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medications and behavior > Exam 1 (CHAPTERS 1-4) 3 > Flashcards

Exam 1 (CHAPTERS 1-4) 3 Flashcards

1
Q

What is the annual rate of depression?

A

10%

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2
Q

What is the lifetime rate of depression?

A

17%

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3
Q

Is depression higher or lower in women vs men?

A

Twice as high in women

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4
Q

When does depression commonly begin?

A

In late adolescence/early adult hood (late being 18/19)

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5
Q

What is the Diagnostic Criteria for Depression?

A

SIGECAPS
1) Sleep - too much or little
2) Interests
3) Guilt
4) Energy - too much or little
5) Concentration
6) Appetite - too much or little
7) Psychomotor - too much or too little
8) Sex or suicide

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6
Q

What are six ways you can treat depression?

A

1) More medication
2) Increase activity level
3) Therapy/counseling (journaling)
4) Transcranial Magnetic Stimulation
5) Electroconvulsive Shock Therapy (for resistant depression)
6) Deep Brain Stimulation (DBS)

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7
Q

What three catecholamines are related to depression? DEN

A

1) Dopamine
2) Serotonin
3) Norepinephrine

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8
Q

What is the Hippocampus related to?

A

Learning and memory

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9
Q

What is the initial evidence for the monoamine hypothesis?

A

Effective drugs increased these levels and drugs that depleted SE and NE caused depression symptoms

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10
Q

What is an example the initial evidence for the monoamine hypothesis?

A

Reserpine for HTN blocks monoamine transport into vesicles leaving them vulnerable for degradation leading to side effect of depression

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11
Q

Where are monoamines prevalent?

A

The limbic system and frontal cortex

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12
Q

What does a deficiency in monoamine neurotransmitters “cause”?

A

Depression

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13
Q

Why was a revision of the monoamine hypothesis needed?

A

Because of the lag time between neurotransmitter changes and change in mood

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14
Q

What is the revised monoamine hypothesis?

A

Monoamine neurons do not produce enough trophic or growth factors which leads to neural degeneration in hippocampus and frontal cortex.

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15
Q

What is the key protein in the revised monoamine hypothesis?

A

Brain-derived neurotropic factor (BDNF) (miracle grow for the brain)

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16
Q

Who’s research is fundamental to the idea of BDNF being a factor in depression?

A

Ronald Duman of yale

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17
Q

What is BDNF?

A

Growth factor for neuron survival, receptor growth, and growth of new neurons

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18
Q

What is the mechanism of the revised Monoamine hypothesis?

A

The Downregulation of monoamine neurons and BDNF

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19
Q

What are 8 ways to increase BDNF?

A

1) Green tea
2) Exercise
3) Fasting
4) Less refined sugar/fat
5) Resveratrol
6) Vitamin D
7) Social enrichment
8) Psychotherapy

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20
Q

CREB has to do with what?

A

Generating proteins

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21
Q

What is the monoamine hypothesis complicated by?

A

Chronic Stress

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22
Q

What does stress lead to and what does that lead to?

A

Stress leads to increased cortisol (stress hormone) which leads to BDNF downregulation through an increase of autoreceptor activity

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23
Q

What do antidepressants do to BDNF levels?

A

They downregulate autoreceptors and activate production of BDNF

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24
Q

What drug makes you eat alot?

A

Remeron

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25
Q

When were tricyclics accidentally discovered and what was their original use.

A

1950s and purpose was schizophrenia

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26
Q

What is the mechanisms of tricyclics?

A

Bind to reuptake transporter for NE and SE which increases duration in synaptic gap immediately. Eventually, presynaptic autoreceptor downregulation and BDNF synthesis upregulation

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27
Q

Imipramine significantly increased what in where?

A

Significantly increased BDNF synthesis in all hippocampai areas examined

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28
Q

What are dirty drugs?

A

Tricyclics, overdose/toxicity is easy to achieve

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29
Q

What are side effects of Tricyclics?

A

Block histamine receptors
block acetylcholine receptors
Overdose potential is high (toxic at 10x)

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30
Q

What happens when histamine receptors are blocked?

A

Drowsiness/fatigue

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31
Q

What happens when acetylcholine receptors are blocked?

A

Anticholinergic effects: dry mouth, dizziness, hypotension, constipation, blurred vision, difficulty concentrating and forming memories.

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32
Q

What were Monoamine Oxidase Inhibitors originally used for and when was the accidental discovery?

A

Found in 1950s used for tuberculosis

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33
Q

What is the mechanisms of Monoamine Oxidase Inhibitors?

A

1) 2 types of enzymes that degradate monoamines (MAO-A & MAO-B)
2) Original MAOIs inhibited both but newer MAOIs are more selective.

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34
Q

What are side effects of MAOIs?

A

1) Sedation/ fatigue, dizziness, movement disorders, blurred vision, decreased libido, dry mouth, weight gain.
2) Serious interaction with foods that contain tyramine

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35
Q

What happens when MAOIs interact with tyramine?

A

1) MAOIs keep liver from metabolizing tyramine
2) Severe headaches, hypertensive crisis, stroke

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36
Q

What foods contain tyramine?

A

Cheese, yogurt, aged meats, some bread, wine, beer, some fruits

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37
Q

SSRIs

A

Selective Serotonin Reuptake Inhibitors

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38
Q

What is another name for Serotonin?

A

5-hydroxytryptophan (5HT)

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39
Q

What is the 1988 SSRIS?

A

fluoxetine (Prozac)

40
Q

What is primary mood-altering effects of drugs linked to 5-HT and attempts to minimize side effects?

A

Serotonin

41
Q

What is the mechanisms of SSRIs?

A

1) To inhibit serotonin reuptake by binding to transporter which then increases duration of 5-HT in synaptic gap.
2) Not specific for receptor subtypes

42
Q

What is the primary therapeutic mechanism of SSRIs?

A

Downregulation of 5-HT1a autoreceptors

43
Q

What are side effects of SSRIs?

A

1) Sexual dysfunction in males, decreased libido, GI problems, decreased appetite, insomnia, and agitation (5-HT2receptors)
2) Serotonin Syndrome
3) Suicide ideation/attempts in kids through age 24

44
Q

What is serotonin Syndrome?

A

Toxic reaction from to much serotonin

45
Q

What are signs of serotonin syndrome?

A

Disorientation, confusion, agitation, mania, hyperthermia, diarrhea, coma, death

46
Q

What do we know about suicide ideation/attempts related to SSRIs?

A

1) Recent analyses found no difference in adolescents taking antidepressants vs. placebo
2) Also prescription rates have decreased and suicide rates have increased

47
Q

What are SNRIs?

A

Serotonin-Norepinephrine Reuptake inhibitors

48
Q

What do SSRIs target?

A

Target serotonin to elevate depressed mood…but what about depressed behavior (fatigue, sleepiness, sleeping too much)

49
Q

What does SNRIs target?

A

NE which promotes arousal

50
Q

What are mechanisms of SNRIs?

A

1) They block 5-HT and NE reuptake transporters along with DA
2) Similar to SSRIs

51
Q

SNRIs are —- to get on and —- to get off of

A

Easy to get on, hard to get off of

52
Q

What do we know about mirtazapine (Remeron) and nefazadone (Serzone)?

A

They are more selective and minimize sexual side effects

53
Q

What does bupropion (Wellbutrin/Zyban) not target?

A

It does not target 5-HT which minimizes side effects and may actually enhance sexual functioning

54
Q

What are side effects of Wellbutrin?

A

Restlessness, agitation, motor tics, decreased appetite, weight loss, abdominal discomfort, and seizures

55
Q

What is St. John’s Wort?

A

Natural remedy

56
Q

What does St. John’s Wort effective for?

A

Mild depression but research comparing it to antidepressants and placebos is inconsistent.

57
Q

What has a Meta-analysis found on St. John’s Wort?

A

It is effective for short term treatment of mild depression

58
Q

What are mechanisms of St. John’s Wort?

A

1) Increases 5-HT and NE by inhibiting reuptake and storage of monoamine but not by binding to transporters
2) May be through increasing intracellular sodium

59
Q

What are side effects of St. John’s Wort?

A

1)Less than antidepressants
2) GI upsets, sedation, restlessness, sexual dysfunction, and headaches

60
Q

What is a caution about St. John’s Wort?

A

Serotonin Syndrome

61
Q

What is an interaction of St. John’s Wort

A

It enhances synthesis of a liver enzyme which metabolizes most drugs, decreasing the duration of action and effectiveness of other drugs.

62
Q

What is the rate of bipolar disorder in men and women?

A

It is equal

63
Q

When does bipolar disorder typically onset?

A

Late adolescence/early adulthood

64
Q

What is the annual prevalence rate?

A

6 million (2.5%)

65
Q

hat is the lifetime percentage?

A

4.4%

66
Q

Is it a simple or complex Diagnosing system?

A

Complex

67
Q

What are Criteria for bipolar disorder (MANIA)?

A

1) Disproportionate/abnormally ELEVATED, EXPANSIVE, or IRRITABLE mood at least one week
2) Must have at least 3 of the items from FIGIPC
3) Causes marked impairment in occupation or social functioning

68
Q

What does ketamine do?

A

puts people into dissociative states

69
Q

What are the criteria for a hypomanic episode

A

1) must have symptoms for 4 days instead of week
2) May not severely impair functioning; no psychotic symptoms

70
Q

Criteria of mixed episode

A

Meet criteria for both manic episode and major depressive episode if symptoms occur nearly every day for 1 week

71
Q

Bipolar 1

A

Manic episode or mixed episodes; major depressive disorder episode not required

72
Q

Bipolar 2

A

1 depressive episode and 1 or more HYPOMANIC episodes

73
Q

Rapid cycling

A

4 or more episodes of mania or depression within 1 year

74
Q

Cyclothmia

A

Hypomanic episodes with symptoms of depression that to not meet diagnosis for major depressive disorder for at least 2 years

75
Q

What is the pathology for bipolar?

A

1) largely unknown

76
Q

Is there a genetic component to bipolar?

A

Yes, there is a large genetic component

77
Q

What is the large genetic component

A

70% monozygatic to 12% dizygotic

78
Q

What genes has bipolar been identified with?

A

5HT transporter and BDNF

79
Q

Are there structural abnormalities that come with bipolar?

A

Yes, there is a neural degeneration which leads to loss of neural tissue which leads to ventricle enlargement to fill up space

80
Q

Where are the structural abnormalities that come with bipolar?

A

Prefrontal cortex, amgydala and striatum (caudate nucleus and putamen in basal ganglia_

81
Q

What is the fist treatment for bipolar?

A

Lithium in 1948

82
Q

Lithium and bipolar

A

1) used as salt substitute but was toxic
2) meant to treat mania but was not approved by FDA until 1970

83
Q

Pharmacokinetics of lithium

A

1) easily absorbed, crosses BBB slowly and is excreted intact from kidneys
2) Therapeutic dose has narrow window and is toxic above levels
3) Blood testing to check for lithium toxicity

84
Q

What are side effects (long term) of lithium?

A

Weight gain, thyroid disease, skin rash, kidney dysfunction, compromised immune functioning

85
Q

What happens when you suddenly decrease lithium use?

A

16-fold increase in suicidality

86
Q

Lithium pharmacodynamics

A

1) Also treats depression and suicide ideation effectively
2) Hypothesized relationship to BDNFactivity
3) Increases 5HT activity in cortex and hippocampus by agonizing autoreceptors and heteroreceptors on dopamine neurons

87
Q

Heteroreceptors

A

Function similar to autoreceptors but activated by a neurotransmitter released by a different neuron

88
Q

How does lithium pharmacodynamics have an antimanic effect?

A

mostly by stabilizing dopamine neurons and modest effects on 5-HT neurons

89
Q

Valproic acid treatment for bipolar/mania

A

1) stimulates BDNF synthesis
2) affects GABA and dopamine
- inhibits GABA reuptake increases inhibition
- increases DA release in prefrontal cortex
3) Inhibits glutamate activity which may underlie mania and seizures
4) less side effects

90
Q

What are side effects of Valproic Acid?

A

Sedation, tremor, ataxia, nausea, and weight gain

91
Q

What is an example of Valproic acid?

A

Depecote

92
Q

What is ataxia?

A

Poor movement (same as lithium toxicity)

93
Q

Gabapentin treatment for bipolar/mania

A

1) approved for seizures but also used for mania and neuropathic pain
2) Designed to mimic GABA (increases GABA)
3) Side effects similar to valproic acid

94
Q

How does Gabapentin mimic GABA?

A

It decreases Calcium influx which decreases glutamate activity in the cortex

95
Q

What is an example of Gabapentin?

A

Neurotin

96
Q

Example of neuropathic pain

A

Diabetic neuropathy such as feet pain

medications and behavior (40 decks)

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