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Pharmacology 2 > Antipsychotics and Bipolar Disorder > Flashcards

Antipsychotics and Bipolar Disorder Flashcards

1
Q

What is schizophrenia?

A

Chronic psychosis with deterioration of functional capacity. The inability to interact mentally and emotionally with other people.

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2
Q

When are the onsets for schizophrenia for the different genders?

A

Males are more at risk than females
Males: 15-24 years
Females: 25-34 years
Genetic predisposition, not fatal

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3
Q

What are the positive symptoms of schizophrenia?

A

Excess cognition

Hallucinations (false sensory perceptions), delusions (fixed false beliefs), disorganized speech

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4
Q

What are the negative symptoms of schizophrenia?

A

Deficits in behaviour
Avolition (lack of desire or motivation), Alogia (poverty of speech), Anhedonia (lack of pleasure in completing tasks that were once pleasurable) and blunted affect (flat mood).

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5
Q

What are the cognitive symptoms of schizophrenia?

A

Declines in attention, language, memory and executive function
Probably present from birth

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6
Q

What are the affective symptoms of schizophrenia?

A

Blunted, inappropriate, odd expression

Often lead to social stigmatization

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7
Q

What is the dopamine hypothesis of schizophrenia?

A

Too much mesolimbic dopamine pathway activity to the nucleus accumbens leads to positive symptoms
Low dopaminergic activity in the mesocortical pathway to the prefrontal cortex leads to neagtive symptoms
All dopamine signals come from the ventral tegmental area

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8
Q

What is the nucleus accumbens responsible for?

A

Motivation, reward, addiction and reinforcing behaviour

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9
Q

What is the prefrontal cortex responsible for?

A

Cognition, communication, social function and stress response

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10
Q

How is the dopamine hypothesis supported?

A

Most antipsychotics strongly block D2 dopamine receptors

Drugs that increase dopaminergic activity can produce psychosis

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11
Q

How doe typical antipsychotics work?

A

Antagonism of the D2 receptors in the mesolimbic pathway, providing effective relief from positive symptoms

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12
Q

What are some examples of typical antipsychotics (FGAs)?

A

Chlorpromazine, Fluphenazine, Haloperidol, Thiothixene

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13
Q

What are the adverse effects of typical antipsychotics related to?

A

Receptor non-selectivity

Blockade of non-mesolimbic D2 dopaminergic pathways

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14
Q

What are some of the adverse effects of typical antipsychotics that come from the antimuscarinic effects?

A

Toxic confusional state, dry mouth, urinary retention

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15
Q

What are some of the adverse effects of typical antipsychotics that come from the alpha 1 adrenergic block?

A

Orthostatic hypotension, dizziness, tachycardia, impotence

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16
Q

What are some of the adverse effects of typical antipsychotics that come from the histamine H1 blockade?

A

Weight gain, sedation

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17
Q

What is the nigrostriatal pathway?

A

The substantia niagra sends D2 dopamine signals to the striatum which controls coordination and voluntary movement

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18
Q

What happens when there is D2 blockade in the nigrostriatal pathway?

A

Extrapyramidal side effects (EPS): Parkinson’s syndrome, Akathisia (slowed movements), Acute dystonic reactions (abnormal muscle spasm), Tardive dyskinesia (unusual movement, blinking, jerking-can be irreversible, no reliable treatment)

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19
Q

What is the tuberoinfundibular pathway?

A

The hypothalamus sends D2 dopamine signals to the pituitary gland, which controls prolactin secretion (keeps it low)

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20
Q

What happens when there is D2 blockade in the tuberoinfundibular pathway?

A

Increased prolactin production causing lactation, amenrrohea and infertility in women
Lactation, impotence, decreased libido and gynecomastia in men

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21
Q

What are some other adverse effects of typical antipsychotics?

A

Pseudodepression, corneal and lens deposits (chlorpromazine), retinal deposits and cardiac arrhythmias in overdose (thioridizine)
Neuroleptic malignant syndrome (severe muscle rigidity, impaired sweating, fever, severe agitation)

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22
Q

What are the advantages of atypical antipsychotics?

A

Block D2 receptors in the nucleus accumbens to decrease positive symptoms
Decreased D2 affinity in the nigrostriatal pathway to decrease extrapyramidal side effects
Blocks 5-HT2 receptors (serotonin-usually stops dopamine) to decrease negative symptoms by increase mesocortical dopamine

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23
Q

What are some examples of atypical antipsychotics?

A

Resperidone, Olanzapine, Quetiapine, Ziprasidone, Clozapine (D4 receptors, not D2), Aripiprazole (D2 partial agonist, serotonin agonist)

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24
Q

What are the adverse effects of atypical antipsychotics?

A

Generally the same side effects as typical antipsychotics but with a lower risk, especially of EPS
Seizures and agranulocytosis (clozapine), weight gain, hyperlipidemia, hyperglycemia, type 2 diabetes (clozapine, olanzapine)
Higher death rate in the elderly with dementia

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25
Q

What are the CYP 3A4 drug interactions with atypical antipsychotics?

A

Clozapine, Quetiapine, Aripiprazole will be decreased by Fluoxetine and Grapefruit juice
Will be increased by St. John’s wort

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26
Q

What about atypical antipsychotics causes weight gain?

A

H1 blockade

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27
Q

What are the CYP 1A2 drug interactions with antipsychotics?

A

Clozapine, Olanzapine, Typical antipsychotics will be decreased by ciprofloxacin
Increased by smoking

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28
Q

What are the CYP 2D6 drug interactions with antipsychotics?

A

Risperidone, Phenothiazine, Typical antipsychotics will be decreased by paroxetine

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29
Q

Which drugs will interact and cause excess sedation with antipsychotics?

A

Anxiolytics, alcohol, antidepressants, antihistamines

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30
Q

Which drugs will interact and cause additive antimuscarinic effects with antipsychotics?

A

Antimuscarinics

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31
Q

What does metoclopramide do when it interacts with antipsychotics?

A

It is a D2 antagonist so it causes extrapyramidal symptoms

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32
Q

What do SSRI antidepressants do when they interact with antipsychotics?

A

Increase serotonin, thus increase dopamine supression in the NGS and EPS

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33
Q

What is mania?

A

A distinct period of dramatically elevated, irritable mood lasting 1 week or more and impairing social functioning

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34
Q

What are some symptoms of mania?

A

Inflated self-esteem, reduced need for sleep, verbosity, racing thoughts, distractibility and risky behaviour

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35
Q

What is hypomania?

A

A briefer duration of manic symptoms. Will be less severe

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36
Q

What are the 2 subtypes of bipolar disorder?

A

Bipolar I: Episodes of sustained mania, usually with intervening depressive episodes
Bipolar II: Major depressive episodes with at least 1 manic episode

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37
Q

How does the prevalence of bipolar disorder differ between the two genders?

A

Bipolar I: Equal rates in males and females, onset is about 21
Bipolar II: More prevalent in females

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38
Q

What causes bipolar disorder?

A

Multiple defects, no solid grasp on the mechanism

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39
Q

What are some non-pharmacological treatments of bipolar disorder?

A

Adjust sleep, nutrition, exercise and stress levels

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40
Q

What are the pharmacological treatment options for bipolar disorder?

A

Mood stabilizers, atypical antipsychotics, adjunct therapy with benzodiazepines

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41
Q

What are some examples of mood stabilizers?

A

Lithium, valproate, lamogitrine, carbamazepine

42
Q

What is the major working hypothesis behind the action of lithium?

A

Lithium affects the IP3/DAG second messenger system by blocking inositol recycling

43
Q

What is lithium used for in bipolar disorder?

A

For manic phase and maintenance
Reduces risk of suicide
Slow onset and better drugs have reduced use

44
Q

What is often given with lithium?

A

Patients with mania possessing psychotic features often recieve adjunct SGA (olanzapine)

45
Q

What are the early adverse effects of lithium?

A

Nausea, vomiting, diarrhea, muscle weakness, polydipsia with polyuria/nocturia, headache, tremor, nephrogenic diabetes insipidus

46
Q

What are the long-term adverse effects of lithium?

A

Renal morphology change, hypothyroidism, weight gain (>10 kg), reduced libido, edema, severe acne, cardiovascular

47
Q

What are some of the problems with lithium?

A

Low therapeutic index, problematic in renal insufficiency

48
Q

Which drugs interact to increase lithium?

A

Thiazide diuretics, NSAIDs, ACE inhibitors, Loop diuretics, Ca channel blockers

49
Q

Which drugs interact to decrease lithium?

A

K-sparing diuretics, Loop diuretics, Ca channel blockers

50
Q

What is carbamazepine used for in bipolar disorder?

A

Manic, depression and maintenance

Better for rapid cycling

51
Q

What are the adverse effects of carbamazepine?

A

Nausea, vomiting, diarrhea, hyponatremia, rash, leukopenia, fluid retention, drowsiness, dizziness, lethargy and headache

52
Q

What is valproate used for in bipolar disorder?

A

Manic

Patients not responsive to lithium, better for rapid cycling

53
Q

What are the adverse effects of valproate?

A

Generally well-tolerated

But with increased doses, nausea, weight gain, diarrhea, vomiting, hair loss, tremor

54
Q

How are antipsychotics used in the treatment of bipolar disorder?

A

Used alone or with mood stabilizers

55
Q

How are benzodiazepines used in the treatment of bipolar disorder?

A

Clonazepam used with a mood stabilzers

Limited by abuse potential if more than acute

56
Q

What drugs are used for the control of depressive episodes of bipolar disorder?

A

Lithium, lamotrigine, antipsychotics, antidepressants

57
Q

Why is lamogitrine used as an alternative to lithium for maintenance?

A

Weight neutral

58
Q

What antipsychotics are used for bipolar depression?

A

Olanzapine and fluoxetine

59
Q

How should antidepressants be used in the treatment of bipolar disorder?

A

Monotherapy may increase cycling between mania and depression
No advantage of monotherapy or combination therapy (with a mood stabilizer)

60
Q

Which drugs are used for maintenance therapy of bipolar disorder?

A

Lithium, Lamogitrine, Valproate, Carbemazepine

And psychotherapy

61
Q

What defines lifetime bipolar disorder?

A

3 or more manic episodes or 1 moderate to severe manic episode

62
Q

What is depression often comorbid with?

A

Anxiety

63
Q

What is reactive (secondary) depression? How is it treated?

A

A temporary reaction to real stimuli (grief, illness)

Treated mostly by psychotherapy

64
Q

What is major diepression?

A

One or more major depressive episodes free of manic, mixed or hypomanic episodes

65
Q

Who is major depression more common in? When is the onset?

A

More common in females, genetic component

Onset is typically 25-44 years old

66
Q

What are some emotional symptoms of major depression?

A

Persistent diminished ability to experience pleasure, loss of interest in usual activities, pessimistic outlook, anxiety

67
Q

What are some physical symptoms of major depression?

A

Chronic fatigue, terminal insomnia, appetite disturbances

68
Q

What are the cognitive symptoms of major depression?

A

Poor concentration, slow thinking, poor short-term memory, confusion

69
Q

What are the psychomotor symptoms of major depression?

A

Slowed physical movements and speech, agitation

70
Q

What are the non-pharmacologic treatment options for major depression?

A

Psychotherapy, electroconductive therapy (patient preference)

71
Q

What is the amine hypothesis?

A

That depression is related to the reduced ability of the synapse to release norepinephrine and serotonin

72
Q

How do most antidepressant drugs work?

A

Enhance synaptic monoamines by blocking normal neurotransmitter reuptake (not that simple based on therapeutic lag)
Long term effects on synaptic strength (presynaptic autoreceptor downregulation)

73
Q

What is the therapeutic lag for antidepressants?

A

The drugs increase the neurotransmitter levels right away but efficacy is delayed 1-4 weeks.

74
Q

What occurs in phase 1 of amine enhancement?

A

Short term (minutes to hours) uptake inhibition causing homeostatic agonist downregulation of the presynaptic receptors to maintain normal agonist:receptor interaction levels, resulting in reduced negative feedback and the phase 2 amine increase

75
Q

What occurs in phase 2 of amine enhancement?

A

Long term (weeks) effects of the phase 1 enhancement which produces further enhanced amine levels to reach therapeutic signifigance

76
Q

What normally happens in the synapse?

A

Pre-synaptic receptors that feedback inhibit to stop amine release.

77
Q

What are some examples of tricyclic antidepressants?

A

Amitriptyline, imipramine, clomipramine

78
Q

How do tricyclic antidepressants work?

A

Mixed norepinephrine and serotonin reuptake inhibitors, great variation in the each blockade potencies
Also some blockade of cholinergic, histaminergic, alpha 1 adrenergic receptors which give the adverse effects

79
Q

What are TCAs also used for?

A

Neuropathic pain

80
Q

What are some adverse effects of TCAs?

A

Sedation,
tremor, insomnia, (increased NE)
seizures, weight gain, sexual disturbances, cardiac arrythmias (overdose)

81
Q

What are the drug interactions with TCAs?

A

CYP 2D6 inhibitors, highly protein bound (can displace other protein bound drugs)
Sedatives, sympathomimetics, antimuscarinics

82
Q

What are some examples of serotonin selective reuptake inhibitors (SSRIs)?

A

Fluoxetine (most drug interactions), Paroxetine, Sertraline (least)

83
Q

How do SSRIs work?

A

Block serotonin reuptake, not NE as much

Drug interactions differ between them

84
Q

What are some adverse effects of SSRIs?

A

Mild, short-lived GI symptoms, headache, sexual dysfunction, fatigue, insomnia, platelet aggregation inhibition
Safer in overdose

85
Q

Why do SSRIs have less side effects than TCAs?

A

Much less cholinergic, histaminergic, adrenergic receptor blockade than TCAs

86
Q

What are some symptoms of paroxetine withdrawal?

A

Short half life=higher chance of physical dependence and withdrawal
Dizziness, nausea, tremor, anxiety

87
Q

What are some drug interactions with SSRIs?

A

Strong CYP 2D6 inhibitors, TCAs, antipsychotics, beta-blockers, low non-SERT interactions

88
Q

What are the advantages of using an SSRI over a TCA?

A

Equal efficacy with milder side effects, more favourable therapeutic index, smaller chance of additive drug interactions (anticholinergics)

89
Q

What are some examples of SNRIs?

A

Venlafaxine

90
Q

How do SNRIs work?

A

Inhibit both serotonin and norepinephrine reuptake (serotonin>NE)
Also weak dopamine reuptake inhibitor
No affinity for muscarinic, alpha 1 or histaminergic, may be useful for depression in conjunction with neuropathic pain

91
Q

What are some adverse effects of SNRIs?

A

Nausea, sweating, dizziness, anxiety, sexual dysfunction, hypertension
May be more dangerous than SSRIs in overdose

92
Q

What are the drug interactions with SNRIs?

A

No pharmacodynamic

Variable protein binding, CYP 2D6

93
Q

What is mirtazapine? How does it work?

A

An atypical antidepressant
Blocks alpha 2 adrenergic receptors, thus increasing norepinephrine release
Potent histamine blocker
Low affinity for muscarinic, alpha 1 adrenergic receptors

94
Q

What are the adverse effects of mirtazapine?

A

Sedation (may be helpful in sleep disturbances), weight gain

Less chance of sexual side effects

95
Q

What is bupropion? How does it work?

A

An atypical antidepressant
Unknown mechanism (doesn’t inhibit NE or serotonin uptake)
Weakly blocks dopamine reuptake, mild stimulant
Low affinity for muscarinic, alpha 1 or histaminergic receptors

96
Q

What can bupropion be used to comorbidly treat with depression?

A

Fatigue, poor concentration, ADHD

97
Q

What are the adverse effects of bupropion?

A

Nausea, headache, dizziness, insomnia, seizures*
Much lower incidence than with TCAs
No sexual dysfunction, weight gain, sedation

98
Q

What are the drug interactions with bupropion?

A

Meds that lower the seizure threshold, L-Dopa

CYP 2D6 inhibitor

99
Q

What are the 1st line treatment options for major depression?

A

SSNRI, SNRI

If it fully remits, maintain for 4-6 months

100
Q

What should be used as 2nd line treatment options?

A

No response: Switch to different SSRI, SNRI, bupropion, mirtazapine
Partial response: switch or augment atypical antipsychotics, bupropion

Pharmacology 2 (23 decks)

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