Pharmacology for psychiatry Flashcards

1
Q

OVERVIEW

i) name the five main classes
ii) are side effects more common or more severe in psych medicines?

A

i) anti depressants, anti psychotics, mood stabilisers, anxiolytics, hypnotics
ii) no

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2
Q

SSRIS

i) name three
ii) give four indications
iii) how many days is their peak action seen in?
iv) which SSRI has the shortest half life and which has the longest?
v) which one most commonly causes agitation as a side effect?

A

i) fluoxetine, paroxetine, sertraline, citalopram
ii) depression, anxiety, panic, OCD, PTSD
iii) peak action seen in 10-14 days
iv) paroxetine has shortest half life (20 hrs) and fluox has longest (2-4 days)
v) fluox most common causes agitation as SE

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3
Q

SSRI DISCONTINUATION SYNDROME

i) when does it occur?
ii) name three symptoms
iii) which SSRI does it most commonly occur with? why?
iv) name three ways its treated

A

i) occurs on cessation of an SSRI - especially when abrupt
ii) agitation, dizziness, nausea, diarrhoea, flu like symptoms
iii) most common with paroxetine as it has the shortest half life
iv) treat by reassure and monitor, reintro drug and taper withdrawal, consider alt antidep/anxiolytic

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4
Q

MIRTAZAPINE

i) what type of antidepressant is it?
ii) which receptor does it act on? what effect does it have?
iii) what else can it help with? is there sexual dysfunction?

A

i) noradrenergic and specific serotonergic antidepressant (NaSSA)
ii) acts on alpha 2 receptors > antagonist (cuts the brake cable on serotonin and NA release)
iii) can help with sleep and anti emetic, no sexual dysfunc

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5
Q

TRICYCLIC ANTIDEPRESSANTS

i) name two that are currently in use
ii) what are they mostly used for?
iii) how does their efficacy compare to SSRIs? are they used first line? why?
iv) what do they bind to (2) what does this therefore lead to
v) what system is targeted and results in side effects

A

i) amitriptyline and imipramine
ii) only really used for depression

iii) similar efficacy to SSRIs in major depression
- not used firsy line due to adverse effects and overdose risk

iv) bind to NA and 5HT reuptake transporters therefore increase monoamine levels in synaptic cleft
v) has pronounced anticholinergic (muscarinic) effects

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6
Q

TRICYCLIC SIDE EFFECTS & OVERDOSE

i) name three anticholinergic effects that may be seen
ii) give three other side effects
iii) which two systems are affected in overdose? give three things that may be seen
iv) are TCAs or SSRIs more hazardous in overdose?

A

i) anticholinergic - dry mouth, constipation, urine retention
ii) psychotropic effects eg agitation, sexual dysfunc, muscle twitches, cardiac arrhythmias
iii) OD can affect neurol and cardio systems - confusion, tachycarida, arrhythmia, hypotension, seizure, coma
iv) TCAs are more hazardous in OD

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7
Q

OTHER ANTIDEPRESSANTS - VENLAFAXINE

i) what type of antidepressant is venlafaxine?
ii) does it have a more or less pronounced dose response effect than other antidepressants?
iii) what may it be particularly effective for
iv) give three side effects
v) name another antidepressant of the same class? what venlafaxine SE doesn’t it have?

A

i) venlafaxine is an SNRI (5HT & NA reuptake inhibitor)
ii) more pronounced dose response effect than other anti deps
iii) can be particularly effective for mixed anx and depress
iv) side effects = hypertension (as NA can inc BP), headache, nausea, discont synd
v) duloxetine is also an SNRI - doesnt have hypertension concerns as NA effect isnt as big

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8
Q

MAOis

i) what do they prevent the action of? what does this therefore lead to?
ii) name three foods they can interact with? which compound in specific is implicated?
iii) how may they affect blood pressure? what may this lead to?
iv) which drugs must they not be combined with? why?

A

i) prevent action of monoamine oxidase therefore preventing bdown of 5HT, DA and NA

ii) interact with most cheeses, red wine, broad beans and fermented sausies
- implicates tyramine (broken down by MAOs)

iii) can have a hypertensive effect which can lead to a hypertensive crisis
iv) cant be combined with SSRIs > leads to serotonin syndrome (excess 5HT around as low uptake and no breakdown)

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9
Q

SUMMARY OF ACTIONS

give an example and the action of

i) SSRI
ii) SNRI
iii) tricyclic
iv) MAOi
v) NaSSA

A

i) SSRI - fluoxetine/paroextine/citalopram
- block reuptake of 5HT into presyn neuron

ii) SNRI - venlafaxine/duloxetine
- block reuptake of 5HT and NA into presyn neuron

iii) tricyclic - amytriptyline
- blocks 5HT and NA reuptake pump

iv) MAOi - phenelzine/moclebamide
- blocks MAO from breaking down 5HT, NA and DA

v) NaSSA - mirtazapine
- inc release of 5HT and NA via alpha 2 receptors in the presyn neuron

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10
Q

TYPICAL ANTIPSYCHOTICS

i) what is their action on which receptor?
ii) are they most effective at addressing positive or negative symptoms?
iii) name a brain area they may work
iv) name three negative symptoms that may worsen on typical APs
v) name two typical APs

A

i) D2 receptor antagonist
ii) reduce positive symptoms
iii) work on NAcc
iv) apathy, lack of motivation, lack of self care may worsen due to action on PFC

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11
Q

SIDE EFFECTS OF TYPICAL APS

i) blockade of which DA pathway results in extra pyramidal side effects
ii) what effect does DA have on prolactin? what does reduced DA therefore cause?
iii) name two associated symptoms with the above

A

i) blockade of nigrostriatal route > EPS
ii) DA inhibits prolactin therefore reducing DA by APs can cause hyper-prolactinaemia
iii) hyper PRL > gynaecomastia and galactorrhea

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12
Q

NT SYSTEMS AND PSYCHOSIS

i) name a drug that has structural resemblance to serotonin?
ii) which receptor can newer APs eg clozapine act on?
iii) name a molecule that can produce schz like symptoms? what receptor doe sit bind to?

A

i) LSD
ii) newer APs can act at 5HT2a
iii) PCP > schz like symptoms - glutamate agonist

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13
Q

ATYPICAL ANTIPSYCHOTICS

i) do they have a more or less potent action at D2 receptors than typicals?
ii) do they cause EPS?
iii) what system do they act on in addition to DA?
iv) which type of side effects are less common than with typicals? name two side effects that are more common with atypicals
v) name two
vi) is there any evidence that they are better than typicals?

A

i) less potent action at D2 than typicals
ii) less propensitiy to cause EPS but do still cause them
iii) also act on 5HT

iv) neurol SEs are less common
- more problems with weight gain and metabolic synd (new onset diabetes) espec with olanzapine

v) risperidone, olanzapine, quetiapine
vi) no

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14
Q

EXTRA PYRAMIDAL SIDE EFFECTS

i) give four examples
ii) what receptors are blocked to cause this?

A

i) parkinsonism (tremor, rigid, cog wheeling), dystonias (fixed deformities), tardive dyskinesia, hyperPRL
ii) DA receptor blockade

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15
Q

CHOLINERGIC/ADRENERGIC R SIDE EFFECTS

i) name three muscarinic (cholinergic) receptor side effects
ii) name three side effects of blocking alpha adrenergic receptors

A

i) constipation, dry eyes/mouth, dizzy, tachycardia, dyspepsia
ii) orthostat hypotension, vertigo, sexual dysfunc, palpitations

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16
Q

CLOZAPINE

i) what type of cases is this reserved for?
ii) which type of side effects may req blood monitoring?
iii) does it have a high or low propensity to cause EPS?
iv) name two SE that may occur
v) name a SE that cant be missed

A

i) reserved for treatment resistant cases
ii) haematological side effects
iii) low propen for EPS
iv) hypersalivation and hypotension
v) make sure to check for constipation > can be fatal (toxic megacolon)

17
Q

RAPID TRANQUILLISATION

i) when may this be warranted?
ii) what should always be tried first?
iii) which route of drug admin should be tried first
iv) name one AP and one benzo that then may be given IM
v) what ultimately needs to be treated?

A

i) in acute agitation/aggression where there is risk of harm to self or others
ii) always try de escalation first
iii) try oral first
iv) then may give AP - halo or olanz / nbenzo - lorazepam/midazolam
v) need to treat underlying cause

18
Q

name four mood stabilisers

A

lithium, valproate, carbamazepine, lamotrigine

19
Q

LITHIUM

i) what does it do?
ii) name two short term and two long term side effects
iii) why is lithium toxicity common? name four symptoms of it
iv) name three prepcipitants for toxicity

A

i) mood stabiliser

ii) short term - polydip/uria, nausea, fine tremor, loose stool
long term - renal impair (important), hypothyroid, weight gain, acne

iii) tox is common as there is a narrow therapeutic window
- signs of tox - coarse tremor, N+V, ataxia, cerebellar signs, confusion

iv) precipitants - dehydration, drug interacts eg thiazides or NSAIDs, deteriorating renal function

20
Q

VALPROATE

i) what is it? in what instance is it mostly effective
ii) which two channels does it inhibit?
iii) which NT does it enhance effects of? which NT does it reduce effect of?
iv) name a side effect that determines when it may be used

A

i) mood stabiliser - good in acute mania but not so effective in depression
ii) inhibits Ca and Na channels
iii) enhances effect of GABA and reduces Glu
iv) teratogenic

21
Q

CARBAMAZEPINE

i) what is it used to treat? is it more or less effective than lithium?
ii) what is one of the major problems?
iii) what does it induce?

A

i) anti manic drug that is less effective than lithium
ii) major prob with drug interactions
iii) induces liver enzymes so can reduce levels of other agents

22
Q

BENZOS

i) name three
ii) give three things they can be used for in psychiatry
iii) which receptor do they bind to?
iv) name two other anxiolytics and where they bind

A

i) diazepam, lorazepam, clonazepam
ii) hypnotics, anxiolytics, minor tranq, ETOH withdraw, anticonvulsants
iii) bind to benzo bind site on GABA A receptor

iv) pregabalin - binds to VG calcium channels in the CNS
buspirone - partial agonist at 5HT1a