Psychiatric Disease Flashcards
Factors affecting risk of developing a psychiatric disease?
Genetics Life events eg divorce, bereavement Individual personality Coping skills Social support Environmental influences such as viruses, toxins and other diseases
What would be a biological predisposing, precipitating and perpetuating factor?
Predisposing - genetics
Precipitating - cannabis use
Perpetuating - not complying with medication
What does depression present with?
2 of the 3 core symptoms
- low mood
- anhedonia (lack pleasure in anything)
- decreased energy
Associated symptoms
- loss of concentration
- decreased appetite
- sleep disturbance
- irritability
- suicidal thoughts
- self harm
What is thought to be the underlying pathology in depression?
Monoamine neurotransmitters eg noradrenaline and serotonin are deficient
Or…
Depletion of or abnormalities in receptors for the monoamine transmitters at the post-synaptic membrane, despite adequate neurotransmitter levels
Name the four classes of anti-depressants and give an example of each
Selective serotonin reuptake inhibitors
- fluoxetine
- citalopram
- paroxetine
- sertraline
Tricyclic anti-depressants
- amitryptiline
- imipramine
- clomipramine
Serotonin-noradrenaline re-uptake inhibitors
- venlafaxine
- duloxetine
Monoamine oxidase inhibitors
Mechanism of action of selective serotonin reuptake inhibitors
Prevent reuptake of serotonin by the pre-synaptic membrane
Increases 5-HT concentration in the synaptic cleft
Absorption, metabolism and elimination of selective serotonin re-uptake inhibitors?
Absorbed from the gut
Metabolised by the liver
Long elimination - once daily dose
ADRs of selective serotonin reuptake inhibitors?
Anorexia
Nausea
Diarrhoea
Mania
Increased social ideation
Tremor
Extra-pyramidal syndromes
When are selective serotonin reuptake inhibitors used?
Moderate to severe depression
What is an important ADR of citalopram?
Torsades de Pointes
How do tricyclics antidepressants (TCAs) work?
Block re-uptake of 5-HT and NA by the pre-synaptic membrane
Absorption, metabolism and half-life of TCAs?
Absorbed in the gut
(Lipid soluble)
Metabolised by the liver
Long half-life
ADRs of TCAs?
CNS:
- sedation
- impaired psychomotor function
- lower seizure threshold
ANS
- reduced glandular secretions
- eye accommodation block
GI
-constipation
CVS
- tachycardia
- postural hypotension
- impaired myocardial contractility
When are TCAs used?
Not a lot
- have many side effects
- can block α-1 adrenoceptors, suppressing NA transmission
Mechanism of action of serotonin-noradrenaline re-uptake inhibitors (SNRIs)?
At low doses, affect 5HT only
At higher doses, block reuptake of noradrenaline also
Absorption and half life of SNRIs?
GI absorption
Short half-life
ADRs of SNRIs?
Same as SSRIs
- anorexia, nausea, diarrhoea
- mania, increased suicidal ideation, tremor, extra-pyramidal syndromes
Plus
- sleep disturbances
- raised BP
- dry mouth
- hyponatraemia
When are SNRIs used?
As second or third line drugs
Mechanism of action of monoamine oxidase inhibitors?
Block degradation of neurotransmitters
When are monoamine oxidase inhibitors used?
Rarely - highly toxic
Which class of anti-depressants can cause withdrawal syndrome if suddenly stopped?
SNRIs (eg venlafaxine, duloxetine)
Define psychosis
When patients are not in touch with reality
What are the positive symptoms in paranoid schizophrenia?
Hallucinations
Disturbances of thinking
Delusions
Behavioural change
What are the negative symptoms seen in paranoid schizophrenia?
Social withdrawal
Unusual speech and though
What are some cognitive symptoms and affective symptoms seen in paranoid schizophrenia?
Cognitive
- selective attention
- poor memory
- reduced abstract though
Affective
- anxiety
- depression
What are hallucinations?
A perception in the absence of an external stimulus eg auditory, olfactory, visual, gustatory, tactile
What is a delusion?
A fixed false belief that is out of keeping with someone’s culture or religious belief
What is thought to be the underlying pathophysiology of paranoid schizophrenia?
There is an excess of dopamine being released by the brain
What are the main dopamine pathways in the brain and what are they important for?
Meso-limbic: emotional response and behaviour
Meso-cortical: arousal and mood
Nigrostriatal: control of movement - damaged in Parkinson’s
Tuberoinfundibular: function of the hypothalamus and pituitary gland
Mechanism of action of drugs used to treat paranoid schizophrenia?
D2 antagonism, blocking the dopamine pathways
Produce sedation and tranquilisation within first few hours and anti-psychotic effects set in within a few days
General ADRs of dopamine antagonists for schizophrenia?
Enhanced negative and cognitive symptoms
Potential dyskinesia
Hyperprolactinaemia
What molecular effects can typical D2 anti-psychotics have?
D2-antagonist in the CNS
Anticholinergic effects
α-adrenergic blockade
Antihistamine effect
What extra-pyramidal side effects can typical anti-psychotics cause?
Parkinsonism
Acute dystonia
Akathasia (constant motion)
Tardive dyskinesia
What is the really serious side effect that typical anti-psychotics can cause?
Neuroleptic malignant syndrome
- severe rigidity, hyperthermia, increased CPK and autonomic lability
- fluctuating consciousness and confusion
- medical emergency, 10% mortality
What are some other ADRs of typical anti-psychotics?
Postural hypotension
Weight gain
Prolactinaemia
Pigmentation
What can an overdose of typical anti-psychotics cause?
CNS depression
Cardiac toxicity - prolonged QTC
Risk of sudden death
Name some typical anti-psychotics
Haloperidol
Chloropromazine
When else is haloperidol used?
In an acute emergency setting for sedation and tranquilisation
Name some atypical anti-psychotics
Olanzipine
Risperidone
Clozapine
Quetiapine
ADRs of atypical anti-psychotics
Better than typical because they’re newer
Excessive weight gain (olanzapine) due to effects on satiety centres, never feel full
Increased prolactin secretion (risperidone)
Extra-pyramidal side effects (less common)
Postural hypotension
Cardiac toxicity (long QT syndrome)
Advantages of atypical anti-psychotics over typical?
Fewer extrapyramidal side effects so more acceptable to the patient
Different preparations eg dissolvable
Some can be taken once a day
Differing side-effect profiles can be matched to the patient’s characteristics
What is anxiety?
A fear out of proportion of the situation so that individuals undergo avoidance of the certain scenario
May have physical symptoms
What are the symptoms of anxiety?
Light-headedness
Shortness of breath
Hot or cold flushes
Fear of dying or going crazy
First line treatment of anxiety?
CBT - gradually increase the exposure threshold by working up stage by stage
When are pharmacological agents used in anxiety?
As adjuncts in severe cases
Which drugs are used for anxiety?
Benzodiazepines (anxiolytics)
Anti-depressants
Anti-psychotics
Mechanism of action of benzodiazepines?
Enhance the effects of GABA by acting on GABA receptors
-bind to BZD receptors of which there are two groups, high affinity and low affinity
-high affinity group is important for the anxiolytics, hypnotic and anti-convulsants effects
Bioavailability of BZDs?
Almost 100%
Reaches max concentrations 30-90 mins after taking them
Distribution of BZDs?
Highly lipid soluble so diffuse through the CNS rapidly
Excretion and half life of BZDs?
Excreted via kidneys
Long half life
ADRs of BZDs?
Drowsiness
Dizziness
Psychomotor impairment
Dry mouth Blurred vision GI upset Ataxia Headache Hypotension Amnesia Restlessness Rash
Effect of taking BZDs in pregnancy?
Can cause a cleft lip
Respiratory depression and feeding difficulties
What are the withdrawal effects of BZDs?
Insomnia
Agitation
Anxiety
-can build up a tolerance
How can BZDs cause death?
Overdose - however they are rare
Respiratory depression
Treatment of a BZD overdose?
Flumazenil - acts as a BZD antagonist on the GABA receptor
Only give if you are sure that no other drug has been taken with the benzodiazepine
What is bipolar characterised by?
Episodes of depression and hypomania and then mania
Symptoms of mania?
Feeling unusually excited, optimistic, happy or irritable
Overactive
Poor concentration and attention span
Rapid speech, jump from one idea to another
Poor judgement eg over-spending
Increased interest in sex
Psychotic symptoms such as hallucinations, grandiose delusions
Which drugs are used in the treatment of bipolar?
Lithium Sodium valproate Carbamazepine Lamotrigine Atypical anti-psychotics
Mechanism of action of lithium?
Theories
-affect electrolytes and channels: may compete with magnesium and calcium ions
- neurotransmitters: increases 5-HT, chronic lithium can reduce 5-HT a receptor sites
- second messenger systems: Li attenuates the effects of certain neurotransmitters on their receptors without altering receptor density
How is the dose of lithium decided?
Narrow therapeutic window so dose needs to start low and be gradually titrated upwards
Levels are monitored at least 3-monthly
What tests need to be checked before starting lithium?
Renal and thyroid function before starting and every six months
How is lithium excreted?
Renally
-nephrotoxic
Uses of lithium?
Prophylaxis of mania and depression in bipolar disorder
Augmentation of anti-depressants in unipolar depression where anti-depressants are not enough
Evidence for reducing suicidality
Best evidence of all mood-stabilisers
ADRs of lithium?
Memory problems Thirst and polyuria Tremor Drowsiness Weight gain Hypothyroidism Nephrotoxic Hair loss Rashes
What can an overdose of lithium cause?
Vomiting and diarrhoea Coarse tremor Dysarthria Cognitive impairment Restlessness Agitation Coma and death
Treatment of a lithium overdose?
Supportive - fluids
Anticonvulsants
Haemodialysis
General mechanisms of action of drugs for psychiatric disease?
Agonists or antagonists of neurotransmitter receptors
Inhibit regulatory enzymes
