22. Drugs used in Psychiatric Disease Flashcards
What are the general action of CNS drugs?
Stimulators or blockers of neurotransmitter release. Or can act as inhibitors of regulatory enzymes.
What is the formulation of psychiatric disorders?
Genetic vulnerability + life events + individual personality/coping skills/social support + environmental influences.
What are the core symptoms of depression?
Low mood, anhedonia (loss of enjoyment in previously enjoyable activities).
What are the secondary symptoms of depression?
Decreased appetite, sleep disturbance, physical aches and pains, irritability, self harm or suicidal ideas/acts, psychotic symptoms.
What is the monoamine hypothesis of depression?
Deficiency of monoamine neurotransmitters (NA and serotonin) so drugs that deplete these could induce depression.
What is the neurotransmitter receptor hypothesis of depression?
Abnormality in the receptors for monoamine transmission leads to depression. So depletion of NTs causes compensatory up regulation of post synaptic receptors.
What is the monoamine hypothesis of gene expression for depression?
Deficiency in molecule functioning.
What are the types of antidepressants?
Monoamine oxidase inhibitors, monoamine uptake inhibitors, others.
What are the types of monoamine uptake inhibitors?
Non-selective noradrenalin and serotonin, selective noradrenaline or serotonin.
What are selective serotonin reuptake inhibitors use for?
Moderate to severe depression (with CBT).
Name an SSRI.
Fluoxetine, citalopram, paroxetine, sertraline.
What are the pharmokinetics of SSRIs? (Absorption, half lives, metabolism).
Absorbed in gut, long half life, metabolised in liver.
What are the ADRs of SSRIs?
Common - anorexia, nausea, diarrhoea. Rare - precipitation of mania, increased suicidal ideation.
Name a tricyclic antidepressant.
Amitryptiline, imipramine, clomipramine, lofepramine.
What are the actions of TCAs?
Inhibit NA uptake so enhanced NA neurotransmission, muscarinic cholinoceptor blockade-reduced cholinergic neurotransmission, alpha-1 adrenoceptor blockade-suppression of NA neurotransmission.
What are the ADRs of TCAs?
CNS - sedation and impairment of psychomotor performance. ANS - reduced glandular secretions. CVS - tachy, postural hypotension. GI - constipation.
Which drug family is more dangerous in OD - SSRIs or TCAs?
TCAs.
Name a pure non-selective monoamine uptake inhibitor (SNRIs).
Venlafaxine, duloxetine.
In what way are SNRIs dose dependent?
Lower doses - serotonin action, higher doses - noradrenline action.
What are the ADRs of SNRIs?
Sleep disturbance, increased BP, dry mouth, hyponatraemia, withdrawal on discontinuation.
What is psychosis?
Lack of contact with reality.
What are the symptoms of paranoid schizophrenia?
Disturbed thinking, hallucinations, delusions, unusual speech-thought disorder, behavioural change, lack of insight.
What is a hallucination?
Perception in the absence of an external stimulus.
What is a delusion?
Fixed false belief that is out of keeping with someone’s culture or religious beliefs.
What is the dopamine theory of schizophrenia?
Amphetamine causes symptoms like positive ones of schizophrenia and dopamine antagonists are the best treatment.
How is the dopamine theory of schizophrenia limited?
It doesn’t account for the negative symptoms.
What are the main dopamine pathways?
Mesolimbic (emotional response and behaviour), mesocortical (arousal and mood), nigrostriatal, tuber-hypophyseal.
What are the effects of D2 antagonists?
Nigrostriatal pathway -> Parkinsonian symptoms; mesocortical -> enhance negative symptoms; tuberoinfundibular -> hyperprolactinaemia; mesolimbic -> massively reduces positive psychotic symptoms.
What is the suggested link between schizophrenia and 5HT function?
Increased 5HT has been linked with disturbed behaviours in schizophrenia.
What is the suggested link between schizophrenia and cortical glutamate function?
Glutamate is an excitatory neurotransmitter, decreased function is associated with schizophrenia.
What are the drugs used in schizophrenia?
First generation - haloperidal, chlorpromazine; atypical antipsychotics - olaznapine, risperideone, quetiapine; clozapine.
What are the actions of all antipsychotics? (From hours to weeks).
Within hours - sedation and tranquilisation.
Hours to days - extrapyramidal side effects.
Days to weeks - antipsychotic effects and activating effect.
Why are atypical antipsychotics more acceptable to patients with schizophrenia?
Less EPSE ADRs, once daily dosing, differing side effect profiles to match some patients.
What are the ADRs of atypical antipsychotics in schizophrenia?
Varies drug-to-drug, EPSE at high doses, weight gain, increased prolactin, sedation.
Which typical antipsychotic is safe in schizophrenic emergencies?
Haloperidol.
What are the ADRs of typical antipsychotics in schizophrenia?
EPSE, neuroleptic malignant syndrome, postural hypotension, weight gain, endocrine changes, pigmentation.
What are the toxicity risks of typical antipsychotics in schizophrenia?
CNS depression, cardiac toxicity, risk of sudden death with high dose.
What makes up an anxiety disorder?
Fear out of proportion to situation leading to avoidance.
What are the physical symptoms of anxiety?
Light headedness, shortness of breath, hot and cold flushes, nausea, palpitations, numbness, pins and needles.
What is the treatment line of anxiety?
Non-pharmacological approaches, treat coexistent disorders, antidepressants, anxiolytics.
Name a benzodiazepine.
Diazepam, lorazepam.
What is the mechanism of action of benzodiazepines in anxiety?
Binds BDZ receptor to have inhibitory effects. Enhances GABA.
Explain what is meant by tolerance and dependence with use of benzodiazepines.
Tolerance - need to increase the dose to achieve the same effect. Dependence on discontinuation of treatment - withdrawal effects.
What are the ADRs of benzodiazepines?
Common - drowsiness, dizziness, pyschomotor impairment. Occasional - dry mouth, blurred vision, GI upset, ataxia, headache, reduced BP. Rare - amnesia, restlessness, rash.
How are cases of overdose of benzodiazepines treated?
Support, flumazenil as antagonist to inverse BDZ receptor agonism.
What is bipolar spectrum disorder?
Depression and hypomania/mania.
What are the symptoms of bipolar spectrum disorder?
Unusually excited/happy/optimistic/irritable, overactive, poor concentration and short attention span, poor sleep, rapid speech, poor judgement, hypersexuality, psychotic symptoms.
What are the mood stabilisers used in bipolar spectrum disorder?
Lithium, sodium valproate, carbamazepine, lamotrigine, antipsychotics.
What is the mechanism of action of lithium?
Competes with Mg and Ca ion channels, increases 5HT but reduces if chronic use, attenuates effects of NT on receptors.
Why does lithium need monitoring?
Due to narrow therapeutic window, need to check: renal function, thyroid function every 6 months.
What are the uses of lithium?
Prophylaxis of mania and depression, augmentation of antidepressants in unipolar depression, reduce suicidality.
What are the ADRs of lithium?
Memory problems, thirst, polyuria, tremor, drowsiness, weight gain.
What are the toxic effects of lithium?
Vomiting, diarrhoea, coarse tremor, dysarthria, cognitive impairment, restlessness, agitation.
How is lithium toxicity treated?
Supportive measures, anticonvulsants, increase fluid intake, haemodialysis.
What are the two groups of dementia medication? Give an example of each.
Acetyl cholinesterase inhibitors - donepezil, galantamine, rivastigmine. NMDA antagonist - memantine.
What is the action of AChE-I in dementia treatment?
Slows progression of Alzheimers.
What are the ADRs of AChE-I?
Nausea, vomiting, anorexia, diarrhoea, fatigue insomnia, headache, bradycardia, worsening COPD, gastric/duodenal ulcers.
What are the ADRs of memantine in dementia?
Hypertension, dyspnoea, headache, dizziness, drowsiness.
