Psych Drugs, Tx and SE's Flashcards

1
Q

What are some typical and atypical antipsychotics? How do they differ in action?

A

Typical - block D2 receptors

  • > Chlorpromazine
  • > Haloperidol

Atypical - block D2, D3, D4, D5 and 5HT receptors, more selective than typical antipsychotics so less SEs

  • > Aripiprazole
  • > Risperidone
  • > Clozapine (acts on D1+D4)
  • > Olanzapine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the normal 1st line treatment for schizophrenia? What are some risks associated with these drugs?

A

1st line for Schizophrenia = atypical antipsychotic due to heavy SEs of typical antipsychotics + relapse risk

However
INCREASED risk of stroke and VTE in the elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the common side effects of typical and atypical antipsychotics? Specific drug SEs/risks?

A

Typical =

  • > EPSEs (acute dystonia, akathisia, parkinsonisms and tardive dyskinesia)
  • > Hyperprolactinaemia

Atypical =

  • > Fewer EPSEs (acute dystonia, akathisia, parkinsonisms and tardive dyskinesia)
  • > Less hyperprolactinaemia (Aripiprazole is good for this, Risperidone is NOT; also makes pregnancy harder)
  • > Olanzapine = metabolic syndrome and hyperglycaemia, weight gain, sedation, anticholinergic
  • > Quetiapine = QT prolongation
  • > Clozapine = agranulocytosis (1%), sedation, weight gain, hyperglycaemia, lithium interaction, lowers seizure threshold, anticholinergic, myocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is an important SHx question to ask when on Clozapine?

A

Smoking + cessation - clozapine levels go up if the patient stops smoking suddenly, so if aware then can adjust accordingly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is neuroleptic malignant syndrome? How is it Ix and managed?

A

Rare but life-threatening side effect of antipsychotics (most likely Haloperidol)

Gradual onset triad (4-11d later) of:

  • Mental status change (Catatonia)
  • Muscular rigidity
  • Autonomic instability (hyperthermia >40degrees, labile BP, high HR, RR and sweating)

Ix:

  • FBC –> Leucocytosis
  • Rigidity –> rhabdomyolysis –> high CK >1000
  • U&Es deranged

Mx:

  • A-E approach
  • Stop antipsychotics
  • Supportive - fluids, dialysis
  • Dantrolene, bromocriptine (muscle relaxant, dopamine agonist)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What relieving drugs can be used for which EPSEs?

A

Acute dystonia (early, sometimes within hours) - anticholinergic e.g. Procyclidine

Akathisia (hours to weeks) - switch drug/lower dose OR
+ Proporanolol/BDZ

Parkinsonism (days-weeks) - switch/lower dose OR anticholinergic e.g. procyclidine

Tardive dyskinesia (months-years) - switch medications (typical or clozapine) OR Tetrabenazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can antidepressants be used to treat? What are the different types of ADs?

A

Includes SSRIs, SNRIS, TCAs, NaSSAs, MAOIs, RIMAs + NARIs

Tx for:

  • Depression
  • Anxiety disorders
  • OCD
  • EDs
  • PDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the ‘discontinuation’ symptoms if you suddenly stop SSRIs?

A
'FIRM STOP':
Flu-like Sx
Insomnia
Restlessness
Mood swings

Sweating
Tummy problems (D&V, pain)
Off balance (Ataxia)
Paraesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do SSRIs work (time taken etc)? What are some specific drug indications? What are some CI drugs to be aware of?

A

SSRIs - block reuptake of 5HT in the synaptic cleft

Initially make you feel worse before you feel better (1-2w) as 5HT immediately increases but glutamate takes longer/initially suppressed and this discrepancy in timing causes slight worsening of Sx. Also increases anxiety, SH and suicide risk so must follow up those with high risk/<30 within 1w, otherwise 2w later!! Takes 2-4/4-6w to work

Specific indications:
Fluoxetine - depression in children/teenagers
Citalolopram - QT prolongation
Sertraline - good in those post-MI/CVD
Paroxetine - higher chance of discontinuation Sx

AVOID:

    • Triptans –> ask if have migraines
    • NSAIDs –> if need to be taken, prescribe PPI also
  • > TCAs, MAOIs, venlafaxine for high suicide risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How long must you take antidepressants for? How are they stopped or switched?

A

Take 4-6w to work, with worsening Sx in first 1-2w

Continue for at least 6m after remission if 1st episode
OR
2 years if a recurrence

Gradually stopped over 4w to avoid discontinuation symptoms

Switching:
Fluoxetine - reduce dose over 2w and wait another 4-7d after stopping before starting another SSRI (due to long half life)
Guidance online for class-switching also

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some SE of SSRIs? What is serotonin syndrome and how is it managed?

A

5 S’s:
Suicide ideation (for 1-2w)
Stomach (N&V, diarrhoea, weight gain, dyspepsia; 5-10d)
Sexual dysfunction
Sleep (insomnia, 5-10d)
Serotonin syndrome (abrupt onset triad of change in mental status i.e. confusion/agitation/coma, neuromuscular changes i.e. jerking/twitching/hyperreflexia and autonomic instability (hyperthermia, hypertension, high HR/RR, sweating) and D&V –> Mx with A-E approach, stop antidepressant, BDZ e.g. Clonazepam and supportive Tx

+++

  • Hyponatremia
  • Akathisia
  • Tremor, dizziness, blurred vision, sweating, headaches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do SNRIs work and what is a common SE?

A

SNRIs - block 5HT and also NA reuptake (at high doses, blocks dopamine reuptake)

Key SE = Headache + SSRI SEs

E.g. Venlafaxine, Duloxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do TCAs work? What are some SEs and CI’s?

A

TCAs - block reuptake of 5HT and NA, at high doses blocks all receptors and used in depression, at low doses blocks H1 and 5HT receptors and used for aiding sleep

Note:

  • Can be fatal in OD - not given to those with suicide risk
  • Do not give alongside MAO medications

SEs:

  • Thrombocytopaenia
  • Cardiac SEs - arrythymias, MI, stroke, postural hypertnesion
  • Anticholinergic - tachycardia, urinary retention, dry mouth, constipation
  • Seizures
  • HYPONATREMIA

E.gs: Amitriptyline, Clomipramine, Imipramine, Lofepramine, Dolulepin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some NaSSA’s and NARI’s ? What SEs do they have?

A

NaSSA - noradrenergic ad specific serotonin antidepressant = Mirtazapine

SEs = sedation, weight gain (indicated when depressed + loss of appetite and insomnia)

NARIs = noradrenaline reuptake inhibitor e.g. Reboxetine, Atomoxetine

SEs = anticholinergic i.e. dry mouth, constipation, sweating, urinary problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are MOAI and RIMA’s? What are some risks/SEs?

A

MAOI - inhibits MAO inside the presynaptic neurone, reduction in use now

  • Risk of hypertensive ‘cheese’ (tyramine) reaction
  • NOT combined with other antidepressants, especially SSRIs, to avoid serotonin syndrome

E.g.s = Phenelzine, Isocarboxacid, Selegiline and Tranylcypromine

SEs = anticholinergic, cheese HTN reaction

RIMAs = reversible inhibitors of MAO e.g. Moclobemide

SEs = agitation/anxiety, sleep disturbance, nausea and HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do BDZ work and what are their effects? What are Z-drugs and SEs?

A

BDZ = enhance GABA transmission by increasing FREQUENCY of the Cl- channels opening f (Barbs no longer used due to danger but inc length of time open)

Effects of BDZ:

  • Anxiolytic
  • Sedative
  • Hypnotic

Z-drugs i.e. Zopiclone are like BDZ which treat insomnia if severe
SEs = increased fall risk, agitation, bitter taste, constipation, hypotonia, dry mouth, risk of dependency

17
Q

What are the positive and negative effects of BDZ? What can be used to reverse its effects?

A

Positive:

  • Wide therapeutic window (Flumanezil is a BDZ antagonist which can reverse effects)
  • Mild effect on REM sleep
  • Doesn’t induce liver enzymes

Negative:

  • Sedation, confusion, anterograde amnesia, ataxia
  • Potentiates other CNS depressants e.g. ALCOHOL
  • Tolerance and dependence risk
  • Cleft lip risk if used in 1st trimester
  • Co-admin with warfarin/heparin increases free plasma concentration
18
Q

What are mood stabilisers used for and what are the side effects and risks of each? What occurs in Li toxicity?

A

Mood stabilisers = Lithium, Valproate, Lamotrigine and Carbemazepine

Used for BPAD and Schizoaffective disorder

Lithium dose = 0.6-1.0mmol/L
SEs:
- Mild tremor
- Benign leucocytosis
- N&V
- Hypothyroidism and Hyperparathyroidism (high Ca)
- Nephrogenic DI
- Weight gain
- N&V
- OD = >1.2mmol/L –> coarse tremor, hyperreflexia, nystagmus, GI and CNS (ataxia, seizureS). May occur if dehydrated, on other drugs like NSAIDs, ACEi and diuretics which interrupt renal excretion, or deliberate OD.
- If suddenly discontinue then will RELAPSE
- Ebstein’s abnormality in pregnancy but weigh risk with patient
- Monitor 12h after first dose, 1w after and weekly until level is steady (~5w) and then 3m lithium levels and 6m U&Es and TFTs

Valproate:

  • Highly teratogenic so not prescribed to women of childbearing age (spina bifida in pregnancy)
  • N&V and diarrhoea
  • Liver failure/DILI
  • Hair loss
  • Weight gain
  • Thrombocytopenia

Lamotrigine:
- Severe skin rash (SJS)

Carbemazepine:

  • Monitoring required
  • Pregnancy use causes spina bifida
  • Induces liver enzymes
19
Q

What is ECT and what are its indications? What are the side effects? What are some CIs?

A

ECT induces a generalised tonic-clonic seizure under GA

  • > Prolonged/Severe mania episode
  • > Severe life-threatening, treatment resistant depression
  • > Catatonia

Absolutely CI in raised ICP!!

SEs:

  • Headache and nausea
  • Muscle aches
  • Cardiac arrhythmia
  • Memory problems (retrograde»>anterograde amnesia)
  • Long-term impact on memory is poorly understood but impairment can occur
20
Q

What are some risk factors and protective factors for suicide?

A

Note: hanging/strangulation is the most common cause

Risk factors:

  • M>F (3:1)
  • Mental illness - BPAD, Depression
  • Young male
  • Occupation (Dr, Vet)
  • Alone/unmarried/divorced or widowed
  • Lower social class
  • Substance abuse

Higher suicide intent after DSH:

  • Preplanning
  • Attempts to conceal
  • Lack of help seeking after previous act
  • Actions - will, note
  • Violent methods

Protective factors:

  • Married
  • Lithium medication
  • Religion/Faith
  • No substance abuse