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HYMS PPT > Psychological > Flashcards

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
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2
Q

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

A

Benzodiazepines - avoid prolonged use

Propranolol

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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

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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

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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)

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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)
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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
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8
Q

Why are SSRIs preferred over TCAs and MAOIs?

A

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

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9
Q

Which SSRIs are most likely to cause serotonin syndrome?

A

Sertraline
Paroxetine
Fluvoxamine

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10
Q

What pharmacological agents are available for sedation?

A

Benzodiazepines:
Diazepam (preferred)
Lorazepam
Chlordiazepoxide

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11
Q

What medications can be given as tranquillisers for patients?

A

Haloperidol
Olanzapine
Lorazepam

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12
Q

How do you manage a benzodiazepine overdose?

A 
Supportive care (ABCDE)
Continue management via IV thiamine (Pabrines)
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13
Q

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

A 
Tremor
Anxiety
Perceptual disturbances
Dysphoria
Psychosis
Seizures
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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
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15
Q

Why is lithium used as a mood stabilising drug?

A

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

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16
Q

What are lithium’s contraindications?

A
  • Significant renal impairment
  • Sodium depletion
  • Dehydration
  • Significant cardiovascular disease
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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
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18
Q

What are examples of SNRIs?

A

Duloxetine

Venlafaxine

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19
Q

What is reboxetine’s mechanism of action?

A

Selective noradrenaline reuptake inhibitor

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20
Q

What are examples of tricyclic antidepressants?

A

Amitriptyline
Imipramine
Lofepramine

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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
Q

Why are antipsychotics contraindicated in dementia patients?

A

Significantly decreased life expectancy by 7 years; increased risk of strokes

26
Q

What is meant by ‘anticholinergic life burden’?

A

Increased risk of dementia, reduced life expectancy, falls, acute confusional states and delirium

27
Q

What are the non-pharmacological choices for managing a patient with psychosis

A
  • Education

- Family/ caregiver support

28
Q

What is an adverse drug reaction?

A

Adverse effects of a drug at its therapeutic doses (NOT therapeutic failure, overdose, drug abuse, non-compliance or medication errors)

29
Q

What is an adverse drug event?

A

Occurrence of event after drug exposure; not necessarily caused by the drug

30
Q

What is the difference between type A and type B adverse drug reactions?

A

Type A - Augmented = exaggerated response to pharmacological action
High incidence, low mortality
Type B - Bizarre

31
Q

Give examples of non-selective NSAIDs

A 
Diclofenac
Aspirin
Ibuprofen
Naproxen
Indomethacin
32
Q

Besides ulcers, what are the mild and severe side effects of NSAIDs?

A

Mild: Heartburn and dyspepsia
Severe: Ulcers, bleeding and perforation

33
Q

What are common adverse effects of cytotoxic drugs?

A

Nausea and vomiting
Hyperuricaemia
Neutropenia

34
Q

What are risks of taking naproxen with ramipril?

A

Drug related AKI from NSAID with additional affected renal function from ramipril

35
Q

What drugs is cytochrome P450 (CYP3A4) responsible for metabolising?

A
  • Calcium channel blockers
  • Benzodiazepines
  • HIV protease inhibitors
  • HMG-CoA-reductase inhibitors (statins)
  • Warfarin
  • Ciclosporin
  • Non-sedating antihistamines
36
Q

What are inhibitors of cytochrome P450?

A
  • Fluconazole
  • Clarithromycin
  • Erythromycin
  • Grapefruit juice
  • Ritonavir
37
Q

What are inducers of cytochrome P450?

A
  • Carbemazepine
  • Rifampicin
  • Rifabutin
  • St. John’s wort
38
Q

How long to inducers take to act on cytochrome P450?

A

Days to weeks

39
Q

How long to inhibitors take to act on cytochrome P450?

A

Rapidly, within days

40
Q

What are common examples of enzyme induction?

A

Combined oral contraceptive + rifampicin

Warfarin + carbamazepine

41
Q

What are common examples of enzyme inhibition?

A

Statins + clarithromycin

Warfarin + amiodarone

42
Q

What are common drug-food interactions?

A

Tetracycline and milk products
Warfarin + vitamin K containing foods
Grapefruit juice + most drugs
Cranberry juice + most drugs

43
Q

How is codeine metabolised?

A

Prodrug that’s demethylated to morphine by CYP2D6

44
Q

What are the consequences of being a CYP2D6 ultra-rapid metaboliser?

A

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
Q

What does 3N mean in the context of a diplotype genotype?

A

There are three alleles present rather than two. This means that there will be an additional copy of one of the genes.

46
Q

What are the consequences of being a CYP2D6 poor metaboliser?

A

Patients may not see any effect of codeine/ it takes a really long time to manifest

47
Q

What scenarios could happen as a result of codeine/CYP2D6 problems?

A

Breastfeeding in a mother who is an ultra metaboliser

48
Q

How would one prevent codeine overdose?

A
  • 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
Q

Why is pancytopenia a possible side effect of mesalazine?

A

Azathioprine induced marrow suppression

50
Q

How is bone marrow toxicity possible at low azathioprine doses?

A

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
Q

What is the difference between pharmacogenetics and pharmacogenomics?

A

Pharmacogenetics - single drug-gene interactions

Pharmacogenomics - effect of multiple genes on drug response (genome wide association)

HYMS PPT (4 decks)

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