Psychiatric Drugs & Management Flashcards
Give examples of predisposing factors for mental illness.
“inclined”
BIOLOGICAL = genetics, gender, head injury
PSYCHOLOGICAL = personality type, conflict
SOCIAL = role, isolation, gender
Give examples of precipitating factors for mental illness.
“catalyst”
BIOLOGICAL = drug use, head injury
PSYCHOLOGICAL = traumatic life experience, coping style
SOCIAL = poverty, isolation
Give examples of perpetuating factors for mental illness.
“make something continue”
BIOLOGICAL = non-compliance with medication, drug abuse
PSYCHOLOGICAL = hopelessness
SOCIAL = social network, work, family
What are the diagnostic requirements of depression?
2 week history of at least 2 of the core symptoms:
- low mood
- anhedonia
- decreased energy
2/3 of the core symptoms indicates mild/moderate depression
3/3 of the core symptoms indicates major depression
The no. of secondary symptoms also indicates the severity:
- decreased appetite
- sleep disturbance
- hopelessness
- reduced libido
- reduced concentration
- irritability
- self harm/suicidal ideas/acts
- can have psychotic symptoms
Outline the pathophysiology of depression.
Hypothesis 1: deficiency of monoamine neurotransmitters (noradrenaline and serotonin)
Hypothesis 2: abnormality in receptors for monoamine transmission (depletion of neurotransmitter —> up-regulation of post-synaptic receptors)
Hypothesis 3: deficiency in molecular functioning distal to the post-synaptic receptor
Outline the pharmacological options for depression. How long are these usually indicated for?
MAO inhibitors
MAO uptake inhibitors: non-selective noradrenaline AND serotonin or selective noradrenaline OR serotonin
- non-selective = pure (SNRIs) or with additional actions (TCAs)
- selective = noradreline (NARIs) or serotonin (SSRIs)
Other e.g. mirtazepine
First-line pharmacological treatment for depression is indicated for at least 1yr before cessation
Give some examples of SSRIs. Describe the pharmacodynamics and ADRs associated with their use. When are they indicated?
e.g. fluoxetine (Prozac), citalopram (most selective), paroxetine (most potent), sertraline
First-line treatment for moderate to severe depression (along with CBT)
Pharmacodynamics:
- almost completely absorbed from the gut
- long elimination half lives (OD)
- metabolised in liver
- max benefit in 4-6wks (WARN ABOUT!)
- reasonably safe in overdose (if taken on their own)
ADRs: COMMON = - anorexia - nausea - diarrhoea RARE = - precipitation of mania due to increasing mood (lowest risk of all anti-depressants) - increased suicidal ideation within 3 days (?increased motivation/concentration/energy) - tremor - extrapyramidal symptoms
Give some examples of TCAs. Describe their pharmacokinetics and pharmacodynamics. Give some examples of ADRs associated with their use.
e.g. amitryptiline (neuropathic nerve pain), imipramine, clomipramine (OCD), lofepramine
Pharmacokinetics (highly toxic, multiple ADRs):
- inhibition of noradrenaline uptake —> sympathomimetics ADRs
- muscarinic cholinoceptor blockade —> anticholinergic ADRs
- alpha-1-adrenoceptor blockade —> sympatholytic ADRs
Pharmacodynamics:
- lipid soluble
- absorbed from gut
- long half life
- metabolised in liver
ADRs:
- CNS = sedation, impairment of psychomotor performance, lowering of seizure threshold, hyporeflexia
- ANS = reduction in glandular secretions, eye accommodation block, constipation, pupil constriction, hypothermia
- CVS = tachycardia, postural hypotension, impair myocardial contractility (put on cardiac monitor)
- GI = constipation
- metabolic acidosis
Give some examples of SNRIs. When are they indicated? Describe their pharmacokinetics and pharmacodynamics. Give some examples of ADRs associated with their use.
e.g. duloxetine, venlafaxine
Second or third-line treatment for depression
Pharmacokinetics:
- low dose = serotonergic actions
- high dose = noradrenergic actions
Pharmacodynamics:
- short half life (may be withdrawal syndrome on discontinuation)
ADRs: same as with SSRIs: COMMON = - anorexia - nausea - diarrhoea RARE = - precipitation of mania due to increasing mood (increased risk compared with SSRIs) - increased suicidal ideation within 3 days (?increased motivation/concentration/energy) - tremor - extrapyramidal symptoms ADDITIONAL (SNRI-specific) = - sleep disturbance - hypertension - dry mouth - hyponatraemia
Give examples of ADRs associated with MAO inhibitors. What dietary considerations are there when using them?
Extremely toxic
ADRs:
- postural hypotension
- weakness
- dizziness
- headache
- fatigue
- agitation
- anxiety
- weight gain
- impotence
Cannot eat certain foods e.g. cheese
Define psychosis. What conditions can have psychosis as a symptom?
Lack of contact with reality
Encompasses hallucinations and delusions
Seen in:
- paranoid schizophrenia
- mania
- severe depression with psychosis
- organic syndromes
- delusional disorders
- delirium
- dementia
Contrast hallucinations and delusions.
HALLUCINATION = perception in the absence of an external stimulus
DELUSION = fixed false belief that is out of keeping with someone’s culture or religious beliefs
Outline the prevalence of paranoid schizophrenia. What are the signs and symptoms?
PREVALENCE = 1% in general population
- 10%+ risk with one parent with paranoid schizophrenia
- 50%+ risk with both parents with paranoid schizophrenia
- 10% will kill themselves
- die 20yrs younger than the general population (without considering increased suicidal risk)
S&S:
- disturbances of thinking
- auditory hallucinations (hear voices OUTSIDE head)
- persecutory delusions
- unusual speech (thought disorder)
- behavioural changes
- lack of insight
- apathy
- asocial
- self-neglect
What is the pathophysiology of paranoid schizophrenia?
DOPAMINE:
- dopamine antagonists (D2) usually the best treatment for schizophrenia but do not treat the negative symptoms (apathy, asocial, self-neglect)
- some evidence of increased dopamine function in schizophrenics
- amphetamine causes symptoms similar to positive symptoms of schizophrenia (hallucinations, delusions)
- changes in dopamine function may be a response to long-term treatment
SEROTONIN:
- implicated in behaviours disturbed in schizophrenia (perception, attention, mood, aggression, sexual drive, appetite, motor behaviours, sleep)
- most anti-psychotic drugs are 5-HT antagonists (e.g. clozapine)
- precursors of 5-HT exacerbate schizophrenia (e.g. tryptophan)
GLUTAMATE:
- PCP (non-competitive NMDA-type glutamate receptor antagonist) induces symptoms very similar to schizophrenia
- post-mortem studies show increased cortical glutamate receptors of increased binding of glutamate receptor ligands
What are the different dopamine pathways in the brain? How are they involved in schizophrenia?
MESOLIMBIC: emotional response and behaviour
(dramatic therapeutic action of dopamine on positive psychotic symptoms)
MESOCORTICAL: arousal and mood
(enhanced negative and cognitive psychotic symptoms)
TUBEROINFUNDIBULAR (hypothalamus and pituitary gland) —> hyperprolactinaemia (lactation, infertility, sexual dysfunction)
NIGROSTRIATAL:
- Parkinson’s disease
- extrapyramidal side-effects
- tardive dyskinesia
