Alcohol Symposium: The Whole World is a Bottle Flashcards
What does a blood pH of 7.21 indicate?
Acidosis Normal is 7.35-7.45
If the blood bicarbonate is low, what is the type of acidosis?
Metabolic
Why might a patient be breathing out excessive CO2?
To compensate for the acidosis
What might a low potassium level mean?
Vomiting or malnourishment (chloride may also be lost in the vomit)
Even if the patient is vomiting, why do they stay acidotic?
Their acid load is much more significant than what they’re vomiting
Why might a urea value within normal range really be high?
The patient has low muscle mass
Why might the creatinine high?
Indicative of AKI
How do you calculate the osmolal gap?
Serum osmolality - (2x Na + Urea + Glucose) = osmolal gap
What may the osmolal gap mean?
“something else in the blood” e.g. ethanol
What does the anion gap help understand?
The difference in the presence of anions and cation
How is the anion gap calculated?
(Na+ + K+) – (HCO3- + Cl-) Normal gap = 8 to 16 mmol/L
What does it mean if the gap is >16 mol/l?
There is/are (an) unmeasured anion(s) present here contributing to the acidosis.
What blood sign would exclude DKA?
Normal glucose
When does alcoholic ketoacidosis occur?
The day after a binge
Which ketone is in excess in AKA?
Beta-Hydroxybutyrate
How is there an increase in Beta-Hydroxybutyrate?
Alcohol metabolism drives the production of NADH. To breakdown NADH to NAD, acetate is converted to beta-hydroxybutyrate.
What is the consequence of the malnutrition of chronic alcohol users?
They have depleted reserve. Ethanol provide calorie intake but glycogen stores will be depleted.
What is another consequence of raised NADH levels?
It impairs hepatic gluconeogenesis and the metabolism of lactate - this drives hypoglycaemia and acidosis
How do you stabilise a patient with AKA?
IV fluids IV thiamine (vit B1) - Pabrinex
You have noticed that the patient has ophthalmoplegia, gait ataxia, and is confused. What do you give next?
(Wernicke’s) Glucose after Pabrinex
How else might you help manage the alcohol withdrawal?
Symptom-triggered diazepam scoring chart
What may Wernicke’s progress to and is it reversible?
Korsokoff’s and NO
Why is thiamine so important and what happens in insufficiency?
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)
Alpha ketoglutarate dehydrogenase requires thiamine as a cofactor in the Krebs cycle. What happens when thiamine is absent and alpha ketoglutarate dehydrogenase builds up?
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)
What is the downside to thiamine administration?
Very little downside to administration (there is the very small chance of anaphylaxis) – if you ever see an unexplained lactic acidosis, give thiamine
What happens if you give glucose before thiamine in the malnourished or thiamine-deficient patient?
You risk driving Wernicke’s Encephalopathy
What is acetaldehyde and why is it so dangerous for the liver?
A metabolite of ethanol It is thought to be particularly toxic especially to hepatic proteins
What are the biochemical signs of fatty liver disease/hepatic steatosis?
- Subclinical hyperbilirubinaemia - Mild elevation of transaminases (AST/ALT) - Gamma GT is elevated in a majority of patients
How does alcoholic hepatitis present?
A diversity of presentations: - Jaundice - Anaemia - Leucocytosis - The hepatic enzymes tend to present in a ratio of AST: ALT >2 (should normally be <1).
What might the biochemical picture of alcoholic hepatitis be?
- 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?
