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Psychiatry > Drugs and treatments in psych > Flashcards

Drugs and treatments in psych Flashcards

1
Q

What is the effect of antidepressants? What are the different types

A
  • Most work on serotonin activity and aim to increase activity at post synaptic receptors
  • Have most of their effects in 2-3 weeks
  • SSRIs most common
  • Others = NSRIs, Mirtazapine, tricyclics, MAOIs
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2
Q

SSRIs
- MOA
- SE

A

MOA - reduce presynaptic reuptake of serotonin after release to increase activity - more serotonin sits in the nerve junction = down reg of post synaptic receptors
SE - agitation and restlessness, nausea and GI disturb (inc peptic ulcer), headache, weight changes, sexual dysfunc

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3
Q

What are some of the different SSRIs? What are some important things to know?

A

Sertraline 50-200mg - safest in cardiac disease
Citalopram 20-40mg - issue w QTC prolongation, ECG before and after, shouldn’t prescribe w other QTC prolongation meds
Fluoxetine 20-60mg - risk of serotonin syndrome
Paroxetine 20-60mg - risk of discontinuation syndrome

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4
Q

What is discontinuation syndrome?

A

Discontinuation syndrome - sweating, shakes, agitation, insomnia, headaches, irritability, N+V, paraesthesia, clonus - when antidepressants stopped suddenly. Paroxetine and venlafaxine trickiest to stop - alt days or half dose or switch to fluoxetine and then stop

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5
Q

NSRIs:
MOA
SE

A

Noradrenaline serotonin reuptake inhibitors - act in the same way as SSRIs but bind to noradrenaline reuptake receptors too.
SE - similar to SSRIs but greater potential for sedation, nausea and sexual dysfunc

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6
Q

What are some examples of NSRIs?

A

Duloxetine 60-120mg
Venlafaxine 75-375mg - more efficacious and can go to a higher dose but caution in heart disease. >225mg dose monitor BP (used to be gold standard antidepressant, probs still is now)

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7
Q

Mirtazapine:
MOA
SEs

A

MOA - acts as 5HT-2 and 5HT-3 antagonist
SE - sedation (strong activity on histamine activity, hence sedation) and weight gain

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8
Q

Tricyclic antidepressants:
- Use
- Warning
- SE

A

Useful for those who don’t respond to SSRIs. Reasonably effective but not tolerated as well as SSRIs.
Have potential for muscarinic and histaminic SEs. Used at low doses for neuropathic pain.
Warning - fatal in overdose due to QTc prolongation and arrhythmias
eg. imipramine

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9
Q

What are muscarinic SEs?

A
  • Dry mouth, difficulty swallowing, thirst
  • Retention
  • Hot, flushed, dry skin
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10
Q

What are histaminic SEs?

A
  • Dry mouth
  • Dizzy and drowsy
  • N+V
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11
Q

What are adrenergic SEs?

A
  • Sweating
  • Tremor
  • Headaches
  • Nausea
  • Dizziness
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12
Q

What do you need to know about MAOIs?

A

Potential for significant and dangerous interactions w other drugs - only prescribed by consultants, possibly more effective for atypical depression.
Potential for tyramine reaction leading to hypertensive crisis.
If change to another antidepressant need 6 weeks washout period - time between stopping one drug and starting another.

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13
Q

Vortioxetine:
- MOA
- SE

A

MOA - serotonergic activity, seratonin reuptake inhibitor and receptor modulator - effective and v well tolerated. Cognitive sx eg. poor con are treated well.
SE - nausea, only at high dose.

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14
Q

How do you decide which antidepressant to use?

A

What has been used before? Was it effective/tolerated?
Sx or comorbidities you may want to address eg. weight loss, insomnia, neuropathic pain.
In new cases - usually SSRI first unless major weight loss and sleep difficulty, then you pick mirtazapine.

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15
Q

What do you do about changing dose or switching antidepressant?

A

For depression - if has no benefit at typical dose after 3 weeks, switch, if partial benefit then increase the dose
For anxiety - increase dose if no initial benefit
For SEs - if they aren’t going to improve then switch

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16
Q

What is serotonin syndrome?

A

Cognitive - headaches, agitation, hypomania, confusions, coma
Autonomic dysfunction - shivering, sweating, hyperthermia, tachy, nausea and diarrhoea
Somatic - myoclonus, hyper reflexia, tremor
Fast onset, caused by SSRIs, SNRIs, tricylic ADs, recreational drugs, opiates
Treat - fluids and monitor, stop seratonergic drugs

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17
Q

How do antipsychotics work?

A
  • Reduce level of dopamine activity at D2 receptors
  • Target mesocortical and mesolimic pathways (glutaminergic)
  • Also affect nigrostriatal (movement) and hypothalamic pit adrenal axis
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18
Q

What are SEs of all antipsychotics?

A
  • Sedation
  • Weight gain
  • Extra pyramidal SEs - bradykinesia, muscle stiffness, tremor, akathisia
  • Acute dystonia - muscle spasms and contractions
  • Oculogyric crisis - spasmodic movements of the eyes, normally into fixed upwards position

Atypical - weight gain and dyslipidaemia, DM
Typical - EPSEs, dizziness, sexual dysfunc

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19
Q

Typical vs atypical antipsychotics

A

Typical - older and more likely to cause extra pyramidal SEs, more likely to bind to more muscarinic and histaminic receptors
Atypical - tend to have more serotonergic activity

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20
Q

What are the typical antipsychotics?

A

Haloperidol
Chlopromazine
Flupenthixol
Zuclopenthixol

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21
Q

What are the atypical antipsychotics?

A

Also called SGAs - second generation antipsyhotics
Clozapine
Olanzapine
Risperidone
Aripiprazole - partial D2 agonist, fewer SEs

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22
Q

What monitoring is needed of antipsychotics?

A

Before prescription - FBC, lipids, LFTs, HbA1c, weight, ECG, BP and pulse
Weekly - weight
3 months - FBC, lipids, LFTs, HbA1c, weight, ECG, BP and pulse
Yearly - FBC, lipids, LFTs, HbA1c, weight, ECG, BP and pulse

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23
Q

Clozapine:
- MOA
- Use
- SE

A

MOA - D2 and 5HT-2 antagonist
Use - most efficacious antipsychotic, used in schizophrenia after 2 other antipsychotics not worked
SE - agranulocytosis (severe leukopenia, close monitoring FBC), gastro intentestinal hypomobility - fatal bowel obstruction and constipation, hypersalivation and urinary incontinence

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24
Q

What is neuroleptic malignant syndrome? CF, RF and supportive treat

A

CF - fever/hyperthermia/sweat, confusion, muscle stiffness, palpitations, autonomic instability due to antipsychotics, usually in first 10 days
Death caused by - rhabdomyolysis, renal fail, seizures
RF - typical antipsychotics and abrupt stopping, high doses, young men
Treat - A+E, stop antipsychotics, fluid resus, reduce temp, may need ICU, VTE prophylaxis

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25
Q

When are anticholinergics used in psych? Give some examples

A

Dopamine:Acetylcholine that causes SEs. If blocking dopamine then will have increased Ach. To treat EPSEs can just use anticholinergics to decrease Ach.
eg. procylidine, benzatropine

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26
Q

What are the different drug classes of anxiolytics?

A

B blockers
Benzos
Pregab
Antidepressants

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27
Q

B blockers:
- MOA
- CI

A

MOA - reduce autonomic nervous system activation, reduce palpitations and tremor (physical sx of anxiety).
Contraindicated in asthma.
eg. propanolol
Not v good for long term anxiety disorders.

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28
Q

Benzos:
- MOA
- Warning

A

MOA - bind to GABA receptors to increase GABA and reduce excitability of neurones - positive allosteric modulators
Warning - big risk of tolerance and dependence. Use cautiously for no more than 6 weeks.
Can cause paradoxical disinhib - people don’t get relaxed but get agitated

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29
Q

Pregab:
- MOA
- Use
- SE

A

MOA - binds to voltage gated Ca channels in neurones = increased GABA conc and reduced neuronal activity.
Use - anxiety, neuropathic pain, epilepsy
Less potential for misuse and dependence than benzos but still can be.
SE - sedation and weight gain

30
Q

What are the hypnotics?

A

Sleeping tablets:
- Benzos - temazepam, lormatazepam
- Nonbenzos - Z drugs, zopiclone
Significant potential for misuse, dependence and rebound insomnia - use for only 2 weeks and take for 5/7 days.

31
Q

What are the mood stabilisers?

A
  • Lithium
  • Anticonvulsants
  • Second generation antipsychotics
    Used to treat bipolar mood disorder.
32
Q

Lithium:
- MOA
- Use
- SEs

A

MOA - unknown
Use - significant evidence to reduce suicide and reduction of self harm, used to augment antidepressants
SEs - GI disturb, fine tremor, polydipsia and polyuria, weight gain, metallic taste, hypothyroid, renal impairment.

33
Q

What is lithium toxicity?

A

Can be intentional overdose but usually w chronic treatment because of reduced drug excretion.
CF - D+V, drowsy, apathy, restless, dysarthria, dizzy, ataxia, not coordinated, muscle twitch, coarse tremor
Severe - hyperrelexia, convulsions, collapse, coma, renal fail, circ collapse, hypokalaemia, death
ECG - T wave inversion most common

34
Q

What is the first line treatment of bipolar disorder?

A

Quetiapine - second gen antipsychotic.
Doses and monitoring the same as psychosis

35
Q

Anticonvulsants as mood stabilisers
eg. and SEs

A
  • Na valproate - teratogenic and check LFTs
  • Carbamazepine
  • Lamotrigine - risk of Stevens Johnson syndrome
  • Pregab
    All have the risk of thrombocytopenia so check FBC.
    SEs - sedation and weight gain
36
Q

What drugs are used for cognitive sx of dementia?

A

AchE inhibs - increase Ach in brain, used for cognitive sx eg. apathy, only for mild and mod dementia
Memantine - used for agitated and challenging behaviour

37
Q

Cholinesterase inhibs:
- SEs
- Monitoring
- Drugs

A

SE - N+D+V, insomnia, muscle cramps, anorexia, bradycardia
Monitor - pulse and ECG before start
eg. donepezil, rivastrigmine, galantamine

38
Q

What drugs are used in ADD and ADHD?

A
  • Methylphenidate - ritalin, most commonly used, combination of immediate and sustained release
  • Dextroamphetamine and lisdexamfetamine
  • Atomoxetine - noradrenaline re uptake inhib, used for prev drug dependence, sexual dysfunc
  • Guanfacine, not for adults
39
Q

Methylphenidate:
MOA
SE

A

MOA - is a stimulant, helps increase activity in frontal lobe, increases dopamine levels by blocking reuptake of dopamine and also NA
SE - tics, seizures, worsening behaviour, sleep issues, loss of appetite, mood changes

40
Q

What are the SEs of dexamfetamine and lisdexamfetamine?

A
  • Dizzy and drowsy
  • Headaches
  • Aggression
  • Decreased appetite
  • N+V+D
41
Q

What is acamprosate?

A

Helps to maintain abstinence from alcohol, decreases cravings. MOA unclear

42
Q

Oral naltrexone

A

Opioid receptor antagonist used to treat alcohol and opioid dependence, helps to prevent relapse.

43
Q

What is ECT?

A

Small doses of electric current used to induce seizures, treatment for severe depression. Is done under GA and also have a muscle relaxant to help prevent soreness from seizure.
ECT administered twice a week for up to 12 treatments, stop the treatment as soon as the pt has maximum benefit. Can be done inpt or outpt.
Electrode can be bilateral or unilateral.

44
Q

What are the indications for ECT?

A
  • Severe depression or difficult to treat depression
  • Catatonia
  • Mania
45
Q

What are the contraindications of ECT?

A
  • Raised intracranial pressure, cerebral aneurysym or recent stroke
  • Recent MI, unstable angina, DVT, uncontrolled HR/BP
  • Acute resp infection
  • Recent food - need 6 hours fasting
  • Unstable fracture, bariatric, cochlear implants
  • Pregnancy, controlled epilepsy
46
Q

What are the side effects of ECT?

A
  • Normal risks of anaesthesia
  • Confusion, headache, status epilepticus, peripheral nerve palsy
  • Stroke, arrhythmia, PE, subconjunctival haemorrhage, broken teeth
  • Memory loss - all types, retrograde, anterograde, geographical orientation, procedural memory
47
Q

What are some other types of neuromodulation?

A

Vagus nerve stimulation and rTMS - transcranial magnetic stim

48
Q

What are the baseline tests before starting lithium?

A
  • Weight, BP and pulse
  • U+Es - lithium renal excretion (don’t prescribe w other drugs that damage kidney)
  • FBC, creatinine, TFT, Ca, TFTs
  • ECG
49
Q

When should lithium levels be checked?

A

First 5 days following starting therapy or changing dose.
Weekly until levels stable for 4 weeks - then every 3 months.
Need to check levels 12 hours after dose

50
Q

What are the target concs of lithium?

A

Acute episode - 0.6-1.0 mmol/L
Prophylaxis of bipolar affective disorder - 0.4-0.8 mmol/L
Toxic range = usually >1.5 mmol/L but can be >1 mmol/L

51
Q

How is lithium toxicity managed and what are the ways to reduce risk?

A

No antidote - stop lithium and monitor levels, supportive treatment normally.
- Correction of fluid and electrolyte balance, may need dialysis if severe enough - cont until no lithium in serum or dialysis fluid
- Monitor ECG

Don’t take lithium w thiazide diuretics, ACEi or NSAIDs

52
Q

Benzodiazepines:
MOA
SE

A

MOA - increase GABA
SE - drowsy, light headed, confusion, unsteady and dizzy, slurred speech, memory problems, sedative

53
Q

Zopiclone:
MOA
SE

A

MOA - modulator of GABA receptor, increasing GABA
SE - bitter/metallic taste in mouth, hangover effect next day, can cause amnesia, falls, delusions and hallucinations

54
Q

What antipsychotics can be used depot?

A

Flupenthixol
Haloperidol
Risperidone
Olanzapine
Aripiprazole

55
Q

What is the monitoring for clozapine?

A

Differential WBC monitoring weekly for 18 weeks then fortnightly for up to a year, then monthly (risk of agranulocytosis)

56
Q

What are some specific treatments of neuroleptic malignant syndrome?

A

Dantrolene (skeletal muscle relaxant for reducing temp), bromocriptine and amantadine (hasten clinical response)
Benzos

57
Q

How does agranulocytosis present?

A

Fever, mouth ulcers, sore throat
Normally in the first 18 weeks of clozapine use

58
Q

How do you manage agranulocytosis?

A

Granulocyte colony stimulating factor (GCSF) can reduce duration of agranulocytosis, if pt becomes febrile or has signs of sepsis/focal infection need to start abx promptly - febrile neutropenia guidelines.

59
Q

What is acute dystonia?

A

Movement disorders characterised by involuntary contractions of muscles, often after taking medications eg. antipsychotics.
Can affect all muscle groups eg. ocular muscles - oculogyric crisis and laryngeal dystonia = larynx.
Can be life threatening so may need emergency care.

60
Q

What is the management of acute dystonias?

A

Antimuscarinics - IV procyclidine
IV benzos are 2nd line

61
Q

What are the principles of psychotherapy?

A
  • Therapeutic relationship
  • Explanation for a pt distress
  • Providing new info about the nature and origins of a persons problems and ways for them to deal w them
  • Development of hope that there can be successs
  • Emotional arousal
62
Q

What are the different forms of psychotherapy available on the NHS?

A
  1. Psychodynamic psychotherapy
  2. CBT
  3. Interpersonal therapy IPT
  4. Family/systemic therapies
63
Q

What is psychodynamic psychotherapy?

A
  • Once/twice weekly for about 4 months to a year but can be longer
  • Therapy addresses transference and defence mechanisms w the aim of resolving unconc conflict
  • An increased understanding of personal problems and behaviours can achieve symptomatic
  • Sessions are unstructured
  • Used for personality disorders, depression, eating disorders and some anxiety disorders
64
Q

What is CBT?

A

Behavioural therapy uses exposure to reduce avoidance and response to a stimulus. Based on conditioning. Used for simple phobias or sexual dysfunctions, anxiety disorders, PTSD, EDs and depression.
Cognitive therapy addresses dysfunc thoughts and beliefs that maintain undesirable emotional states and behaviours - problem orientated, 6-15 weekly sessions w homework tasks. Identifies and challenges negative thoughts. Used in depression, anxiety and EDs.

65
Q

What is IPT?

A

Interpersonal therapy - link between onset of depressive sx and current interpersonal problems as a focus for treatment. Addresses current relationships.

66
Q

What are family and systemic therapies?

A

Target the system that generates problematic behaviour eg. family unit. Most commonly used for managing children but can also be used in EDs.

67
Q

What are some barriers to the therapeutic relationship?

A
  • Therapist not following the core conditions - empathy, congruence and unconditional positive regard
  • Poor/no boundaries
  • Language barriers
  • Previous trauma or attachment issues
  • Substance use
68
Q

What is transferance?

A

The unconcious transfer of feelings and attitudes from the past onto the therapist.
eg. irritated at the therapist because they remind you your abusive father

69
Q

What is counter transferance?

A

The feelings the therapist has in relation to the patient/ Therapists have to undergo their own therapy to counteract that. How does the patient make you feel and why is this important?

70
Q

ID vs ego vs super ego

A

ID - primitive desires
Ego - rational stable part of the personality
Super ego - ethical moral standards you have taken on

Psychiatry (6 decks)

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