what happens in insufficiency?

Answer 23

It is a cofactor in many metabolic processes Can cause a build up of lactic acid, amongst other things (chronic alcohol misusers are prone to be deficient in as alcohol blocks duodenal uptake of thiamine and interferes with thiamine storage and conversion)

Question 24

Alpha ketoglutarate dehydrogenase requires thiamine as a cofactor in the Krebs cycle. What happens when thiamine is absent and alpha ketoglutarate dehydrogenase builds up?

Answer 24

It has been linked to mitochondrial damage causing cellular necrosis, and triggering apoptosis (cell death) – cells in the cerebellum are particularly sensitive to this (hence the motor control issues)

Question 25

What is the downside to thiamine administration?

Answer 25

Very little downside to administration (there is the very small chance of anaphylaxis) – if you ever see an unexplained lactic acidosis, give thiamine

Question 26

What happens if you give glucose before thiamine in the malnourished or thiamine-deficient patient?

Answer 26

You risk driving Wernicke’s Encephalopathy

Question 27

What is acetaldehyde and why is it so dangerous for the liver?

Answer 27

A metabolite of ethanol It is thought to be particularly toxic especially to hepatic proteins

Question 28

What are the biochemical signs of fatty liver disease/hepatic steatosis?

Answer 28

• Subclinical hyperbilirubinaemia - Mild elevation of transaminases (AST/ALT) - Gamma GT is elevated in a majority of patients

Question 29

How does alcoholic hepatitis present?

Answer 29

A diversity of presentations: - Jaundice - Anaemia - Leucocytosis - The hepatic enzymes tend to present in a ratio of AST: ALT >2 (should normally be <1).

Question 30

What might the biochemical picture of alcoholic hepatitis be?

Answer 30

• Ratio of AST: ALT >2 - Markedly elevated gGT - Elevated bilirubin - Note low Mg, low PO4, and low K mentioned earlier. Chronic alcohol misusers tend to be malnourished. ?Refeeding risk?

Question 31

Question 32

Question 33