Biochemistry of Alcohol Abuse Flashcards
What is the classic triad of refeeding syndrome?
Low magnesium, low phosphate and low potassium
Booze, malnutrition and disease
Who is at risk of refeeding syndrome?
1 or more of - BMI less than 16kg/m, unintentional weight loss greater than 15%, no nutritional intake for more than 10 days and low Mg, K and phosphate
2 or more - BMI <18.5kg/m, unintentional weight loss more than 10kg, no nutritional intake for more than 5 days and history of alcohol and drugs
What will relocate or deplete electrolytes in refeeding syndrome?
Alcohol abuse
Drugs like insulin, antacids and diuretics
What is the timeline of refeeding syndrome?
Normal eating - starvation - reintroduction of calories
Anabolism - catabolism - anabolism
Describe cellular uptake in refeeding syndrome
Potassium, phosphate and magnesium decrease in malnutrition
ECF is apparently normal (low or normal) mg and PO4 in serum
ICF Mg and PO4 used up during starvation
What are the physical signs of low magnesium uptake?
Confusion, delirium, tremors, seizures, tachyarrhythmias, tetany, Chvostek sign, Trousseau sign and ECG changes
What are the ECG changes in low magnesium uptake?
Widening QRS complexes
Peaking T waves
Prolonged PR interval
What are associated biochemical abnormalities in low magnesium uptake?
Hypokalaemia
Hypocalcaemia
Low parathyroid levels
Low vitamin D levels
Describe how insulin drives cellular uptake of potassium
Insulin is used to treat hyperkalaemia to drive potassium into cells
Minima urinary conc. of potassium is 2.5mmol/l - even if whole body is deplete
Move potassium out of cells into blood which can mask the worsening potassium depletion
What are the physical exam findings of hypokalaemia?
Weakness and decreased muscle tone
What are some complications of prolonged hypokalaemia?
Polyuria due to nephrotic DI and rhabdomyolysis
What are the ECG findings of hypokalaemia?
Ventricular tachycardia, atrial tachycardias, PR interval prolongation, P wave amplitude increased, P waves width increased, u waves, T wave inversion and ectopic
What happens when glucose is reintroduced in hypophosphatemia?
Massive reuptake in phosphate for ATP production
What are the neurological implications of hypophosphatemia?
Seizures, coma, delirium and osmotic demyelination
What are the cardiac and MSK implications of hypophospatemia?
Impaired cardiac contractibility and cardiomyopathy
Weakness, ileus and proximal myopathy
What are the haematological implications of hypophosphatemia?
Increased propensity for haemolysis
What is the treatment of refeeding syndrome?
Reintroduce calories slowly
Expect electrolyte redistribution - phosphate often drops the fastest
Replace electrolytes IV
Give thiamine (Vitamin B1)
When does alcoholic ketoacidosis occur?
Tends to occur after a day of massive binge drinking
Describe alcoholic ketoacidosis
Can look like DKA with normal glucose
Lipolysis is increased as increased cortisol and catecholamines
Generates fatty acids which drive ketone production
What ketone is produced in alcoholic ketoacidosis?
Beta-hydroxybutyrate
What is the affect of increased FFAs?
Inhibits processing of acetyl CoA in Krebs cycle which further drives ketone production
What is the effect of raised NADH?
Reduces gluconeogenesis
What is the treatment for AKA?
Fluids
Dextrose slowly
Thiamine
Correct electrolyte imbalance - watch for refeeding syndrome
What is the triad of Wernicke’s/ Korsakoff’s?
Gate ataxia or imbalance, ophthalmoplegia/ nystagmus and confusion
What is the effect of lack of thiamine?
Krebs cycle stalls, switch from aerobic to anaerobic respiration
This produces far less ATP and lactate is the bi-product - focal acidosis (areas involved in motor control and cognition)
How much thiamine is stored in the liver?
5-10 day supply