Clinical Case Studies Week 5 (Depression, Psychosis + Schiz, Dementia) Flashcards
What does the psychological treatment of depression consist of?
Structured problem-solving strategies
Stress management strategies
CBT
Interpersonal psychotherapy (IPT)
Short-term dynamic therapy
Which SSRI/SNRI will have withdrawal effects? Why? What are these withdrawal effects?
Fluvoxamine, paroxetine, and venlafaxine as these have short half lives.
Withdrawal effects for SSRIs and SNRIs: Dizziness, nausea, paraesthesia, anxiety, agitation, tremor, sweating, confusion, electric shock-like sensations
When do SSRI doses need adjustment?
Doses usually need adjustment in hepatic impairment
What differentiates escitalopram from other SSRIs?
Escitalopram - causes less sedation, sexual dysfunction and no agitation or weight gain due to high receptor selectivity
Explain the following drug interactions and precuations for SSRI
A) Platelet aggregation
B) Hyponatraemia risk
C) QT interval prolongation/arrhythmia risk
A)
- Caution with other drugs that effect clotting → bleeding risk (esp GI)
- E.g. Warfarin + SSRIs may increase anticoagulant effect and risk of bleeding; monitor INR and ↓ warfarin dose as needed.
B)
- Increase risk with other drugs causing this effect.
C)
- ↑ risk with other drugs causing this effect.
What type of impairment affects SNRI (metabolism)?
Dosage adjustments required in renal impairment (CrCl < 30ml/min)
Hepatic impairment - variable recommendations depending on the agent (duloxetine contraindicated)
What are the adverse effects of SNRIs? how do they differ from SSRIs?
Similar adverse effects and precautions to SSRIs due to serotonergic actions
Suicide risk, serotonin syndrome, hyponatraemia, risk of bleeding, narrow angle glaucoma
> narrow angle glaucoma is a NA side effect
Cardiac effects
Use cautiously in patients with cardiac disease
Increases in BP reported with desvenlafaxine, duloxetine (infrequent) & venlafaxine
Control hypertension before starting desvenlafaxine or venlafaxine
Lipid effects
Elevations have occured with desvenlafaxine, use with caution
When is agomelatine contraindicated?
Contraindicated in hepatic impairment or if aminotransferase concentration is > 3 X ULN.
> Caution if aminotransferases are already elevated or other risk factors for hepatic damage
> Additive hepatotoxic effects with other drugs
When are TCAs used? What do they have a role in? When are they potentially lethal?
Used generally after unsuccessful trials of at least 2 first-line treatments
- Have a role in severe melancholic depression
- Potentially lethal in overdose!!! (cardiotoxicity)
Precatuons of TCA?
suicide risk, CV disease, elderly, epilepsy (lowers seizure threshold like all antidepressants), hyperthyroidism
What makes vortioxetine desirable?
Can be stopped without tapering
For serotonin toxicity:
A) What are mild symptoms
B) What are the moderate symptoms
C) What are the severe symptoms
A)
- Mydriasis, shivering, sweating, mild tachycardia
B)
- disorientation, excitement, rigidity, tachycardia, hyperthermia (> 40) tremor, clonus, hyperreflexia
C)
- Delirium, hypertension, hyperthermia, muscle rigidity, tachycardia
What are te TWO treatment options for serotonin toxicity?
Cyproheptadine: 12mg single dose or 4 to 8mg tds
Chlorpromazine: 12.5 to 50mg slow IV infusion over 30 to 50min
How to commence antidepressants?
Generally commence antidepressants with a low dose and gradually increase over 2 to 4 weeks
When is the full effect of antidepressants seen?
Full effects may take 4 to 8 weeks but improvement seen within 1 to 3 weeks
How long to continue drug treatment for after a single episode of major depression?
Continue drug treatment for 4 to 12 months after a single episode of major depression
> high risk of relapse
How to adjust treatment for depression medication?
Increase dose if full response not achieved (check adherence before adjusting therapy)
- Up to maximum possible dose
- Depending on side effects
Assess respone after 2 to 4 weeks
If a change is necessary can switch to an antidepressant from the same or a different class
What to do for patients who fail to respond to antidepresasnt therapy? What are the key questions in assessing failure to respond to psychotropic drugs?
Is diagnosis correct
Has the patient been taking their medication regularly
Have possible underlying medical causes been identified and treated
Is the patient reacting adversely to a current medication
Have the drug dose and duration of administration been adequate
Have relevant psychosocial or personality factors been addressed
Have alcohol or other substance use problems been addressed n
Could an interacting drug be compromising the response
What are the FOUR options in treatment of resistant patients (refractory depression)?
Switching antidepressants
Augmentation strategies
Antidepressant polypharmacy
Electroconvulsive therapy (ECT)
For switching antidepressants;
A) What requires long washout periods?
B) TCAs and most SSRI (except fluoxetine) clear the drugs from the body within how long?
C) For other switches, what needs to be considered?
A)
- Specified long washout periods are mandatory for irreversible MAOIs
- Non selective irreversible MAOI and serotonin toxicity drug stays in body 2-3 weeks after it has been ceased –> severe HTN and serotonin toxicity
B)
around 5 days, the half life is around 20-30 hours
C)
Potential for withdrawal effects and need for tapering dose of agent being ceased
Half life of drug & continued effects → potential for interaction/toxicity during switch if the drug has a long half life
Clinical urgency for change/potential for relapse and exacerbation
What two antidepressants are most common for withdrawal effects? What is the general rule for discontinuing a drug?
Paroxetine and venlafaxine
Halve the dose every week until the daily dose is half of the lowest unit available, then stop after 1 week
What can rapid withdrawal of the more potently anticholinergic tricyclic antidepressants (TCAs) (eg amitriptyline) result in?
Cholinergic rebound (agitation, headache, sweating, gastrointestinal symptoms), parkinsonism and problems with balance.
> sailvation, lacrimation, urination, diarrhoea, GI distress, emesis SLUDGE = cholinergic effects
What is Electro-convulsive therapy (ECT)?
Delivery of an electric current to induce a seizure for a therapeutic response (uni or bilateral)
- Indicated for severe and unresponsive forms of depression
- Response rate of 50 to 80%
How often is ECT given? What is done to prevent high relapse rate? What are the side effects?
- Treatments given 3 times weekly or ↓ if cognitive impairment emerges
- 6 to 14 treatments (up to 24 treatments)
Relapse rate high
- Maintain recovery with pharmacotherapy (that has not been previously ineffective), lithium or mood stabiliser or combination
Side effects
- Memory loss, muscle aches and pains, headaches, transient confusion
How does exercise alleviate symptoms of depression?
↑ energy
Improve sleep
Positive distraction
Social support
↑ sense of control and self-esteem
May change levels of neurotransmitter
Trials have demonstrated regular exercise to be equally effective as antidepressants in mild to moderate depression
> decrease risk of developing depression
Key Messages about depression
- Depression may result in significant disability
- Depression may be associated with a number of medications and medical conditions, in particular co-morbid psychiatric illnesses
- Pharmacotherapy is indicated in moderate to severe MDD only
- SSRIs are first line (in general) – need to consider what is best for the individual
- Drug choice should be based on patient preference, past history of response, adverse effect profile, potential for toxicity in overdose, potential for drug interactions
- Consider interactions due to CYP450 enzymes
- Monitor for serotonin syndrome
- Avoid withdrawal syndrome
- Observe washout periods when switching antidepressants to reduce adverse effects
- There is little evidence to support combinations of antidepressants, although the risk of adverse events is well documented
Pyschosis from this card onwards …
What to do if EPSE occurs?
ideally reduce antipsychotic dose or switch to alternative antipsychotic
What treatment for the following EPSE?
A) Dystonias - stiffness, uncontrolled muscular spasms
B) Akathisia - inner restlessness, strong desire or compulsion to move
C) Parkinsonism - tremor and/or rigidity, mask- like face, shuffling gait, slow movements
D) Tardive Dyskinesia - involuntary abnormal movements of face, tongue, lips, hands or feet
A)
benzatropine (oral, inj), trihexyphenidyl (benzhexol)
B)
propranolol, clonazepam
C)
benzatropine, trihexyphenidyl
D)
Can be irreversible. Stop antipsychotic (preferred)
Treatment poor efficacy – tetrabenazine, Ginkgo biloba
What is first line treatment in schizophrenia?
2nd Generation Antipsychotics (SGAs)
More metabolic adverse effects
More expensive
Pharmacalogy of aripiprazole? What is it used to agument?
Is a dopamine system stabiliser (increased dopamine output when conc are low and decreased dopamine output when conc. are high)
- Less sedation, weight gain and prolactin elevation
- Good 1st choice antipsychotic
- Doesn’t provide sedation if patient acutely unwell
- May cause insomnia, akathisia and/or activation
> often used to augment other antipsychotics
> to reduce weight gain e.g. clozapine, olanzapine
> to reduce prolactin e.g. risperidone
Pharmacology of brexpiprazole
Indicated only in schizophrenia
May have positive effects on mood
Well tolerated – little weight gain, prolactin elevation, akathisia
Pharmaclogy of lurasidone
Take with food to increase absorption
Low incidence weight gain, small rise in prolactin
Theorised to improve mood & be useful in bipolar
Reports of increased irritability/rage
Pharmacology of olanzapine
Sedating – may be beneficial in acute psychosis
WEIGHT GAIN +++
Metabolic syndrome major concern. For this reason falling out of favour as long term treatment