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Pharma ESA4 > Psychiatric Disease > Flashcards

Psychiatric Disease Flashcards

1
Q

What are the general actions of CNS drugs?

A

Agonists/antagonists of neurotransmitter receptors

Inhibitors of regulatory enzymes

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2
Q

What are the key transmission/modulatory CNS pathways?

A 
Noradrenaline
Dopamine
Serotonin
GABA
Acetylcholine
Glutamate
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3
Q

What factors can affect psychiatric disorders?

A 
Genetic vulnerability
Life events
Individual personality
Coping skills/social support
Environmental influences (viruses, toxins, drugs, health)
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4
Q

What are the secondary symptoms of depression?

A 
Decreased appetite
Sleep disturbance
Hopelessness
Poor concentration
Irritability
Self harm/suicidal ideas or acts
Reduced libido
May have psychotic symptoms
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5
Q

Why are monoamine oxidase inhibitors (MAOIs) not often given? (MAOIs inhibit destruction of neurotransmitters)

A

Dietary restrictions (tyramine, found in a lot of foods), which if broken can manifest as severe hypertension with a risk of death.

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6
Q

What are the three theories of depression cause?

A 
Monoamine hypothesis (deficit of serotonin/noradrenaline)
Neurotransmitter receptor hypothesis (malformations of receptor shape for neurotransmission)
Monoamine hypothesis of gene expression (deficiency in molecular functioning)
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7
Q

What are SSRIs used to treat?

A

Moderate to severe depression (first line)

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8
Q

Which SSRIs are given?

A

Fluoxetine
Citalopram (most selective)
Paroxetine (most potent)
Sertraline

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9
Q

Should SSRIs be given alone?

A

No - Psychiatric therapy in conjunction for max effectiveness (eg: CBT)

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10
Q

What are the pharmokinetic features of SSRIs?

A

Almost totally absorbed from the gut
Long elimination half-life lives (dose once daily)
Metabolised in liver

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11
Q

What are the side effects of SSRIs?

A

(common)
Anorexia, nausea, diarrhoea
(Rare)
Precipitation of mania, increased suicidal ideation, tremor, extrapyramidal syndromes
Reasonably safe in overdose if taken alone

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12
Q

What are TCAs?

A

Tricyclic antidepressants
(Not first line)
Amitriptyline, imipramine, clomipramine, lofepramine

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13
Q

What are the effects of TCAs?

A

Inhibition of noradrenaline uptake (↑ transmission)
Muscarinic cholinoceptor blockade (↓ transmission)
Alpha 1 adrenoreceptor blockade (suppresses transmission)

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14
Q

What are the pharmokinetics of TCAs?

A

As SSRIs

Lipid soluble

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15
Q

What are the side effects of TCAs?

A

Sedation, impairment of psychomotor performance, low seizure threshold
Reduction in glandular secretions, eye accomodation block
Tachycardia, postural hypertension, ↓myocardial contractility
Constipation
MORE dangerous in overdose

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16
Q

What are SNRIs?

A

Serotonin and noradrenaline uptake inhibitors
(Second/third line)
Eg: venlafaxine and duloxetine
Can be anxiolytic at high doses

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17
Q

What are the side effects of SNRIs?

A

As with SSRIs
Sleep disturbance, ↑BP, dry mouth, hyponatremia
Short half life, thus potential for withdrawal on discontinuation

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18
Q

What are the symptoms of schizophrenia?

A 
Disturbance of thinking
Hallucinations
Delusions
Unusual speech-thought disorder
Behavioural changes
Lack of insight
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19
Q

What is the dopamine theory of schizophrenia?

A

Excess dopaminergic pathway stimulation in schizophrenia
(Dopamine antagonists are best schizophrenia treatment, BUT other methods (eg amphetamine) only cause positive symptoms, not negative, and dopamine antagonists don’t treat negative symptoms)

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20
Q

What are the main dopaminergic pathways?

A

Mesolimbic ()
Mesocortical ()
Nigrostriatal
Tuberoinfundibular

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21
Q

What does the mesolimbic pathway handle?

A

Emotional response and behaviour

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22
Q

What does the mesocortical pathway handle?

A

Arousal and mood

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23
Q

What are the effects of blocking D2 receptors?

A

Mesolimbic: ↓ positive psychotic symptoms
Mesocortical: ↑ negative and cognitive psychotic symptoms
Nigrostriatal: tardive dyskinesia, extrapyramidal side effects
Tuberoinfundibular: hyperprolactinaemia (lactation, infertility, sexual dysfunction)

24
Q

Is schizophrenia associated with increased 5HT function?

A

Yes - 5HT-2A antagonists are effective antipsychotics

5HT implicated in behaviours disturbed during schizophrenia (appetite, mood, attention, aggression, sexual drive)

25
Q

Is schizophrenia associated with decreased cortical glutamate function?

A

Post mortems show ↑ cortical glutamate receptors and binding of receptor ligands in cortex, basal ganglia, and hippocampal formation.
However, no current treatments targeting this system.

26
Q

What are the actions of antipsychotics?

A

Sedation, tranquillisation (in hours)
Antipsychotic (days to weeks)
(Side effects - ↑ negative symptoms in weeks (unlikely in typical antipsychotics), extrapyramidal in hours to days (unlikely in atypical antipsychotics))

27
Q

What are the benefits of atypical antipsychotics?

A

Less extrapyramidal side effects
Different preparations - dissolvable
Some only need one dose daily

28
Q

Which atypical antipsychotics are usually given?

A

Risperidone
Quetiapine
Olanzapine

29
Q

What are the side effects of atypical antipsychotics?

A 
Sedation
Can have extrapyramidal side effects at high doses
Very drug to drug:
Olanzapine - weight gain
Risperidone - increased prolactin
30
Q

What is clozapine?

A

The most effective antipsychotic, atypical.

However, severe side effects thus given as third line agent.

31
Q

What are the side effects of clozapine?

A 
Severe constipation
Sedation
Hypersalivation
Extreme weight gain
Neutropenia/agranulocytosis
32
Q

What is haloperidol?

A

A typical antipsychotic
Safe to give in emergencies (side effects well known)
Sedating effect

33
Q

What is the range of action of haloperidol?

A

Dopamine receptor blockade
Anticholinergic effects
Alpha-adrenergic blockade
Antihistamine effects

34
Q

What are the side effects of haloperidol?

A 
Extrapyramidal: 
Parkinsonism, acute dystonia, akathisia, tardive dyskinesia
Neuroleptic malignant syndrome: 
Severe rigidity, hyperthermia, ↑CPK, autonomic lability
Postural hypertension
Weight gain
Pigmentation
Hyperprolactinaemia
35
Q

What are the toxic effects of haloperidol?

A

CNS depression
Cardiac toxicity
Risk of sudden death with high dose

36
Q

What is anxiety?

A

Fear out of proportion to the situation
Manifests in: avoidance, fear, light headedness, shortness of breath, hot and cold flush, nausea, palpitations, numbness, pins and needles

37
Q

How is anxiety treated?

A

Non pharmacologically at first (CBT)
Treat coexisting disorders
Drugs - antidepressants, anxiolytics, very occasionally antipsychotics

38
Q

What are the principle neurotransmitter systems involved with anxiety?

A

GABA
Serotonin
Noradrenaline

39
Q

What are benzodiazepines? (Eh: diazepam, lorazepam)

A

Exerts effects through binding to high affinity BDZ receptor, which normally forms a GABA-BDZ complex.
Full agonist at these receptor sites, enhancing GABA.

40
Q

What issues are there with benzodiazepines?

A

Highly addictive (dependence leads to withdrawal)
Negative side effects
Reduced benefit over time (tolerance)

41
Q

What are the pharmokinetics of benzodiazepines?

A

Readily bioavailable following oral administration
Rapid acting: 30-90 minutes
Highly lipid soluble, allowing for rapid CNS diffusion
Renally excreted
Long half life

42
Q

What are the side effects of benzodiazepines?

A

Common:
Drowsiness, dizziness, psychomotor impairment
Occasional:
Dry mouth, blurred vision, GI upset, ataxia, headache, ↓BP
Rare:
Amnesia, restlessness, rash

43
Q

What is bipolar disorder?

A

A psychiatric disorder consisting of episodes of depression and hypomania/mania

44
Q

Which drugs act as mood stabilisers?

A 
Lithium
Sodium valproate
Carbamezepine
Lamotrigine
Antipsychotics
45
Q

What is the action of lithium?

A

Unknown
May compete with Mg/Ca ions in ion channels
↑5HT
Attenuates effect of some neurotransmitters on their receptors

46
Q

What are the pharmokinetics of lithium?

A

Renally excreted
Slowly release preparations once daily
Levels need to be monitored and taken 12 hours after last oral dose
Check renal and thyroid function every 6 months and before starting

47
Q

What are the uses of lithium?

A

Prophylaxis of mania and depression in bipolar disorder
Augmentation of antidepressants in unipolar depression
Reduces suicidality
Best evidence as a mood stabiliser

48
Q

What are the side effects of lithium?

A 
(Hypothyroidism, hair loss, rashes)
Memory problems (52%)
Thirst (42%)
Polyuria (38%)
Tremor (34%)
Drowsiness (24%)
Weight gain (18%)
49
Q

What are the toxic effects of lithium?

A

Monitor blood levels closely
Vomiting, diarrhoea
Coarse tremor, dysarthria
Cognitive impairment, restlessness, agitation

50
Q

Which antiepilieptics work as mood stabilisers?

A

Sodium valproate
Lamotrigine
Carbamezepine

51
Q

What is the chief side effect of antiepilieptic mood stabilisers?

A

Teratogenic if taken during pregnancy

52
Q

Which groups of drugs are used to treat dementia?

A

Acetylcholine cholinesterase inhibitors
(Donepezil, galantamine, rivastigmine)
NDMA antagonists
(Memantine)

53
Q

What are AChE-I drugs used to treat?

A

Mild to moderate dementia

54
Q

What does ACh handle?

A

Arousal, memory, attention, mood

55
Q

What are the side effects of AChE-Is?

A

Nausea, vomiting, diarrhoea, gastric/duodenal ulcers
Fatigue, insomnia, headache
Bradycardia
Worsens COPD

56
Q

What is memantine used to treat?

A

Moderate to severe dementia

NDMA receptor antagonist

57
Q

What are the side effects of memantine?

A

Usually well tolerated

Hypertension, dyspnoea, headache, dizziness, drowsiness

Pharma ESA4 (8 decks)

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