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Year 2 > CLASP-Alcohol > Flashcards

CLASP-Alcohol Flashcards

1
Q

How many units is considered binge drinking?

A

6 units

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2
Q

What is the recommended daily allowance for mothers breastfeeding?

A

no more than 2 units per day

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3
Q

How do you calculate units?

A

e.g. 70cl of 40% vodka:

40/1000 x 700 = 28 units.

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4
Q

What is the drink driving limit in scotland?

A

10.9mM e.g. 50mg per 100ml of blood.

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5
Q

Does alcohol have a positive or negative inotropic effect on the cardiovascular system? And what does this mean?

A

NEGATIVE- has decreased contractility of the heart meaning that the heart has to beat faster.

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6
Q

What is the effect of alcohol on the CNS?

A

it is a CNS depressant

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7
Q

How does alcohol depress the CNS?

A

it increases the levels of GABBA which is an inhibitor of neurotransmitters.

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8
Q

What is the pathogenesis of alcoholic hepatitis?

A

parenchymal inflammation and hepatocyte damage. Scar tissue replaces healthy tissue (fibrosis).

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9
Q

What cells mediate fibrosis in the liver?

A

hepatic stellate cells.

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10
Q

Is alcoholic hepatitis reversible?

A

yes- with abstinence

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11
Q

What are the features of portal hypertension?

A

variceal bleeding, ascites, splenomegaly, peritonitis, hepatic encephalopathy

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12
Q

What are the features of alcoholic ketoacidosis?

A

low sugar, high glucagon, high ketones (beta-hydroxybutyrate) and excess NADH.

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13
Q

What does excess NADH cause?

A

it inhibits gluconeogenesis by preventing oxidation of lactate to pyruvate and will cause lactate to accumulate. the consequences may be hypoglycaemia and lactic acidosis. it also inhibits fatty acid oxidation which generated NADH for ATP but NADH needs are already met by ethanol metabolism. this is why triacylglycerols accumulate in the liver to cause a fatty liver.

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14
Q

Why does Wernickes syndrome occur?

A

Thiamine deficiency

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15
Q

What are the features of Wernickes syndrome?

A

known alcoholic, that is a bit shaky with jerky eye movements but can hold a conversation.

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16
Q

what is the treatment for Wernickes?

A

Thiamine replacement.

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17
Q

What is the risk associated with Wernickes?

A

it can lead to Korsakoff syndrome

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18
Q

What is the triad in Wernickes-Korsakoff syndrome?

A

Ocular dysfunction (nystagmus), confusion and ataxic gait.

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19
Q

what is the treatment for Wernickes-Korsakoff syndrome?

A

Thiamine replacement over 5 days.

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20
Q

What is Korsakoff syndrome?

A

it is a progression from Wernickes-Korsakoff syndrome and involves cerebral atrophy which is irreversible.

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21
Q

What are the symptoms of Korsakoff syndrome?

A

Anterograde amnesia- inability to retain new information.
Retrograde amnesia- episodic memory.
Confabulation- replacement of new memories with those that are false.

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22
Q

What cardiomyopathy is most related to alcoholism

A

dilated cardiomyopathy

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23
Q

What arrhythmias are most common in acute alcoholic episodes?

A

AF and SVT.

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24
Q

What arrhythmia is most associated with Holiday Heart Syndrome?

A

SVT

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25
Q

What is holiday heart syndrome?

A

Binge drinking on an otherwise healthy heart causing abnormal heart rhythms (SVT)

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26
Q

What is the treatment of Holiday Heart?

A

nothing- it spontaneously resolves on its own

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27
Q

What is Steatohepatitis and how does it happen?

A

it is a fatty liver caused by excess NADH (inhibits fatty acid oxidation)

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28
Q

What is a clinical sign of thiamine deficiency?

A

Beriberi syndrome

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29
Q

What is Wet Beriberi syndrome?

A

Affects the CVS- causes fast HR, SOB and leg swelling

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30
Q

What is dry Beriberi syndrome?

A

affects the CNS- causes numbness of the hands and feet, confusion, trouble moving legs and pain.

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31
Q

What is the most common lobe affected by aspiration pneumonia?

A

right lower lobe.

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32
Q

What are the organisms commonly found in aspiration pneumonia?

A

Klebsiella, strep penumoniae, staph aureus, and haemophilus influenzae.

33
Q

What is honeycombing?

A

it is a characteristic of aspiration pneumonia which is partially digested cell walls.

34
Q

What is the treatment for aspiration pneumonia?

A

Co-amoxiclav and metronidazole

35
Q

What is the treatment for methanol posioning?

A

Ethanol and dialysis

36
Q

What is Veisalgia Cephalgia?

A

hangover headache which can occur from 4 to 24 hours after drinking.

37
Q

What are Congeners?

A

they are a by-product of fermentation that add taste and aroma to alcoholic drinks. They are more present in dark liquors and red wine.

38
Q

What is Dupeytren’s Contracture?

A

benign fibrosis of palmar fascia of the fingers.

39
Q

What are Grey Turner’s and Cullen’s sign indicative of?

A

Pancreatitis

40
Q

What is the management of alcohol withdrawal?

A

Benzodiazepines (diazepam)

41
Q

What is Antabuse (disulfriam) used for?

A

Prescribed to recovering alcoholics to help them abstain from drinking. if they drink alcohol when taking this it will make them sick.

42
Q

Why is bicarbonate low in methanol poisoning?

A

because methanol produces a high acidic load which uses up all the bicarbonate.

43
Q

What is used in acute cases to treat alcoholics?

A

Pabrinex (thiamine) and Diazepam

44
Q

What are the markers of liver damage?

A

ALT, AST, ALP, GGT

45
Q

What are markers of liver function?

A

bilirubin, albumin, prothrombin time

46
Q

What does an isolated raised GGT show?

A

That the cause is alcohol

47
Q

What is the embryological remnant of the ligamentum teres?

A

Umbilical vein

48
Q

What borders the hepatocytes?

A

Space of Disse

49
Q

What 5 structures exist in the portal tract/triad?

A

proper hepatic artery, hepatic vein, bile ducts, lymphatics & vagus nerve

50
Q

What is the oxidation sequence of alcohol?

A

Ethanol-> acetylaldehyde -> acetate

51
Q

What are the enzymes involved in the oxidation of alcohol?

A

alcohol dehydrogenase and aldehyde dehydrogenase.

52
Q

Where is ethanol first metabolised?

A

in the stomach.

53
Q

What effect does food have on alcohol absorption?

A

Food increases portal flow which causes faster metabolism of ethanol, however, it also slows gastric emptying and can bind alcohol to its constituents slowing down absorption.

54
Q

Where does metabolism of alcohol occur?

A

majority is in the liver which small amounts in the pancreas and brain.

55
Q

Does alcohol easily cross the plasma membrane?

A

yes- it is amphipathic (has both hydrophobic and hydrophillic qualities)

56
Q

What is the breakdown of methanol?

A

Formaldehyde-> formic acid -> acidosis (causing blindness and renal failure)

57
Q

Why is there competitive inhibition of methanol and ethanol?

A

Because they are both metabolised by alcohol dehydrogenase.

58
Q

Where is alcohol absorbed?

A

Mostly in the small intestine (80%) with the rest in the stomach.

59
Q

Are aerated drinks absorbed quicker?

A

Yes

60
Q

Which drugs cause faster alcohol absorption?

A

Antihistamines, domperidone, metoclopramide.

61
Q

Is alcohol involved in lipid synthesis?

A

Yes- it converts NAD to NADH which stimulates lipid synthesis.

62
Q

What are the effects on glucose when drinking alcohol?

A

alcohol affects glucose metabolism causing hypoglycaemia.

63
Q

What are the alternative pathways that are activated when drinking alcohol?

A

MEOS & CP450

64
Q

What is the effect of the CP450?

A

Releases free radicals that damages tissues and exacerbates oxidative stress.

65
Q

What enzyme are south east asians commonly deficient in?

A

Aldehyde dehydrogenase

66
Q

At what blood alcohol level is there blurred vision, falls and heightened emotional responses?

A

100-200

67
Q

At what blood alcohol level are you worried about them falling into a coma?

A

300-400

68
Q

What blood alcohol level is fatal and why?

A

500+. they lose control of basic functions resulting in respiratory depression/arrest.

69
Q

How do people “build a tolerance” to alcohol?

A

thought to be due to the upregulation of alcohol dehydrogenase

70
Q

At what rate is alcohol removed from the blood?

A

15mg/100ml/hr

71
Q

Why do women get drunk faster than men?

A

they have more lean mass (fat) and blood level for their BMI and have lower levels of alcohol dehydrogenase.

72
Q

What types of cancers have an increased risk via alcohol?

A

Breast, bowel, mouth/throat/oesophageal, stomach and liver.

73
Q

What screening tool is used for those who are alcohol dependent?

A

AUDIT

74
Q

What are delirium tremors and when do they occur?

A

72-96 hours after the last drink. they are confusion, hallucinations, tachycardia, sweating, hypertension, body tremors and seizures.

75
Q

What is the treatment of DT’s?

A

pabrinex and benzodiazepines

76
Q

What is the breakdown of haem?

A

Haem -> iron + biliverdin -> unconjugated bilirubin

77
Q

What enzyme breaks down haem to biliverdin?

A

Haem oxygenase

78
Q

What enzyme breaks down biliverdin to bilirubin?

A

biliverdin reductase

Year 2 (10 decks)

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