This document summarizes various psych drugs including antidepressants, mood stabilizers, antipsychotics, and anxiolytics/hypnotics. It describes how antidepressants like SSRIs work to increase serotonin and norepinephrine levels. It also discusses the mechanisms and side effects of different classes of antidepressants and mood stabilizers. The summary outlines conventional and atypical antipsychotics indicating their uses and side effects. Finally, it reviews anxiolytic benzodiazepines and their therapeutic indications as well as risks like dependence.
1. Psych Druuuuugs
• Anti depressants
• Mood Stabilisers
• Anti psychotics
• Anxiolytics and Hypnotics
2. Anti depressants
• How do they work?
Increase levels of good mood chemicals (serotonin and
noradrenaline)
• Where do they work?
In the presynaptic cleft
Specific Serotonin Reuptake Inhibitor (SSRI)
Noradrenaline reuptake inhibitor (NRI)
Tricyclic antidepressant (TCA)
Mono Amine Oxidase Inhibitor (MAOI)
Reversible Inhibitor of Mono amine oxidase A (RIMA)
3. In more detail…..
• So serotonin and noradrenaline are
MONOAMINE NEUROTRANSMITTERS (made
at the presynaptic cleft)
4.
5. Selective Serotonin Reuptake
Inhibitors (SSRI’S)
FLUOXETINE
SERTRALINE
PAROXETINE
CITALOPRAM
Side effects:
• Nausea
• Vomiting
• Anxiety
• Agitation
• Insomnia
• Loss of appetite
• Sexual dysfunction
Anorgasmia &
delayed ejaculation
Contra-indication:
MANIA
11. Mono Amine Oxidase Inhibitors (MAOI)
MAOI’s:
PHENELZINE
TRANYLCYPROMINE
ISOCARBOXAZID
RIMA’s:
MOCLOBEMIDE
Side effects:
Similar to TCA
12. Mono Amine Oxidase Inhibitors
(MAOI) Side effects
• Accumulation of monoamine neurotransmitter
• ‘Life Threatening Hypertensive Crisis’
• How can we prevent this happening?
• Reduce other amines in the body (amines found in
certain foods and drugs)
• TYRAMINE rich foods: strong cheese, yeast and protein
extract (marmite, Bovil, oxo) CHEESE CRISIS
• TYRAMINE rich drugs: adrenaline, noradrenaline,
amphetamines, cocaine, dopamine, decongestants
• FOOD RESTRICTIONS WHEN ON MAOI’s
13. SEROTONIN SYNDROME
• When SSRI’s are administered simultaneously
with MAOI’s or (MAOI’s with opiates)
SYMPTOMS: (occurs in a few minutes)
• AGITATED
• FEVER
• SWEATING
• INCREASE HR
• MYOCLONUS
• OVER RESPONSIVE REFLEXES
14. Contra indications for starting MAOI
• Phaeochromocytoma
• Cerebrovascular Disease
• Hepatic Imparement
• Mania
18. Mood stabiliser - Lithium
• How does it work?
• Before you start taking it….
• Check patient medications before prescribing..
• How long does it take to start working?
• Common side effects?
• Lithium Toxicity
• Monitoring
• Contraindications
20. Antipsychotics
Conventional (typical) antipsychotics
• Cause EPSE because blocks dopamine D2
Receptors in other parts of the brain
Atypical antipsychotics
• First line treatment for schizophrenia
Because has less effect on dopamine D2
Receptors so fewer EPSE’s
21. Indications (psych)
• Schizophrenia
• Schizoaffective disorder
• Delusional Disorder
• Depression or mania with psychotic features
• Delirium
• Behavioural disturbance in dementia
• Severe agitation
22. Non psych indications
• Motor tics (tourettes)
• Nausea and vomiting
• Intractable hiccups and pruritus
24. Clinical side effects of using
conventional/typical antipsychotics
Because of non-specific blocking of receptors –
Has similar side effects to TCA’s
Chemoreceptor
trigger zone
29. Indication of Benzo’s
• Anxiety
• Alcohol withdrawal
• Akathisia
• Acute mania or psychosis
• Epilepsy prophylaxis
• (any reason someone might need to CHILL
out)
30. Side effects
• Drowsy, ataxia (using machinery/driving)
• Can depress respiration centre so caution in
chronic resp patients
• Risk of developing dependence
• OVERDOSE
• USE WITH OTHER DRUGS (ESP ALCOHOL)
31. Benzo’s
• Temazepam SA oral
• Oxazepam SA oral
• Lorazepam SA oral, IV, IM
• Diazepam LA oral, PR, IV, IM
• Chlordiazepoxide LA oral
There are 2 chemicals involved with mood: serotonin and noradrenaline. When these chemicals are in the synaptic cleft they lighten the mood and when they leave the synaptic cleft (are reabsorbed) they no longer have an effect on mood. Therefore the aim of antidepressants is to keep these chemicals in the synaptic cleft for as long as possible.
These drugs selectively inhibit the serotonin reuptake pumps on the presynaptic cleft
FLUOXETINE
SERTRALINE
PAROXETINE
CITALOPRAM
This drug selectively blocks the presynaptic noradrenaline reuptake pump
Eg REBOXETINE
TCA’s block the reuptake of noradrenaline and serotonin reuptake pumps on the presynaptic cleft.
Also blocks the muscarinic, histaminergic and alpha adrenergic receptors (which is why there are quite a few side effects with TCA’s)
Muscarinic acetylcholine causes an effect on secretory exocrine glands and on smooth cardiac muscle:
secretion from salivary glands and stomach
Slows heart rate
Reduces contractile force of atrium
Reduces conduction velocity of av node
Eye accommodation
Commonly causes vaso constriction of arteries and veins so when stimulated causes blood pressure to be normal. If alpha adrenergic receptor is blocked then causes postural hypotension (dizziness and syncope)
MOA = an enzyme that breaks down monoamine neurotransmitters (serotonin and noradrenaline)
Non selective and irriversible inhibition of monoamine oxidise A and B (there are 2 isomers of monoamine neurotransmitters)
RIMA (reversible inhibitor of monoamine oxidase A)
Works by selectively and reversibly inhibiting monoamine oxidase A
Inhibition of monoamine oxidase A means there is an accumulation of monoamine neurotransmitter
As there is lots of monoamine neurotransmitter it means that the metabolism of other amines is affected and they are not broken down, meaning that as MAOI binds irriversibly amine levels can accumulate to DANGEROUSLY high levels.
The high levels of amine causes a MASSIVE release in norodrenaline and this causes a LIFE THREATENING HYPERTENSIVE CRISIS
CHEESE CRISIS = strong cheese can cause high levels of tyramine – early warning sign = a throbbing headache
RIMA’s REVERSIBLY INHIBIT MAOA so the drug is displaced when amine levels increase so no food restrictions required.
Shouldn’t start TCA or SSRI for 2 weeks after stopping MAOI
(give it 3 weeks for clomipramine and imipramine)
Shouldn’t start MAOI for 1-2 weeks after stopping another antidepressant
3 weeks for clomipramine and imipramine
5 weeks for fluoxetine
Small vascular tumour in the adrenal gland) causing uncontrolled release of adrenaline and noadrenaline causing increase in BP and HR palpatations and headache
Cerebrovascular disease
Hepatic imparement
Mania!!
Both conventional and atypical antipsychotics have extra- pyramidal side effects because of the effect on other dopamine D2 receptors in other parts of the brain.
Have Dopamine receptors located in these other areas…means their normal function is stopped
Mesolimbic pathway – these receptors are involved in delusions, hallucinations, thought disorder, euphoria and drug dependance
So BLOCKING OF THESE RECEPTORS = TREATMENT FOR PSYCH SYMPTOMS
2) Mesocortical pathway – mediates cognitive and negative symptoms of schizophrenia so
BLOCKING OF THESE RECEPTORS MEANS WORSENING OF NEGATIVE AND COGNITIVE SYMPTOMS OF SCHIZO
3) Nigrostriatal pathway (basal ganglia)– controls motor movement so if blocked get EPSE – parkinsonium symptoms, acute dystonia, akathisia, tardive dyskinesia, neuroleptic malignant syndrome (rare but life threatening condition – a reaction to neuroleptic medication – get fever, muscle rigidity, fever, altered mental status and autonomic dysfunction)
4) Tuberoinfundibular pathway – controls prolactin secretion. (Dopamine inhibits prolactin secretion)
So if blocked get: HYPERPROLACTINAEMIA, GALACTORRHOEA (BREAST MILK PRODUCTION), AMENNORRHOEA, SEXUAL DYSFUNCTION.
5) CHEMORECEPTOR TRIGGER ZONE: so when this is functioning normally is allows you to feel sick and to be sick. Blocking the pathway means that you cant be sick so is an anti-emetic
Clozapine – very effective antipsychotic but there is a risk of life threatening bone marrow supression due to a side effect being agranulocytosis and it is only used for ‘treatment-resistant schizophrenia’ Also can cause seizures at a high dose and hypersalivation
Olanzapine
Resperidone
Benzodiazephines bind to specific benzo receptors in the GABA A receptor which causes increased affinity of the complex of GABA. So get an increase affinity for chloride ions into the neurone which causes hyperpolarisation of the post synaptic membrane (therefore preventing depalarisation and an action potential)
Alcohol, opiates, barbituates TCA, antihistamines may enhance the effect of benzo’s and cause resp depression
Lorasewpam only benzo with predicatable absorption when given IM.
ANTIDEPRESSANTS – SSRI, NRI, TCA, MAOI’s, RIMA (REVERSIBLE INHIBITOR OF MA),
MOOD STABILISER
ANTI PSYCHOTIC – TYPICAL (CONVENTIONAL) AND ATYPICAL
ANXIOLYTIC / SEDATIVE – LA AND SA BENZOS