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Psychiatry > Antipsychotic medication > Flashcards

Antipsychotic medication Flashcards

1
Q

The difference in MoA of typical and atypical anti-psychotics

A
  • Typical (1st generation) → bind to numerous dopamine receptors in different parts of the brain
  • Atypical (2nd generation)→ bind to specific dopamine receptors in specific areas of the brain
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2
Q

Examples of typical antipsychotics

A
  • Chlorpromazine
  • Haloperidol
  • Thioridazine
  • Trifluoperazine
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3
Q

Main SEs of typical vs atypical anti-psychotics

A

Typical: extrapyramidal SEs

Atypical: weight-gain, metabolic SEs

*however e.g. atypical may also cause EPSEs but are less likely to do so and typical may also cause metabolic SEs but again, are less likely to do so

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4
Q

Simple general prescribing profile of anti-psychotic meds (3 steps)

A
  • 1st line : an atypical
  • 2nd line: another atypical or a typical
  • 3rd line: Clozapine (treatment resistant)
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5
Q

Mesocortical pathway

  • location
  • symptoms
  • problem of dopamine
A

Mesocortical Pathway

  • projects from the ventral tegmentum (brain stem) to the cerebral cortex
  • negative symptoms and cognitive disorders (lack of executive function) arise in this pathway
  • problem here for a psychotic patient, is too little dopamine
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6
Q

Relationship of anti-psychotics and dopamine pathways

A
  • An excess of dopamine is hypothesised to be strongly linked to schizophrenia
  • There are 4 main dopaminergic pathways in the brain
  • blocking dopamine in these pathways would result in a reduction in dopamine and a reduction is symptoms
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7
Q

Tuberoinfundibular pathway

  • location
  • SEs
A

Tuberoinfundibular Pathway

  • projects from the hypothalamus to the anterior pituitary
  • dopamine release inhibits/regulates prolactin release-blocking dopamine in this pathway will predispose patient to metabolic problems (metabolic syndrome)
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8
Q

Pathophysiology of metabolic syndrome

A
  • Interference in the dopaminergic pathways of the tuberoinfundibular pathway (from the hypothalamus to pituitary)
  • Metabolic syndrome → range of metabolic problems: hyperprolactinaemia, hyperglycaemia, diabetes, obesity
  • All of these are caused/worsened by atypical antipsychotic medication
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9
Q

Mesolimbic pathway

  • location
  • symptoms created by this pathway
  • dopamine and symptoms of psychosis
A

Mesolimbic Pathway

  • projects from the dopaminergic cell bodies in the ventral tegmentum to the limbic system
  • positive symptoms come from this pathway (hallucinations, delusions, and thought disorders)
  • there is too much dopamine in this region, which contributes to psychotic symptoms
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10
Q

Nigrostriatal pathway

  • location
  • role of this pathway
  • what happens when anti-psychotics are used
A

Nigrostriatal Pathway:

  • projects from the dopaminergic cell bodies in the substantia nigra to the basal ganglia
  • this pathway is involved in movement regulation
  • dopamine suppresses acetylcholine activity. Dopamine hypoactivity can cause Parkinsonian movements, akathisia and dystonia

These are extra pyramidal side effects (EPSE) – a collection of dystonia, akathisia, parkinsonism caused by a reduction in dopamine in this pathway

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11
Q

What dopamine receptors are there?

A

Dopamine receptors – are in 2 main groups:

  • D1+D5
  • D2/3/4

*D2 and D4 dysfunction are more strongly associated with psychosis

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12
Q

Why can we use anti-psychotics in nausea and vomiting?

A
  • hyperactive dopaminergic activity on D2 receptors in the mesolimbic pathway is responsible for the positive symptoms of schizophrenia (hallucinations, delusions, paranoia)
  • D2 receptors also in the chemoreceptor trigger zone, this accounts for their use in nausea and vomiting
  • All antipsychotics, esp. chlorpromazine, have some sedative effect = good for acute psychomotor agitation
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13
Q

Is only dopamine and its excess responsible for psychosis?

A

A complex interaction of dopamine, serotonin, noradrenaline and other neurotransmitters is involved in the pathological neurochemistry of psychosis.

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14
Q

Risperidone

  • type of antipsychotic
  • SEs
A

Risperidone:

  • atypical but functions more like a typical antipsychotic at doses greater than 6mg
  • Increased extrapyramidal side effects
  • Most likely atypical to induce hyperprolactinemia
  • Weight gain and sedation (dosage dependent)
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15
Q

Olanzapine

  • type of anti-psychotic
  • SEs
A

Olanzapine:

  • atypical
  • Weight gain even with short term use
  • May cause hypertriglyceridemia, hyperglycemia and hypercholesterolemia
  • May cause hyperprolactinemia and transaminitis (2% )
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16
Q

Quetiapine

  • type of antipsychotic
  • SEs
A

Quetiapine:

  • atypical
  • May cause transaminitis (6% of all patients)
  • May be associated with weight gain, though less than seen with olanzapine
  • May cause hypertriglyceridemia, hyperglycemia and hypercholesterolemia, however less than olanzapine
  • Most likely to cause orthostatic hypotension
17
Q

Why Aripiprazole is considered ‘atypical atypical’ anti-psychotic?

A

Aripiprazole: (Atypical atypical!!)

  • Unique mechanism of action (D2 partial agonist)
18
Q

Advantages and interactions of Aripiprazole

A
  • 5HT2 agonist →Low EPS, no QT prolongation, low sedation
  • YP2D6 (fluoxetine and paroxetine), 3A4 (carbamazepine and ketoconazole) interactions
19
Q

Are atypical anti-psychotics SEs free?

A
  • All atypicals can cause QT prolongation
  • Atypicals are not ‘side effect free’ they can cause many unpleasant and serious side effects – they are just less likely to cause EPSE’s, and whilst there is little that can be done to reverse some EPSEs
20
Q

High potency typical anti-psychotics

  • MoA
  • main SEs
  • (3) examples
A

High potency typical antipsychotics

MoA: bind to the D2 receptor with high affinity

*as a result they have higher risk of extrapyramidal side effects (EPSE).

Examples: Fluphenazine, Haloperidol, Pimozide

21
Q

Low potency anti-psychotics

  • receptor interactions
  • SEs
  • (2) examples
A

Low potency typical antipsychotics

  • have less affinity for the D2 receptors but tend to interact with nondopaminergic receptors
  • this results in more cardiotoxic and anticholinergic adverse effects including sedation, hypotension
  • Examples include Chlorpromazine and Thioridazine
22
Q

Use of atypical anti-psychotics

A

Typical antipsychotics

  • not frequently used due to the likelihood of EPSEs
  • they may be used short-term to help sedate agitated patients
  • Haloperidol is commonly used as an IM injection, with Lorazepam (benzodiazepine) as a method of rapid tranquillisation
23
Q

What meds do we use if rapid tranquillisation is needed?

A

Haloperidol is commonly used as an IM injection, with Lorazepam (benzodiazepine) as a method of rapid tranquillisation

24
Q

What drug do we use in treatment-resistant schizophrenia?

A

Clozapine

  • may be associated with weight gain (though less than seen with olanzapine)
  • may cause hypertriglyceridemia, hyperglycemia and hypercholesterolemia, (however less than olanzapine)
  • agranulocytosis (lowered white cell count) can occur in 1% of cases
25
Q

How can clozapine cause agranulocytosis?

A
  • Unclear how Clozapine causes agranulocytosis
  • The theory is that:

Clozapine produces a nitrenium ion (a toxic metabolite) which binds with neutrophil proteins and interacts with myeloid precursor cells and mature neutrophils resulting in agranulocytosis.

26
Q

Contraindications to Clozapine use

A
  • hypersensitivity to clozapine (or any of its component)
  • history of agranulocytosis or severe granulocytopenia with clozapine
  • uncontrolled epilepsy
  • severe central nervous system depression
  • comatose state
  • paralytic ileus
  • myeloproliferative disorders
  • use of other agents that may potentially cause agranulocytosis
27
Q

Potential SEs of clozapine

A
  • agranulocytosis
  • seizures
  • myocarditis
  • constipation
  • metabolic syndrome and weight gain (through less than olanzapine)
28
Q

What are extrapyramidal pathways?

A

The extrapyramidal pathways

  • part of the spinal tracts that control movement
  • they don’t run through the pyramidal tracts of the medulla (hence the name)
  • they help regulate voluntary movement through the lower motor neurons
29
Q

Timescale of extra-pyramidal SEs that may occur with anti-psychotic treatments

A
30
Q

Oculogyric crisis

  • what’s that
  • features
  • causes
  • management
A

An oculogyric crisis is a dystonic reaction to certain drugs or medical conditions

Features

  • restlessness, agitation
  • involuntary upward deviation of the eyes

Causes

  • antipsychotics
  • metoclopramide
  • postencephalitic Parkinson’s disease

Management

  • IV antimuscarinic: benztropine or procyclidine
31
Q

What’s tardive dyskinesia?

A
  • rare, late occurring
  • set of irreversible movement SEs (facial and motor problems)
  • result of long term treatment with Typical Antipsychotics (very rare with atypicals)
  • 30% of people on typical got Tardive dyskinesia and 70% of those had irreversible side effects
32
Q

What’s a neuroleptic malignant syndrome and what’s cause of it?

A

Neuroleptic malignant syndrome

  • rare but dangerous condition seen in patients taking antipsychotic medication
  • mortality of up to 10% and
  • can also occur with atypical antipsychotics, also occur with dopaminergic drugs (such as levodopa) for Parkinson’s disease, usually when the drug is suddenly stopped or the dose reduced
33
Q

Pathophysiology of neuroleptic malignant syndrome

A

The pathophysiology is unknown but one theory is that:

Dopamine blockade induced by antipsychotics triggers massive glutamate release and subsequent neurotoxicity and muscle damage.

34
Q

Features of neuroleptic malignant syndrome

A

It occurs within hours to days of starting an antipsychotic and the typical features are:

  • pyrexia
  • muscle rigidity
  • autonomic lability: typical features include hypertension, tachycardia and tachypnoea
  • agitated delirium with confusion

A raised creatine kinase is present in most cases. AKI secondary to rhabdomyolysis) may develop in severe cases. A leukocytosis may also be seen

35
Q

Management of neuroleptic malignant syndrome

A
  • stop antipsychotic
  • patients should be transferred to a medical ward if they are on a psychiatric ward and often they are nursed in intensive care units
  • IV fluids to prevent renal failure
  • dantrolene may be useful in selected cases
    • thought to work by decreasing excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor, and decreasing the release of calcium from the sarcoplasmic reticulum
  • bromocriptine, dopamine agonist, may also be used

Psychiatry (8 decks)

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