WEEK 3: MEDICATIONS Flashcards
1
Q
ANTIPSYCHOTIC MEDICATIONS
A
- Treat psychotic symptoms (not its underlying causes) - predominately the positive symptoms (delusions, hallucinations, thought disorder)
- Based on the dopamine hypothesis, the antipsychotic activity appears to be related to the dopamine blocking activity in the brain
- Typical antipsychotics have an affinity to D1 and D2 receptors
- Atypical antipsychotics high affinity with D2 & 5-HT receptors
- The side effects are results of the dopamine antagonism
2
Q
TYPICAL OR FIRST GENERATION ANTIPSYCHOTICS (OLDER)
A
- Each group of typical antipsychotics equally effective for reducing/eliminating positive symptoms
- Poor side effect profile- became a cause for concern because of effect on quality of life and their link with non-adherence, high risk for EPSE
- May be prescribed for treatment of agitation in addition to regular antipsychotics. E.g. Chlorpromazine
- Still commonly used in long acting injection (depot) form E.g. Zuclopenthixol, Fluphenazine & Haloperidol decanoate
3
Q
TYPICAL ANTIPSYCHOTICS
A
- Long acting IMIs (commonly used in community settings)
- Zuclopenthixol, Flupenthixol, Haloperidol, Fluphenazine
- Medium acting IMI (Used in acute situations e.g. acute inpatient setting)
- Zuclopenthixol Acetate ‘Clopixol Acuphase’
- Side effects: Restlessness, tremor, muscle stiffness, constipation, weight gain, EPSEs, neuroleptic malignant syndrome
4
Q
ATYPICALS OR 2ND GENERATION ANTIPSYCHOTICS (NEWER)
A
- Efficacy similar to typical antipsychotics in reducing positive symptoms
- Better side effect profile, less neurological side effects- however other S/Es metabolic issues
- Usually the treatment of choice for psychotic symptoms
- Efficacy similar to older antipsychotics- but more effective in reducing negative symptoms of psychosis
5
Q
CLOZAPINE
A
- Atypical antipsychotic- far more effective than any other antipsychotic BUT has potentially very severe side effects that limit its use to people with ‘treatment resistant schizophrenia’
- Most common SEs- increased appetite, sedation, hyper salivation, low BP, dizziness
- Serious SEs- agranulocytosis, myocarditis, seizures, hepatotoxicity, diabetes, severe constipation and potential bowel obstruction
- Clinical protocols established, regular blood tests (FBC) cardiac monitoring (ECG and echo), metabolic monitoring, be aware of potential toxicity with smoking cessation (dose may need to be reduced)
6
Q
SIDE EFFECTS: EXTRAPYRAMIDAL (EPSEs)
A
- Caused by dopamine antagonists- causing motor disturbances
- The extrapyramidal system is part of the motor system involved in coordination of movement
- Much more common with older antipsychotic medications, however still potential risk with risperidone and amisulpride
7
Q
SIDE EFFECT: NEUROLEPTIC MALIGNANT SYNDROME
A
- Rare and potentially life threatening condition characterised by fever, rigidity, tremor, sympathetic nervous system dysregulation and creatine kinase (CK) elevation
- Managed by discontinuing medication and monitoring and immediate medical intervention (usually in a general hospital) if suspected
- Both typical and atypical antipsychotics can cause NMS
8
Q
SIDE EFFECTS: METABOLIC SYNDROME
A
- Weight gain and the development of metabolic syndrome associated with atypical antipsychotics; serious issue
- Weight gain usually occurs in the first 4-12 weeks of treatment and associated with abdominal obesity and enhanced adiposity (linked with increased morbidity and mortality)
- Metabolic syndrome made up of a cluster of abnormalities
- Abdominal obesity, Hypertension, Hyperlipidaemia, Hyperglycaemia
- When experienced together, lead to an increased risk of diabetes and cardiovascular disease
9
Q
FIRST EPISODE PSYCHOSIS
A
- For FEP, “start low, go slow”
- Start with one of these atypical antipsychotics: Amisulpride, Aripiprazole, Quetiapine, Risperidone, Ziprasidone
- Importance of non-pharmacological approaches (like with anyone with a psychotic illness)
- Tops 5 goals of young people with FEP: employment, education, housing, relationships and health
- Working with the family of the person with FEP
10
Q
SMOKING AND ANTIPSYCHOTIC MEDICATION
A
- Smoking may increase the metabolism of some antipsychotic medications (e.g. clozapine, olanzapine, haloperidol)
- Plasma levels of both clozapine & olanzapine may be reduced by up to 50% in people who smoke tobacco
- Need to be aware of the potential increase in the levels if the person stops smoking abruptly
- Higher doses of the these medications are required to achieve the same therapeutic effect in smokers, compared to non smokers
11
Q
THEORIES OF DRUG ACTION
A
- Important neurotransmitters that act on neurons, the brain’s information processing units
- 100 billion neurons and 1 trillion glia in the brain
- GABA→ Gamma-aminobutyric acid- main inhibitory neurotransmitter
- Glutamate→ Main excitatory neurotransmitter
- Monoamines→ Dopamine: Noradrenaline (aka norepinephrine); Serotonin
- Others→ Acetylcholine; Histamine; Endogenous cannabinoids; Endogenous opioids
12
Q
THEORIES OF DRUG ACTION
A
Agonist→ enhances or mimics transmitter action
- Binds to receptor
- Inhibits reuptake
- Inhibits enzymatic breakdown
Antagonist→ Prevents transmitter action
- Block receptor
Direct effects on ion channels
- Most anticonvulsant drugs work this way
13
Q
FACTORS THAT DETERMINE THE RESPONSE TO A DRUG
A
- Genetic predisposition and epigenetic modulation
- Pharmacokinetics- How drugs are absorbed and metabolised - Liver is important
- Pharmacodynamics- How drugs interact with their brain and body targets (brain receptors important)
- Environmental influences→ e.g. diet- St John’s wort
- Pharmacogenomics→ Personalised response- epigenetics- whether genes are turned on or off- Cytochrome CYP2D6 gene affects drug metabolism
14
Q
DRUGS USED IN MOOD DISORDERS AND ANXIETY
A
- Antidepressants→ SSRIs/ SNRIs, MAOIs/TCA’s, NASSA’s
- Mood stabilisers→ Lithium, Valproate, Carbamazepine, Lamotrigine
- Anxiolytics and Sedatives→ Benzodiazepines, Z drugs, Antihistamines
15
Q
ANTIDEPRESSANT MEDICATION- Types
A
- SSRIs→ selective serotonin reuptake inhibitors
- SNRIs → Serotonin and noradrenaline reuptake inhibitors
- Noradrenaline reuptake inhibitors
Tricyclics - MAOI- Monoamine oxidase inhibitors
- Melatonergic antidepressants
- RIMA’s → Reversible inhibitors of MAO
- Tetracyclics
- Tricyclic analogue of mianserin NaSA