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Psychopharmacology Flashcards

1
Q

What two classes can mental illness be differentiated into?

A

Psychosis

Neurosis

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2
Q

Characteristics of psychosis

A

Less common but more serious

Characterised by a radical loss of touch with reality

The patient has no insight into their problem

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3
Q

Characteristic of neurosis

A

Common mental health problems

Severe forms of normal emotional experiences like depression, anxiety or panic

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4
Q

What are hallucinations?

A

When someone sees, hears, smells, tastes or feels things that don’t exist outside their mind

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5
Q

What are delusions?

A

A person has an unshakeable belief in something untrue which cannot be explained by cultural beliefs

Can be persecutory or grandiose

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6
Q

What can the symptoms of psychosis be split into?

A

Positive - change in behaviour or thoughts; hallucinations or delusions

Negative - withdrawal of lack of social function; reduction in speech or social withdrawal

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7
Q

What are the causes of psychosis?

A

Psychological causes

General medical causes

Drug induced

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8
Q

Historical methods of treating psychosis

A

Shock therapy

Psychosurgery

Fever therapy to treat neurosyphilis

Insulin induced coma and convulsion

Electroconvulsive shock therapy

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9
Q

When was the birth of psychopharmacology?

A

1950s

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10
Q

Describe the development of the first anti-psychotic drug

A

Promethazine was an anti-histamine causing sedation

Scientists argued that modifying this drug would remove its effect on sedation, but would make positive symptoms decrease since patients were less sensitive to external stimuli

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11
Q

How was Promethazine modified to test its effect as an anti-psychotic?

A

Chemically altered through addition of chlorine

Make Chlorpromazine

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12
Q

Was Chlorpromazine successful?

A

Yes

Induced a different type of sedation that made patients less reactive to external stimuli

Decreasing hallucinations and delusions

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13
Q

What is Chlorpromazine an example of?

A

Class I, typical antipsychotic

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14
Q

Mechanism of action of Chlorpromazine

A

Binds to dopamine 2 receptor

Blocks dopamine - dopamine antagonist

Causing a sedative-like effect on patients

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15
Q

What is something about the mechanism of action of Chlorpromazine the clinicians did not notice?

A

Promethazine causes sedation through acting on the histamine 1 receptor

When modifying this compound, the target receptor was also changed

Chlorpromazine was shown to act through the D2 receptor

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16
Q

Describe the dopaminergic hypothesis of psychosis

A

Hypothesis that believes that dopamine causes psychosis

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17
Q

What are the two main factors relating dopamine to psychosis?

A

Dopamine antagonists reduce signs and symptoms of psychosis

Drugs that enhance the release of dopamine in the brain can induce hallucination

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18
Q

Example of a drug that induces release of dopamine in the brain

A

Amphetamine

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19
Q

What did the dopamine hypothesis of psychosis lead to?

A

The development of receptor antagonists for treatment of psychosis

Especially D2 receptor antagonists

Chlorpromazine, Haloperidol

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20
Q

What is the problem with targeting dopamine as a therapy for psychosis?

A

Dopamine has actions on a lot of different neural pathways

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21
Q

What are the brain’s main dopaminergic pathways?

A

Mesolimbic: hyperactive in schizophrenia, leads to the positive symptoms

Mesocortical: hypoactive in schizophrenia, leads to the negative symptoms

Nigrostriatal pathway: extrapyramidal motor control

Hypothalamus-pituitary pathway: hypothalamus inhibits prolactin through dopamine release

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22
Q

What dopaminergic pathway do you want to target in psychosis?

A

Mesolimbic pathway

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23
Q

Components of the mesolimbic pathway

A

Dopaminergic neuron originates in the substantia nigra and synapses on the nucleus accumbens

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24
Q

Are dopamine antagonist effects used for psychosis therapy limited to target the mesolimbic pathway?

A

No

Their effects on other brain pathways lead to unwanted side-effects

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25
Q

What are the non-neurological effects of dopamine antagonists?

A

Increased prolactin with consequent breast swelling and galactorrhea

Through blockage of the dopaminergic tuberoinfundibular pathway

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26
Q

What are the extrapyramidal effects of dopamine antagonists?

A

Motor symptoms:

  • tremor
  • rigidity
  • dystonia
  • tardive dyskinesia
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27
Q

Ways to control the motor symptoms of dopamine antagonists

A

The balance between cholinergic and dopamine transmission is important in the extrapyramidal system

Increased acetylcholine in relation to dopamine further worsens the motor side-effect presentation of D2 antagonists

Anticholinergic drugs can reduce the extrapyramidal side effects of D2 antagonists

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28
Q

D2 antagonists have a significant effect on negative symptoms of schizophrenia

TRUE or FALSE

A

FALSE

D2 antagonists have no significant effect of negative symptoms

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29
Q

Drugs targeting the negative symptoms of psychosis

A

Second generation of antipsychotics

Atypical antipsychotics

Antagonise the 5HT2A receptors

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30
Q

Example of atypical antipsychotics

A

Olanzapine

Risperidone

Clozapine

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31
Q

Mechanism of action of Clozapine

A

5HT2A antagonist

No extrapyrimidal effect

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32
Q

Cause of schizophrenia

A

No clear cause

There is a significant genetic component (10-15% of first-degree relatives share the condition)

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33
Q

What do PET scans of schizophrenics show?

A

Increased D2 receptors in the nucleus accumbens

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34
Q

Apart from the negative effects of dopamine blockade in the mesolimbic and hypothalamic axes, what neurological side-effects result from blocking the nigrostriatal pathway?

A

Apathy

Depression

Decreased initiative

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35
Q

Which separate receptors do antipsychotic drugs have effects on?

A

a-adrenoceptors: hypotension

Muscarinic receptors: urinary retention

H1 receptors: sedation

5-HT receptors: weight gain

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36
Q

Why do antipsychotic drugs have effects on many receptors?

A

Because their structure targets lots of receptors

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37
Q

What are typical antipsychotics?

A

Those that inhibit the D2 receptors

Aim to control the positive symptoms

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38
Q

What are atypical antipsychotics?

A

Those that target the D2 and 5HT2A receptors

Negative symptoms

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39
Q

Why do atypical antipshycotics have less of extrapyramidal effects?

A

5HT2A inhibits the release of dopamine in parts of the brain that need the neurotransmitter

Inhibiting 5HT2A therefore increases the concentration of dopamine at this site

Drugs which block both 5HT2A and D2 therefore cause less side-effects

40
Q

Importance of neurosis

A

Not as serious as psychosis, but has a high social cost due to its prevalence

41
Q

Why are emotions important in humans?

A

Represents an important mechanism that makes sure we make correct decisions

42
Q

What are the two main types of neurosis?

A

Mod disorders

Anxiety disorders

43
Q

What is the treatment of neurosis conditions?

A

Support is the first and main treatment

Pharmacological approaches are second line

44
Q

What two categories can anxiety disorders be split into?

A

Specific

Generalised

45
Q

What are the two types of symptoms of anxiety?

A

Psychological symptoms

Physical symptoms

46
Q

Subtypes of specific anxiety disorder

A

Phobia - patient is fearful of a specific thing

Panic disorder - patient is fearful of death

OCD - patient believes something will happen if they don’t perform a specific task

PTSD - experiences of a severe condition causes false memories leading to stress

47
Q

What is generalised anxiety disorder?

A

Not related to a specific fear

Associated with insomnia

48
Q

What part of the brain is associated with fear?

A

Fear stems from the amygdala

Hyperactivated in fear

49
Q

How can the amygdala be targeted in anxiety?

A

Inhibition of hyperactivation of the amygdala through hyperpolarisation of the cell

Hyperpolarisation achieved through opening of chloride channels

50
Q

Drug targeting chloride channels of the amygdala

A

Benzodiazepine

51
Q

Mechanism of action of Benzodiazepine

A

Cholinergic GABA channels cause cell hyperpolarisation

Benzodiazepines bind on a separate receptor next to the GABA binding site to increase the affinity of GABAa for its receptor

52
Q

Other drugs separate to benzodiazepines also causing anxiolytic effects

A

Serotonin agonists

B-adrenoceptor antagonists

Antihistamines

Barbituates

53
Q

Which serotonin receptors are targeted in anxiety?

A

5-HT1a

54
Q

Where do 5HT1a receptors occur in the brain?

A

Cerebral cortex

Amygdala

55
Q

Nature of 5-HT1a receptors

A

Auto-inhibitory

Result in decreased firing

56
Q

How are serotonin receptors targeted in anxiety?

A

5-HT1a agonists

Activate the presynaptic serotonin receptors

Particularly in the dorsal raphe nucleus of the midbrain

57
Q

How do b-adrenoceptor antagonists help in anxiety?

A

Reduce some of the peripheral manifestations of anxiety

58
Q

Mechanism of action of barbituates

A

Increase channel opening of GABAa beyond that seen with GABA istelf

59
Q

Use of Barbituates

A

Clinical use has been severely restricted due to their low TI and dependence

Still used in anaesthesia and epilepsy

60
Q

What are hypnotics?

A

Drugs used to treat insomnia

61
Q

Link between anxiety and insomnia

A

Both can be treated with CNS depressants

Both can be treated using the same drugs in different concentrations

62
Q

Disadvantage of benzodiazepines

A

Due to brain plasticity, tolerance to benzodiazepines develops quickly

Withdrawal from drug leads to worsening symptoms due to the compensatory mechanisms

63
Q

When are benzodiazepines used?

A

Short term conditions

  • pre-surgery anxiety
  • grief reaction
  • epilepsy
64
Q

What is the best therapy for anxiety patients?

A

Cognitive behaviour therapy

65
Q

What are the two types of mood disorders?

A

Unipolar depression

Bipolar depression

66
Q

Characteristics of depression

A

Low mood

No pleasure, appetite or sexual drive

Longer than 2 months

67
Q

Subtypes of depression

A

Seasonal depression - related to season

Postpartum depression

Endogenous depression - nothing is wrong, but don’t know why

68
Q

Neurological basis behind depression

A

Poorly understood

Monoamine theory explains that depression is caused by a functional deficit of noradrenaline and 5-HT in the forebrain

69
Q

Evidence backing the monamine theory of depression

A

Inhibition of NA or 5-HT reuptake improves mood

Inhibition of MAO improves mood

Drugs which deplete monoamine stores cause depression

70
Q

Evidence against the monamine theory of depression

A

Some drugs have antidepressant effect without affecting NA/5-HT transmission

There is a 2-4 week delay in the clinical action of antidepressants despite immediate effects on neurotransmission

71
Q

Which part of the brain contains serotonin receptors important for mood?

A

Raphe nucleus

72
Q

What are the 3 main types of antidepressants?

A

Those that inhibit the reuptake of monoamines

MAO inhibitors

Atypical

73
Q

Targets for preventing the uptake of serotonin

A

Uptake 1 transporter

Selective serotonin transporter

74
Q

Targets for preventing the uptake of noradrenaline

A

Uptake 1 transporter

75
Q

Drugs that target the uptake 1 transporter

A

Tricyclic antidepressants

76
Q

Drugs that target the selective serotonin transporters

A

Selective serotonin receptor inhibitors

77
Q

What is the advantage of SSRIs over TCADs?

A

SSRIs specifically target serotonin

Not many side-effects, whereas people can overdose on TCADs

Also works for anxiety disorders

Less side-effects due to fewer effects on off-target receptors

78
Q

What is the goal of drugs inhibiting the reuptake of serotonin and noradrenaline?

A

Increases the concentration of these transmitters in the synaptic cleft

Increases stimulation of postsynaptic transmission

79
Q

What is the goal of MAO inhibitors?

A

Increase the concentration of serotonin and noradrenaline in the synaptic cleft

Through oxidation

80
Q

What is the major side-effect of MAO inhibitors?

A

Cheese reaction

81
Q

Explain what is meant by the cheese reaction

A

Tyramine is a naturally occuring amine which causes hypertension

The liver contains a lot of MAO to destroy tyramine

When taking MAO inhibitors, this is inhibited too

Patients with MAO inhibitors cannot consume wine or cheese, because they will develop hypertension

82
Q

What is the difference between older and newer MAO inhbitors?

A

Older MAOIs bind covalently and therefore have a longer duration of action

Newer MAOIs are more selective to MAO-A and therefore have fewer side effects

83
Q

What are atypical antidepressants?

A

Combine actions of MAOIs and reuptake inhibitors

Less well characterised mechanism of action

84
Q

What is the main drug used to treat bipolar depression?

A

Lithium

Prophylaxis

85
Q

Describe the discovery of lithium chloride as a therapy for bipolar depression

A

Hypertension was a big issue in the mid-1900s

Scientists wanted to replace salt with Lithium Chloride

They noticed that upon consumption, people looked seemed relaxed

They tried to see its effect on bipolar through an injection

This was shown to be effective at reducing episodes of mania

86
Q

Mechanism of action of lithium chloride

A

Inhibits the formation of IP3

Modifies the membrane potential an ionic balance

87
Q

Why must administration of lithium chloride be carefully controlled?

A

Patients can overdose

Increased incidence of diabetes in individuals

88
Q

Examples of psychomotor stimulants

A

Amphetamines

MDMA

Cocaine

89
Q

Mechanisms of action of amphetamines and cocaine

A

Raise the synaptic concentrations of NA, DA and 5-HT

Through:

  • stimulation of release into synaptic cleft
  • inhibition of neuronal uptake
  • inhibition of MAO
  • inhibition of vesicular uptake
90
Q

Actions of amphetamines and cocaine

A

Euphoria

Elation

Improved concentration

Appetite suppression

Inhibition of REM sleep

91
Q

Are the physical withdrawal symptoms of cocaine and amphetamines pronounced?

A

No

92
Q

What pathway is particularly involved in the action of amphetamines and cocaine

A

Dopamine pathways

93
Q

Mechanisms of action of methylxanthines

A

Inhibits PDE, increasing the concentration of cAMP

Potentiates responses mediated by b-adrenoceptors and D1 receptors

94
Q

What causes the behavioural effects of methylxanthines?

A

Antagonism on adenosine receptors

95
Q

What is a unique feature of caffeine?

A

On top of inhibiting PDE, it also enhances release of NTs by blocking presynaptic receptors

96
Q

Uses of methylxanthines

A

Asthma

Pharmacology (13 decks)

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