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Psychiatry > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Which drugs most effectively diffuse across the BBB?

A

Hydrophobic / lipophilic drugs

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2
Q

Name the clinical uses of antidepressant drugs

A
  • moderate to severe depression
  • dysthymia
  • generalised anxiety disorder
  • panic disorder, OCD, PTSD
  • premenstrual dysphoric disorder
  • bulimia nervosa
  • neuropathic pain
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3
Q

Name the groups of antidepressant drugs

A
  • monoamine oxidase inhibitors

- monoamine reuptake inhibitors; tricyclics, SSRIs and SNRIs

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4
Q

Name examples of monoamine neurotransmitters

A
  • noradrenaline
  • 5-HT
  • dopamine
  • phenelzine
  • imipramine
  • fluoxetine
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5
Q

The rostral nucleus in the mid brain has what roles?

A
  • mood
  • sleep
  • feeding behaviour
  • sensory perception
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6
Q

The caudal raphe nucleus in the midbrain plays what role?

A

A role in pain and analgesia

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7
Q

What are the two mid brain nuclei involved in serotonin projection pathways?

A
  • rostral nucleus

- caudal raphe nucleus

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8
Q

What is the precursor of serotonin?

A

Tryptophan

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9
Q

Describe what happens at the serotonergic synapse normally

A
  • tryptophan is converted to 5-OH-tryptophan via tryptophan hydroxylase
  • then converted to 5-HT via L-AA decarboxylase
  • 5-HT stored in vesicles in presynaptic neuron, then released into synaptic cleft
  • a transporter will reuptake serotonin into presynaptic cell and either resolve it back into vesicles or it catalyses to 5-HIAA to be disposed of
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10
Q

What areas of the brain are involved in noradrenaline projection pathways?

A
  • locus coeruleus
  • lateral tegmental area
  • radiates widely to cortical and subcortical areas
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11
Q

What is the precursor of noradrenaline?

A

Tyrosine

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12
Q

Describe what occurs at the noradrenergic synapse normally

A
  • tyrosine is converted to DOPA via tyrosine hydroxylase
  • DOPA is converted to DA via L-AA decarboxylase
  • then converted to NA via DA beta-hydroxylase
  • stored in vesicles in presynaptic neuron, released into synaptic cleft to act on post synaptic alpha and beta receptors
  • a specific transporter is used for reuptake of NA and either stored in vesicles or converted to MHPG for disposal
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13
Q

Name examples of monoamine oxidase inhibitors

A
  • phenelzine

- moclobemide

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14
Q

What is the mode of action of monoamine oxidase inhibitors?

A
  • irreversible (phenelzine) or reversible (moclobemide) inhibitors of MAO-A and B
  • increases concentrations of neurotransmitters (NA and 5-HT) in the synaptic cleft so less is transported back into the presynaptic neurone
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15
Q

Describe the side effects of monoamine oxidase inhibitors

A
  • cheese reaction / hypertensive crisis
  • potentiates effects of other drugs (e.g. barbiturates) by decreasing their metabolism
  • insomnia
  • postural hypotension
  • peripheral oedema
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16
Q

Why does the ‘cheese reaction’ / hypertensive crisis occur with use of monoamine oxidase inhibitors?

A
  • caused by inhibition of MAO-A in gut (and liver) by irreversible inhibitors preventing breakdown of dietary tyramine and by multiple drugs that potentiate amine transmission (e.g. pseudoephedrine, other antidepressants)
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17
Q

Name examples of a tricyclic antidepressant

A
  • Imipramine
  • dosulepin
  • amitriptyline
  • lofepramine
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18
Q

Describe the mode of action of tricyclic antidepressants

A
  • blocks the reuptake of monoamines into presynaptic terminals
  • so the NTs are not easily taken back up into the presynaptic neurone, so in in synaptic cleft for longer in larger concentrations so more time to enact effect on post synaptic receptors
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19
Q

Describe the common side effects of tricyclic antidepressants

A
  • anticholinergic; blurred vision, dry mouth, constipation, urinary retention
  • sedation
  • weight gain
  • cardiovascular; postural hypotension, tachycardia, arrhythmias
  • cardiotoxic in overdose
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20
Q

Name examples of selective serotonin reuptake inhibitors (SSRIs)

A
  • fluoxetine
  • citalopram / escitalopram
  • sertaline
  • paroxetine
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21
Q

What is the mode of action of SSRIs?

A

Selectively inhibit reuptake of 5-HT from the synaptic cleft

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22
Q

What are the common side effects of SSRIs?

A
  • nausea
  • headache
  • worsened anxiety
  • transient increase in self harm and suicidal ideation in <25 years
  • sweating / vivid dreams
  • sexual dysfunction
  • hyponatraemia (in elderly)
  • discontinuation effects
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23
Q

Name examples of SNRIs

A
  • venlafaxine

- duloxetine

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24
Q

What is the mode of actions of SNRIs?

A
  • block the reuptake of monoamines (noradrenalne and 5-HT) into presynpatic terminals
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25
Q

What are the side effects of SNRIs?

A
  • similar to SSRIs

- lack major receptor blocking actions (e.g. anticholinergic) so more limited range of side effects than tricyclics

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26
Q

Name the NA selective antidepressant drugs

A
  • reboxetine
  • maprotiline
  • desipramine
  • reboxetine
  • protriptyline
  • nortriptyline
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27
Q

Name the non-selective antidepressant drugs

A
  • amitriptyline
  • imipramine
  • clomipramine
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28
Q

Name the 5-HT selective antidepressants

A
  • venlafaxine
  • paroxetine
  • fluvoxamine
  • sertaline
  • fluoxetine
  • citalopram
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29
Q

Name an example of a dopamine uptake inhibitor (atypical antidepressant)

A

Bupropion

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30
Q

Describe the features of mirtazapine (atypical antidepressant)

A
  • mixed receptor effects, blocks alpha2, 5-HT2 and 5-HT3
  • side effects; weight gain and sedation
  • but can block serotonergic side effects if given with SSRIs
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31
Q

Lithium ions and sodium ions are indistinguishable to the renal tubules. What will the effect of dehydration be on lithium levels?

A

Increase lithium levels

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32
Q

What is the mode of action of lithium?

A

May block the phosphatidylinositol pathway (second messenger system) or inhibit glycogen synthase kinase 3-beta or modulate NO signalling

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33
Q

What needs to be monitored in patients on lithium treatment?

A
  • 12hr post dose blood levels must be monitored because of narrow therapeutic index
  • target range is 0.4-1.0mmol/L with higher end of range being associated with better response
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34
Q

What are the side effects of lithium?

A
  • dry mouth / strange taste
  • polydipsia and polyuria
  • tremor
  • hypothyroidism
  • long term reduced renal function
  • nephrogenic diabetes insipidus (decreased renal function over years)
  • weight gain
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35
Q

What are the toxic effects of lithium?

A
  • vomiting
  • diarrhoea
  • ataxia / coarse tremor
  • drowsiness / altered conscious level
  • convulsions
  • coma
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36
Q

Name examples of anticonvulsants that can be used as mood stabilisers

A
  • valporic acid
  • lamotrigine
  • carbamazepine
37
Q

What is the mode of action of the anticonvulsants used as mood stabilisers?

A
  • very unclear

- perhaps potentiate GABA transmission and therefore block overactive pathways (kindling model of bipolar disorder)

38
Q

What are the side effects of valporates?

A
  • drowsiness
  • ataxia
  • cardiovascular effects
  • induces liver enzymes
  • teratogenicity (neural tube defects)
39
Q

What are the side effects of carbamazepine?

A
  • drowsiness
  • ataxia
  • cardiovascular effects
  • induces liver enzymes
40
Q

What are the side effects of lamotrigine?

A

Very small risk of stevens-johnson syndrome

41
Q

Name examples of antipsychotics that can be used as mood stabilisers

A
  • quetiapine
  • aripiprazole
  • olanzapine
  • lurasidone
42
Q

What is the mode of action of the antipsychotics used as mood stabilisers?

A

Dopamine antagonism and 5-HT antagonism

43
Q

What are the side effects of the antipsychotics as mood stabilisers?

A
  • sedation
  • weight gain
  • metabolic syndrome
  • extra-pyramidal side effects (aripiprazole)
44
Q

Name examples of drugs that are used to treat anxiety

A
  • benzodiazepines
  • antidepressants
  • buspirone
  • pregabalin
  • beta blockers (propranolol)
45
Q

Name neurotransmitters involved in amygdala centred circuits

A
  • 5HT
  • GABA
  • glutamate
  • CRF (corticotrophin releasing factor)
  • NE (norepinephrine)
  • voltage gated ion channels
46
Q

Describe the features of GABA

A
  • main inhibitory transmitter in the brain
  • reduces activity of neurones in amygdala and cortico-striatal-thalamic-cortical circuit
  • benzodiazepines (anxiolytic) enhance GABA action i.e. increased inhibitory response
47
Q

Name the main GABA receptors

A
  • GABA-A
  • GABA-B
  • GABA-C
48
Q

GABA-A is the target of what substances?

A
  • benzodiazepines
  • barbiturates
  • alcohol
49
Q

Name examples of first generation anti-psychotics

A
  • chlorpromazine
  • haloperidol
  • zuclophenthixol
  • flupentixol
  • trifluperazine
  • prochloperazine
  • perphenazine
  • sulpiride
    (amisulpiride)
50
Q

Name examples of second generation anti-psychotics

A
  • clozapine
  • olanzapine
  • quetiapine
  • risperidone
  • paliperidone
  • lurasidone
    (amisulpiride)
51
Q

Name an example of a third generation anti-psychotic

A

Aripriprazole (dopamine partial agonist)

52
Q

What are the different dopamine receptors?

A
  • D1
  • D2
  • D3
  • D4
  • D5
53
Q

Where are D1 receptors found?

A
  • neostriatum
  • cerebral cortex
  • olfactory tubercle
  • nucleus accumbens
  • limbic and striatal areas
54
Q

Where are the D2 receptors found?

A
  • neostriatum
  • olfactory tubercle
  • nucleus accumbens
  • limbic and striatal areas
55
Q

Name agonists and antagonists of D2 receptors

A

Agonist;
- bromocriptine

Antagonist;

  • raclopride
  • haloperidol
56
Q

Where are D3 receptors found?

A
  • nucelus accumbens

- island of calleja

57
Q

Where are D4 receptors found?

A
  • midbrain

- amygdala

58
Q

Name an antagonist of D4 receptors

A

Clozapine

59
Q

Where are D5 receptors found?

A
  • hippocampus

- hypothalamus

60
Q

When does dopaminergic side effects occur?

A

When 60-80% of the dopamine receptors are blocked

61
Q

Name dopaminergic side effects

A
  • extrapyramidal side effects; acute dystonic reaction, parkinsonism, tardive dyskinesia
  • neuroleptic malignant syndrome
  • hyperprolactinaemia
  • akathesia / restless legs
  • anticholinergic effects
  • 5HT2; metabolic syndrome
  • antiadrenergic; postural hypotension, hepatotoxicity, prolonged QTc interval, photosensitivity
62
Q

Describe the features of acute dystonic reaction as a dopaminergic side effect

A
  • onset in minutes
  • increasing muscle tone
  • energetic
  • torticolis
  • oculogyric crisis
  • tongue protrusion
63
Q

Describe the features of parkinsonism as a dopaminergic side effect

A
  • bradykinesia
  • cogwheeling rigidity
  • resting tremor
  • shuffling gait
  • dead pan facial expression
64
Q

Describe the features of tardive dyskinesia as a dopaminergic side effect

A
  • long term often permanent
  • involuntary repetitive oro-facial movements
  • blinking, grimacing, pouting, lip smacking common
  • may involve limbs and or trunk
65
Q

How are extra-pyramidal side effects treated?

A

Ach inhibitors help to bring Ach concentration down to match that of dopamine so that the system is balanced again (e.g. procyclidine, trihexyphenidyl, orphenadrine)

66
Q

Describe the features of neuroleptic malignant syndrome

A
  • rare, onset over 24-72 hours, lasts for days untreated
  • fatal in up to 20 or 30% if not treateed
  • clinical picture; increasing muscle tone, pyrexia, changing pulse / BP >rhabdo > ARF > coma > death
  • investigations > CK
67
Q

Describe the treatment of neuroleptic malignant syndrome (dopaminergic side effect)

A
  • stop antipsychotic (consider onward management of their schizophrenia)
  • rapid cooling, renal support
  • skeletal muscle relaxants e.g. dantroline
  • dopamine agonists e.g. bromocriptine
68
Q

Describe the features of akathisia (dopaminergic side effect)

A
  • affects up to 20% of patients
  • manifests within days-weeks of treatment
  • pacing
  • rocking from foot to foot
  • unable to sit or stand still
  • poor sleep as a result
  • links to increased suicide risk
69
Q

What is the treatment of akathisia (dopaminergic side effect)

A
  • 1st line; beta blockers, e.g. propranolol

- 2nd line; benzodiazepines e.g. clonazepam

70
Q

What are the main types of side effects with the first generation antipsychotics?

A

extra-pyramidal side effects

71
Q

What are the main types of side effects with the second generation antipsychotics?

A
  • weight gain

- sedation

72
Q

Describe the side effect for clozapine

A
  • agranulocytosis> neutropenic sepsis (weekly bloods for 3 months then monthly thereafter)
  • myocarditis
  • constipation > gastric paresis > obstruction > perforation
  • weight gain; average 10kg in 3 months
  • sedation
  • sialorrhoea
  • strict monitoring regimens in place
73
Q

What drugs are available as depot?

A
  • haloperidol
  • zuclopenthixol
  • flupenthixol
  • risperidone
  • paliperidone
  • aripiprazole
  • olanzapine
  • clozapine
74
Q

The D1 receptor family (D1 and D5) have what role?

A

Stimulate cAMP

75
Q

The D2 receptor family (D2, D3, D4) have what role?

A
  • inhibit adenylyl cyclase
  • inhibit voltage activated Ca2+ channels
  • open K+ channels
76
Q

What is the effect of GABA binding to its binding site?

A

Allows for chloride to pass through the channel which prevents an action potential - inhibitory action

77
Q

What is the action of benzodiazepines?

A
  • bind at a separate site to GABA
  • increases the likelihood that GABA binding will activate the receptor a/o increase the effect that GABA has when bound
  • positive allosteric modulator; acts as agonists at the allosteric modulatory site but have no action on its own
  • ^ frequency of opening allows more chloride to pass through which hyperpolarises the membrane potential and makes it less likely the neurone will fire an action potential
78
Q

What are the pharmacological effects of benzodiazepines?

A
  • reduce anxiety and aggression
  • hypnosis / sedation
  • muscle relaxation
  • anticonvulsant effect
  • anterograde amnesia
79
Q

What are the clinical uses of benzodiazepines?

A
  • acute treatment of extreme anxiety
  • hypnosis
  • alcohol withdrawal
  • mania
  • delirium
  • rapid tranquilisation
  • premedication before surgery or during minor procedures
  • status epilepticus
80
Q

Describe the symptoms of benzodiazepine withdrawal

A
  • abdominal cramps
  • increased anxiety, panic attacks
  • muscle tension, chest pain, palpitations, sweating, shaking
  • blurred vision
  • depression
  • insomnia, nightmares
  • dizziness
  • headaches
  • inability to concentrate
  • nausea and vomiting
  • tingling in hands and feet
  • restlessness
  • sensory sensitivity
81
Q

Describe the process of withdrawing benzodiazepines

A
  • transfer patient to equivalent daily dose of diazepam / chlordiazepam preferably taken at night
  • reduce dose every 2-3weels in steps of 2 or 2.5mg
  • reduce dose further, if necessary in smaller steps
  • stop completely; time needed for withdrawal can vary from about 4 weeks to a year or more
82
Q

How do antidepressants treat anxiety?

A
  • acutely; SSRIs increase extracellular serotonin
  • chronically; anxiolytic properties appear (hence time taken until clinical effectiveness observed)
  • not fully understood
83
Q

Name the antidepressants used in anxiety and in what conditions

A 
SSRIs; 
- panic disorder, OCD, PTSD, phobias 
- GAD (escitalopram, paroxetine) 
Tricyclics (clomipramine, imipramine);
- 2nd line for panic disorder (unlicensed), OCD 
Venlafaxine (SNRI);
- GAD 
Moclobemide (MAOI)
- social anxiety disorder
84
Q

Describe the management of GAD

A
  • psychoeducation
  • self help / psychoeducation groups
  • high intensity psychological intervention (CBT) OR drug treatment (SSRI)
  • SNRI
  • pregabalin
  • combination of CBT and drug treatment
85
Q

Describe the management of panic disorder

A
  • self help
  • CBT OR SSRI if long standing or no benefit from CBT (do not use benzodiazepines, avoid propranolol, buspirone, bupropion)
  • tricyclics (clomipramine, desipramine, imipramine, lofepramine)
  • continue treatment for 6 months
86
Q

Describe the management of OCD

A
  • low intensity psychological intervention (CBT and ERP)
  • more intensive psychological intervention or SSRI (if effective, continue for 1 year)
  • consider increase in dose after 4-6 weeks
  • SSRI plus CBT and ERP - clomipramine
  • augmentation with antipsychotic or clomipramine plus citalopram
87
Q

Describe the management of PTSD

A
  • mild and <4 weeks from trauma; watchful waiting
  • within 3 months of trauma; brief psychological intervention, hypnotic medication for sleep disturbance
  • more than 3 months; trauma focussed CBT or eye movement desensitisation and reprocessing
  • limited evidence for drug treatment
88
Q

Describe the management of social anxiety

A
  • individual CBT
  • SSRI (escitalopram or sertraline), review at 12 weeks
  • SSRI plus CBT
  • alternative SSRI or SNRI
  • MAOI (moclobemide)

Psychiatry (13 decks)

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