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psychiatry > pharmacology in psychiatry (longer) > Flashcards

pharmacology in psychiatry (longer) Flashcards

1
Q

What are the general pharmacology strategies?

A

Indication
- diagnosis & identify target symptoms

Choice of agent and dosage
- agent with acceptable side effect profile and use lowest effective dose (delayed response for many psych meds and drug-drug interactions)

Management

  • adjust dosage
  • use adjunctive and combination therapies
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2
Q

What are the indications for antidepressants?

A
  • depression (unipolar/bipolar)
  • organic mood disorders
  • schizoaffective disorder
  • anxiety disorders (OCD, panic, social phobia, PTSD)
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3
Q

What is selection of antidepressant based on?

A
  • Past history of response
  • Side effect profile
  • Coexisting medical conditions
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4
Q

How long before symptoms start to improve on antidepressants?

A

There is a delay typically of 2-4 weeks after a therapeutic dose is achieved before symptoms improve.

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5
Q

What should be done if no improvement is seen on antidepressants?

A

switch to another antidepressant or augment with another agent.

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6
Q

How should antidepressants be used prophylactically?

A
  • First episode continue for 6mth to a year
  • Second episode continue for 2 years
  • Third episode discuss life long
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7
Q

What are the classifications of antidepressants?

A
  • Tricyclics (TCAs)
  • Monoamine Oxidase Inhibitors (MAOIs)
  • Selective Serotonin Reuptake Inhibitors (SSRIs)
  • Serotonin/Noradrenaline Reuptake Inhibitors (SNRIs)
  • Novel antidepressants
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8
Q

What side effects can TCAs have?

A
  • Antihistaminic, anticholinergic, antiadrenergic
  • Lethal in overdose (even 1 week supply can be lethal)
  • Prolonged QT complex
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9
Q

Describe the components of tertiary TCAs

A

have tertiary amine side chains

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10
Q

Why do tertiary TCAs have more side effects than others?

A

Side chains are prone to cross react with other types of receptors which leads to more side effects

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11
Q

Give examples of tertiary TCAs.

A
  • Imipramine,
  • Amitriptyline
  • Doxepin,
  • Clomipramine
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12
Q

What are secondary TCAs?

A

They are often metabolites of tertiary amines

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13
Q

Give examples of secondary TCAs

A
  • Desipramine

- Nortriptyline

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14
Q

What side effects do secondary TCAs have?

A

Same as tertiary TCAs but less severe

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15
Q

What is the mechanism of secondary TCAs?

A

Primarily block noradrenaline

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16
Q

What is the mechanism of monoamine oxidase inhibitors?

A

Bind irreversibly to monoamine oxidase thereby preventing inactivation of amines such as norepinephrine, dopamine and serotonin leading to increased synaptic levels

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17
Q

What are MAOIs particularly effective in?

A

Resistant depression

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18
Q

What side effects do MAOIs have?

A
  • Orthostatic hypotension
  • Weight gain
  • Dry mouth
  • Sedation
  • Sexual dysfunction
  • Sleep disturbance
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19
Q

What is the cheese reaction?

A

Hypertensive crisis can develop when MAOI’s are taken with tyramine-rich foods or sympathomimetics

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20
Q

When can serotonin syndrome develop?

A

take MAOI with meds that increase serotonin or have sympathomimetic actions

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21
Q

What are the symptoms of serotonin syndrome?

A
  • Abdominal pain
  • Diarrhoea
  • Sweats
  • Tachycardia
  • HTN
  • Myoclonus
  • Irritability
  • Delirium
  • Can lead to hyperpyrexia, cardiovascular shock and death
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22
Q

How is serotonin syndrome avoided?

A

wait 2 weeks before switching from a SSRI to an MAOI.

exception of fluoxetine where need to wait 5 weeks because of long half-life.

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23
Q

What is the mechanism of SSRIs?

A

They block presynaptic serotonin reuptake

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24
Q

What are SSRIs used for?

A

Anxiety and depression symptoms

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25
Q

What side effects do SSRIs have?

A
  • GI upset
  • Sexual dysfunction
  • Anxiety
  • Restlessness
  • Nervousness
  • Insomnia
  • Fatigue or sedation
  • Dizziness
  • Cardiotoxicity (very little risk in overdose)
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26
Q

What are the symptoms of SSRI associated activation syndrome?

A
  • nausea
  • anxiety
  • panic
  • agitation
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27
Q

Why does activation syndrome occur with SSRIs?

A

Increase in serotonin

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28
Q

What are the symptoms of SSRI associated discontinuation syndrome?

A
  • Agitation
  • Nausea
  • Disequilibrium
  • Dysphoria
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29
Q

How long can SSRI associated activation syndrome last?

A

2-10 days

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30
Q

When is SSRI discontinuation syndrome more likely to occur?

A

More common with shorter half life drugs so consider switching to fluoxetine

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31
Q

What type of drug is paroxetine?

A

SSRI

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32
Q

What are the disadvantages of paroxetine?

A
  • Sedating, wt gain, more anticholinergic effects

- Likely to cause a discontinuation syndrome

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33
Q

What type of drug is sertraline?

A

SSRI

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34
Q

What are the advantages of sertraline?

A
  • weak drug-drug interactions
  • short half life with lower build-up of metabolites
  • less sedating
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35
Q

What are the disadvantages of sertraline?

A

max absorption requires a full stomach

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36
Q

What type of drug is fluoxetine?

A

SSRI

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37
Q

What are the advantages of fluoxetine?

A
  • long half-life –> little discontinuation syndromes.

- initially activating so may provide increased energy

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38
Q

What are the disadvantages of fluoxetine?

A
  • long half life –> active metabolite may build up
  • significant drug-drug interactions so may not be a good choice in pts already on a number of meds
  • initial activation may increase anxiety and insomnia
  • more likely to induce mania
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39
Q

What type of drug is citalopram?

A

SSRI

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40
Q

What is the mechanism of SNRIs?

A

Inhibit both serotonin and noradrenergic reuptake like the TCAS but without the antihistamine, antiadrenergic or anticholinergic side effects

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41
Q

What are SNRIs used for?

A
  • Depression
  • Anxiety
  • Neuropathic pain
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42
Q

What type of drug is venlafaxine?

A

SNRI

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43
Q

What are the advantages of venlafaxine?

A
  • minimal drug interactions

- short half life (avoids build-up - good for geriatric populations)

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44
Q

What are the disadvantages of venlafaxine?

A
  • increase in diastolic BP
  • cause bad discontinuation syndrome
  • sexual side effects in >30%
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45
Q

What type of drug is duloxetine?

A

SNRI

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46
Q

What are the advantages of duloxetine?

A
  • efficacy for the physical symptoms of depression

- far less BP increase

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47
Q

What are the disadvantages of duloxetine?

A
  • drug interactions (CYP2D6 and CYP1A2 inhibitor)
  • cannot break capsule as active ingredient not stable within the stomach
  • higher drop out rate
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48
Q

What type of drug is mirtazapine?

A

Novel antidepressant

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49
Q

What are the advantages of mirtazapine?

A
  • different mechanism of action to SSRIs.

- can be utilised as a hypnotic at lower doses

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50
Q

What are the disadvantages of mirtazapine?

A
  • weight gain (increases serum cholesterol)

- very sedating at lower doses

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51
Q

What are the indications for mood stabilisers?

A
  • bipolar
  • cyclothymia
  • schizoaffective
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52
Q

What is the only medication to reduce suicide rate?

A

Lithium

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53
Q

What is lithium effective for?

A

long-term prophylaxis of both mania and depressive episodes in bipolar patients

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54
Q

What factors predict a positive response to lithium?

A
  • Prior long-term response or family member with good response
  • Classic pure mania
  • Mania is followed by depression
55
Q

What should be done before starting lithium?

A
  • baseline bloods - U&E and TSH

- pregnancy test

56
Q

How should lithium use be monitored?

A
  • steady state achieved after 5 days
  • check 12 hours after last dose
  • once stable check level 3 months
  • TSH and creatinine 6 months.
57
Q

What is the goal with lithium use?

A

Blood level between 0.6-1.2

58
Q

What are the side effects of lithium?

A
  • GI distress: reduced appetite, nausea/vomiting, diarrhoea
  • thyroid abnormalities
  • nonsignificant leukocytosis
  • polyuria/polydypsia secondary to ADH antagonism
  • interstitial renal fibrosis
  • hair loss, acne
  • reduces seizure threshold, cognitive slowing, intention tremor
59
Q

How does lithium toxicity present?

A

mild: vomiting, diarrhoea, ataxia, dizziness, slurred speech, nystagmus
moderate: nausea, vomiting, anorexia, blurred vision, clonic limb movements, convulsions, delirium, syncope
severe: generalised convulsions, oliguria, renal failure,

60
Q

What type of drug is valproic acid (Depakote)?

A

Anticonvulsant

61
Q

What factors predict a positive response to valproic acid?

A
  • rapid cycling patients (females>males)
  • comorbid substance issues
  • mixed patients
  • comorbid anxiety disorders
62
Q

How does valproic acid compare to lithium?

A
  • Valproic acid is as effective as Lithium in mania prophylaxis but is not as effective in depression prophylaxis.
  • Better tolerated than lithium
63
Q

What should be done before starting valproic acid?

A
  • Baseline LFTs
  • Pregnancy test
  • FBC
64
Q

Why should valproic acid be avoided in women of child bearing age?

A

Can cause neural tube defects

65
Q

How should valproic acid use be monitored?

A
  • Steady state achieved after 4-5 days

- Check 12 hours after last dose and repeat CBC and LFTs

66
Q

What is the goal of valproic acid use?

A

Target blood level 50-125

67
Q

What are the side effects of valproic acid?

A
  • thrombocytopenia and platelet dysfunction
  • nausea, vomiting, weight gain
  • sedation, tremor
  • hair loss
68
Q

What is the first line agent for acute mania and mania prophylaxis?

A

Carbamazepine

69
Q

What type of drug is carbamazepine (tegretol)?

A

Anticonvulsant

70
Q

What is carbamazepine indicated for?

A

Rapid cyclers and mixed patients

71
Q

What should be done before carbamazepine is started?

A
  • Baseline LFTs
  • FBC
  • ECG
72
Q

How should carbamazepine be monitored?

A
  • Steady state achieved after 5 days

- Check 12 hours after last dose and repeat CBC and LFTs

73
Q

What is the goal of carbamazepine used?

A

Blood levels 4-12mcg/ml

74
Q

Why should carbamazepine levels be checked after 1 month?

A

adjust dosing after around a month because induces own metabolism.

75
Q

What are the side effects of carbamazepine?

A
  • rash
  • nausea, vomiting, diarrhoea
  • sedation, dizziness, ataxia, confusion
  • aplastic anaemia and agranulocytosis (<0.002%)
  • water retention (–> hyponatremia_
  • drug-drug interactions
76
Q

What type of drug is lamotrigine (lamictal)??

A

Anticonvulsant

77
Q

What are the indications for lamotrigine?

A
  • Mania

- Neuropathic/chronic pain

78
Q

What should be done before starting lamotrigine?

A

Baseline LFTs

79
Q

How should lamotrigine be initiated and titrated?

A
  • start with 25 mg daily X 2 weeks
  • increase to 50mg X 2 weeks
  • then increase to 100mg
  • faster titration has a higher incidence of serious rash
80
Q

What happens if a patient stops taking their lamotrigine?

A

If the patient stops the med for 5 days or more have to start at 25mg again!

81
Q

What are the side effects of lamotrigine?

A
  • Nausea/vomiting
  • Sedation, dizziness, ataxia and confusion
  • TEN and Stevens Johnson’s syndrome
  • Blood dyscrasias (rare)
82
Q

What drugs can increase lamotrigine levels?

A
  • VPA (doubles concentration, so use slower dose titration),
  • Sertaline
83
Q

Why should lamotrigine be discontinued if ANY rash develops?

A

character/severity of the rash is not a good predictor of severity of reaction

84
Q

What are the indications for antipsychotic drug use

A
  • schizophrenia
  • schizoaffective disorder
  • bipolar disorder- for mood stabilization and/or when psychotic features are present
  • psychotic depression
  • augmenting agent in treatment resistant anxiety disorders
85
Q

What are the key pathways affected by dopamine in the brain?

A
  • Mesocortical
  • Mesolimbic
  • Nigrostriatal
  • Tuberoinfundibular
86
Q

Describe the mesocortical pathway and its role in mood disorders.

A
  • Projects from the ventral tegmentum (brain stem) to the cerebral cortex.
  • This pathway is felt to be where the negative symptoms and cognitive disorders (lack of executive function) arise.
  • Problem here for a psychotic patient, is too little dopamine.
87
Q

Describe the mesolimbic pathway and its role in mood disorders.

A
  • Projects from the dopaminergic cell bodies in the ventral tegmentum to the limbic system.
  • This pathway is where the positive symptoms come from (hallucinations, delusions, and thought disorders).
  • Problem here in a psychotic patient is there is too much dopamine.
88
Q

Describe the nigrostriatal pathway and its role in mood disorders.

A
  • Projects from the dopaminergic cell bodies in the substantia nigra to the basal ganglia.
  • This pathway is involved in movement regulation.
  • Remember that dopamine suppresses acetylcholine activity. -Dopamine hypoactivity can cause Parkinsonian movements i.e. rigidity, bradykinesia, tremors), akathisia and dystonia.
89
Q

Describe the tuberoinfundibular pathway and its role in mood disorders.

A
  • Projects from the hypothalamus to the anterior pituitary.
  • Remember that dopamine release inhibits/regulates prolactin release.
  • Blocking dopamine in this pathway will predispose your patient to hyperprolactinemia (gynecomastia/ galactorrhea/ decreased libido/ menstrual dysfunction).
90
Q

What is the mechanism of typical antipsychotics?

A

D2 dopamine receptor antagnoists

91
Q

Give examples of high potency typical antipsychotics.

A
  • Fluphenazine
  • Haloperidol
  • Pimozide
92
Q

Explain the effects of high potency typical antipsychotics.

A
  • High potency typical antipsychotics bind to the D2 receptor with high affinity.
  • As a result they have higher risk of extrapyramidal side effects
93
Q

Explain the effects of low potency typical antipsychotics.

A
  • Low potency typical antipsychotics have less affinity for the D2 receptors
  • They tend to interact with nondopaminergic receptors resulting in more cardiotoxic and anticholinergic adverse effects including sedation, hypotension
94
Q

Give examples of low potency typical antipsychotics.

A
  • Chlorpromazine

- Thioridazine

95
Q

What is the mechanism of atypical antipsychotics?

A

Serotonin-dopamine 2 antagonists (SDAs)

96
Q

In what way are atypical antipsychotics considered atypical?

A

They are considered atypical in the way they affect dopamine and serotonin neurotransmission in the four key dopamine pathways in the brain.

97
Q

What type of drug is risperidone (Risperdal)?

A

Atypical antipsychotic

98
Q

In what forms is risperidone available?

A
  • Regular tablet
  • IM depot forms
  • Rapidly dissolving tablet
99
Q

What are the side effects of risperidone?

A
  • Increased extrapyramidal side effects (dose dependent)
  • Most likely atypical to induce hyperprolactinemia
  • Weight gain and sedation (dosage dependent)
100
Q

How does the function of risperidone change at doses greater than 6mg?

A

Functions more like a typical antipsychotic at doses greater than 6mg

101
Q

What type of drug is olanzapine (Zyprexa)?

A

Atypical antipsychotic

102
Q

In what forms is olanzapine available?

A
  • Regular tablet
  • Immediate release IM
  • Rapidly dissolbing tab
  • Depo form
103
Q

What are the side effects of olanzapine?

A
  • Weight gain (can be as much as 30-50lbs with even short term use)-Hypertriglyceridemia, hypercholesterolemia, hyperglycemia (even without weight gain)
  • Hyperprolactinemia (< risperidone)
  • Abnormal LFT’s (2% of all patients)
104
Q

What type of drug is quetiapine (Seroquel)?

A

Atypical antipsychotic

105
Q

In what form is quetiapine available?

A

Regular tablet only

106
Q

What are the side effects of quetiapine?

A
  • Abnormal LFTs

- Weight gain (

107
Q

What type of drug is aripiprazole (abilify)?

A

Atypical aripiprazole

108
Q

In what forms if aripiprazole available?

A
  • Regular tablets
  • Immediate release IM formulation
  • Depo form
109
Q

What is the mechanism of ariprprazole?

A

Unique mechanism of action as a D2 partial agonist

110
Q

What are the possible interactions of ariprprazole?

A
  • CYP2D6 (fluoxetine and paroxetine), 3A4 (carbamazepine and ketoconazole) interactions that the manufacturer recommends adjusted dosing.
  • Could cause potential intolerability due to akathisia/activation.
111
Q

What is aripiprazole not associated with?

A
  • Weight gain

- QT prolongation

112
Q

What type of drug is clozapine (clozaril)?

A

Atypical antipsychotic

113
Q

What form is clozapine available in?

A

Regular tablet only

114
Q

Who is clozapine reserved for?

A

Treatment resistant patients because of side effect profile but this stuff works

115
Q

What are the side effects of clozapine?

A
  • Agranulocytosis
  • Increased risk of seizures
  • Sedation, weight gain abnormal LFTs
  • Increased risk of hypertriglyceridemia, hypercholesterolemia, hyperglycemia, including nonketotic hyperosmolar coma and death with and/or without weight gain
116
Q

Due to its association with agranulocytosis, what should be done monitoring wise for clozapine use?

A

Requires weekly blood draws for 6 months then fortnightly for 6 months

117
Q

What is the commonest psychotic symptom?

A

Lack of insight

118
Q

What problem can psychosis present in terms of medication?

A
  • People with psychotic illnesses relapse most commonly due to non compliance
  • Only 30% of patients take medication as prescribed
119
Q

What should be considered after a 3rd episode of schizophrenia?

A
  • There is a clear link to reduced functioning, lower IQ and negative symptoms
  • Consider long acting IM
120
Q

Give examples of adverse effects of antipsychotics.

A
  • Tardive dyskinesia

- Neuroleptic malignant syndrome

121
Q

What is tardive dyskinesia?

A

-Involuntary muscle movements that may not resolve with drug

122
Q

How does neuroleptic malignant syndrome present?

A

Characterised by:

  • Severe muscle rigidity
  • Fever
  • Altered mental status
  • Autonomic instability
  • Elevated WBC, CPK and LFTs
  • Potentially fatal
123
Q

What extrapyramidal side effects are associated with antipsychotic use?

A
  • Acute dystonia
  • Parkinson syndrome
  • Akathisia
124
Q

What agents can be used for extrapyramidal symptoms?

A
  • Anticholinergics such as benztropine, trihexyphenidyl, diphenhydramine
  • Dopamine facilitators such as Amantadine
  • Beta-blockers such as propranolol
125
Q

What are anxiolytics used to treat?

A
  • Panic disorder
  • GAD
  • Substance-related disorders and their withdrawal
  • Insomnias
  • Parasomnias
126
Q

What treatment regime is common in anxiety disorders?

A

In anxiety disorders often use anxiolytics in combination with SSRIS or SNRIs for treatment.

127
Q

What type of drug is buspirone (buspar)?

A

Non-benzodiazepine anti-anxiety drug

128
Q

What are the advantages of buspirone?

A
  • Good augmentation strategy- Mechanism of action is 5HT1A agonist. It works independent of endogenous release of serotonin.
  • No sedation
129
Q

What are the disadvantages of buspirone?

A
  • Takes around 2 weeks before patients notice results.
  • Will not reduce anxiety in patients that are used to taking BZDs because there is no sedation effect to “take the edge off.
130
Q

What type of drug are benzodiazepines?

A

Anti-anxiety CNS depressants

131
Q

What are benzodiazapines used to treat?

A
  • Insomnia
  • Parasomnias
  • Anxiety disorder
  • Often used for CNS depressant withdrawal protocols ex. ETOH withdrawal
132
Q

What are the side effects of benzodiazapines?

A
  • Somnolence
  • Cognitive deficits
  • Amnesia
  • Disinhibition
  • Tolerance
  • Dependence
133
Q

How do you deal with treatment resistance with antidepressants?

A
  • Start with SSRI
  • Combine SSRI with SNRI
  • Adjunctive treatment with lithium
  • Adjunctive treatment with atypical antipsychotic
  • ECT
134
Q

What are the classes of mood stabiliser?

A
  • Lithium
  • Anticonvulsants
  • Antipsychotics

psychiatry (23 decks)

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