Psychological Flashcards

1
Q

What are the treatment options for patients with generalised anxiety disorder?

A
Sertraline = first-line (SSRI) 
Alternative = serotonin norepinephrine reuptake inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the treatment options for patients with acute anxiety disorder?

A

Benzodiazepines - avoid prolonged use

Propranolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the mechanism of action for benzodiazepines?

A

Propagator of GABA neurotransmission; binds to GABA-A receptors, increases affinity of GABA to its receptor which then increases GABA-A’s opening frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How should you prescribe benzodiazepines?

A

Avoid where possible
Maximum 2-4 weeks use
Anxiety must be severe, disabling or causing the patient unacceptable distress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How should you prescribe SSRIs?

A

Therapeutic doses are approx the same for anxiety as what you’d prescribe for depression.
Time to onset varies by patient but usually it’s 4 weeks - continue initial therapeutic dose for 4-6 weeks and INCREASE DOSE if no response is shown (don’t switch meds)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the side effects of SSRIs?

A
  • Sexual dysfunction
  • GI abnormalities (nausea & diarrhoea)
  • Insomnia
  • Anorexia with weight loss
  • Withdrawal on discontinuation
  • Serotonin syndrome (tachycardia, agitiation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the features of SSRI toxicity?

A

Onset: days - week after new SSRI/ increase in current SSRI dose

  • Autonomic instability
  • Mental status change
  • Inducible muscle clonus (via excessive 5-HT1A and 5-HT2A stimulation)
  • Hyperreflexia
  • Muscle rigidity
  • Hyperthermia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why are SSRIs preferred over TCAs and MAOIs?

A

SSRIs are significantly less toxic (MAOIs caused most cases historically)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which SSRIs are most likely to cause serotonin syndrome?

A

Sertraline
Paroxetine
Fluvoxamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What pharmacological agents are available for sedation?

A

Benzodiazepines:
Diazepam (preferred)
Lorazepam
Chlordiazepoxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What medications can be given as tranquillisers for patients?

A

Haloperidol
Olanzapine
Lorazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do you manage a benzodiazepine overdose?

A
Supportive care (ABCDE)
Continue management via IV thiamine (Pabrines)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What features would you expect to see in benzodiazepine dependence syndrome?

A
Tremor
Anxiety
Perceptual disturbances
Dysphoria
Psychosis
Seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How would you manage benzodiazepine withdrawal?

A
  • Benzodiazepine with a prolonged clinical effect (Diazepam = first-line)
  • Titrate to effect
  • Once symptoms are controlled, gradually taper down dose over several months
    N.B. It’s almost impossible to get patients off benzos successfully
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is lithium used as a mood stabilising drug?

A

Suspected to be linked to sodium transporters, reduction in suicide risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are lithium’s contraindications?

A
  • Significant renal impairment
  • Sodium depletion
  • Dehydration
  • Significant cardiovascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the side effects associated with lithium?

A
  • Nausea and diarrhoea
  • CNS effects: tremor, ataxis, dysarthria, mild cognitive impairment
  • Hypothyroidism
  • Diabetes insipidus
  • Overdose from its narrow therapeutic window
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are examples of SNRIs?

A

Duloxetine

Venlafaxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is reboxetine’s mechanism of action?

A

Selective noradrenaline reuptake inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are examples of tricyclic antidepressants?

A

Amitriptyline
Imipramine
Lofepramine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is mirtazapine’s mechanism of action?

A

Presynaptic alpha2-adrenoreceptor blocker

22
Q

What are examples of classic monoamine oxidase inhibitors?

A

Phenelzine

Tranylcypromine

23
Q

What is agomelatine’s mechanism of action?

A

Melatonin receptor agonist and serotonin receptor antagonist

24
Q

How should a patient be monitored prior to starting antipsychotic medication?

A
  • Weight
  • Waist circumference
  • Pulse & blood pressure
  • ECG if cardiovascular risk factors are identified
  • Fasting blood glucose/ HbA1c/ blood lipid profile & prolactin levels
  • Assessment of any movement disorders
  • Assessment of nutritional status, diet & level of physical activity
25
Why are antipsychotics contraindicated in dementia patients?
Significantly decreased life expectancy by 7 years; increased risk of strokes
26
What is meant by 'anticholinergic life burden'?
Increased risk of dementia, reduced life expectancy, falls, acute confusional states and delirium
27
What are the non-pharmacological choices for managing a patient with psychosis
- Education | - Family/ caregiver support
28
What is an adverse drug reaction?
Adverse effects of a drug at its therapeutic doses (NOT therapeutic failure, overdose, drug abuse, non-compliance or medication errors)
29
What is an adverse drug event?
Occurrence of event after drug exposure; not necessarily caused by the drug
30
What is the difference between type A and type B adverse drug reactions?
Type A - Augmented = exaggerated response to pharmacological action High incidence, low mortality Type B - Bizarre
31
Give examples of non-selective NSAIDs
``` Diclofenac Aspirin Ibuprofen Naproxen Indomethacin ```
32
Besides ulcers, what are the mild and severe side effects of NSAIDs?
Mild: Heartburn and dyspepsia Severe: Ulcers, bleeding and perforation
33
What are common adverse effects of cytotoxic drugs?
Nausea and vomiting Hyperuricaemia Neutropenia
34
What are risks of taking naproxen with ramipril?
Drug related AKI from NSAID with additional affected renal function from ramipril
35
What drugs is cytochrome P450 (CYP3A4) responsible for metabolising?
- Calcium channel blockers - Benzodiazepines - HIV protease inhibitors - HMG-CoA-reductase inhibitors (statins) - Warfarin - Ciclosporin - Non-sedating antihistamines
36
What are inhibitors of cytochrome P450?
- Fluconazole - Clarithromycin - Erythromycin - Grapefruit juice - Ritonavir
37
What are inducers of cytochrome P450?
- Carbemazepine - Rifampicin - Rifabutin - St. John's wort
38
How long to inducers take to act on cytochrome P450?
Days to weeks
39
How long to inhibitors take to act on cytochrome P450?
Rapidly, within days
40
What are common examples of enzyme induction?
Combined oral contraceptive + rifampicin | Warfarin + carbamazepine
41
What are common examples of enzyme inhibition?
Statins + clarithromycin | Warfarin + amiodarone
42
What are common drug-food interactions?
Tetracycline and milk products Warfarin + vitamin K containing foods Grapefruit juice + most drugs Cranberry juice + most drugs
43
How is codeine metabolised?
Prodrug that's demethylated to morphine by CYP2D6
44
What are the consequences of being a CYP2D6 ultra-rapid metaboliser?
The enzyme will increase the bioavailability of the metabolised drug and increase the patient's risk of overdose More side effects and a shorter than expected duration of pain control
45
What does 3N mean in the context of a diplotype genotype?
There are three alleles present rather than two. This means that there will be an additional copy of one of the genes.
46
What are the consequences of being a CYP2D6 poor metaboliser?
Patients may not see any effect of codeine/ it takes a really long time to manifest
47
What scenarios could happen as a result of codeine/CYP2D6 problems?
Breastfeeding in a mother who is an ultra metaboliser
48
How would one prevent codeine overdose?
- Don't take codeine first (take standard dose of morphine) | - Don't take oxycodone, hydrocodone or tramadol as they're all prodrugs and therefor use CYP2D6
49
Why is pancytopenia a possible side effect of mesalazine?
Azathioprine induced marrow suppression
50
How is bone marrow toxicity possible at low azathioprine doses?
Thiopurine methyltransferase (TMPT) is the drug needed to break down 6-MP (active drug) into breakdown products but it could be mutated and have low activity resulting in 6-MP build-up.
51
What is the difference between pharmacogenetics and pharmacogenomics?
Pharmacogenetics - single drug-gene interactions | Pharmacogenomics - effect of multiple genes on drug response (genome wide association)