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Medications and Behavior > Exam 1 (CHAPTERS 1-4) 3 > Flashcards

Exam 1 (CHAPTERS 1-4) 3 Flashcards

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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
When were tricyclics accidentally discovered and what was their original use.
1950s and purpose was schizophrenia
26
What is the mechanisms of tricyclics?
Bind to reuptake transporter for NE and SE which increases duration in synaptic gap immediately. Eventually, presynaptic autoreceptor downregulation and BDNF synthesis upregulation
27
Imipramine significantly increased what in where?
Significantly increased BDNF synthesis in all hippocampai areas examined
28
What are dirty drugs?
Tricyclics, overdose/toxicity is easy to achieve
29
What are side effects of Tricyclics?
Block histamine receptors block acetylcholine receptors Overdose potential is high (toxic at 10x)
30
What happens when histamine receptors are blocked?
Drowsiness/fatigue
31
What happens when acetylcholine receptors are blocked?
Anticholinergic effects: dry mouth, dizziness, hypotension, constipation, blurred vision, difficulty concentrating and forming memories.
32
What were Monoamine Oxidase Inhibitors originally used for and when was the accidental discovery?
Found in 1950s used for tuberculosis
33
What is the mechanisms of Monoamine Oxidase Inhibitors?
1) 2 types of enzymes that degradate monoamines (MAO-A & MAO-B) 2) Original MAOIs inhibited both but newer MAOIs are more selective.
34
What are side effects of MAOIs?
1) Sedation/ fatigue, dizziness, movement disorders, blurred vision, decreased libido, dry mouth, weight gain. 2) Serious interaction with foods that contain tyramine
35
What happens when MAOIs interact with tyramine?
1) MAOIs keep liver from metabolizing tyramine 2) Severe headaches, hypertensive crisis, stroke
36
What foods contain tyramine?
Cheese, yogurt, aged meats, some bread, wine, beer, some fruits
37
SSRIs
Selective Serotonin Reuptake Inhibitors
38
What is another name for Serotonin?
5-hydroxytryptophan (5HT)
39
What is the 1988 SSRIS?
fluoxetine (Prozac)
40
What is primary mood-altering effects of drugs linked to 5-HT and attempts to minimize side effects?
Serotonin
41
What is the mechanisms of SSRIs?
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
What is the primary therapeutic mechanism of SSRIs?
Downregulation of 5-HT1a autoreceptors
43
What are side effects of SSRIs?
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
What is serotonin Syndrome?
Toxic reaction from to much serotonin
45
What are signs of serotonin syndrome?
Disorientation, confusion, agitation, mania, hyperthermia, diarrhea, coma, death
46
What do we know about suicide ideation/attempts related to SSRIs?
1) Recent analyses found no difference in adolescents taking antidepressants vs. placebo 2) Also prescription rates have decreased and suicide rates have increased
47
What are SNRIs?
Serotonin-Norepinephrine Reuptake inhibitors
48
What do SSRIs target?
Target serotonin to elevate depressed mood...but what about depressed behavior (fatigue, sleepiness, sleeping too much)
49
What does SNRIs target?
NE which promotes arousal
50
What are mechanisms of SNRIs?
1) They block 5-HT and NE reuptake transporters along with DA 2) Similar to SSRIs
51
SNRIs are ---- to get on and ---- to get off of
Easy to get on, hard to get off of
52
What do we know about mirtazapine (Remeron) and nefazadone (Serzone)?
They are more selective and minimize sexual side effects
53
What does bupropion (Wellbutrin/Zyban) not target?
It does not target 5-HT which minimizes side effects and may actually enhance sexual functioning
54
What are side effects of Wellbutrin?
Restlessness, agitation, motor tics, decreased appetite, weight loss, abdominal discomfort, and seizures
55
What is St. John's Wort?
Natural remedy
56
What does St. John's Wort effective for?
Mild depression but research comparing it to antidepressants and placebos is inconsistent.
57
What has a Meta-analysis found on St. John's Wort?
It is effective for short term treatment of mild depression
58
What are mechanisms of St. John's Wort?
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
What are side effects of St. John's Wort?
1)Less than antidepressants 2) GI upsets, sedation, restlessness, sexual dysfunction, and headaches
60
What is a caution about St. John's Wort?
Serotonin Syndrome
61
What is an interaction of St. John's Wort
It enhances synthesis of a liver enzyme which metabolizes most drugs, decreasing the duration of action and effectiveness of other drugs.
62
What is the rate of bipolar disorder in men and women?
It is equal
63
When does bipolar disorder typically onset?
Late adolescence/early adulthood
64
What is the annual prevalence rate?
6 million (2.5%)
65
hat is the lifetime percentage?
4.4%
66
Is it a simple or complex Diagnosing system?
Complex
67
What are Criteria for bipolar disorder (MANIA)?
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
What does ketamine do?
puts people into dissociative states
69
What are the criteria for a hypomanic episode
1) must have symptoms for 4 days instead of week 2) May not severely impair functioning; no psychotic symptoms
70
Criteria of mixed episode
Meet criteria for both manic episode and major depressive episode if symptoms occur nearly every day for 1 week
71
Bipolar 1
Manic episode or mixed episodes; major depressive disorder episode not required
72
Bipolar 2
1 depressive episode and 1 or more HYPOMANIC episodes
73
Rapid cycling
4 or more episodes of mania or depression within 1 year
74
Cyclothmia
Hypomanic episodes with symptoms of depression that to not meet diagnosis for major depressive disorder for at least 2 years
75
What is the pathology for bipolar?
1) largely unknown
76
Is there a genetic component to bipolar?
Yes, there is a large genetic component
77
What is the large genetic component
70% monozygatic to 12% dizygotic
78
What genes has bipolar been identified with?
5HT transporter and BDNF
79
Are there structural abnormalities that come with bipolar?
Yes, there is a neural degeneration which leads to loss of neural tissue which leads to ventricle enlargement to fill up space
80
Where are the structural abnormalities that come with bipolar?
Prefrontal cortex, amgydala and striatum (caudate nucleus and putamen in basal ganglia_
81
What is the fist treatment for bipolar?
Lithium in 1948
82
Lithium and bipolar
1) used as salt substitute but was toxic 2) meant to treat mania but was not approved by FDA until 1970
83
Pharmacokinetics of lithium
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
What are side effects (long term) of lithium?
Weight gain, thyroid disease, skin rash, kidney dysfunction, compromised immune functioning
85
What happens when you suddenly decrease lithium use?
16-fold increase in suicidality
86
Lithium pharmacodynamics
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
Heteroreceptors
Function similar to autoreceptors but activated by a neurotransmitter released by a different neuron
88
How does lithium pharmacodynamics have an antimanic effect?
mostly by stabilizing dopamine neurons and modest effects on 5-HT neurons
89
Valproic acid treatment for bipolar/mania
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
What are side effects of Valproic Acid?
Sedation, tremor, ataxia, nausea, and weight gain
91
What is an example of Valproic acid?
Depecote
92
What is ataxia?
Poor movement (same as lithium toxicity)
93
Gabapentin treatment for bipolar/mania
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
How does Gabapentin mimic GABA?
It decreases Calcium influx which decreases glutamate activity in the cortex
95
What is an example of Gabapentin?
Neurotin
96
Example of neuropathic pain
Diabetic neuropathy such as feet pain

Medications and Behavior (40 decks)

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