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Psychiatry Mix > Antipsychotics > Flashcards

Antipsychotics Flashcards

1
Q

What are some other names for antipsychotics?

A

neuroleptics or major tranquilisers

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2
Q

What are antipsychotics typically used for?

A
  • psychosis, including schizophrenia,
  • and also in delirium

( quetiapine may be used for anxiety)
(bipolar, OCD, tourettes, huntingtons)

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3
Q

How are antipsychotics usually grouped?

A

typical antipsychotics (first generation) (aka FGA) and

atypical antipsychotics (second generation) (aka SGA).

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4
Q

Name 4 FGA?

A 
First generation anti-psychotics e.g: 
(try fly high)
- trifluoperazine 
- fluphenazine (depot (long acting) injection),  
- haloperidol,

(cheating thieves low)

  • chlorpromazine,
  • thioridazine
  • clopenthixol
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5
Q

Name 7 SGA?

A

Atypical antipsychotics e.g:

  • clozapine,
  • risperidone,
  • sertindole,
  • aripiprazole,
  • zotepine,
  • olanzapine,
  • quetiapine
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6
Q

It is said antipsychotic have what 4 important qualities?

A
  • Sedation
  • Anticholinergic activity
  • Extrapyramidal activity
  • Hypotensive effects

The drugs vary in how much they affect these areas. SGA/atypical are better at combating negative symptoms.

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7
Q

What is the pharmacologic mechanism shared by all antipsychotics?

A

D2 receptor blockage is the only pharmacological property shared by all antipsychotic drugs.

many also have effects on acetylcholine, noradrenaline, histamine and serotonin pathways leading to wide ranging side-effects.

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8
Q

What are the main dopamine pathways and what symptoms are they responsible for / do they control?

A

(antipsychotics are D2 antagonists)

[a]. Mesolimbic pathway: HIGH dopamine gives POSITIVE symptoms – delusions, hallucinations, disorganized speech/thinking and disorganized or catatonic behaviour

[b]. Mesocortical pathway: LOW dopamine gives NEGATIVE symptoms – Alogia, affective flattening, avolition etc.

[c]. Nigrostriatal pathway: Controls motor movement (blockade gives motor symptoms)

[D]. Tuberoinfundibular pathway: releases dopamine to reduce prolactin secretion.

(also in the CTZ)

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9
Q

What clinical implications does partial agonist on D2 receptors have?

A

Improved negative and positive symptoms, EPSE, prolactin changes.

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10
Q

What clinical implications does partial agonist on 5HT-1A receptors have?

A

Improved negative symptoms

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11
Q

What clinical implications does antagonist on 5HT-2A receptors have?

A

Sexual dysfunction; reduced EPSE and improved negative symptoms.

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12
Q

What clinical implications does antagonist on alpha-ADR-1 receptors have?

A

Postural hypotension, dizziness, reflex tachycardia

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13
Q

What clinical implications does antagonist on H1 receptors have?

A

Sedation, increased appetite, weight change, hypotension

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14
Q

What clinical implications does antagonist on M1 receptors have?

A

Minimal impact on blurred vision, dry mouth, constipation, urinary retention, sinus tachycardia

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15
Q

General differences between FGAs and SGAs?

A

FGAs:

  • predominantly D2 action
  • more EPSE
  • prolactin elevation
  • muscarinic cholinergic blocking
  • less effect on negative symptoms

SGAs:

  • lower D2 affinity
  • high serotonin/dopamine binding ratio
  • reduced EPSE
  • more metabolic syndrome effects
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16
Q

Name at least two FGAs (max 6)

A

CHLOPROMAZINE, HALOPERIDOL, trifluoperazine, fluphenazine, zuclopenthixol and flupentixol

17
Q

Name 6 SGAs

A

CLOZAPINE, amisulpride, risperidone, olanzapine, quetiapine, and aripiprazole

18
Q

What are 10 important antipsychotic side effects to know about?

A
  1. Extrapyramidal side-effects (EPSEs).
  2. Neuroleptic malignant syndrome (NMS).
  3. Prolonged QT (a risk factor for occasionally fatal ventricular arrhythmia). If
    >500, refer for cardiological assessment.
  4. Hyperprolactinaemia (with osteoporosis) and sexual dysfunction.
  5. Metabolic syndrome - weight gain, diabetes, dyslipidaemia (elevated
    triglyceride and low HDL cholesterol level) and hypertension.
  6. Decreased seizure threshold.
  7. Anticholinergic effects – constipation etc.
  8. Hyponatraemia (syndrome of inappropriate secretion of antidiuretic
    hormone (SIADH).
  9. Photosensitivity.
  10. Agranulocytosis and myocarditis (clozapine)
19
Q

What is clozapine licensed for?

A

Licensed for treatment-resistant schizophrenia. Can improve positive/negative symptoms of psychosis, affective symptoms, cognitive symptoms and manic symptoms (in treatment resistant bipolar disorder).

These effects are due to its receptor affinity binding profile – histaminergic, muscarinic, adrenergic, serotonergic and dopaminergic receptors.

20
Q

What are 5 important side effects of clozapine?

A

• NEUTROPENIA/agranulocytosis – (concomitant use of lithium can increase the white cell-count)

  • Myocarditis and cardiomyopathy: ECG is required before treatment commencement.
  • Tachycardia
  • Seizures
  • Hypersalivation

(requires regular blood tests due to its side-effect profile especially bone marrow suppression)

21
Q

How is clozapine started? (7)

A
  1. Register with clozapine monitoring service
  2. Baseline BMI, waist, fasting lipid and glucose, LFTs, U&Es, FBC, prolactin, CPK, BP+HR, ECG
  3. start at low dose 12.5mg and titrate up. BP+HR daily during titration
  4. FBC weekly for 18 weeks, then fortnightly until 52 weeks (neutropenia)
  5. Miss dose by 48hrs means recommence titration
  6. Aim for plasma level to reach 350ug/L
  7. Repeat some of step 2 monitoring
22
Q

What monitoring is required on clozapine?

A

Baseline BMI, waist, fasting lipid and glucose, LFTs, U&Es, FBC, prolactin, CPK, BP+HR, ECG.

FBC weekly for 18 weeks, then fortnightly until 52 weeks (neutropenia)

10-16wks, 6 and 12 month, yearly: BMI, waist, fasting lipid and glucose; LFTs and U+Es(not at 6 months);

ECG : baseline and 10-16wks only

BP+HR: daily during titration, weekly for 18wks, then monthly/max 3 monthly

23
Q

What blood test do you check is you suspect neuroleptic malignant syndrome (NMS)?

A

CPK

24
Q

What are the symptoms of NMS?

A
  • Fever
  • Rigidity
  • Delirium
  • Fluctuating bp and HTN
  • Tachycardia
  • Sweating
  • Extrapyramidal side effects (EPSE’s)
  • Bloods: creatinine kinase – very high!

Similar to serotonin syndrome but NMS has:

  • normal pupils (not dilated)
  • hypOreflexia

Rare, but is a medical emergency and can be life-threatening. It results in death in about 10% of cases. Treat hyperthermia.

25
Q

What causes NMS?

Treatment?

A

Genetic variant of the D2 receptor, results in abnormal blockade of D2 in the striatum and hypothalamus.
It causes fever, rigidity, hypertension, sweating, urinary incontinence, altered consciousness. Death: PE, DIC, renal failure from rhabdomyolysis.

Withdraw treatment immediately, and give a dopamine agonist. Ice packs for hyperthermia. Ventilator support. Benzos for agitation. Dantrolene relax muscles.

Symptoms can take longer than 2 weeks to disappear.

26
Q

What are two dystonic movements causes by antipsychotics and how could you treat then?

A

Oculogyric spasm and torticollis

oral, IM or IV anticholinergics e.g. procyclidine 5-10mg

27
Q

What is akathisia?

Treatment?

A

Subjective unpleasant state of motor restlessness. It has been linked to violence and suicide.

non-selective beta-blocker such as propranolol, small dose of clonazepam or the antihistamine cyproheptadine

28
Q

What is tardive dyskinesia?

A

Wide variety of movements: lip smacking, chewing, tongue protrusion, choreiform hand movements, pelvic thrusting and severe orofacial movements

caused by super-sensitivity of dopamine receptors due to prolonged therapy with dopamine-blocking drugs.

29
Q

What antipsychotics are more likely to raise prolactin? What symptoms can be experienced?

A

Risperidone and paliperidone have potent prolactin-elevating effect.

Lead to galactorrhoea, gynaecomastia, hypogonadism, infertility, oligomenorrhoea/amenorrhoea and sexual dysfunction

30
Q

What are some EPSE?

A

1) Akathisia – restlessness
2) Acute dystonia – Often bizarre and unwanted muscle movements e.g. tongue protrusion, torticollis (a head tilt to one side, also with chin lift) and oculogyric crisis (abnormal rotation of the eyeballs).
3) Parkinsonism – tremor, rigidity, ‘mask-like’ faces, bradykinesia
4) Tardive dyskinesia - seen later on. More likely to persist even when treatment withdrawn.

These result from D2 blockade in the nigrostriatal pathways.

Psychiatry Mix (8 decks)

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