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Year 3 Drugs > Mental Health Drugs > Flashcards

Mental Health Drugs Flashcards

1
Q

Tricyclic anti-depressant examples

A

Amitriptyline, lofepramine

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2
Q

Tricyclic anti-depressant indications

A
  1. Second line treatment for moderate - severe depression where SSRIs ineffective
  2. Treatment for neuropathic pain (not licensed)
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3
Q

Tricyclic anti-depressant MOA

A
  • Inhibits neuronal re-uptake of serotonin and noradrenaline from synaptic cleft, increasing their availability for neurotransmission
  • Block a wide range of receptors including muscarinic, histamine, alpha-adrenergic and dopamine - accounts for extensive adverse effects profile
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4
Q

Tricyclic anti-depressant contraindications

A

Used with caution in people at high risk of side effects:

  • Elderly
  • CVD
  • Epileptics
  • Constipated
  • Prostatic hypertrophy
  • Raised intra-ocular pressure
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5
Q

Tricyclic anti-depressant side effects

A
  1. Blockade of anti-muscarinic receptors: dry mouth, urinary retention, blurred vision
  2. Blockade of alpha-adrenergic receptors: sedation and hypotension
  3. Cardiac adverse effects: arrhythmias, prolonged QT and QRS
  4. Neurological changes: convulsions, hallucinations and mania
  5. Dopamine receptor blockade: breast changes, sexual dysfunction
  6. Extrapyramidal symptoms: tremor, dyskinesia
  7. Overdose: hypotension, arrhythmias, convulsions, coma, respiratory failure
  8. Sudden withdrawal: GI upset, neurological and flu-like symptoms, sleep disturbance
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6
Q

Tricyclic anti-depressant interactions

A
  1. MOA inhibitors: both increase serotonin and noradrenaline at synapse - precipitates hypertension, hyperthermia, serotonin syndrome
  2. Augment anti-muscarinic, sedative, hypotensive adverse effects of other drugs
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7
Q

Tricyclic anti-depressant patient information

A

Takes a few weeks to notice improvements
Symptoms may worsen initially
Discuss psychological therapies
Treatment must be continued for 6 month minimum

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8
Q

SSRIs examples

A

citalopram, fluoxetine. sertaline, escitalopram

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9
Q

SSRIs indications

A
  1. 1st line for moderate / severe depression
  2. Mild depression after failure of psychological therapy
  3. OCD
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10
Q

SSRIs MOA

A
  • Preferentially inhibit neuronal re-uptake of serotonin from the synaptic cleft, increasing its availability for neurotransmission
  • Differ to tricyclics: do not inhibit noradrenaline uptake, cause less blockade of other receptors
  • Efficacy between 2 classes similar but SSRIs preferred due to fewer adverse effects
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11
Q

SSRIs contraindications

A

Prescribed with caution where particular risk of adverse effects:

  • epilepsy
  • peptic ulcer disease

Young people:

  • decreased efficacy
  • increased risk of self-harm and suicidal thoughts

Metabolised by liver so reduced dose in hepatic impairment

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12
Q

SSRIs side effects

A
  1. Common: GI upset, appetite and weight disturbance, hypersensitivity reactions (skin rashes)
  2. Elderly: hyponatraemia which may present as confusion and reduced consciousness
  3. Increased suicidal thoughts and behaviours
  4. Lower seizure threshold
  5. Citalopram prolongs the QT interval so can predispose to arrhythmias
  6. Increased risk of bleeding
  7. Serotonin syndrome: when taken at high doses / combined with other anti-depressants / overdose. Triad consisting of:
    -autonomic hyperactivity
    -altered mental state
    -neuromuscular excitation
    Usually responds to withdrawal of treatment and supportive therapy.
  8. Sudden withdrawal: GI upset, neruological and flu-like symptoms, sleep disturbance
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13
Q

SSRIs interactions

A
  1. MOIs: both increase synaptic serotonin levels = serotonin syndrome.
  2. NSAIDs / aspirin: increased risk of GI bleed, must offer gastroprotection
  3. Anti-coagulants: increased risk of bleeding
  4. Other drugs that prolong QT interval e.g. antipsychotics
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14
Q

SSRIs patient info

A

Takes a few weeks to notice improvements
Symptoms may worsen initially
Discuss psychological therapies
Treatment must be continued for 6 month minimum

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15
Q

Benzodiazepines examples

A

Diazepam, lorazepam, midazolam, chlordiazepoxide

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16
Q

Benzodiazepines indications

A
  1. 1st line management of seizures and status epilepticus
  2. 1st line management of alcohol withdrawal reactions
  3. Sedation for interventional procedures if general anaesthesia is unnecessary / undesirable
  4. Short term management of severe anxiety
  5. Short term management of severe insomnia
17
Q

Benzodiazepines MOA

A
  • Targets GABAa: a Cl- channel that opens in response to binding of GABA, the main inhibitory neuron
  • Opening the channel allows Cl- ions to flow into cell making it more resistant to depolraisation
  • Benzodiazepines facilitate and enhance the binding of GABA to GABAa
  • This depresses synaptic transmission and clinically reduces anxiety, causes sleepiness and sedation, and is anti-convulsive.
  • Alcohol also acts on GABAa - chronic users become tolerant to its presence. Abrupt cessation precipitates excitatory state of alcohol withdrawal. Benzodiazepines can be used to withdraw in a more controlled way.
18
Q

Benzodiazepines administration

A
  • Water-based solution
  • Oil-in-water emulsion
  • IV if equipped to deal with over-sedation
19
Q

Benzodiazepines contraindications

A
  1. Elderly: more susceptible to effects so require lower doses
  2. Respiratory impairment
  3. Neuromuscular disease e.g. myasthenia grvis
  4. Liver failure: can cause hepatic encephalopathy - if essential e.g. alcohol withdrawal, choose lorazepam as less liver dependent
20
Q

Benzodiazepines side effects

A
  • Drowsiness, sedation and coma
  • Overdose: cardiorespiratory depression, loss of airway reflexes = airway obstruction and death
  • Tolerance
  • Abrupt cessation = withdrawal reaction similar to alcohol
21
Q

Benzodiazepines interactions

A
  • Additive effect to other sedatives e.g. opiates and alcohol
  • Use cP450 enzymes so use in addition to inhibitors may increase their effects
22
Q

Benzodiazepines patient info

A
  • Only short-term measure
  • Discuss risks of dependence
  • Should not drive or operate machinery after taking
  • Sleepiness may persist
23
Q

Acetylcholinesterase inhibitors examples

A

Donepezil, galantamine, rivastigmine

24
Q

Acetylcholinesterase inhibitor indications

A
  1. To slow progression of Alzheimer’s disease
25
Q

Acetylcholinesterase inhibitors MOA

A
  • Inhibits acetylcholinesterase enzyme responsible for the breakdown of acetylcholine in the synaptic cleft
  • This leaves more acetylcholine available for cholinergic function
  • Effects may lessen as disease course progresses as fewer neurones remain functionally intact
26
Q

Acetylcholinesterase inhibitors administration

A

Oral, 5mg increase to 10mg

27
Q

Acetylcholinesterase inhibitors contraindications

A

Use with caution in:

  • asthma
  • COPD
  • sick sinus syndrome
  • supra-ventricular conduction abnormalities
  • increased risk of peptic ulcers
28
Q

Acetylcholinesterase inhibitors side effects

A
  • Nausea
  • Vomiting and diarrhoea
  • Difficulty sleeping
  • Muscle cramps
  • Decreased appetite
29
Q

Acetlycholinesterase inhibitors patient information

A

Take at bedtime

Year 3 Drugs (9 decks)

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