Psychopharmacy Flashcards
Antipsychotics - dopamine pathways
Nigrostriatal
Mesolimbic
Mesocortical
Tuberoinfundibular
Antipsychotics - dopamine hypothesis
1) hyperactivity of the mesolimbic dopamine pathways cause positive symptoms of schizophrenia
2) deficiency of dopamine in the nigrostriatal pathway accounts for negative and cognitive symptoms of schizophrenia
Antipsychotics - mechanism of action
Block dopamine receptors in the mesolimbic pathway
Antipsychotics - typical antipsychotic examples
Haloperidol
Flupentixol
Chlorpromazine hydrochloride
Antipsychotics - atypical antipsychotic examples
Clozapine Quetiapine Olanzapine Aripiprazole Risperidone
Antipsychotics - indications
Schizophrenia
Schizoid personality disorder
Bipolar affective disorder
Antipsychotics - movement disorder adverse effects
Acute dystonia (e.g. torticollis) Tardive dyskinesia (hyperkinetic involuntary movements) Akathisia (restlessness, tension) Pseudoparkinsonism (tremor, rigidity, bradykinesia)
Antipsychotics - adverse autonomic effects
Antiadrenergic
- QTc prolonged and arrhythmias (torsade des pointes)
Anticholinergic
- dry mouth, blurred vision, constipation and urine trouble
Antipsychotics - adverse effects
Movement disorders Autonomic effects Neuroleptic malignant syndrome Convulsant activity Pigmentation Metabolic effects - weight gain - endocrine (hyperprolactinaemia, decreased libido, sexual dysfunction and menstrual irregularities) Hypersensitivity - cholestatic jaundice - skin reactions (urticaria/eczema)
Clozapine - indications
Treatment resistant schizophrenia
Clozapine - side effects
Less extrapyramidal side effects than typical antipsychotics
Agranulocytosis
Weight gain
Clozapine - smoking risk
Smoking reduces the concentration of clozapine in the plasma
Smoking cessation causes an increase in clozapine levels in the plasma
- can cause dose related side effects (sedation, dizziness, hypersalivation, tachycardia, postural hypotension, constipation and seziures)
Mood stabilisers - available in UK
Lithium
Carbamazepine
Valproate
Mood stabilisers - indications
Acute mania/hypomania in bipolar
Prophylaxis in bipolar and schizoaffective disorders
Prophylaxis in recurrent depressive illness
Augment antidepressant therapy in acute depressive illness
Treating depression in bipolar
Mood stabilisers - what are the expected effects on the patient when using mood stabilisers
Decreased mental and physical overactivity
Improves psychotic features
Prevents exhaustion, sleep deprivation and poor fluid intake
Bipolar disorder - management
Mania/hypomania - lithium, carbamazepine or valproate
Antipsychotics
2nd line mood stabiliser - lamotrigine or gabapentin
Benzodiazepine - lorazepam or clonazepam
ECT
Lithium - predictors of poor response
Rapid cycling or chronic depression (rapid cycling is 4 distinct periods of abnormal mood within a year)
Mixed affective states
Alcohol/drug misuse
Mood-incongruent psychotic features
Lithium - therapeutic range
0.4 - 1 mmol/l
Lithium - precautions
TFTs, U&Es, ECG prior to commencement
Can cause tricuspid valve deformity and affect thyroid function in fetus
Drug interactions
- NSAIDs, thiazide diuretics
Can cause dehydration
- diarrhoea and night sweats
Lithium - adverse effects
Nausea/vomiting Diarrhoea Cognitive dulling Hypothyroidism Renal tubular necrosis - renal failure - this can cause a progressive decrease in renal clearance - eGFR checked every 3 months Tremor Muscle weakness Weight gain Hyperparathyroidism Nephrogenic diabetes insipidus - causes rise in serum ADH, causing thirst and polyuria - inhibits the ADH sensitive adenylate cyclase in the kidney Lithium toxicity
Lithium toxicity - signs and symptoms
Fine tremor - progresses to coarse tremor Nausea and vomiting Dizziness Dysarthria Drowsiness Confusion Fits Coma Death
Lithium toxicity - management
Aim is to reduce absorption and increase clearance of lithium
- diuresis with IV fluid
- gastric lavage
- bowel irrigation
- national poisons information service
Antidepressants - basic principles of prescribing
Provide dose most likely to be effective
Withdraw gradually and be aware of discontinuation syndrome
Continue treatment for 4-6 months after resolution of symptoms (for single episodes)
Antidepressants - monoamine theory of depression
Depression is due to relative or absolute deficiency in monoamines, receptor sensitivity or certain receptor sites in the brain
- noradrenaline
- dopamine
- serotonin
Antidepressants - classes
Tricyclic antidepressants e.g. amitriptyline
Selective serotonin reuptake inhibitor e.g. sertraline, fluoxetine
Serotonin and noradrenaline reuptake inhibitor
Monoamine oxidase inhibitor
Antidepressants - time for efficacy
MAOI, SNRI, SSRI - around 6 weeks to take effect
TCA - 6-7 days
SSRI - 1st line treatment
Citalopram followed by sertraline
Safe in overdose and can be given in heart disease
SSRI - side effects
Nausea Anorexia Dry mouth Diarrhoea/constipation Insomnia Dizziness Anxiety Fatigue Tremor Somnolence Sweating Delayed oragasm/anorgasmia
SSRI - overdose (serotonin syndrome)
Myoclonus Nystagmus Headache Tremor Irritable Confused Agitated Hypomania Coma Pyrexial Sweating Diarrhoea Arrhythmia Death
SSRI - mechanism of action
Inhibition of presynaptic reabsorption of serotonin
Increased availability of serotonin at the synaptic cleft, so it can bind to the postsynaptic receptor, and normal action occurs
SNRI - mechanism of action
Inhibition of presynaptic reabsorption of serotonin and norepinephrine
Increased availability of serotonin and norepinephrine at the synaptic cleft, so it can bind to the postsynaptic receptor, and normal action occurs
TCA - mechanism of action
Stops reuptake of monoamines at presynaptic cleft
Block the action of acetylcholine
