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Psychopharmacology Flashcards

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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
What are the non-neurological effects of dopamine antagonists?
Increased prolactin with consequent breast swelling and galactorrhea Through blockage of the dopaminergic tuberoinfundibular pathway
26
What are the extrapyramidal effects of dopamine antagonists?
Motor symptoms: - tremor - rigidity - dystonia - tardive dyskinesia
27
Ways to control the motor symptoms of dopamine antagonists
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
28
D2 antagonists have a significant effect on negative symptoms of schizophrenia TRUE or FALSE
FALSE D2 antagonists have no significant effect of negative symptoms
29
Drugs targeting the negative symptoms of psychosis
Second generation of antipsychotics Atypical antipsychotics Antagonise the 5HT2A receptors
30
Example of atypical antipsychotics
Olanzapine Risperidone Clozapine
31
Mechanism of action of Clozapine
5HT2A antagonist No extrapyrimidal effect
32
Cause of schizophrenia
No clear cause There is a significant genetic component (10-15% of first-degree relatives share the condition)
33
What do PET scans of schizophrenics show?
Increased D2 receptors in the nucleus accumbens
34
Apart from the negative effects of dopamine blockade in the mesolimbic and hypothalamic axes, what neurological side-effects result from blocking the nigrostriatal pathway?
Apathy Depression Decreased initiative
35
Which separate receptors do antipsychotic drugs have effects on?
a-adrenoceptors: hypotension Muscarinic receptors: urinary retention H1 receptors: sedation 5-HT receptors: weight gain
36
Why do antipsychotic drugs have effects on many receptors?
Because their structure targets lots of receptors
37
What are typical antipsychotics?
Those that inhibit the D2 receptors Aim to control the positive symptoms
38
What are atypical antipsychotics?
Those that target the D2 and 5HT2A receptors Negative symptoms
39
Why do atypical antipshycotics have less of extrapyramidal effects?
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
Importance of neurosis
Not as serious as psychosis, but has a high social cost due to its prevalence
41
Why are emotions important in humans?
Represents an important mechanism that makes sure we make correct decisions
42
What are the two main types of neurosis?
Mod disorders Anxiety disorders
43
What is the treatment of neurosis conditions?
Support is the first and main treatment Pharmacological approaches are second line
44
What two categories can anxiety disorders be split into?
Specific Generalised
45
What are the two types of symptoms of anxiety?
Psychological symptoms Physical symptoms
46
Subtypes of specific anxiety disorder
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
What is generalised anxiety disorder?
Not related to a specific fear Associated with insomnia
48
What part of the brain is associated with fear?
Fear stems from the amygdala Hyperactivated in fear
49
How can the amygdala be targeted in anxiety?
Inhibition of hyperactivation of the amygdala through hyperpolarisation of the cell Hyperpolarisation achieved through opening of chloride channels
50
Drug targeting chloride channels of the amygdala
Benzodiazepine
51
Mechanism of action of Benzodiazepine
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
Other drugs separate to benzodiazepines also causing anxiolytic effects
Serotonin agonists B-adrenoceptor antagonists Antihistamines Barbituates
53
Which serotonin receptors are targeted in anxiety?
5-HT1a
54
Where do 5HT1a receptors occur in the brain?
Cerebral cortex Amygdala
55
Nature of 5-HT1a receptors
Auto-inhibitory Result in decreased firing
56
How are serotonin receptors targeted in anxiety?
5-HT1a agonists Activate the presynaptic serotonin receptors Particularly in the dorsal raphe nucleus of the midbrain
57
How do b-adrenoceptor antagonists help in anxiety?
Reduce some of the peripheral manifestations of anxiety
58
Mechanism of action of barbituates
Increase channel opening of GABAa beyond that seen with GABA istelf
59
Use of Barbituates
Clinical use has been severely restricted due to their low TI and dependence Still used in anaesthesia and epilepsy
60
What are hypnotics?
Drugs used to treat insomnia
61
Link between anxiety and insomnia
Both can be treated with CNS depressants Both can be treated using the same drugs in different concentrations
62
Disadvantage of benzodiazepines
Due to brain plasticity, tolerance to benzodiazepines develops quickly Withdrawal from drug leads to worsening symptoms due to the compensatory mechanisms
63
When are benzodiazepines used?
Short term conditions - pre-surgery anxiety - grief reaction - epilepsy
64
What is the best therapy for anxiety patients?
Cognitive behaviour therapy
65
What are the two types of mood disorders?
Unipolar depression Bipolar depression
66
Characteristics of depression
Low mood No pleasure, appetite or sexual drive Longer than 2 months
67
Subtypes of depression
Seasonal depression - related to season Postpartum depression Endogenous depression - nothing is wrong, but don't know why
68
Neurological basis behind depression
Poorly understood Monoamine theory explains that depression is caused by a functional deficit of noradrenaline and 5-HT in the forebrain
69
Evidence backing the monamine theory of depression
Inhibition of NA or 5-HT reuptake improves mood Inhibition of MAO improves mood Drugs which deplete monoamine stores cause depression
70
Evidence against the monamine theory of depression
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
Which part of the brain contains serotonin receptors important for mood?
Raphe nucleus
72
What are the 3 main types of antidepressants?
Those that inhibit the reuptake of monoamines MAO inhibitors Atypical
73
Targets for preventing the uptake of serotonin
Uptake 1 transporter Selective serotonin transporter
74
Targets for preventing the uptake of noradrenaline
Uptake 1 transporter
75
Drugs that target the uptake 1 transporter
Tricyclic antidepressants
76
Drugs that target the selective serotonin transporters
Selective serotonin receptor inhibitors
77
What is the advantage of SSRIs over TCADs?
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
What is the goal of drugs inhibiting the reuptake of serotonin and noradrenaline?
Increases the concentration of these transmitters in the synaptic cleft Increases stimulation of postsynaptic transmission
79
What is the goal of MAO inhibitors?
Increase the concentration of serotonin and noradrenaline in the synaptic cleft Through oxidation
80
What is the major side-effect of MAO inhibitors?
Cheese reaction
81
Explain what is meant by the cheese reaction
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
What is the difference between older and newer MAO inhbitors?
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
What are atypical antidepressants?
Combine actions of MAOIs and reuptake inhibitors Less well characterised mechanism of action
84
What is the main drug used to treat bipolar depression?
Lithium Prophylaxis
85
Describe the discovery of lithium chloride as a therapy for bipolar depression
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
Mechanism of action of lithium chloride
Inhibits the formation of IP3 Modifies the membrane potential an ionic balance
87
Why must administration of lithium chloride be carefully controlled?
Patients can overdose Increased incidence of diabetes in individuals
88
Examples of psychomotor stimulants
Amphetamines MDMA Cocaine
89
Mechanisms of action of amphetamines and cocaine
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
Actions of amphetamines and cocaine
Euphoria Elation Improved concentration Appetite suppression Inhibition of REM sleep
91
Are the physical withdrawal symptoms of cocaine and amphetamines pronounced?
No
92
What pathway is particularly involved in the action of amphetamines and cocaine
Dopamine pathways
93
Mechanisms of action of methylxanthines
Inhibits PDE, increasing the concentration of cAMP Potentiates responses mediated by b-adrenoceptors and D1 receptors
94
What causes the behavioural effects of methylxanthines?
Antagonism on adenosine receptors
95
What is a unique feature of caffeine?
On top of inhibiting PDE, it also enhances release of NTs by blocking presynaptic receptors
96
Uses of methylxanthines
Asthma

Pharmacology (13 decks)

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