Drugs used in Psychiatric Disorders Flashcards
1
Q
How do anxiety disorders present clinically?
A
- psychologically as fear
- physiologically as heart palpitations, chest pain, shortness of breath, GIT disturbances (IBS), headaches, dizziness, tense muscles and insomnia
2
Q
What drugs are used for anxiety disorders?
A
- Benzodiazepines
- SSRIs
3
Q
What drugs are used for depression?
A
- Selective serotonin re uptake inhibitors (SSRIs) : fluoxetine, sertraline
- Tricyclic Antidepressants (TCA) : imipramine, amitriptyline
- Serotonin Norepinephrine Re uptake inhibitors (SNRIs) : venlaflaxine
- Noradrenergic and Specific Serotonergic Antidepressants (NaSSAs) : mirtazapine
4
Q
What is the mechanism of action of benzodiazepines?
A
- relief acute anxiety symptoms by causing CNS depression through potentiation of GABA neurotransmitter which decreases neuronal excitability
- they potentiate GABA actions by binding to specific benzodiazepine sites in CNS and increase frequency of chloride channel opening but this process is GABA dependent and chloride channels cannot be open in GABA absence. so when patient overdoses on benzodiazepine, their body can still regulate chloride channels bcs GABA is main controller
- GABA binding to receptor normally leads to chloride influx into cells which causes cell relaxation. chloride influx makes the cell more hyper-polarised (negative because anions) so the cell will be more relaxed
- GABA is an inhibitory neurotransmitter that acts as a modulator of impulse transmission so it inhibits excitation of other neurons
5
Q
What are the different types of benzodiazepines?
A
- short acting : midazolam (2-4 hrs DOA)
- intermediate acting : lorazepam, alprazolam (8 hrs DOA)
- longer acting : diazepam, clonazepam (>12 hrs DOA)
6
Q
What is the pharmacokinetics of benzodiazepines?
A
- orally have fast onset of 0.5-1 hr (drug can be abused because of this fast calming effect)
- midazolam, lorazepam and diazepam can be given as IV bolus before scope procedures so that patient will go to sleep
7
Q
How are benzodiazepines metabolised?
A
- by glucuronidation metabolism at the liver
- excretion by the kidneys
8
Q
What are the adverse effects of benzodiazepines?
A
- CNS : increased drowsiness, decreased motor skill and increased reaction time so cannot drive when taking medication. anterograde amnesia where pt cannot rmb events that occur AFTER taking the drug (memory disturbance profound in IV sedation)
- CVS : decreased blood pressure and decreased respiration but this is rare and mild
- paradoxical effects : excitement, rambling about unimportant things, irritability, hallucination often of sexual nature and outbursts of rage. violent behaviour attributed to decreased inhibition of benzodiazepine receptors which enables suppression of violent behaviour
- cannot be taken during pregnancy because benzodiazepines can cross placental barrier and lead to floppy child syndrome where the baby’s limbs will not have any tone at all
- chronic use of more than one month can lead to tolerance such that a higher dose is needed for same therapeutic effect so there can be dependence and withdrawal effects after
9
Q
What are the causes of insomnia?
A
- anxiety
- depression
- caffeine/ drug induced insomnia
- drug withdrawal like after chronic use of alcohol or sleeping pills
10
Q
What drugs can treat insomnia?
A
- Benzodiazepine hypnotics like diazepam, lorazepam and midazolam can induce sleep. although they induce sleep, there will be reduced REM and deep stage 3 non-REM sleep when compared to natural sleep (ironical). half lives range from 2-24 hrs
- non benzodiazepine hypnotics include zolpidem and zopiclone. they act on benzodiazepine sites just like benzodiazepines. have comparable hypnotic effect to benzodiazepines but shorter half lives of 2-4 hours. their adverse effects include withdrawal anxiety and there is abuse potential.
11
Q
What is the clinical presentation of depression?
A
- feeling of shame/guilt
- suicidal thoughts
- psychomotor retardation where head always down and not very active
- appetite can be up or down
- concentration, energy, mood, interest, sleep decreased
- these symptoms persist for at least 2 weeks and they interfere with normal functioning
12
Q
What are some non-pharmacological treatment for depression?
A
- cognitive behavioural therapy
- counselling
- relaxation
13
Q
What is the biochemical theory of depression?
A
- there is deficiency in monoamines leading to reduced motivation so can treat depression with SSRI monoamine replacement (dopamine, serotonin and noradrenaline)
- noradrenaline responsible for : energy, interest, motivation, mood and emotions, cognitive function
- dopamine responsible for : reward, impulsiveness, sex, appetite, aggression, mood and emotions, cognitive function
- serotonin responsible for : sleep, drive, motivation, sex, appetite, aggression, mood and emotions, cognitive function
*excess dopamine can cause anxiety and irritability
14
Q
What is the mechanism of action of Antidepressants?
A
- SERT is a transporter for serotonin re-uptake on pre-synaptic neurons
- TCA, SSRI, SNRI all block SERT so there will be extra serotonin (all 3 drugs) and norepinephrine (SERT and TCA only) in synapse
- NaSSAs like mirtazapine inhibit the presynaptic alpha-2-adrenergic receptors, which causes an increased release of serotonin and norepinephrine
- presence of increased neurotransmitters lead to increased bran derived neurotrophic factor which is needed to protect neurons from damage and enhances neuron growth
15
Q
What are the adverse effects of SSRIs?
A
- anxiety for first few days
- weight loss/weight gain
- headache
- nausea
- sexual dysfunction
- hyponatremia
- no fatality in overdose same as benzodiazepines
