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Psychiatry > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the common side effects of adrenergic/noradrenergic receptors?

A 
Sweating
Tremor
Headaches
Nausea 
Dizziness

Fight/flight

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2
Q

What are the common side effects of muscarinic receptors?

A

Dry mouth, difficulty swallowing, thirst
Difficulty urinating, urinary retention
Hot and flushed skin
Dry skin

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3
Q

What are the common side effects of histamine?

A

Dry mouth
Drowsiness
Dizziness
Nausea and vomiting

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4
Q

What are anti-depressants?

A

Most work on serotonin activity, aiming to increase post synaptic response.
Most have their effect in 2-3wks
Commonly use SSRIs.
Also can use SNRIs, Mirtazapine, Tricyclics, MAOIs.

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5
Q

How do SSRIs work?

A

Bind to reuptake receptors.
Increase serotonin activity by reducing the presynaptic reuptake of serotonin after release.
So more serotonin in the synapse.
Leading to down regulation of post-synaptic receptors 2-3wks later

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6
Q

What are the side effects of SSRIs?

A

Sense of restlessness, agitation on initiation (therefore use benzodiazepines)
Nausea
GI disturbance
Headache

Last longer and are more important for people-
Weight changes- most lead to weight loss.
Sexual dysfunction- difficulty experiencing arousal and orgasm.
Less common- bleeding (some serotonin receptors in GI tract platelets) and suicidal ideation (age related)

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7
Q

What is suicide ideation?

A

Anti-depressants usually increase energy levels before decreasing the suicidal thoughts/suicidality.
Therefore in the initial steps of taking the anti-depressants there is a high risk of suicide. So clinicians should follow up pts after 2wks of prescribing.
More pronounced in men and younger generation.

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8
Q

What are the doses of SSRIs?

A

Sertraline 50-200mg. Therapeutic dose starts at 100mg. Safest in cardiac disease.
Citalopram- 20-40mg. Ecitalopram 10-20mg. Be weary of QTc prolongation therefore avoid if other drugs have the potential for that.
Fluoxetine 20-60mg. Be weary of serotonin syndrome when switching since long half life.
Paroxetine 20-60mg. Be weary of discontinuation syndrome since short half life.

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9
Q

What are SNRIs?

A

Act as SSRIs, but bind to noradrenaline reuptake receptors as well.
Evidence base for neuropathic pain

Two types-
Duloxetine (UK liscensed for neuropathic pain) 60-120mg
Venlafaxine 75-375mg. Caution at higher doses in heart disease, can cause HTN at higher doses so ensure monitoring if 225mg+

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10
Q

What are the side effects for SNRIs?

A

Same as SSRIs but also

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11
Q

What is mirtazapine?

A

5H2/3 antagonist
Strong histaminic activity- causing sedation
Major side effects weight gain and sedation.
Side-effects occur at low and high doses, therefore not dose dependent.
These ‘side effects’ can be used for therapeutic advantage i.e. pt lost weight and struggle to sleep. Most pt take this early evening/night.

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12
Q

What are tricyclics?

A

Used less due to tolerance
All have potential to give muscarinic and histaminic side effects.
More fatal in overdose- QTc prolongation and arrhythmias
Used at low dose for neuropathic pain

Newer- lofepramine and nortriptylines tolerated better than older amitryptilines.

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13
Q

What are MAOIs?

A

Type A work on serotonin more.
Type B work on dopamine more.
More effective for atypical depression- pt sleeps more and eats more.

Irreversible- more dangerous phenelzine, isocarboxazid
Reversible- less dangerous moclobamide trabycypromine.

Risk of tyramine reaction. Too much tyramine leads to more adrenaline and hypertensive crisis. Therefore need to avoid cheese, wine, pickled meats and tyramine products.
Need to be careful when changing to another antidepressant, may require a washout period of 6wks.

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14
Q

Vortioxetine

A

Newer antidepressant
All sorts of serotonergic activity, sometimes will agonise, sometimes antagonise.
Well tolerated, better than other antidepressants.
Most common side effect is nausea.
Improves difficult to treat cognitive symptoms. Post depression, some people find cognitively they’re still not well I.e. difficulty concentrating, poor memory etc.

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15
Q

Which antidepressant should we use?

A

Which have already been used for the pt?
Was this effective before? Was it tolerated before?
Are there any particular co-morbidities we wish to address? I.e. weight loss, insomnia, neuropathic pain.
What does the pt want? Sometimes there is a placebo affect if the pt believes a certain medication will work.

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16
Q

What to use

A

If new case, with no previous treatment- start with SSRIs.
If there is major weight loss or major sleep difficulty then use mirtazipine.
If there is comorbid neuropathic pain then consider SNRIs.

In most cases start with SSRI, if no effect then change SSRI, if no effect then change SNRI venlaflaxine or mirtazapine.

Starting SSRI, usually sertraline.
If the Pt wants a certain drug and there are no contraindications then start it.

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17
Q

Should you increase the dose or switch the antidepressant?

A

Give someone lowest therapeutic dose initially.
Wait 4wks for an effect.
If no effect on the lowest therapeutic dose, increasing the dose is unlikely to give a therapeutic effect.
Switch the medication.

BUT
If there has been a significant change, but the pt is not in complete remission.
Increase the dose.

For anxiety conditions (particularly OCD), consider increasing the dose higher, before giving up and switching.

If there are significant side effects within the first few weeks encourage the side effects will get better then the benefits will begin to appear. If however these side effects are causing a real problem for the pt, switch.

18
Q

What is discontinuation syndrome?

A

Antidepressants are not addictive. BUT they can be difficult to stop.
If you stop taking them abruptly some can develop a withdrawal symptoms.
Syndrome is characterised by- sweating, shaking, agitation, insomnia, headaches, irritability,y parades this, clonus, N+V
This is influenced by half life, the shorter the half life the more difficult.
Also when stopping quickly from a high dose

Paroxetine and venlaflaxine are trickiest to stop. So reduce slowly.
Can take in alternate day, snap tablets in half.
Sometimes switch to fluoxetine (longer half life), then reduce the fluoxetine.

19
Q

What is serotonin syndrome?

A

Very vague presentation
Cognitive- headache, agitation, hypothermia, confusion, coma
Autonomic- shivering, sweating, hyperthermia, tachycardia, nausea and diarrhoea.

Treatment usually supportive i.e. fluids.

20
Q

What are antipsychotics?

A

AKA neuroleptic
All work by reducing the level of dopamine activity at D2 receptors.
Target dopaminergic pathways include mesocrotical, mesolimbic
Unwanted effects can come from nigrostriatal (movement/extrapyramidal side effects) and tu

21
Q

What are the two main classes?

A

Typical- (first generation) more likely to give extra pyramidal side effects. Mind more to muscarinic and histaminic receptors
Atypical- (second generation), bind more to serotonin receptors.

22
Q

What are examples of typical antipsychotics?

A
23
Q

What are examples of atypical

A

Clozapine-has many side effects but works well in difficult cases
Aripriazole- works as a partial agonist therefore has fewer side effects. (Has longest half life and longer to have an effect).

24
Q

What are the side effects of antipsychotics.

A

Potential for sedation, weight gain, QTc prolongation.

Typical (more likely to cause)-
Extra pyramidal- bradykinesia, muscle stiffness and tremor, tardive dyskinesia (involuntary spasm of mouth, pharynx, oropharynx), akathisia (urge to move).
Dizziness
Sexual dysfunction

Atypical (more likely to cause)-
Weight gain
Dyslipidaemia and diabetes

25
Q

How do we monitor antipsychotics?

A

FBC- bone turnover affected
Lipids- can cause dyslipidae,is
LFTS- can cause hepatitis
HbA1c- can cause diabetes

26
Q

What is neuroleptic malignant syndrome?

A

Rare life threatening reaction to antipsychotics.
Fever, confusion, muscle rigidity, sweating, autonomic instability.

Death usually due to rhabdomyolysis, renal failure, seizures

Risk factors include high potency dopamine antagonists (typical antipsychotics) in antipsychotic naive, high doses, young men (more likely to be physically restrained than women and resist an injection)

27
Q

How to treat NMS

A 
NB NMS has high CK compared to SSyndro,e
Emergency A+E
Stop antipsychotics
Give benzo for acute behavioural disturbance
Fluid resus
Reduce temp
O2 if necessary
Rhabdomyolysis treated with fluid and
28
Q

EPSE of antipsychotics

A

Occur due to ratio between Ach and dopamine.
Reducing Ach activity, will reduce EPSE.
If too much Ach symptoms, can’t increase dopamine, therefore reduce Ach.
Use procyclidine (don’t give if history of misuse)
Benzo
Trihexphenidyl
May exacerbate tardic dyskinesia

29
Q

What are acute dystopias

A

Sustained, painful muscle spasms, producing twisted abndomrl posture.
Most common in neck, Jaw, oculogyric crisis (neck arched and eyes rolled back)
Stop antipsychotics
Give IM (usually) or IB procyclidine
Then continue with oral procyclidine for 1-2 days post dystonisd,
May have to use long term to avoid EPSE

30
Q

What is clozapine?

A

D2 antagonist, 5HT-2 antagonist
Most effacCious antipsychotic

Should be used in schizophrenia after two other antipsychotics not been effective.
Potential for agranulocytosis. Therefore needs. Close monitoring FBC, weekly initially for 18wks then fortnightly for 1 year, then monthly. Can’t issue without a FBC.

Potential for gastrointestinal hypo-mobility- constipation so potentially fatal bowel obstruction (toxic mega colon).

Other side effects include hypersalivation and urinary incontinence.
The dose is titration upward over two weeks (I.e. very gradually) and vital signs monitored due to potential for autonomic dysregulstion I.e. could die from VF arrest.

31
Q

How is agranulocytosis treated?

A

Stop clozapine and any other potentially marrow suppressing drugs I.el sodium valproate.
Avoid other antipsychotics where possible, if can’t then give aripriprazole, since least likely to suppress.
Contact consuktant haematologist.
Avoid sources of infection, consider prophylactic broad spectrum Abx
Sometimes lithium is used to increase WCC and neutrophil count, may be better at maintaining high neutrophil count, compared to G-CSF.
G-CSFncan be given, but need to give doses regularly, which can be painful.

32
Q

What are anxiolytics?

A 
Reduce anxiety
Beta blockers
Benzodiazepines
Pregabalin
Antidepressants
33
Q

What are beta blockers?

A

Reduce autonomic nervous system activation.
Bio-psycho-feedback
Often misused by performers (professional musicians, actors) and the drug of choice of snooker players.
Most of the used in psychiatry is propanolol- dangerous in overdose, can lead to cardiac arrhythmias.
Contraindicated in asthma
Limited in effectiveness for enduring anxiety disorders

34
Q

What are benzodiazepines?

A

Meant to be used in short term
Longer half life- less of a dependence
Diazepam (long t1/2) and lorazepam (short)
Bind to GABA receptors, changing the shape and therefore increasing the effect so reduce neurone excitability.
Significant potential for tolerance and dependence
Significant potential for misuse
Use very cautiously and for no more than 6wks
Occasionally cause paradoxical disinhibition- at lower doses.

35
Q

What is pregabalin?

A

Binds go voltage CC on neurones
This increases threshold potential, so makes neurones less excitable
Used in anxiety, neuropathic pain and epilepsy
Less potential for misuse and dependence (and tolerance) than

36
Q

Use of antidepressants for anxiety disorder?

A
37
Q

What are hypnotics?

A

Benzodiazepines- Temazepam, lormatezepam, nitrazepam
Non- benzodiazepines -
Act in very similar way (positive allosteric modulators) but are structurally different to benzodiazepines. Also called Z drugs

Probably not much difference between two groups (Z drugs usually favoured)
Significant potential for misuse, dependence, rebound insomnia.
Use for only 2wks, and take for only 5 out ofn

38
Q

What is lithium?

A

One of the most effective mood stabilisers.
MOA aid unknown- does all sorts of things in the brain, notably lowering NA

Nearly all tab,et

39
Q

What are the side effects of lithium

A

Do U+E and TFTs at 3 months and one year

40
Q

Drug in ADDand ADHD

A

If a person is bouncing off the walls the theory is they’re under stimulated in some way, so are constantly doing things to achieve stimulation. Therefore give stimulants to treat ADHD.
Normally take a tablet which has short and long release within the same tablet.

41
Q

NARI

A

Noradrenaline reuptake inhibitor

Not really in exams

Psychiatry (12 decks)

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