Biochemistry of Alcohol Abuse Flashcards

1
Q

What is the classic triad of refeeding syndrome?

A

Low magnesium, low phosphate and low potassium
Booze, malnutrition and disease

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2
Q

Who is at risk of refeeding syndrome?

A

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

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3
Q

What will relocate or deplete electrolytes in refeeding syndrome?

A

Alcohol abuse
Drugs like insulin, antacids and diuretics

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4
Q

What is the timeline of refeeding syndrome?

A

Normal eating - starvation - reintroduction of calories
Anabolism - catabolism - anabolism

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5
Q

Describe cellular uptake in refeeding syndrome

A

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

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6
Q

What are the physical signs of low magnesium uptake?

A

Confusion, delirium, tremors, seizures, tachyarrhythmias, tetany, Chvostek sign, Trousseau sign and ECG changes

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7
Q

What are the ECG changes in low magnesium uptake?

A

Widening QRS complexes
Peaking T waves
Prolonged PR interval

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8
Q

What are associated biochemical abnormalities in low magnesium uptake?

A

Hypokalaemia
Hypocalcaemia
Low parathyroid levels
Low vitamin D levels

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9
Q

Describe how insulin drives cellular uptake of potassium

A

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

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10
Q

What are the physical exam findings of hypokalaemia?

A

Weakness and decreased muscle tone

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11
Q

What are some complications of prolonged hypokalaemia?

A

Polyuria due to nephrotic DI and rhabdomyolysis

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12
Q

What are the ECG findings of hypokalaemia?

A

Ventricular tachycardia, atrial tachycardias, PR interval prolongation, P wave amplitude increased, P waves width increased, u waves, T wave inversion and ectopic

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13
Q

What happens when glucose is reintroduced in hypophosphatemia?

A

Massive reuptake in phosphate for ATP production

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14
Q

What are the neurological implications of hypophosphatemia?

A

Seizures, coma, delirium and osmotic demyelination

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15
Q

What are the cardiac and MSK implications of hypophospatemia?

A

Impaired cardiac contractibility and cardiomyopathy
Weakness, ileus and proximal myopathy

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16
Q

What are the haematological implications of hypophosphatemia?

A

Increased propensity for haemolysis

17
Q

What is the treatment of refeeding syndrome?

A

Reintroduce calories slowly
Expect electrolyte redistribution - phosphate often drops the fastest
Replace electrolytes IV
Give thiamine (Vitamin B1)

18
Q

When does alcoholic ketoacidosis occur?

A

Tends to occur after a day of massive binge drinking

19
Q

Describe alcoholic ketoacidosis

A

Can look like DKA with normal glucose
Lipolysis is increased as increased cortisol and catecholamines
Generates fatty acids which drive ketone production

20
Q

What ketone is produced in alcoholic ketoacidosis?

A

Beta-hydroxybutyrate

21
Q

What is the affect of increased FFAs?

A

Inhibits processing of acetyl CoA in Krebs cycle which further drives ketone production

22
Q

What is the effect of raised NADH?

A

Reduces gluconeogenesis

23
Q

What is the treatment for AKA?

A

Fluids
Dextrose slowly
Thiamine
Correct electrolyte imbalance - watch for refeeding syndrome

24
Q

What is the triad of Wernicke’s/ Korsakoff’s?

A

Gate ataxia or imbalance, ophthalmoplegia/ nystagmus and confusion

25
Q

What is the effect of lack of thiamine?

A

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)

26
Q

How much thiamine is stored in the liver?

A

5-10 day supply