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Imperial > 25. Psychiatric Disorders & Psychopharmacology > Flashcards

25. Psychiatric Disorders & Psychopharmacology Flashcards

1
Q
A
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2
Q

What equation is used to determine the number of grams of alcohol per 100 ml?

A

ABV% x 0.78 = g/100 mL

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3
Q

What equation is used to calculate the number of units in a given volume of alcohol?

A

ABV% x volume (ml)/1000

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4
Q

What is the recommended weekly allowance of alcohol for men and women?

A

<14 units

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5
Q

What is the legal driving limit for alcohol?

A

80 mg/100 ml

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6
Q

Where is alcohol absorbed in the GI tract?

A

20% - stomach 80% - small intestine

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7
Q

What determines the speed of onset of the effects of alcohol?

A

The speed of onset of the effects of alcohol is proportional to the rate of gastric emptying

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8
Q

What proportion of alcohol is metabolised?

A

90% (the remaining 10% stays unmetabolised)

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9
Q

Out of the alcohol that is metabolised, what proportion is metabolised in the liver? Where does the rest of the metabolism take place?

A

85% - Liver 15% - Stomach

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10
Q

State two enzymes in the liver that are involved in metabolising alcohol.

A

Alcohol dehydrogenase Mixed function oxidase NOTE: these both convert alcohol to acetaldehyde

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11
Q

What is an important feature of mixed function oxidase?

A

It can be induced if you constantly expose yourself to alcohol – it is the reason for alcohol tolerance

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12
Q

Why would one large dose of alcohol give a higher plasma ethanol concentration than several small doses?

A

The liver enzymes that are responsible for metabolising alcohol are saturable Giving a large dose at once is more likely to saturate the enzymes

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13
Q

Describe the metabolism of alcohol in the stomach. How does this differ in women compared to men?

A

The stomach contains alcohol dehydrogenase, which is responsible for15% of alcohol metabolism Women have 50% less alcohol dehydrogenase in their stomachs than men

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14
Q

State one other reason why women, in general, can’t tolerate alcohol as well as men?

A

Women have a body water composition of about 50% Men have a body water composition of about 59-60% so a given amount of alcohol will be more dilute in a man compared to a woman

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15
Q

Describe the metabolism of acetaldehyde.

A

Acetaldehyde is toxic and must be metabolised further It is metabolised by aldehyde dehydrogenase to produce acetic acid

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16
Q

Name a drug that is used as an alcohol aversion therapy. Explain why it is used for this purpose.

A

Disulfiram – it is an aldehyde dehydrogenase inhibitor so it promotes the build up of acetaldehyde, which is responsible for most of the negative feelings associated with drinking

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17
Q

Why do some people (particularly Asians) tend to tolerate alcohol badly?

A

There is a common genetic polymorphism in the aldehyde dehydrogenase gene meaning that some people (particularly Asians) can’t convert acetaldehyde to acetic acid as efficiently so acetaldehyde builds up and makes them feel bad

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18
Q

Describe the pharmacological potency of alcohol.

A

Low pharmacological potency

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19
Q

What are the three major CNS targets of alcohol and what effectsdoes alcohol have on these targets?

A

GABA – alcohol increases allopregnenolone production (which facilitates the opening of chloride channels) – thus enhancing GABA action NMDA – alcohol decreases NMDA receptor function Ca2+ channels – alcohol reduces Ca2+ channel function meaning that there is less calcium influx, which negatively affects neurotransmitter exocytosis

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20
Q

Explain the counter-intuitive effects of alcohol on the central reward pathway.

A

GABA will reduce dopamine release and NMDA will increase dopaminerelease However, alcohol enhances GABA and reduces NMDA activity

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21
Q

Name a few specific parts of the brain that are affected by alcohol and state how they are responsible for features of alcohol intoxication.

A

Hypothalamus – controls appetite, emotions, temperature Reticular activating system – impairs consciousness Hippocampus – amnestic effects Cerebellum – movement and coordination Basal ganglia – perception of time

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22
Q

Describe and explain the effects of alcohol on cutaneous vasculature.

A

Alcohol causes vasodilation (this is thought to be due to acetaldehyde) It causes decrease calcium influx and increased prostaglandins –> vasodilation

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23
Q

Describe and explain the effects of alcohol of alcohol on heart rate.

A

Alcohol decreases the sensitivity of baroreceptors This means decreased baroreceptor firing –> decreased parasympathetic firing + decreased inhibition of sympathetic firing –> INCREASED HEART RATE

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24
Q

Describe the effects of alcohol on the endocrine system.

A

Alcohol inhibits vasopressin release from the neurohypophysis This means that alcohol is a powerful diuretic

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25
Q

How can chronic alcohol abuse lead to dementia?

A

Chronic alcohol caused cortical atrophy and a loss of cerebral white matter –> dementia

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26
Q

How can chronic alcohol abuse lead to ataxia?

A

Chronic alcohol can cause cerebellar cortex degeneration

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27
Q

State an important syndrome that is caused by chronic alcohol use.

A

Wernicke-Korsakoff Syndrome

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28
Q

Describe and explain how chronic alcoholism can cause this syndrome.

A

Wernicke-Korsakoff syndrome is caused by thiamine (vitamin B1) deficiency Chronic alcoholics tend to have a bad diet Thiamine is an important cofactor in the generation of ATP within cells The lack of thiamine impairs the Krebs’ cycle and leads to the build up of oxidative stress within the cells The oxidative stress can cause mitochondrial damage and apoptosis Wenicke’s Encephalopathy – caused by mitochondrial injury Korsakoff’s Psychosis – cell apoptosis in the brain – this is irreversible and the patient will probably die

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29
Q

What are the chronic effects of alcohol on the liver?

A

Alcohol metabolism in the liver uses up NAD+ so it depletes the liver’s NAD+ stores and increases NADH This inhibits beta-oxidation of lipids in the liver so you get an accumulation of fat in the liver It also interferes with the Krebs’ cycle because, without NAD+, glucose can’t be converted to pyruvate, and pyruvate can’t be converted to Acetyl CoA Pyruvate is converted to lactate Acetyl CoA is converted to ketone bodies

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30
Q

How can chronic alcohol abuse cause hepatitis?

A

Chronic use of cytochrome P450 enzymes in metabolising alcohol can generate oxygen free radicals, which can cause mitochondrial injury and inflammatory changes

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31
Q

How can chronic alcohol abuse cause cirrhosis?

A

If the inflammation persists, fibroblasts could be recruited, which lay down connective tissue and cause cirrhosis

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32
Q

What are the potentially beneficial effects of chronic alcohol use at moderate levels?

A

Decreased mortality from coronary artery disease Increase HDL Increase tPA/decreased platelet aggregation NOTE: it is thought that polyphenols are responsible for these effects

33
Q

Describe the chronic effects of alcohol on the GI tract.

A

Alcohol is partly metabolised in the GI tract to generate acetaldehyde (toxic) The acetaldehyde can directly damage the gastric mucosa leading to ulceration There is some evidence that alcohol can be carcinogenic in the stomach

34
Q

Describe the chronic effects of alcohol on the endocrine system.

A

Alcohol can increase ACTH secretion (causes Cushing’s type appearance) Decrease testosterone

35
Q

Why do you get the following symptoms when hungover: a. Nausea b. Headache c. Restlessness and muscle tremors d. Polyuria and polydipsia

A

a. Nausea Gastric irritation –> vagus –> vomiting centre b. Headache Vasodilation c. Restlessness and muscle tremors Rebound increase in CNS activity once the alcohol (depressant) wears off d. Polyuria and polydipsia Inhibition of ADH secretion

36
Q

What are the four main proteins that make up the GABA-A receptor?

A

GABA receptor protein Benzodiazepine receptor protein Barbiturate receptor protein Chloride channel protein

37
Q

What protein links the GABA receptor proteins and the benzodiazepine receptor protein?

A

GABA modulin

38
Q

Describe the normal physiological action of GABA.

A

GABA binds to the GABA receptor protein GABA modulin links the GABA receptor protein and the benzodiazepine receptor protein This results in opening of the chloride ion channel

39
Q

Name a competitive antagonist of the GABA receptor protein.

A

Biciculline

40
Q

Name a competitive antagonist of the benzodiazepine receptor protein.

A

Flumazenil

41
Q

What are the two main effects of benzodiazepines that facilitate GABA neurotransmission?

A

They facilitate the GABA-mediated opening of the chloride channel They facilitate the binding of GABA to its receptor protein (increase theaffinity of GABA to the GABA binding site) – this is reciprocated

42
Q

What are the three main effects of barbiturates that facilitate GABA neurotransmission?

A

They enhance the normal physiological action of GABA They enhance GABA binding to the GABA receptor protein (NOT reciprocated) At higher concentrations, barbiturates can have a direct action on the chloride channel

43
Q

What is the key difference in the mechanism of action of barbiturates and benzodiazepines?

A

Benzodiazepines – increase the frequency of chloride channel opening Barbiturates – increase the duration of chloride channel opening

44
Q

What is the relative difference in selectivity between barbiturates and benzodiazepines?

A

Barbiturates are LESS selective This may explain why barbiturates induce surgical anaesthesia and why barbiturates are less safe than benzodiazepines NOTE: barbiturates also reduce excitatory transmission

45
Q

Name a barbiturate that is used as an anaesthetic.

A

Thiopentone

46
Q

Name three barbiturates and benzodiazepines that are used as anti-convulsants.

A

Diazepam Clonazepam Phenobarbital

47
Q

Name a benzodiazepine that is used as an anti-spastic.

A

Diazepam

48
Q

What are two other clinical uses of benzodiazepines and barbiturates?

A

Anxiolytics Hypnotics

49
Q

Define anxiolytic.

A

Remove anxiety without impairing mental or physical activity

50
Q

Define sedative.

A

Reduce mental and physical activity without producing loss of consciousness

51
Q

Define hypnotic.

A

Induces sleep

52
Q

What structure is common to all barbiturates?

A

Six-membered ring (4 carbons and 2 nitrogens)

53
Q

Barbiturates have been largely superseded by benzodiazepines. Which barbiturate is still used relatively commonly?

A

Amobarbital

54
Q

What is the half-life of this drug?

A

20-25 hours

55
Q

What are the unwanted effects of barbiturates?

A

Low safety margin (overdose can be lethal) Alters natural sleep (reduced REM) Enzyme inducers Potentiate the action of other CNS depressants (e.g. alcohol) Tolerance Dependence

56
Q

What structure is common to all benzodiazepines?

A

They are tricyclic

57
Q

What are the three key benzodiazepines?

A

Diazepam Oxazepam Temazepam

58
Q

What is the difference between all the benzodiazepines that are in clinical use?

A

Their pharmacokinetics

59
Q

Describe the administration of benzodiazepines.

A

Well absorbed per orally Peak plasma concentration after about 1 hour

60
Q

When would you give IV benzodiazepines?

A

Treatment of status epilepticus

61
Q

Describe the distribution of benzodiazepines.

A

Bind strongly to plasma proteins Highly lipid soluble

62
Q

Describe the metabolism of benzodiazepines.

A

Extensively metabolised in the liver

63
Q

Describe the excretion of benzodiazepines.

A

Excreted in the urine as glucuronide conjugates

64
Q

Describe the duration of action of benzodiazepines.

A

Varies a lot This allows classification as short-acting and long-acting benzodiazepines

65
Q

What makes long-acting benzodiazepines have a long duration of action?

A

They have slower metabolism They generate active metabolites

66
Q

Name two short-acting benzodiazepines.

A

Oxazepam Temazepam

67
Q

Name a long-acting benzodiazepine.

A

Diazepam

68
Q

Describe the metabolism of oxazepam.

A

It is metabolised straight to its glucuronide conjugate (t1/2 = 8 hours)

69
Q

Describe the metabolism of temazepam.

A

Metabolised to oxazepam and then to the glucuronide conjugate

70
Q

Describe the metabolism of diazepam.

A

Metabolised via temazepam and oxazepam to the glucuronide conjugate Some diazepam is metabolised to nordiazepam and then oxazepam

71
Q

Name three drugs that are used as anxiolytics.

A

General rule – long-acting benzodiazepines Diazepam Chlordiazepoxide Nitrazepam

72
Q

Under what condition would you use a short-acting benzodiazepine as an anxiolytic?

A

Hepatic impairment – this means that the benzodiazepines and metabolised more slowly – drug of choice = oxazepam

73
Q

Name two drugs that are used as sedatives/hypnotics.

A

General rule – short-acting benzodiazepines Oxazepam Temazepam

74
Q

Name a long acting drug that might be used as a sedative/hypnotic.

A

Nitrazepam (t1/2 = 28 hours)

75
Q

What are the advantages of benzodiazepines over barbiturates?

A

Wide margin of safety  Overdose causes prolonged sleep (but this is rousable)  Flumezanil can be given IV if a patient has overdosed Mild effect on REM sleep Do NOT enhance liver enzymes

76
Q

What are the unwanted effects of benzodiazepines?

A

Sedation Confusion Ataxia Potentiate other CNS depressants (e.g. alcohol) Tolerance Dependence Free plasma concentration of benzodiazepines can be increased by giving aspirin and heparin

77
Q

Name a sedative/hypnotic that isn’t a benzodiazepine. What class of drug does this fall into?

A

Zopiclone – this is a cyclopyrrolone and it’s short-acting (t1/2 = 5 hours) NOTE: it acts on the benzodiazepine receptor but it is not a benzodiazepine This has fewer hangover effects but dependency is still an issue

78
Q

What drug is used to control the physical symptoms of anxiety?

A

Propranolol

79
Q

Name a new drug that has started being used as an anxiolytic.

A

Buspirone – 5HT1A agonist This has relatively few side effects and causes less sedation than benzodiazepines Downside: slow onset of action (maximal anxiolytic effects are not seen for a number of days/weeks)

Imperial (23 decks)

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