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Year 4 - Mental Health > Psychopharmacology > Flashcards

Psychopharmacology Flashcards

1
Q

what is the MOA of SSRIs?

A

inhibit serotonin reuptake in presynaptic neurone, increasing post-synaptic serotonergic neurone activity

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2
Q

name examples of SSRIs and if they have any particular indications

A
  • CITALOPRAM: 1st line in depression
  • FLUOXETINE: 1st line in depression, preferred in younger pts, longets 1/2 life
  • SERTRALINE: indicated in cardiac disease
  • PAROXETINE: most potent, greater risk of discontinuation syndrome
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3
Q

name the common and/or severe side effects of SSRIs

A

Common:

  • nausea, diarrhoea
  • headache
  • weight changes
  • sexual disturbances
  • restlessness

Severe:

  • hyponatraemia/SIADH
  • arrhythmias/prolonged QT (esp. citalopram/escitalopram)
  • serotonin syndrome
  • discontinuation syndrome (less with fluoxetine as longer 1/2 life)
  • suicidal ideation
  • CNS Sx: tremor, EPS
  • increased risk bleeding
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4
Q

how long should antidepressants be continued?

A

6 months post-remission, should be discontinued gradually over 4 weeks

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5
Q

describe the symptoms of discontinuation syndrome. How could you prevent this?

A
  • increased mood changes
  • restlessness and insomnia
  • GI symptoms: pain, cramping, vomiting, diarrhoea
  • unsteadiness
  • sweating
  • paraesthesia

Decrease dose gradually over 4 weeks, can bridge with fluoxetine as long 1/2 life

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6
Q

can SSRIs be safely used in pregnancy?

A

Weight up costs and benefits

  • can cause congenital cardiac defects in 1st trimester (esp. paroxetine)
  • can cause persistent pulmonary HTN of the newborn in 3rd trimester
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7
Q

name an example of a NaSSA. What is its MOA? Main ADRs?

A

MIRTAZAPINE: presynaptic a2 adrenoR blocker… increases adrenergic and serotonergic neurotransmission.

  • sedation
  • increased appetite/weight gain
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8
Q

What is the main MOA of antipsychotics?

A

D2 R antagonists - main therapeutic effect via dopamine blockage in mesolimbic pathway (decrease +ve effects within days/weeks).
Atypicals have lesser dopamine antagonism activity less EPSE.

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9
Q

Name examples of atypical antipsychotics and any features specifically associated

A
  • aripiprazole: often used 1st line as fewer side effects (partial D2 antagonist)
  • risperidone
  • quetiapine: more sedating
  • amisulpiride
  • olanzapine
  • clozapine: greatest efficacy high risk of agranulocytosis (esp in first 4 mths), hypersalivation
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10
Q

Name examples of typical antipsychotics

A
  • haloperidol
  • chlorpromazine
  • sulpiride
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11
Q

Compare the side effect profile of typical vs atypical antipsychotics

A

Typical

  • EPSE prominent
  • hyperprolactinaemia

Atypical
- metabolic Sx prominent - increased appetite, weight gain, hyperlipidaemia

Both

  • neuroleptic malignant syndrome
  • prolonged QT interval (can lead to arrhythmias eg torsade de pointes or VF)
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12
Q

Why can antipsychotics cause hyperprolactinaemia? What are the possible effects of this?

A

Dopamine usually inhibits prolactin release via D2 Rs in tubuloinfundibular pathway so dopamine antagonism results in increased dopamine release.

In males: gynaecomastia, galactorrhoea, hypogonadotropic hypogonaidsm (ED, decreased libido, infertility).

In females: galactorrhoea, hypogonadotropic hypogonadism (amenorrhoea, decreased libido, infertility).

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13
Q

What are EPSE? Describe examples.

A

Group of movement disorders caused by disruption of dopamine pathways in basal ganglia.

  1. Acute dystonia
    - onset: hours to days
    - painful and lasting muscle spasms predominantly of head, neck and tongue
    - e.g. torticollis, facial grimacing, oculogyric crisis, tongue protrusion or twisting
  2. Pseudoparkinsonism
    - onset: week 1
    - bradykinesia, coarse tremor, rigidity
  3. Akathisia
    - onset: week 1-8
    - restlessness
  4. Tardive dyskinesia
    - onset: months to years
    - involuntary movements of mouth and tongue, limbs face or respiratory muscles after chronic use of antipsychotics
    - e.g. repetitive chewing and lip smacking, choreic movements
    - irreversible
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14
Q

explain the pathophysiology of acute dystonias. How would you manage a patient presenting acutely?

A

Result from an imbalance between dopaminergic and cholinergic neurotransmission - nigrostriatal D2 receptor blockade leads to an excess of striatal cholinergic output.

Management:

  1. PROCYLCIDINE IM/IV - antimuscarinic
  2. If Tx with antimuscarinic is ineffective IV DIAZEPAM can be given for life-threatening acute dystonia (e.g. laryngeal dystonia)
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15
Q

what are the risk factors for developing acute dystonias?

A
  • male
  • young age (children esp. susceptible)
  • previous episode of acute dystonia
  • FHx of dystonia
  • higher potency D2 R antagonists used at higher doses
  • recent cocaine use
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16
Q

how would you manage a patient who has developed tardive dyskinesia?

A
  1. discontinuation of antipsychotic drug
    - switch to atypical
    - dose reduction may initially worsen condition
  2. possible medications:
    - TETRABENAZINE - most common s/e is depression
    - CLONAZEPAM (benzodiazepine)

TD Sx do improve in about 1/2 pts who stop antipsychotics. May resolve completely if signs caught early but may be irreversible.

17
Q

what are the risk factors for the development of tardive dyskinesia?

A
  • typical antipsychotics at high dose
  • longer duration of Tx
  • age >50 yrs
  • African descent
18
Q

how would you manage a patient on antipsychotics who presents with akathisia?

A
  1. dose reduction or switch to an atypical antipsychotic

2. PROPRANOLOL

19
Q

how would you manage a patient on antipsychotics who presents with pseudoparkisnoism?

A
  1. dose reduction or switch to an atypical antipsychotic
  2. medication
    - anticholinergic agent e.g. PROCYCLIDINE
    - AMANTADINE (weak dopamine agonist with modest antiparkinsonian effects)
20
Q

describe the clinical features of neuroleptic malignant syndrome

A

Usually occur within 2 weeks of 1st dose.

  • tetrad of: fever + muscle rigidity + autonomic instability (eg tachycardia, labile BP, diaphoresis) + mental status changes (eg confusion, delirium)
  • rhabdomyolysis
  • elevated creatine kinase + leucocytosis

(FALTER: Fever + Autonomic instability + Leucocytosis + Tremor + Elevated enzymes (CK, transaminases) + Rigor)

21
Q

how would you manage a patient presenting with neuroleptic malignant syndrome?

A
  1. discontinuation of antipsychotic drug (usually lasts 5-7 days after discontinuation)
  2. supportive measures e.g. ICU care
  3. pharmacotherapy (no proven effective treatment)
    - DANTROLENE (ryanodine R antagonist): prevents release of Ca2+ from sarcoplasmic reticulum of striated muscle… reduced muscle rigidity and hyperthermia
    - BROMOCRIPTINE: D2 R agonist
22
Q

what are the main s/e of lithium?

A
  • fine tremor (one of most common, can be treated with propranolol if persistent)
  • polyuria, polydipsia, nephrogenic DI
  • nausea, vomiting and diarrhea (is a salt so affects fluid balance)
  • weight gain
  • metallic taste, dry mouth
  • muscle weakness
  • ECG changes e.g. T wave depressions, U waves, sinus bradycardia
  • hypothyroidism, goitre
  • hyperparathyroidism + hypercalcaemia
  • leucocytosis
23
Q

which tests would you perform before prescribing lithium?

A
  • weight/BMI
  • U&Es inc. calcium
  • eGFR
  • TFTs
  • FBC
  • ECG - if CVD or risk factors for it
24
Q

what is the pathophysiology of lithium-induced DI? How would it present? How would you manage?

A
  • Lithium interferes with ADH signaling… reduces aquaporins on collecting duct cell’s surface… fewer water molecules reabsorbed and kidneys unable to concentrate urine… increased free water excretion.
  • Clinical features: polyuria, nocturia, polydipsia (increased risk of dehydration and subsequent Li toxicity).
  • Management: amiloride
25
Q

Is lithium safe in pregnancy?

A

No, esp. in 1st trimester. Associated with cardiac defects, e.g. Ebstein’s anomaly.

26
Q

how would a patient with lithium toxicity present?

A
  • vomiting and diarrhoea
  • coarse tremor, ataxia, dysarthria, fasiculations
  • drowsiness, coma, seizures
27
Q

describe possible complications of lithium toxicity

A
  • seizures and coma
  • ventricular tachycardia
  • renal failure
  • SILENT (syndrome of irreversible lithium-effectuated neurotoxicity) - after cessation of lithium >2 mths: truncal ataxia, ataxic gait, scanning speech, incoordination
28
Q

how would you manage a patient presenting with lithium toxicity?

A

Mild:

  • stop lithium and check level
  • encourage fluids, stop diuretics, monitor U&Es and renal function

Moderate-sever:

  • consider whole bowel irrigation for severe, acute ingestions
  • IV fluids
  • benzodiazepines if seizures
  • haemodialysis if seizures, coma, renal insufficiency + [Li+] >4
29
Q

describe the MOA of benzodiazepines

A

Act on GABA Rs to enhance inhibitory effects of GABA - post-synaptic inhibition causes hypnotic and anxiolytic effect

30
Q

name examples of benzodiazepines and the typical doses used to treat anxiety

A

lorazepam: 0.5 - 4 mg
diazepam: 6 - 30 mg

31
Q

suggest possible side effects of benzodiazepines

A
  1. CNS depression: confusion, drowsiness, depression
  2. respiratory depression
  3. tremor, vertigo, ataxia
  4. paradoxical increase in aggression, suicidal ideation
  5. dependence
  6. withdrawal syndrome (seizure trigger if abrupt)
32
Q

name a contraindication for benzodiazepines

A

pregnancy - neonatal withdrawal symptoms or resp. depression, cleft lip/palate

Year 4 - Mental Health (12 decks)

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