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4th Year Drugs > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

Name 4 SSRIs

A

Fluoxetine
Sertraline
Paroxetine
Citalopram

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2
Q

What is the mechanism by which SSRIs work?

A

Presynaptic blockage of serotonin reuptake pumps.

Increases postsynaptic binding

Do NOT inhibit NA reuptake

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3
Q

What are the indications for SSRIs?

A

Depression - 1st line moderate to severe
Anxiety disorders
OCD
Bulimia nervosa (fluoxetine)

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4
Q

What are the SEs of SSRIs?

A

8 S’s

  • Stress (anxiety/worry) - early
  • stomach upset/bleeding - early
  • Size (weight gain)
  • Sexual dysfunction
  • Skin rash (hypersensitivity)
  • Suicidal thoughts
  • Seizure threshold reduced
  • Serotonin syndrome - triad of altered mental state, neuromuscular excitability, autonomic hyperactivity (hyperthermia)
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5
Q

What are the CIs for SSRIs?

A
  • Mania
  • Under 18s (except Fluoxetine) - reduced efficacy, increased risk of suicidal thoughts and self harm
  • Epileptics - lowers seizure threshold
  • Peptic ulcer disease - increased risk of bleeding
  • Hepatic impairment - metabolised by liver
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6
Q

Why are there fewer SEs for SSRIs vs TCAs?

A

Because SSRIs do not block other receptors (dopamine, histamine, cholinergic, alpha-adrenergic), resulting in associated SEs

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7
Q

What are the drug interactions of SSRIs? (Citralopram, sertraline, fluoxetine)

A
  • Do not combine with other serotonin increasing drugs,
  • > e.g. MAOIs, TCAs - serotonin syndrome and potential overdose (convulsions, coma and cardiotoxicity- arrythmias)
  • Avoid combo with drugs that prolong QT duration
  • Increase plasma conc of TCA’s
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8
Q

How long should antidepressant drugs be taken for?

A

6 Months

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9
Q

What should be avoided wren taking anti-depressants?

A
  • St John’s wort
  • alcohol
  • reduce caffeine
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10
Q

How are SSRIs metabolised?

A

Liver

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11
Q

What are the discontinuation Sx’s of SSRIs?

A

FINISH Sx

  • flu like symptoms
  • insomnia
  • nausea
  • imbalance
  • sensory disturbance
  • hyper-arousal
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12
Q

What are the symptoms of serotonin syndrome?

A

HARMED

  • hyperthermia
  • autonomic instability
  • rigidity
  • myoclonus
  • encephalopathy
  • diaphoresis
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13
Q

Name 4 tricyclic antidepressants

A

Amitriptyline
Clomipramine
Imipramine
Lofepramine

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14
Q

What is the mechanism by which TCAs work?

A
  • blocks pre-synaptic 5-HT and noradrenaline re-uptake . Also blocks dopamine, histamine, alpha-adrenergic and muscarinic/cholinergic receptors.

Increases availability for post-synpatic transmission.

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15
Q

What are the indications for TCAs?

A
  • 2nd Line for moderate-severe depression where SSRIs not effective
  • Anxiety disorders and OCD

Tx option for neuropathic pain (not licensed for use), narcolepsy

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16
Q

What are the SEs for TCAs?

A

Brain - hallucinations, convulsions, mania

CV - arrthymias, prolongs QT and QRS (TOXIC in overdose)

Anticholinergic - dry mouth, constipation, urinary retention, blurred vision (can’t see, can’t pee, can’t shit, can’t spit)

Alpha-adrenergics - postural hypotension

Histamine - sedating, weight gain

Dopamine blockage - breast changes/gynaecomastia, sexual dysfunction, extrapyramidal Sx (PAAT: parkinson sx, akathisia, Acute dystonias, tardive dyskinesia)I

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17
Q

What are the CIs for TCAs?

A
  • CV disease
  • Elderly
  • Mania
  • Epileptics (reduces seizure threshold)
  • Prostatic hypertrophy - urinary retention
  • Glaucoma
  • Hepatic impairment
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18
Q

What are the potential interactions of TCAs?

A

Should not be combined with MAO inhibitors/SSRIs or any other drugs that increase 5-HT/NA - serotonin syndrome

Should also not be combined with drugs that block dopamine, muscarinic, histamine or hypotensive drug

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19
Q

How are TCAs metabolised?

A

Liver

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20
Q

Name 3 Monoamine oxidase inhibitors

A

Phenelzine
Tranylcypromine
Moclobemide

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21
Q

What is the mechanism by which MAOIs work?

A

Non selective and irreversible inhibition of monoamine oxidase A and B (degrades monoamines in synaptic cleft)

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22
Q

What are the indications for MAOIs?

A

Depression (atypical/resistant - hypersomnia, overeating, anxiety)

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23
Q

What are the SEs of MAOIs?

A 
Postural hypotension
GI
Headache/dizzy
Hepatocellular necrosis (rare)
Monoaminergic crisis
- Hypertensive crisis (see interactions)
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24
Q

What are the CIs for MAOIs?

A
  • Mania
  • Hepatic dysfunction
  • Phaeochromocytoma (risk of hypertensive crisis)
  • Cerebrovascular disease
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25
Q

What are the interactions of MAOIs? What is the mechanism?

A
  • MAO A blockage -> amine NT accumulation and impairs food-amine metabolism.

High amines = hypertensive crisis, hyperpyrexia and psychosis.

∴ Avoid in combo with:

  • Sympathomimetics e.g. cough/decongestant meds
  • SSRIs and TCAs (also increased risk of serotonin syndrome)
  • Levodopa
  • Opioid analgesics
  • Tyramine containing foods (e.g. cheese, beer, marmite)
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26
Q

How long should you leave it before starting another anti-depressant after MAOI? Why?

A

2 weeks after stopping - Due to irreversible MAO inhibition

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27
Q

Name one serotonin-NA reuptake inhibitor (SNRI)

A

Venlafaxine

Duloxetine

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28
Q

What is the mechanism by which SNRIs works?

A

Presynaptic blockage of both 5-HT and NA reuptake pumps

Negligible effects on dopamine, histamine, alpha-adrenergic and cholinergic receptors.

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29
Q

What are the indications for SNRIs?

A
  • Major depression where SSRIs are not effective/tolerated

- GAD

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30
Q

Wha are the SEs of SNRIs?

A
  • GI upset (dry mouth, nausea, constipation)
  • PALPITATIONS
  • Changes in weight/appetite
  • CNS disturbances (e.g. headache, abnormal dreams, insomnia, confusion)
  • reduces seizure threshold
  • Hyponatraemia
  • Serotonin syndrome
  • Suicidal thoughts (increases motivation) and behaviour
  • Major discontinuation Sx
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31
Q

What are the CIs for SNRIs?

A
  • Elderly
  • Hepatic and renal impairment
  • CV disease - prolongs QT duration, increase risk of arrhythmias
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32
Q

What are the potential interactions for SNRIs?

A

Avoid combo with other antidepressants (serotonin syndrome)

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33
Q

What type of antidepressant is mirtazapine?

A

Noradrenergic and specific serotonergic antidepressant (NaSSA)

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34
Q

What is the mechanism by which mirtazapine works?

A

Presynaptic alpha 2 receptor blockage (results in increased release of NA and serotonin from presynaptic neurons)

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35
Q

What are the indications for mirtazapine?

A
  • Major depression where SSRIs are not effective/tolerated

- GAD

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36
Q

What are the SEs of mirtazapine?

A
  • Increased appetite, weight gain and sedation (histamine antagonism)
  • Headache and dry mouth

Rarely…

  • Dizziness
  • Postural hypotension
  • Tremor
  • Peripheral oedema
  • Hyponatraemia
  • Serotonin syndrome
  • (Negligible anticholinergic effects)
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37
Q

What are the CIs for mirtazapine?

A

Elderly
Mania
Hepatic and renal impairment
CV disease (increased risk of arrythmias)

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38
Q

What are the potential drug interactions for mirtazapine?

A

Combo with other antidepressant classes - serotonin syndrome

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39
Q

When should mirtazapine be taken?

A

At night - minimise/take advantage of it’s sedative effects.

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40
Q

What type of drug is lithium?

A

Mood stabiliser

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41
Q

What is the mechanism by which lithium exerts its action?

A

Not really known

Might modulate the neurotransmitter-induced activation of second messenger systems

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42
Q

What are the indications for lithium?

A
  • Acute Mania
  • Prophylaxis of bipolar affective disorder (relapse prevention)
  • Tx of resistant depression (lithium augmentation)
  • Other: adjunct to antipsychotics in schizoaffective disorders and schizophrenia
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43
Q

What are the SEs of lithium?

A

75% patients on lithium will experience some SEs

  • Leucocytosis/lethargy
  • Insipidus (polyuriabpolydipsia)
  • Tremor (fine)/Teratogenicity (Epstein’s abnormality - malformation of tricuspid valve in 1st T. Also causes floppy baby syndrome, hypothyroidism, and polyhydraminos)
  • Hypothyroidism
  • Increased weight
  • Vomiting
  • Metallic taste

Long term SEs:
kidney - 10-20 % have morphological kidney changes (>1% develop kidney failure after 10yrs)
Hypothyroidism (5-35%) - more in women (6-18 months after starting)

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44
Q

When should lithium be discontinued in pregnancy?

A

Mild/stable forms of bipolar: taper dose and stopped pre pregnancy

Moderate risk of relapse: lithium should be tapered and discontinued during first trimester

Severe bipolar with high risk of relapse: lithium = maintained during pregnancy (with informed consent, appropriate counselling of risk to foetus, prenatal diagnosis and echo at 16-18 weeks gestation)

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45
Q

What is the therapeutic ranger for lithium? What are the signs of toxicity?

A

Narrow therapeutic range (0.5-1.0 mmol/

Cause of toxicity
Drugs: ACEi, NSAIDs, diuretics
- Renal failure
- UTI
- Dehydration
  1. 5-2 mmol/L Toxic
    - N&V, apathy, coarse tremor, ataxia, muscle weakness

> 2 mmol/L Very Toxic
- nystagmus, dysarthria (diff speaking), impaired consciousness, hyperactive, tendon reflexes, oliguria, hypotension (precede circulatory collapse), myoclonus jerks, convulsions, coma

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46
Q

What is the Tx for lithium toxicity?

A

Supportive - adequate hydration, renal function and electrolyte balance.

If convulsions - anti-convulsions

If renal failure - dialysis

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47
Q

What investigations should be completed prior to lithium Tx?

A
  • lithium levels
  • FBCs and U&Es (renal function and electrolyte balance)
  • TFTs
  • ECG - cardiac abnormalities
    – pregnancy test (if female)
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48
Q

How is lithium metabolised?

A

Renally

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49
Q

What are the CIs for lithium?

A
  • Pregnant/breastfeeding (8x increased risk of Ebstein’s anomaly in first trimester during the first trimester of pregnancy)
  • Renal impairment (older adults, dehydration)
  • Hypothyroid
  • Cardiac impairment
  • Neurological conditions e.g. Parkinson’s/Huntingdon’s
50
Q

What are the potential drug interactions of lithium?

A

Clearance of lithium = decreased with renal impairment and sodium depletion

∴ diuretics (esp thiazides), NSAIDs and ACEi increase lithium levels

-Antipsychotics may synergistically increase lithium-induced NEUROTOXICITY

51
Q

How should lithium Tx be monitored?

A

Lithium is long term treatment to stabilise patients mood. Regular review by psychiatrist to determine whether the dose and/or formulation is adequate

Initially

  • check lithium level after 5days of initial dose (titration up as required until suitable maintenance dose).
  • Review frequently (weekly) at beginning of treatment to determine lithium level until therapeutic level = stable for 4 weeks
  • lithium levels should be checked every 3 months
  • U&Es and TFTs checked every 6 months due to SEs on these organs

Need to inform doctor that taking lithium (due to multiple interactions)!!

52
Q

What is the mechanism by which sodium valproate works?

A

Weak inhibitor of Na channels -> stabilises resting membrane potentials and reduce neuronal excitability

Increases brain content of GABA (principle inhibitory NT) - reduces neuronal excitability

53
Q

What are the indictions for sodium valporate?

A
  • Epilepsy (1st for generalised or absence seizures, 2nd for focal seizures)
  • 2nd line - Bipolar disorder (acute Tx/prophylaxis against recurrence)
54
Q

What are the SEs of sodium valporate?

A
  • Valproate
  • Appetite increase/weight gain
  • Liver failure (monitor LFTs during 1st 6 months)
  • Pancreatitis
  • Reversible hair loss (grows back curly)
  • Oedema
  • Ataxia
  • Teratogenicity, Tremor, Thrombocytopaenia
  • Encephalopathy (due to hyperammonaemia) / Enzyme inducer
55
Q

What are the CIs for sodium valporate?

A
  • Pregnant women (1st tremester)
  • Hepatic/renal impairment
  • Porphyria
56
Q

What are the potential drug interactions of Sodium valporate?

A
  • CYP450 INHIBITOR - increases concentration/risk of toxicity of drugs metabolised by CYP450 e.g. warfarin - sodium valproate metabolised by CYP450
  • drugs that induce CYP450 reduces sodium valproate concentration and increases risk of seizures (e.g. carbamezapine, phenytoin)
  • Drugs that lower seizure threshold e.g. SSRIs, anti-psychotics, tricyclic antidepressants, tramadol
57
Q

What is the mechanism by which carbamazepine exerts its action?

A

Inhibits neuronal Na channels - stabilising resting membrane potentials and reducing neuronal excitability

Block synaptic tranmission in trigeminal nucleus

Stabilise mood - reducing electrical kindling in temporal lobe and limbic system

58
Q

What are the indications for carbamezapine?

A
  1. Epilepsy - 1st for focal seizures (with/without 2o generalisation) and generalised seizures
  2. Trigeminal neuralgia - 1st line
  3. Bipolar disorder - option for prophylaxis in pts resistant/intolerant to other meds
59
Q

What are the SEs of carbamezapine?

A
  • GI upset
  • Neurological effects - dizziness/ataxia
  • Carbamezapine hypersensitivity (mac-pap skin rash)
  • Antiepileptic hypersensitivity syndrome - severe skin reactions (SJS), fever, lymphodenopathy, haemotological abnormalities/pancytopaenia (↓WCC), ↑LFTs
60
Q

Why shouldn’t pregnant mothers take carbamezapine?

A
  • Teratogenic (neural tube defects, cardiac, urinary tracts abnormalities, cleft palate)
61
Q

What are the CIs to carbamezapine?

A
  • pregnancy - high folic acid supplements
  • Hepatic, renal or cardiac impairment (increased risk of toxicity)
  • Antiepileptic hypersensitivity syndrome
62
Q

What are the important interactions of carbamezaine?

A

CYP450 inducer - ↓ efficacy and concentration of P450 drugs e.g. warfarin

↑Concentration and adverse effects with P450 inducers

Efficacy ↓ with drugs that lower seizure threshold (e.g. SSRIs, TCAs, antipsychotics)

63
Q

How is carbamezapine metabolised?

A

Hepatic (P450)

64
Q

What type of drug is lamotrigine?

A

Anti-convulsants/mood stabiliser

65
Q

What is the mechanism by which lamotrigine works?

A

Blocks Na channels - stabilising neurons and reducing neuronal excitability

66
Q

What are the indications for lamotrigine?

A
  1. 2nd line for generalised seizures (inc Lennox-Gestault and tonic-clonic seizures)
  2. Bipolar disorders - stabilises mood and reduces depression
67
Q

What are the SEs of lamotrigine?

A
  • GI - N&V
  • Neuro - confusion, agitation, drowsiness, ataxia, diplopia, nystagmus
  • STEVEN JOHNSON SYNDROME - therefore titrate dose
68
Q

What are the CIs for lamotrigine?

A
  • Can be SAFELY used in pregnancy!!
  • Hypersensitivity reactions - rash
  • Steven Johnsons syndrome (serious reaction)
  • Renal and hepatic impairment (increased risk of toxicity)
69
Q

What are the important drug interactions for lamotrigine?

A
  • Efficacy reduced by drugs that lower seizure threshold - e.g. SSRIs, tricyclics, anti-psychotics, tramadol
  • Metabolised by CYP450 - concentration increased by (CYP450 inhibitors and reduced by CYP450 inducers
70
Q

Name 3 first generation (typical) antipsychotics

A

Haloperidol
Chlopromazine
Prochlorperazine

71
Q

What is the mechanism by which first generation antipsychotics work?

A

Block post-synaptic dopamine D2 receptors

72
Q

What are the three main dopaminergic pathways in the CNS? WHat else has D2 receptors?

A
  • Mesolimbic/mesocortical
  • Nigrostriatal pathway
  • Tuberohypophyseal pathway
  • Chemoreceptor trigger zone
73
Q

What does the mesolimbic/mesocortical pathway comprise? what is the effect of blocking this pathway?

A

Runs between the midbrain and the limbic/frontal system

Considered main determinant of antipsychotic effects

Overactivity of mesolimbic system (high dopamine) = positive symptoms seen in schizo

Mesocortical dysfunction (high dopamine levels) = negative and cognitive symptoms seen in schizo

74
Q

What does the the nigrostriatal pathway comprise/ What is the effect of blocking this pathway?

A

Connects the substantia nigra with the corpus striatum of the basal ganglia

Extrapyramidal effects

75
Q

What does the tuberohypophyseal pathway comprise? What is the effect of blocking this pathway?

A
  • Connects hypothalamus with pituitary gland
  • Hyperprolactinaemia (menstrual disturbance, galactorrhoea, breast pain, gynaecomastia)
  • Temperature dysregulation(?)
76
Q

What are the main SEs of the first generation anti-psychotics? (haloperidol, chlorpromazine, prochlorperazine)

A 
EXTRAPYRAMIDAL EFFECTS 
EARLY
- Parkinsonism 
- acute dystonic reactions
- Akathisia (inner restlessness)
- Neuroleptic malignant syndrome 
LATE
- Tardive dyskinesia - pointless, involuntary, repetitive movements e.g. lip smacking

OTHERS

  • drowsiness
  • ↓ BP
  • ↑QT + arrythmias
  • Erectile dys
  • Hyperprolactinaemia Sx
77
Q

What are the CIs for first generation anti psychotics?

A

Elderly
Dementia
Parkinson’s disease - extrapyramidal effects

78
Q

What are the important drug interactions of first generation antipsychotics?

A

Drugs that…

  • prolong QT interval e.g. amiodarone, macrolides
  • Opioids
  • Enhance CNS depression
  • Lower seizure threshold
79
Q

How are anti-psychotics metabolised?

A

Liver

80
Q

How should Neuroleptic malignant syndrome be managed? What is the cause?

A
  • Stop antipsychotics (IV dialysis?)
  • ↓ temp, vent support
  • Start dopaminergic and anti-cholinergic drugs
  • ↓agitation e.g. benzos
  • Restart anti-P hesitantly
  • ↓dopamine levels due to D2 blockage
81
Q

Name 4 second generation anti-psychotic drugs?

A

Quetiapine
Olanzapine
Risperidone
Clozapine

82
Q

What is the mechanism by which second generation anti-psychotics exert their action?

A

Block post synaptic dopamine receptors

83
Q

What are the main difference between 1st generation and second generation antipsychotics? What are the proposed mechanisms for this difference?

A

Improved efficacy in treatment-resistant schizophrenia (especially clozapine) and against negative symptoms

Lower risk of extra pyramidal Sx

Possible mechs: higher affinity for other receptors (particularly 5-HT2a receptors) looser binding to D2 receptors (in the case of clozapine/quetiapine)

84
Q

What are the indications for 2nd generation antipsychotics?

A
  1. Urgent Tx of severe psychomotor agitation
  2. 1st line for Schizophrenia - esp pt’s who do not tolerate 1st generation (extrapyramidal Sx), where -ve Sx are prominent , Tx resistant
  3. Bipolar disorder (acute episodes)
85
Q

What are the important SEs of 2nd generation anti psychotics?

A
  • Sedation
  • Dry mouth, blurred vision, constipation, urinary retention- ACh binding - (‘can’t see, can’t pee, can’t shit, can’t spit’)
  • Extrapyramidal effects (H2 blocking of nigrostriatal pathway) - ↑ in 1st generation
  • Metabolic disturbance (↑weight, DM, ↑lipid) - ESP the ‘-PINES’
  • Prolong QTc/arrhythmias (alpha-1 binding)
  • Hyperprolactinaemia (esp respiridol) - H2 blocking of tuberphypophyseal pathway - lactation, gynaecomastia, sexual dysfunction (amenorrhea/infertility)
86
Q

When is clozapine indicated?

A

Tx resistant schizophrenia - where 2 other antipsychotics have been tried for sufficient amount of time (ie not because patient stopped/did not tolerate)

87
Q

What are the specific side effects of clozapine?

A
  • Agranulocytosis ~1%
  • QTc prolongation/arrhythmias
  • life threatening constipation (prescribe 2 laxatives)
  • hypersalivation
  • sedation
  • postural hypertension
  • Weight gain etc
88
Q

What are the CIs to 2nd generation antipsychotics?

A

CV disease
Parkinson’s/dementia
Clozapine - severe heart disease or Hx of neutropenia

89
Q

What are the important drug interactions of 2nd generation anti-psychotics?

A
  • Other sedating drugs
  • Do not combine with other dopamine-blocking meds
  • Drugs that prolong QT interval (e.g. amiodarone, quinine, macrocodes, SSRIs)
90
Q

How are 2nd antipsychotic medication monitored?

A

Blood tests (FBC, U&E, creatine, LFTs) at start of Tx and periodically thereafter (weekly then monthly FBCs for clozapine)

  • Metabolic and CV SEs (weight, lipid profile, fasting blood glucose)
91
Q

What is the speed of action of antipsychotics for: Tranquilizing effects
Side effects
Anti-psychotic effects

A

Tranquillising - Hours
SEs - Hours to days
Anti-psych - Days to weeks

92
Q

What type of drugs are benzodiazepines?

A

anxiolytic (i.e. ↓ anxiety)

hypnotic (i.e. sedative)

93
Q

Name 5 benzos

A 
Diazepam
Temezepam
Lorazepam
Chlordiazepoxide
Midazolam
94
Q

What is the mechanism by which benzos work?

A
  • Benzos facilitate and ENHANCE binding of GABA to GABAa receptor
  • Widespread depressant effect of synaptic transmission → Causes ↓ anxiety, sleepiness, sedation, anti-convulsant effects
  • Ethanol also acts on same receptor - benzo = Tx for alcohol withdrawal
95
Q

What are the indications for benzos?

A
  1. 1st line - seizures/status epilepticus
  2. 1st line - alcohol withdrawal
  3. Common sedative for intervention procedures
  4. Short term Tx for severe anxiety
  5. Short term Tx for severe insomnia
  6. Akathisia, muscle spasms
96
Q

What are the important SEs of Benzos?

A
  • Drowsiness → Sedation → Coma (dose dependent) (AVOID DRIVING/MACHINERY)
  • Few weeks use (>4 weeks) - DEPENDENCE
  • Withdrawal reaction (similar to alcohol) with abrupt cessation
  • OVERDOSE: Airway obstruction → death
97
Q

What are the CIs for benzos?

A
  • Elderly
  • Respiratory impairment/neuromuscular disease
  • Liver failure (may precipitate hepatic encephalopathy)
98
Q

What is the best benzo for alcohol withdrawal and why?

A

Lorazepam - depends less on liver for elimination

99
Q

What are the important drug interactions with benzos?

A

Additive sedative effect - avoid with alcohol and opioids

  • Metabolised by CYP450 - CYP450 inhibitors may increase effects
100
Q

What type of drugs are the Z drugs?

A

Hypnotics

101
Q

Name 2 Z drugs?

A

Zopiclone

Zolpidem

102
Q

What is the mechanism by which Z drugs work?

A

Similar to benzos - enhance GABA binding to GABAa receptor

  • Widespread depressant effect of synaptic transmission - ↓anxiety, sleepiness, sedation

(NOT anticonvulsant as only taken ORALLY)

103
Q

How long is the length of Z drug action?

A

Short

104
Q

What are the indications for Z drugs?

A

Short term Tx of severe insomnia

105
Q

What are the SEs of Z drugs?

A
  • Daytime sleepiness (don’t drive/do complex tasks)
  • Rebound insomnia when stopped
  • CNS effects - headache, confusion, nightmares, amnesia
  • Zopiclone - taste disturbance
  • Zolpidem - GI upset
  • PROLONGED USE (>4 weeks) - dependence and withdrawal effects if stopped
  • OVERDOSE - drowsiness, coma, resp depression
106
Q

What are the CIs for Z drugs?

A
  • Elderly (caution)
    X Obstructive sleep apnea
    X Resp muscle weakness
    X Resp depression
107
Q

What are the important interactions of Z drugs?

A
  • Enhance sedative effects of antihistamines, alcohol, opioids
  • Enhance hypotensive effects of antihypertensive meds
  • Metabolised by CYP450 - inhibitors ↑, inducers ↓
108
Q

What is neuroleptic malignant syndrome?

A

RARE, LIFE THREATENING
- insidious onset (4-11 days from initiation/change in dopamine antagonist)

  • rigidity (lead pipe)
  • confusion
  • autonomic dysfunction (↑BP)
  • pyrexia

↑WCC, ↑CPK (muscle activity), ↑LFTs

109
Q

Name 3 anti-cholinesterase inhibitor

A

DONEPEZIL
Rivastigmine
Galantamine

110
Q

What is the mechanism by which anticholinesterase inhibitors exert their action?

A

Alzheimer’s - mechanism ↓ACh in the brain

Donepezil - reversible, non-competitive inhibitor of anticholinesterase. ↓ ACh hydrolysis in brain, ↑ availability for neurotrans.

111
Q

What are the indications for donepezil?

A

1st line for mild-moderate Alzheimers

112
Q

What are the CIs for donepezil?

A

Cholinergic effects!

  • Asthma/COPD
  • sick sinus syndrome/supravent conduction abnormalities
  • Peptic ulcers
  • Antipsychotic Tx
113
Q

What are the SEs of donepezil?

A
  • Insomnia/weird dreams
  • Hallucinations
  • Agitation/aggression
  • Fatigue
  • Dizziness/drowsiness
  • Urinary incontinence
  • N/V/D
  • Muscle cramps
  • Rash/urticaria
114
Q

How does electroconvulsive therapy works?

A

Unknown mechanism - release of NTs and hypothalamic/pituitary hormones?

115
Q

What are the indications for ECT?

A

DEPRESSION

  • life threatening/suicidal
  • psychotic features/stupor
  • treatment resistant

MANIA (severe)

SCHIZOPHRENIA - catatonic, +ve Sz, schizoaffective

SEVERE POSTNATAL DEPRESSION

116
Q

How is ECT administered?

A

2-3x per week (between 4-12 Txs. Can be more)

Bilateral or unilateral placement

Charge should be sufficient to induce generalised seizure lasting ~15secs

117
Q

What do anaesthetists administer before ECT? Why?

A

Administered by an anaesthetist

Short acting induction agent eg methohexital - should last approx 5 mins. Not painful.

Muscle relaxant

118
Q

What are the SEs of ECT?

A

Mortality - 1 in 50,000

Loss of memory - short term/autobiographical (reduced with unilateral ECT)

Confusion headache, nausea, muscle pain - 80% pts

119
Q

What are the important drug interactions to consider with ECT?

A

SEIZURE LOWERING eg antidepressants, antipsychotics

SEIZURE INCREASING - eg benzos, anticonvulsants

120
Q

What are the CIs for ECT?

A

No absolute CIs!!

Caution with…

  • heart disease
  • raised intracranial pressure
  • risk of cerebral bleeding
  • poor anaesthetic risk

4th Year Drugs (7 decks)

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