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Pharmacology - Fall > Lecture 10 - Antidepressants, Bipolar, & Antipsychotics > Flashcards

Lecture 10 - Antidepressants, Bipolar, & Antipsychotics Flashcards

1
Q

What is reactive (secondary) depression?

A

Temporary reaction to real stimuli (grief, illness)

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2
Q

What is the treatment for reactive depression?

A

Psychotherapy

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3
Q

What is bipolar disorder?

A

Recurrent major depressive episodes w/ intervening manic, hypomanic, or mixed episodes

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4
Q

What is major depression?

A

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

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5
Q

Which gender is major depression more common in?

A

Females

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6
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
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7
Q

What are some physical symptoms of major depression?

A
  • Chronic fatigue
  • Terminal insomnia (waking up very early and not being able to fall back asleep)
  • Appetite disturbances
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8
Q

What are some cognitive symptoms of major depression?

A
  • Poor concentration, slow thinking, poor short-term memory

- Confusion

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9
Q

What are some psychomotor symptoms of major depression?

A
  • Slowed physical movements and speech

- Agitation

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10
Q

What is needed for a diagnosis of depression?

A

At least 5 symptoms every day for 2 weeks

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11
Q

What are some non-pharm therapies for major depression?

A
  • Psychotherapy

- ECT

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12
Q

What is the amine hypothesis?

A

Depression is related to decreased synaptic levels of NE and serotonin

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13
Q

How are most antidepressants believed to work?

A

Enhance synaptic amines by blocking normal NT reuptake processes

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14
Q

What is phase 1 amine enhancement?

A

Short term (minutes to hours); uptake inhibition

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15
Q

What is phase 2 amine enhancement?

A
  • Long term (weeks) effects of phase 1 enhancement

- Produces further enhanced amine levels to reach therapeutic significance

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16
Q

What does phase 1 amine enhancement cause?

A

Homeostatic agonist down-regulation of pre-synaptic receptors that feedback inhibit to stop amine release, to maintain “normal” agonist-to-receptor interaction levels, causing decreased negative feedback and increased phase 2 amines

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17
Q

Pre-synaptic receptor downregulation correlates w/ _____

A

Improved mood

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18
Q

What are examples of TCAs?

A

Amitriptyline and imipramine

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19
Q

What is the mechanism of TCAs?

A
  • Mixed NE and serotonin reuptake inhibitors

- Also some blockade of cholinergic, histaminergic, alpha 1 adrenergic receptors causing adverse effects

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20
Q

What are TCAs also used for?

A

Neuropathic pain

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21
Q

What is the symptom of TCA overdose?

A

Cardiac arrhythmias

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22
Q

What are drug interactions w/ TCAs?

A
  • CYP 2D6 inhibitors

- Sedatives, antimuscarinics, sympathomimetics

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23
Q

What are examples of SSRIs?

A

Fluoxetine, paroxetine, sertraline, and citalopram

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24
Q

What is the mechanism of SSRIs?

A

Block serotonin reuptake much more than NE

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25
Q

Are SSRIs more effective than TCAs?

A

No

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26
Q

What are some advantages to SSRIs over TCAs?

A
  • Have much less cholinergic, histaminergic, and adrenergic receptor blockade so milder side effects
  • Much more favourable therapeutic index
  • Smaller chance of additive drug interactions
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27
Q

What are symptoms of paroxetine withdrawal?

A
  • Dizziness
  • Nausea
  • Tremor
  • Anxiety
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28
Q

What are drug interactions w/ SSRIs?

A

Strong CYP 2D6 inhibitors, TCAs, antipsychotics, beta-blockers interfere w/ metabolism

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29
Q

What are examples of SNRIs?

A

Venlafaxine, duloxetine, and desvenlafaxine

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30
Q

What is the mechanism of SNRIs?

A
  • Inhibit both NE and serotonin reuptake
  • Weak dopamine reuptake inhibitors
  • No affinity for alpha 1 adrenergic, muscarinic, or histaminergic
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31
Q

What are advantages to SNRIs over SSRIs/TCAs?

A
  • May be useful for depression w/ neuropathic pain

- Fewer drug interactions

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32
Q

What are examples of atypical antidepressants?

A
  • Mirtazapine

- Bupropion

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33
Q

What is the mechanism of mirtazapine?

A
  • Blocks alpha 2 receptors, thus increases NE release
  • Low affinity for muscarinic, alpha 1 receptors
  • Potent histamine receptor blocker
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34
Q

What are drug interactions w/ mirtazapine?

A

None known

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35
Q

What are advantages to mirtazapine?

A
  • As tolerable as SSRIs
  • Anxiolytic/sedative effect can be useful
  • Minimal cholinergic/adrenergic drug interactions
    • Weight gain major drawback
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36
Q

What is the mechanism of bupropion?

A
  • Doesn’t inhibit NE or serotonin reuptake
  • Weakly blocks dopamine reuptake
  • Mild stimulant
  • Low affinity for muscarinic, histaminergic, and alpha 1 receptors
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37
Q

What are some drug interactions w/ bupropion?

A
  • Meds that lower seizure threshold (L-Dopa)

- CYP 2D6 inhibitors

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38
Q

What are some advantages to bupropion?

A
  • As tolerable as SSRIs
  • Stimulant effects may be helpful
  • May offer relief from SSRI/SNRI-induced sexual dysfunction or weight gain
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39
Q

What are some examples of monoamine oxidase inhibitors?

A
  • Phenelzine
  • Tranylcypromine
  • Moclobemide
40
Q

What does MAO-A do?

A

Breaks down NE and serotonin

41
Q

What does MAO-B do?

A

Breaks down dopamine

42
Q

Tranylcypromine is a ____ inhibitor

A

MAO-A and B

43
Q

Moclobemide is a ____ inhibitor

A

MAO-A

44
Q

When are MAO inhibitors used?

A

Px unresponsive to other treatment due to side effects or food/drug interactions

45
Q

What are some drug interactions w/ MAO inhibitors?

A

Serotonin syndrome w/ TCAs, SSRIs, or SNRIs

46
Q

Pharmacologic therapy is effective in majority of major depression px after ______

A

Therapeutic lag period

47
Q

What are the first line treatments for major depression?

A

SSRIs and SNRIs

48
Q

What is schizophrenia?

A

Chronic psychosis w/ deterioration of functional capacity

49
Q

Which gender does schizophrenia affect more often?

A

Males

50
Q

What are some positive symptoms of schizophrenia?

A
  • Delusions (most common)
  • Hallucinations
  • Disorganized speech
51
Q

What are some negative symptoms of schizophrenia?

A
  • Avolition - lack of motivation, desire, and persistence
  • Alogia - poverty of speech
  • Anhedonia - inability to feel pleasure
  • Lack of emotional response
52
Q

What are some cognitive symptoms of schizophrenia?

A

Decrease in attention, language, memory, executive function

53
Q

Which symptoms of schizophrenia are likely present before any others?

A

Cognitive symptoms

54
Q

What are affective symptoms of schizophrenia?

A

Blunted, inappropriate, odd expression

55
Q

How do positive schizophrenia symptoms result?

A

Too much mesolimbic dopamine pathway activity

56
Q

How do negative schizophrenia symptoms result?

A

Low doapminergic activity in mesocortical pathway

57
Q

What occurs in the mesolimbic pathway?

A

Dopamine binds to nucleus accumbens, which controls motivation, reward, addiction, and reinforcing behaviour

58
Q

What occurs in the mesocortical pathway?

A

Dopamine D1 binds to prefrontal cortex, controlling cognition, social function, and stress response

59
Q

What do most antipsychotics block?

A

D2 dopamine receptors (mesolimbic system)

60
Q

Which drugs can produce psychosis?

A

Drugs that increase dopaminergic activity

61
Q

What is the mechanism for typical antipsychotics?

A

Antagonism of D2 receptors in mesolimbic system

62
Q

Which symptoms are relieved w/ typical antipsychotics?

A

Positive

63
Q

What are examples of typical antipsychotics?

A
  • Chlorpromazine
  • Fluphenazine
  • Haloperidol
  • Thiothixene
64
Q

What causes adverse effects of typical antipsychotics?

A

Receptor non-selectivity and blockade of non-mesolimbic D2 dopaminergic pathways

65
Q

What is the most important alpha 1 blocker side effect?

A

Orthostatic hypotension

66
Q

What does D2 blockade in the nigrostriatal pathway cause?

A

Extrapyramidal side effects (Parkinson’s syndrome or pseudo-parkinsonism, restlessness, acute dystonic reactions)

67
Q

What occurs in the nigrostriatal pathway?

A

Dopamine D2 goes from substantia nigra to striatum

68
Q

What occurs in the tuberoinfundibular pathway?

A

Dopamine goes from hypothalamus to pituitary

69
Q

What does D2 blockade in the tuberoinfundibular pathway cause?

A

Increased prolactin production

70
Q

What effect does dopamine normally have on prolactin?

A

Suppresses prolactin release

71
Q

What is a symptom of thioridizine overdose?

A

Cardiac arrhythmias

72
Q

What are advantages of atypical antipsychotics?

A
  • Block D2 in nucleus accumbens causing decrease in positive symptoms
  • Decreased D2 in nigrostriatal system causes decreased EPS
  • Block serotonin receptors causing decreased negative symptoms
73
Q

How can you decrease negative symptoms?

A

By increasing mesocortical dopamine

74
Q

What is the mechanism of clozapine?

A

Seems to have greater effect at D4 and little effect at D2 receptors

75
Q

What is aripiprazole used as?

A

An enhancer for antidepressants

76
Q

What is the mechanism of aripiprazole?

A

D2 partial agonist

77
Q

What are the adverse effects of atypical antipsychotics?

A

Same as typical antipsychotics but w/ lower risk

78
Q

What is a major side effect of clozapine?

A

Seizures

79
Q

Which CYP enzymes is clozapine metabolized by?

A

1A2 and 3A4

80
Q

What is an activator of CYP 1A2?

A

Smoking

81
Q

How long does mania last?

A

Over a week

82
Q

What is hypomania?

A

Briefer duration and less severe manic symptoms

83
Q

What is bipolar 1 disorder?

A

Episodes of sustained mania, usually w/ intervening depressive episodes

84
Q

What is bipolar 2 disorder?

A

Major depressive episodes w/ at least 1 manic episode

85
Q

What is the mechanism of bipolar disorder?

A

Multiple defects, not fully understood

86
Q

What are some non-pharm treatments for bipolar disorder?

A

Adjust sleep, nutrition, exercise, or stress levels

87
Q

What are some examples of mood stabilizers?

A
  • Lithium
  • Valproate
  • Lamotrigine
  • Carbamazepine
88
Q

What are some pharmacologic treatments for bipolar disorder?

A
  • Mood stabilizers
  • Atypical antipsychotics
  • Adjunct therapy w/ BZDs
89
Q

Which treatments can control manic episodes?

A
  • Lithium, valproate, carbamazepine
  • Atypical antipsychotics
  • BZDs
90
Q

Which treatments can control depressive episodes?

A
  • Lithium
  • Lamotrigine
  • Antipsychotics
  • Antidepressants
91
Q

What effects does lithium have?

A
  • Decreased serotonin reuptake
  • Decrease dopamine synthesis
  • Increased GABAergic activity
  • Increased glutamate reuptake
  • Decreased neuronal Ca reuptake
92
Q

Lithium has a ___ therapeutic index

A

Low

93
Q

What is carbamazepine used for?

A

Manic and depressive episodes and maintenance

94
Q

What is the BZD of choice for bipolar disorder?

A

Clonazepam

95
Q

Which antipsychotics are best for depressive episodes of bipolar disorder?

A

Olanzapine and fluoxetine together

96
Q

Which treatments are used for maintenance therapy of bipolar disorder?

A
  • Lithium
  • Lamotrigine
  • Valproate
  • Carbamazepine
  • Psychotherapy

Pharmacology - Fall (15 decks)

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