mental health + neurology Flashcards

1
Q

tricyclic antidepressants:

  • example? 1
  • mechanism of action?
A

amitryptyline

  • inhibit neuronal reuptake of serotonin + noradrenaline
  • block a wide array of receptors (muscarinic, histamine, a adrenergic, dopamine) -> lots of adverse effects
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2
Q

tricyclic antidepressants:

  • example?
  • indications? 2
A
  • amitryptaline
    1) second-line for depression (if SSRIs not effective)
    2) neuropathic pain (though not licensed for this)
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3
Q

tricyclic antidepressants side effects:

  • example?
  • due to anti-muscarinic actions? 4
  • due to blockage of histamine and alpha adrenergic receptors? 2
  • due to dopamine receptor blockage? 3
  • cardiac effects?2
  • serious brain effects? 3
  • effects of sudden withdrawal? 4
A

anti-muscarinic:

  • dry mouth
  • constipation
  • blurred vision
  • urinary retention

antihistamine + alpha receptors

  • sedation
  • hypotension

anti-dopamine

  • breast changes
  • sexual dysfunction
  • rarely: extra-pyramidal symptoms (tremor, dyskinesia)

cardiac:

  • arrhythmias
  • ECG changes (incl prolongation of QT + QRS durations)

brain:

  • convulsions
  • hallucinations
  • mania

overdose is very dangerous!!! can be fatal!!

sudden withdrawal:

  • GI upset
  • neuro symptoms
  • flu-like symptoms
  • sleep disturbance
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4
Q

tricyclic antidepressants:

  • example?
  • relative contraindications? 6
A

amitriptyline

  • elderly
  • cardiovascular disease
  • epilepsy
  • constipation
  • prostatic hypertrophy
  • raised intraoccular pressure

basically those more likely to get side effects!

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5
Q

tricyclic antidepressants:

  • example?
  • important interaction?
  • possible result?
A

amitriptyline

  • monoamine oxidase inhibitors

as both increase serotonin + noradrenaline levels at synapse

  • can precipitate HTN + hyperthermia or serotonin syndrome

nb tricyclic antidepressants can increase anti-muscarinic, sedative or hypotensive effects of other drugs

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6
Q

serotonin syndrome:

  • what is it?
  • when most likely to get?
  • symptoms? 3
A

too much serotonin -> excessive nerve cell activity

  • when starting, or increasing dose of, medications which increase serotonin levels at the synapse (many anti-depressants)
  • confusion
  • agitation/restlessness
  • headache
  • dilated pupils
  • high heart rate
  • increased BP
  • loss of muscle coordination or twitching muscles
  • muscle rigidity
  • diarrhoea
  • heavy sweating
  • increased temp
  • shivering
  • goose bumps
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7
Q

info for patients on tricyclic antidepressants:

  • advise to patients? 3
  • warnings to patients? 3
A
  • get psychological therapy as well
  • may take a couple of weeks for symptoms to improve
  • continue for 6 months after feeling better
  • about side effects
  • not to stop suddenly
  • not to overdose
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8
Q

SSRIs:

  • examples? 4
  • mechanism of action?
A
  • citalopram
  • excitalopram
  • fluoxetine
  • sertraline

preferentially inhibit the reuptake of serotonin out of the synaptic cleft back into pre-synaptic neuron

nb differ from tricyclic antidepressants as have no effect on noradrenaline reuptake and cause less blockage of other receptors
- so have same efficacy but SSRIs have fewer side effects!

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9
Q

SSRIs:

  • examples? 4
  • indications? 3
A
  • citalopram
  • escitalopram
  • fluoxetine
  • sertraline

1) 1st line treatment for moderate-to-severe depression (+ in mild depression if psychological treatments fail)
2) panic disorder
3) OCD

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10
Q

SSRIs:

  • examples? 4
  • common GI side effects?
  • common neuro/psych side effects?
  • other common side effects? 3
  • particular side effect of citalopram?
  • effect of overdose?
  • effects of sudden withdrawal? 4
A
  • citalopram
  • escitalopram
  • fluoxetine
  • sertraline
  • GI upset
  • appetite + weight disturbance (loss or gain)
  • suicidal thoughts and behaviour
  • SSRIs lower the seizure threshold
  • hypersensitivity reaction (incl skin rash)
  • hyponatraemia
  • increase bleeding risk

citalopram
- can cause long Q-T interval (predisposing to arrhythmias)

overdose -> serotonin syndrome

sudden withdrawal:

  • GI upset
  • neuro symptoms
  • flu-like symptoms
  • sleep disturbance
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11
Q

SSRIs:

  • examples? 4
  • relative contraindications? 5 (incl why)
A
  • citalopram
  • escitalopram
  • fluoxetine
  • sertraline
  • epilepsy (lowers seizure threshold)
  • peptic ulcer disease (increase bleeding risk)
  • young people (poor efficacy + have higher risk of suicide + self harm)
  • elderly (more likely to get side effects, use lower dose)
  • hepatic impairment (as metabolised by liver)
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12
Q

SSRIs:

  • examples? 4
  • severe interaction? 1
  • relative interactions? 3
A
  • citalopram
  • escitalopram
  • fluoxetine
  • sertraline
  • monoamine oxidase inhibitors (may cause serotonin syndrome)
  • NSAIDs (prescribe PPI to protect gastro)
  • anticoagulants (increase bleed risk)
  • antipsychotics (as also prolong Q-T interval)
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13
Q

SSRIs:

  • what to tell patients?
  • which SSRIs should be prescribed for people on lots of meds?
A
  • warn about possible side effects
  • symptoms should improve over 2 weeks or so
  • carry on for 6 months after feeling better
  • don’t stop suddenly
  • don’t overdose
  • citalopram
  • escitalopram
    (appear to have fewer drug interactions)
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14
Q

benzodiazepines

  • examples? 5
  • suffix?
  • how do they differ?
  • mechanism of action?
  • mechanism of action for alcohol withdrawal?
A
  • diAZEPAM
  • temAZEPAM
  • lorAZEPAM
  • chlordiAZEpoxide
  • midAZolam
  • azepam
  • differ mainly in duration of action!

facilitate + enhance binding of GABA to the GABAa receptor

  • > widespread depressant effect on synaptic transmission
  • reduced anxiety
  • sleepiness
  • sedation
  • anticonvulsant effects

alcohol is also a GABAa agonist
- in chronic use, patient becomes tolerant to its presence

therefore abrupt cessation -> excitatory state of alcohol withdrawal
- treated with a benzodiazepine which can be withdrawn in a more controlled manor

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15
Q

benzodiazepines:

  • examples? 5
  • indications? 5
A
  • diAZEPAM
  • temAZEPAM
  • lorAZEPAM
  • chlordiAZEpoxide
  • midAZolam

1) seizures + status epileptics (1st line)
2) alcohol withdrawal (1st line)
3) sedation for interventional procedures (where GA is unnecessary or undesirable)
4) SHORT TERM for severe anxiety
5) SHORT TERM for severe insomnia

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16
Q

benzodiazepines:

  • examples? 5
  • adverse effects? 3
  • long-term effect?
  • effect of sudden withdrawal?
A
  • diAZEPAM
  • temAZEPAM
  • lorAZEPAM
  • chlorAZEpoxide
  • midAZolam
  • drowsiness
  • sedation
  • coma

relatively little respect depression (as opposed to opiate OD) but loss of airway reflexes can -> airway obstruction + death

dependence can develop (if on for weeks)

  • withdrawal reaction similar to alcohol
17
Q

benzodiazepines:

  • examples? 5
  • relative contraindications? 4
  • best one for alcohol withdrawal?
A
  • diAZEPAM
  • temAZEPAM
  • lorAZEPAM
  • chlordiAZEpoxide
  • midAZolam
  • elderly (greater effect)
  • significant respect impairment
  • neuromuscular disease (e.g. myasthenia gravis)
  • liver failure (may precipitate hepatic encephalopathy)

if use is essential (e.g. alcohol withdrawal) use LORAZEPAM as affects the liver the least

18
Q

benzodiazepines:

  • examples? 5
  • interactions? 2
A
  • diAZEPAM
  • temAZEPAM
  • lorAZEPAM
  • chlordiAZEpoxide
  • midAZolam
  • alcohol + opiods (add to deating effect)
  • cytochrome P450 inhibitors (will increase effect of benzodiazepine)
19
Q

benzodiazepines:

  • advice for treatment of anxiety or insomnia? 2
  • general advice for usage? 2
A
  • only a short term measure
  • try not to use every day and use for max of 4 weeks
  • no operating of heavy machinery
  • sleepiness may persist into following day
20
Q

acetyl cholinesterase inhibitors:

  • examples? 3
  • indication?
  • mechanism of action?
A
  • donepezil (aricept)
  • galantine (reminyl XL)
  • rivastigmine (Exelon)
  • mild/moderate dementia

stops the reuptake of ACh back into the presynaptic neuron -> more Ach in synapse (bit like SSRIs with seratonin)

has been shown to slow progression of disease

nb can also be used in Parkinson’s, myasthenia gravis + glaucoma

21
Q

acetyl cholinesterase inhibitors:

  • examples? 3
  • absolute contraindications? 3
  • relative contraindications? 4
A
  • donezepil
  • galantine
  • rivastigamine
  • pregnancy + breast feeding
  • severe hepatic failure
  • severe renal failure
  • CVD disease (may cause bradycardia, esp take care in sick sinus syndrome + supra ventricular conduction disorders
  • peptic ulcer disease (may make worse)
  • COPD + asthma (may cause bronchoconstriction)
  • epilepsy (may lower seizure threshold)
22
Q

acetylcholinesterase inhibitors:

  • examples? 3
  • side effects? 11
A
  • donezepil
  • galantine
  • rivastigamine
  • nausea + vomiting
  • diarrhoea
  • frequent urination
  • weight loss
  • muscle cramps
  • fatigue
  • fainting
  • hypertension
  • headache
  • insomnia
  • hallucinations + abnormal dreams
23
Q

acetylcholinesterase inhibitors:

  • examples? 3
  • interactions?
A
  • donezepil
  • galantine
  • rivastigamine

***look up in BNF

24
Q

L-dopa

  • examples? 2 (+ brand names)
  • indication?
  • mechanism of action?
A
  • co-carELDOPA (sinemet)
  • co-benELDOPA (madopar)

later Parkinson’s disease

  • dopaminergic drugs (which target dopamine receptors in brain) such as ropinirole and prmipexol are used early in disease

lack of dopamine/dopamine producing cells in substantial Niagara in Parkinson’s

L-dopa is a dopamine precursor which can cross blood-brain barrier

nb can be used to treat secondary Parkinsonism but priority is correcting underlying cause (e.g. drug)

25
Q

L-dopa:

  • examples? 2 (+ brand names)
  • relative contraindications? 3
A
  • co-carELDOPA (sinemet)
  • co-benELDOPA (madopar)
  • elderly
  • existing cognitive or psychiatric disease (risk of confusion + hallucinations)
  • CVD (risk of hypotension)
26
Q

L-dopa:

  • examples? 2 (+ brand names)
  • side effects? 6
A
  • co-carELDOPA (sinemet)
  • co-benELDOPA (madopar)
  • nausea
  • drowsiness
  • hypotension
  • confusion
  • hallucinations
  • dyskinesia

nb pschizophrenia is thought to be dt too much dopamine

big problem is low therapeutic range (on-off effect) - range gets smaller as disease progresses

27
Q

L-dopa

  • examples? 2 (+ brand names)
  • interactions? 2
A
  • co-carELDOPA (sinemet)
  • co-benELDOPA (madopar)
  • antipsychotics (esp 1st gen)
  • metoclopramide (anti-emetic)

these are both dopamine antagonist so have opposite effect to L-dopa

28
Q

L-dopa

  • what to co-prescribe
  • how to reduce on-off effect? 2
  • monitoring required? 1
A

peripheral dopa-decarboxylase (nb ‘co-‘ part of drug name shows these drugs are already combined)
- reduces conversion to dopamine outside brain, reduces side effect of nausea and increases therapeutic effect

  • use dopamine agonists first (ropinirole, pramipexol) for as long as possible before using L-dopa
  • make sure patients get doses at the correct time of day (for them) and review doses + timings regularly
  • blood pressure (watch for hypotension)
29
Q

anti epileptics:

  • examples? 5
  • indications? (be specific about each one)
A

phenytoin

  • status epilepticus (where benzodiazepines are ineffective)
  • reduce freq of seizures in epilepsy (though other drugs are preferred

sodium valproate

  • generalised and absence seizures (1st line)
  • focal seizures (2nd line)
  • bipolar (acute treatment of mania + prophylaxis against recurrence)

carbamazepine

  • focal seizures +/- secondary generalisation (1st line)
  • primary generalised seizures (1st line)
  • trigeminal neuralgia (1st line)
  • bipolar disorder, prophylaxis (2nd/3rd line)

lamotrigine

  • focal seizures
  • tonic-clonic seizures

levitaracetam
- focal seizures

30
Q

anti epileptics

- mechanism of action of 3 commonest?

A

sodium valproate

  • weak inhibitor of neuronal Na channels (raising threshold for an AP)
  • increases brain content of GABA

phenytoin

  • inhibitor of neuronal Na channels (raising threshold for an AP)
  • has same effect on cardiac purkinje fibres -> side effects

carbamazepine
- inhibitor of neuronal Na channels (raising threshold for an AP)

nb all of these are not completely understood

31
Q

anti-epileptics:

  • effect of each of 3 commonest on foetuses?
  • other contraindications for 3 commonest?
A

sodium valproate:

  • neural tube defects, craniofacial, cardiac + limb abnormalities + developmental delay
  • HIGHLY TERATOGENIC (often not given to pre-menopausal women)

phenytoin:

  • foetal hydantoin syndrome
  • craniofacial abnormalities and low IQ
  • nb these can be, in theory, protected against w high dose folic acid

carbamazepine:

  • neural tube defects, cardiac + urinary tract abnormalities + cleft palate
  • can be partially protected against w high dose folic acid

sodium valproate:

  • hepatic impairment
  • severe renal impairment

phenytoin

  • low therapeutic index
  • hepatic impairment (reduce dose)
  • anti epileptic hypersensitivity syndrome

carbamazepine

  • anti epileptic hypersensitivity syndrome
  • hepatic, renal or cardiac disease
32
Q

anti-epileptics:

  • side effects of 3 commonest? (+ rarer/more serious ones)
  • names of two others
A

sodium valproate
- GI upset (nausea, heartburn, diarrhoea)
- neuro + psych effects (tremor, ataxia + behavioural disturbances)
- thrombocytopenia
- transient increase in liver enzymes
= hair loss (hypersensitivity), grows back curlier
= severe liver injury + pancreatitis
= bone marrow failure
= anti epileptic hypersensitivity syndrome

phenytoin
- change in appearance (skin coarsening, acne, hirsutism, gum hypertrophy)
- neuro effects, cerebellar toxicity (nystagmus, ataxia + discoordination) + impaired cognition or consciousness
- osteomalacia (as induce vit D metabolism)
= haematological disorders (as induce folic acid metabolism)
= hypersensitivity (rash to anti epileptic hypersensitivity reaction)
= phenytoin toxicity (i.e. overdose) -> death by CV collapse + resp depression

carbamazepine
- GI upset (nausea + vomiting)
- neuro effects (esp dizziness + ataxia)
- oedema + hyponatraemia (dt ADH-like effect)
= hypersensitivity (rash to anti epileptic syndrome)

  • lamotrigine
  • levitaracetam
33
Q

anti epileptic hypersensitivity syndrome:

  • which drugs can lead to it? 2
  • when does it occur?
  • symptoms? 4
  • mortality?
A
  • phenytoin
  • carbamazepine

nb can v v v rarely be caused by other things

usually within 2 months of starting treatment

  • severe skin reactions (e.g. Steven Johnson syndrome, toxic epidermal necrolysis)
  • fever
  • lymphadenopathy
  • systemic effect (haematological, hepatic, renal)
  • mortality is 10%
34
Q

anti-epileptics, interactions:

  • sodium valproate? 4
  • phenytoin? 4
  • carbamazepine? 4
A

sodium VALproate

  • it is a P450 INHIBITOR (increases plasma conc of other drugs)
  • also affected by P450 interactions (so conc increases with inhibitors + conc decreases with inducers)
  • drugs that lower seizure threshold (SSRIs, tricyclic antidepressants, antipsychotics, tramadol)
  • aspirin (competes for protein binding, increases plasma conc)

PHENytoin
- it is a P450 INDUCER (decreases plasma conc of other drugs)
- also affected by P450 interactions (so conc increases with inhibitors + conc decreases with inducers)
carbamazepine
- drugs that lower seizure threshold (SSRIs, tricyclic antidepressants, antipsychotics, tramadol)
- other anti epileptic drugs

CARbamazepine:
- it is a P450 INDUCER (decreases plasma conc of other drugs)
- also affected by P450 interactions (so conc increases with inhibitors + conc decreases with inducers)
carbamazepine
- drugs that lower seizure threshold (SSRIs, tricyclic antidepressants, antipsychotics, tramadol)
- other anti epileptic drugs

35
Q

sodium valproate:

  • what to co-prescribe?
  • when to take?
  • what symptoms of adverse reactions to look out for? 7
  • what to monitor? 2
  • driving rules w epilepsy? 2
A
  • contraceptives (for women of child-bearing age)
  • nb risk of foetal abnormality is 10% (folic acid can reduce this)
  • with food (reduce GI side effects)

liver poisoning:

  • lethargy
  • loss of appetite
  • vomiting
  • abdo pain

blood abnormalities:

  • bruising
  • high temp
  • mouth ulcers
  • compare seizure freq before + after treatment
  • LFTs (especially when changing treatment
  • can’t drive within 12months of a seizure
  • can’t drive within 6 months of changing or stopping meds
36
Q

phenytoin:

  • what to co-prescribe?
  • when to take?
  • what symptoms of adverse reactions to look out for? 3
  • what to monitor? 2
  • driving rules w epilepsy? 2
A
  • contraceptives (for women of child-bearing age)
  • take with food (and don’t miss a dose!!)
  • skin rashes
  • bruising
  • signs of infection (high temp, sore throat)
  • compare seizure freq before + after treatment
  • plasma phenytoin conc (therapeutic index is low)

nb during IV treatment, monitor BP, ECG, RR + O2 sats to check for adverse reactions

  • can’t drive within 12months of a seizure
  • can’t drive within 6 months of changing or stopping meds
37
Q

carbamazepine:

  • what to co-prescribe?
  • what symptoms of adverse reactions to look out for? 6
  • what to monitor? 1
  • driving rules w epilepsy? 2
A
  • contraceptives (for women of child-bearing age)
  • skin rashes
  • bruising
  • bleeding
  • high temp
  • mouth ulcers (blood probs)
  • reduced appetite or abdominal pain (liver toxicity)
  • compare seizure freq before + after treatment
  • can’t drive within 12months of a seizure
  • can’t drive within 6 months of changing or stopping meds