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Management of Disorders > Psychopharmacology > Flashcards

Psychopharmacology Flashcards

1
Q

What factors predict poor adherence to medication?

A

▪️ Psychological problems and/or cognitive impairment
▪️ Complexity of treatment
▪️ Inadequate follow up
▪️ Poor insight
▪️ Side effect profile
▪️ Barriers to care
▪️ Culture, religion, stigma

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2
Q

How can we check for and improve adherence?

A

▪️ Blood tests - check for metabolites
▪️ Check pill bottle
▪️ Use injections when at high risk of non-adherence (LAI)
▪️ Depot = special preparation for slow release

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3
Q

What are orodispersible tablets?

A

Tablets that disintegrate in the mouth within a minute in the presence of saliva due to super disintegrants in formulation

May improve compliance

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4
Q

When can antipsychotic long acting injections NOT be used and why?

A

When antipsychotic-naïve:
▪️ Plasma levels will increase over several weeks without increasing dose due to accumulation
▪️ Increased risk of AE

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5
Q

What do you need to enquire about when deciding on the right medication?

A

▪️ Allergies
▪️ Vitamins and herbs
▪️ Old and OTC drugs
▪️ Interactions
▪️ Dependence
▪️ Use of street drugs
▪️ Family history

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6
Q

What happens when a tablet is swallowed?

A

▪️ Sits for ~45 minutes in stomach
▪️ Absorbed into bloodstream from small intestine
▪️ Transferred to liver through portal vein

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7
Q

What happens to a medication in the liver?

A

▪️ Chemically processes it into active and inactive metabolites
▪️ Ratio determines bioavailability of the drug (duration and intensity)
▪️ Mediated through cytochrome 450 (system of enzymes)

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8
Q

What happens when rate of metabolism of active metabolites in the liver is increased (e.g., enzyme induction)?

A

Decreased duration and intensity

(Unless metabolising a pro-drug into a drug)

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9
Q

What factors might affect drug metabolism?

A

▪️ Age (slower in foetal, neonatal, and elderly)
▪️ Genetic variation
▪️ Ethnicity and sex
▪️ Enterohepatic circulation
▪️ Nutrition
▪️ Intestinal flora
▪️ Diseases such as liver, kidney or heart

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10
Q

What factors are known to affect clozapine metabolism and why is it important to consider these?

A

▪️ Some SSRIs such as fluoxetine (increased seizure risk)
▪️ Smoking - induces metabolism

If metabolism is increase, e.g. by smoking, may be at risk of toxicity is smoking ceased

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11
Q

What is the key consideration when creating a drug for the CNS?

A

That it can cross the blood-brain barrier

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12
Q

What is the difference between an antagonist and an inverse agonist?

A

Antagonists prevent action of agonists/block receptors BUT have no activity of their own

(An inverse agonist blocks the action of an agonist AND exerts its own opposite effect)

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13
Q

What was the first typical antipsychotic developed in the 50s?

A

Chlorpromazine (Thorazine)

(Saw big decrease in no. of inpatients)

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14
Q

Malfunction of which neurotransmitter system is primarily implicated in depression?

A

The monoaminergic neurotransmitter system

(serotonin?)

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15
Q

What is typically the first line of treatment for depression of at least moderate severity?

A

SSRIs (e.g., fluoxetine, paroxetine, sertraline)

(Effective in ~50%, after as quickly as 1-2 weeks)
(Best com

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16
Q

What are the main side effects associated with SSRIs?

A

▪️ Headaches
▪️ Sexual dysfunction
▪️ Hyponatraemia
▪️ Gastrointestinal bleeds
▪️ Increased risk of suicidal thoughts in younger people?

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17
Q

What are discontinuation symptoms?

A

▪️ Symptoms experienced after stopping a drug, often explained by ‘receptor rebound’
▪️ Usually within 5 days but depends on half-life
▪️ Usually mild and self-limiting

(E.g., diarrhoea on discontinuation of antidepressant with potent anticholinergic effects)

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18
Q

When is risk of discontinuation symptoms the greatest?

A

With short half-life drugs (e.g., paroxetine), thus just missing doses may be enough to trigger symptoms

(If severe, taper off gradually)

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19
Q

What are NaSSAs?

A

Noradrenergic and Specific Serotonergic Antidepressants (e.g. mirtazapine)

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20
Q

What do NaSSAs do?

A

▪️ Alpha 2 antagonism (adrenergic)
▪️ Blocks 3 serotonin receptors and histamine 1
▪️ Leads to increased release of noradrenaline and serotonin

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21
Q

What are the benefits of NaSSAs?

A

▪️ As effective as SSRIs
▪️ Anxiolytic and sleep-restoring
▪️ No sexual dysfunction
▪️ Improves appetite (may make weight gain more likely

22
Q

What are SNRIs?

A

Serotonin and Noradrenaline Re-uptake Inhibitors (e.g., Venlafaxine)

Low dose = inhibition of serotonin uptake
Higher dose = inhibition of noradrenaline re-uptake

23
Q

When should SNRIs be used and why?

A

▪️ Reserved for 2nd line treatment
▪️ Risk of hypertension so blood pressure should be checked regularly

24
Q

When are pharmacological interventions typically considered for anxiety?

A

As a second option is psychological therapy is not effective

25
Q

What are benzodiazepines and when/how should they be used?

A

▪️ GABA enhancers - inhibition!
▪️ Only for when anxiety is severe, disabling or causing extreme distress
▪️ At the lowest effective dose for as short as possible due to potential physical dependence and withdrawal

26
Q

What should you do when prescribing SSRIs and SNRIs for generalised anxiety?

A

Start at half the normal starting dose and titrate upwards as tolerated

27
Q

What is pregabalin licensed for?

A

Generalised Anxiety Disorder

28
Q

What interventions should be considered for panic disorder?

A

▪️ SSRI = first line
▪️ Encourage self-help based on CBT
▪️ AVOID benzodiazepines

29
Q

What interventions should be considered for generalised anxiety disorder?

A

▪️ SSRI = first line
▪️ SNRIs and pregabalin = alternative choices
▪️ Benzos not beyond 2-4 weeks
▪️ High intensity psychological intervention and self-help

30
Q

What interventions should be considered for cases of OCD with moderate-severe functional impairment?

A

▪️ SSRI and/or intensive CBT
▪️ Clomipramine if SSRIs fail
▪️ Add antipsychotic if still suboptimal response, or combine clomipramine with citalopram

31
Q

What should you consider when prescribing medication for sleep?

A

▪️ Behavioural strategies to improve sleep hygiene (e.g, alcohol, pain, caffeine, other medications)
▪️ Intermittent and short-term dosing at lowest effective dose if necessary

32
Q

What might you prescribe someone who has difficulties falling asleep?

A

Zolpidem because it has a short-half life

Temazepam also has a short half life but has increased risk of dependence

33
Q

What might you prescribe someone who has difficulties maintaining sleep?

A

Zopiclone because of its long half-life so longer lasting

34
Q

What is promethazine?

A

An antihistamine with sedative properties

35
Q

What is melatonin?

A

A hormone produced by the pineal gland in a circadian manner
▪️ Rises in evening ~2 hours before sleep, enabled by darkness
▪️ Involved in induction of sleep and synchronisation of circadian system

36
Q

What are the main dopamine pathways in the brain that antipsychotics act on?

A

▪️ Mesolimbic (delusions and hallucinations)
▪️ Mesocortical (cognitive and affective symptoms)
▪️ Tuberoinfundibular (prolactin secretion)
▪️ Nigrostriatal (movements

(Latter two both NORMAL in SCZ)
(5th = thalamic?)

37
Q

What do typical, first generation antipsychotics do?

A

D2 receptor antagonism to improve positive symptoms in psychosis

BUT block reward circuits leading to apathy, anhedonia, and EPSEs

(e.g., haloperidol, chlorpormazine)

38
Q

What are atypical, second generation antipsychotics?

A

▪️ Rapid dissociation from dopamine receptors
▪️ 65-75% D2 blockade
▪️ Additional properties such as serotonin antagonism, D2 partial agonism, and serotonin partial agonism

(e.g., olanzapine, risperidone, quetiapine, aripiprazole)

39
Q

What are the pros and cons of atypical antipsychotics?

A

▪️ Reduced extrapyramidal symptoms
▪️ Increased effectiveness for negative symptoms
▪️ Last longer

BUT more metabolic side effects such as weight gain and diabetes

40
Q

What can be used for refractory schizophrenia?

A

Clozapine

(Must have already tried 2 different antipsychotics)

41
Q

What should you consider when prescribing clozapine?

A

▪️ Dose-dependent adverse effects
▪️ Most common and severe at the beginning
▪️ Monitor blood levels to ensure still in therapeutic range
▪️ Monitor white blood cell count to avoid fatal side effects such as agranulocytosis
▪️ Increased risk of seizures

42
Q

What should you take baseline measurements of when starting antipsychotics?

A

▪️ Full blood count (FBC)
▪️ Urea and electrolytes (U&Es)
▪️ Liver function tests (LFTs)
▪️ Electrocardiogram (whenever dose increases)
▪️ Blood pressure

43
Q

What additional factor should you monitor if prescribing risperidone, amisulpiride or sulpiride?

A

Prolactin

44
Q

What additional factors should you monitor if prescribing olanzapine?

A

Plasma glucose and blood lipids

45
Q

What is the mainstay treatment for bipolar disorder?

A

▪️ Antipsychotics (e.g., olanzapine)
▪️ Mood stabilisers (incl lithium, sodium valproate, carbamazepine)
▪️ Possibly sedatives/anxiolytics in addition (e.g., benzodiazepines)

46
Q

What is the first line treatment for rapid cycling type bipolar disorder?

A

Lithium, either with or without valproate
▪️ If neither, try alternative antipsychotics such as lamotrigine

(Lithium = second messenger systems and gene regulation, valproate = boosts GABA)

47
Q

What might partly explain the association between epilepsy and depression?

A

Depletion of serotonin

48
Q

What should be considered when using pharmacological interventions for psychiatric symptoms in neurological illness?

A

▪️ Psychiatric side effects (e.g., with ASM)
▪️ Pharmacokinetic interactions (e.g., fluoxetine may increase ASM plasma levels, causing toxicity)
▪️ Pharmacodynamic interactions (may overlap with psychotropic adverse effects)
▪️ Dose-related risk of seizures in some psychotropics

49
Q

What percentage of people with PD experience depression and what should be considered when treating this?

A

▪️ ~25%, predicts greater decline
▪️ SSRIs = first line
▪️ BUT when combined with selegiline may risk serotonin syndrome

50
Q

How might you treat someone with PD-related psychosis?

A

▪️ Typically secondary to dopaminergic meds
▪️ If have insight and not distressed by hallucinations, don’t treat with additional psychotropics
▪️ Consider adjusting dopamine agonist
▪️ Consider cholinesterase inhibitor or atypical antipsychotic with low affinity - most evidence for clozapine

51
Q

What are the main considerations when treating NPS in MS?

A

▪️ Depression = most common
▪️ SSRIs or Neudexta (dextromethorphan and quinidine)
▪️ Steroid treatment might cause affective disorder
▪️ Modafinil or amantadine for sleep?
▪️ Be careful not to worsen cognition

Management of Disorders (28 decks)

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