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Imperial > 25. Psychiatric Disorders & Psychopharmacology > Flashcards

25. Psychiatric Disorders & Psychopharmacology Flashcards

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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
How can chronic alcohol abuse lead to dementia?
Chronic alcohol caused cortical atrophy and a loss of cerebral white matter --\> dementia
26
How can chronic alcohol abuse lead to ataxia?
Chronic alcohol can cause cerebellar cortex degeneration
27
State an important syndrome that is caused by chronic alcohol use.
Wernicke-Korsakoff Syndrome
28
Describe and explain how chronic alcoholism can cause this syndrome.
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
29
What are the chronic effects of alcohol on the liver?
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
30
How can chronic alcohol abuse cause hepatitis?
Chronic use of cytochrome P450 enzymes in metabolising alcohol can generate oxygen free radicals, which can cause mitochondrial injury and inflammatory changes
31
How can chronic alcohol abuse cause cirrhosis?
If the inflammation persists, fibroblasts could be recruited, which lay down connective tissue and cause cirrhosis
32
What are the potentially beneficial effects of chronic alcohol use at moderate levels?
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
Describe the chronic effects of alcohol on the GI tract.
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
Describe the chronic effects of alcohol on the endocrine system.
Alcohol can increase ACTH secretion (causes Cushing’s type appearance) Decrease testosterone
35
Why do you get the following symptoms when hungover: a. Nausea b. Headache c. Restlessness and muscle tremors d. Polyuria and polydipsia
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
What are the four main proteins that make up the GABA-A receptor?
GABA receptor protein Benzodiazepine receptor protein Barbiturate receptor protein Chloride channel protein
37
What protein links the GABA receptor proteins and the benzodiazepine receptor protein?
GABA modulin
38
Describe the normal physiological action of GABA.
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
Name a competitive antagonist of the GABA receptor protein.
Biciculline
40
Name a competitive antagonist of the benzodiazepine receptor protein.
Flumazenil
41
What are the two main effects of benzodiazepines that facilitate GABA neurotransmission?
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
What are the three main effects of barbiturates that facilitate GABA neurotransmission?
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
What is the key difference in the mechanism of action of barbiturates and benzodiazepines?
Benzodiazepines – increase the frequency of chloride channel opening Barbiturates – increase the duration of chloride channel opening
44
What is the relative difference in selectivity between barbiturates and benzodiazepines?
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
Name a barbiturate that is used as an anaesthetic.
Thiopentone
46
Name three barbiturates and benzodiazepines that are used as anti-convulsants.
Diazepam Clonazepam Phenobarbital
47
Name a benzodiazepine that is used as an anti-spastic.
Diazepam
48
What are two other clinical uses of benzodiazepines and barbiturates?
Anxiolytics Hypnotics
49
Define anxiolytic.
Remove anxiety without impairing mental or physical activity
50
Define sedative.
Reduce mental and physical activity without producing loss of consciousness
51
Define hypnotic.
Induces sleep
52
What structure is common to all barbiturates?
Six-membered ring (4 carbons and 2 nitrogens)
53
Barbiturates have been largely superseded by benzodiazepines. Which barbiturate is still used relatively commonly?
Amobarbital
54
What is the half-life of this drug?
20-25 hours
55
What are the unwanted effects of barbiturates?
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
What structure is common to all benzodiazepines?
They are tricyclic
57
What are the three key benzodiazepines?
Diazepam Oxazepam Temazepam
58
What is the difference between all the benzodiazepines that are in clinical use?
Their pharmacokinetics
59
Describe the administration of benzodiazepines.
Well absorbed per orally Peak plasma concentration after about 1 hour
60
When would you give IV benzodiazepines?
Treatment of status epilepticus
61
Describe the distribution of benzodiazepines.
Bind strongly to plasma proteins Highly lipid soluble
62
Describe the metabolism of benzodiazepines.
Extensively metabolised in the liver
63
Describe the excretion of benzodiazepines.
Excreted in the urine as glucuronide conjugates
64
Describe the duration of action of benzodiazepines.
Varies a lot This allows classification as short-acting and long-acting benzodiazepines
65
What makes long-acting benzodiazepines have a long duration of action?
They have slower metabolism They generate active metabolites
66
Name two short-acting benzodiazepines.
Oxazepam Temazepam
67
Name a long-acting benzodiazepine.
Diazepam
68
Describe the metabolism of oxazepam.
It is metabolised straight to its glucuronide conjugate (t1/2 = 8 hours)
69
Describe the metabolism of temazepam.
Metabolised to oxazepam and then to the glucuronide conjugate
70
Describe the metabolism of diazepam.
Metabolised via temazepam and oxazepam to the glucuronide conjugate Some diazepam is metabolised to nordiazepam and then oxazepam
71
Name three drugs that are used as anxiolytics.
General rule – long-acting benzodiazepines Diazepam Chlordiazepoxide Nitrazepam
72
Under what condition would you use a short-acting benzodiazepine as an anxiolytic?
Hepatic impairment – this means that the benzodiazepines and metabolised more slowly – drug of choice = oxazepam
73
Name two drugs that are used as sedatives/hypnotics.
General rule – short-acting benzodiazepines Oxazepam Temazepam
74
Name a long acting drug that might be used as a sedative/hypnotic.
Nitrazepam (t1/2 = 28 hours)
75
What are the advantages of benzodiazepines over barbiturates?
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
What are the unwanted effects of benzodiazepines?
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
Name a sedative/hypnotic that isn’t a benzodiazepine. What class of drug does this fall into?
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
What drug is used to control the physical symptoms of anxiety?
Propranolol
79
Name a new drug that has started being used as an anxiolytic.
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)

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