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Drugs and Psychopharmacology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What effects do sedatives have on GABA?

A

Sedatives make GABA work overtime. By upping its level of activity in the CNS, sedatives allow GABA to produce a much stronger effect on your brain activity.

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2
Q

Sedative drugs binding site:

A

GABA (w/ a variety of subtype receptors)

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3
Q

Benzodiazepines facilitate the

A

binding of GABA

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4
Q

Benzodiazepines act on __ and bind at __ and __.

A

amygdala; insula and orbital-frontal cortex

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5
Q

What is the amygdala responsible for?

A

anxiety

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6
Q

What are the insula and orbital-frontal cortex responsible for, respectively?

A

behavior and fear related responses

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7
Q

What is the difference between anxiety and panic?

A

duration and intesity

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8
Q

Are Benzodiazepines GABA agonist?

A

yes

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9
Q

When are benzodiazepines NOT used?

A

-panic
-PTSD
-GAD (generalized anxiety disorder)
-when fine motor skills are involved
-if a person uses alcohol
-for mid-adolescents

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10
Q

GABAergic

A

any chemical that modifies the effects of GABA in the body or brain

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11
Q

Benzodiazepines chemically block:

A

GABA-A

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12
Q

True or False: Benzodiazepines are low in toxicity.

A

true

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13
Q

About how many benzodiazepines are available in the US?

A

15 to 20

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14
Q

What are the most commonly used benzodiazepines?

A
  1. Ativan
  2. Volume
  3. Xanax
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15
Q

When does benzodiazepine peak concentration?

A

1 hour

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16
Q

How many stages do benzodiazepines go through to be metabolized? List the steps.

A

3 steps:
1. oxidatively metabolized by the cytochrome P450 enzymes
2. conjugated with glucuronide
3. excreted almost entirely in the urine

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17
Q

What are benzodiazepines metabolized into?

A

nordiazepam, oxazepam, and temazepam

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18
Q

What is considered a low dose of benzodiazepines?

A

5 to 10 mg

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19
Q

Buspar/Buspirone

A

-antianxiety
-serotonin drug
-5HT1AA agonist
-treats anxiety and depression
-used to treat GAD

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20
Q

What are some benefits of taking Buspar/Buspirone?

A

-doesn’t produce a lot of sedative effects
-very little cognitive effects
-can be taken w/ alcohol
-very little potential for addiction
-most of the drug is metabolized at first pass

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21
Q

About what percent of Buspar/Buspirone makes it into the bloodstream?

A

~5%

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22
Q

How can the efficacy of Buspar/Buspirone be improved?

A

by drinking grapefruit juice

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23
Q

What are the 4 main antidepressants?

A
  1. MAO inhibitors
  2. tricyclics
  3. SSRI
  4. SNRI
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24
Q

What are the 2 different types of depression?

A
  1. major depressive disorder
  2. dysthymic disorder/persistent depressive disorder
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25
Q

What are the major differences between major depressive disorder and dysthymic disorder/persistent depressive disorder?

A
  1. duration
  2. intensity

major depressive disorder: high in intensity but doesn’t last long

dysthymic disorder/persistent depressive disorder: symptoms not as intense but they are long-term/chronic

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26
Q

MAO

A

monoamine oxidate
-works really well
-monoamines are inhibited
-the only antidepressant meds that work inside the membrane

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27
Q

__ is the only antidepressant that works inside the membrane. What is their location? Why is this an issue?

A

MAO inhibitors; Located mainly in the terminal button but can be found all over. This is an issue because this means that MAO would be inhibited everywhere (this can also be a good thing too though)

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28
Q

MAO inhibitors: Neurotransmitters make it to the membrane in a __ quantity meaning __.

A

large; brain fires better

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29
Q

MAO inhibitors are very well tolerated as long as __.

A

patients watch what they eat and other meds aren’t crossed

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30
Q

What types of foods should be avoided when taking MAO inhibitors? Why?

A

Cheese, nuts, and alcohol should be avoided because the body will be unable to break it down.

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31
Q

In MAO inhibitors, the covalent bond is easily breakable or unbreakable? What does this bond look like?

A

The bond is unbreakable;
MAO—covalent bond—drug

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32
Q

MAO inhibitors prevent

A

monoamine oxidase from removing the neurotransmitters norepinephrine, serotonin, and dopamine from the brain

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33
Q

Tricyclics

A

-3 ring structure
-“dirty drugs”

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34
Q

Why are tricyclics called “dirty” drugs?

A

they attach to different neurotransmitters all over the brain

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35
Q

What are the main neurotransmitters that tricyclics bind to?

A

acetylcholine, serotonin, and muscarinic receptors

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36
Q

What is the major issue with tricyclics?

A

side effects

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37
Q

What are some side effects of taking tricyclics?

A

-Drowsiness
-Blurred vision
-Constipation
-Dry mouth
-Drop in blood pressure
-Urine retention

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38
Q

How long does it take for tricyclics to show effects?

A

about 3 weeks

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39
Q

SSRIs

A

-only target serotonin
-weight loss frequently reported
-selectively blocks serotonin

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40
Q

Why are SSRIs a better treatment option?

A

They’re cheaper and safer to use, and people are more likely to stay on these drugs.

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41
Q

SNRIs

A

-only block norepinephrine

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42
Q

When are SNRIs more likely to be used?

A

When there is no response to SSRIs or they do not work for the patient.

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43
Q

What are the major symptoms of depression?

A
  1. behavior
  2. emotional
  3. physical
  4. cognitive
  5. motivational
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44
Q

What symptom of depression are we more likely to associate with?

A

emotional

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45
Q

When one is experiencing physical depression symptoms, what is the best approach?

A

medication

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46
Q

When one is experiencing cognitive depression symptoms, what is the best approach?

A

psychotherapy

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47
Q

What is the overall best approach to treating depression?

A

a combination of medication and psychotherapy

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48
Q

What are you looking for when diagnosing depression?

A

-issues with sex
-cognitive symptoms (what they think/how they think)
-issues with substance

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49
Q

What is first assessed when diagnosing/treating depression?

A

duration and trigger

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50
Q

Endogenous Depression

A

-the person “always kind of felt this way”
-responds better to medication
-persistent depression
-assumed to be within

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51
Q

Reactive Depression

A

-response to something
-trigger
-very common
-produces very serious depressive episodes

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52
Q

What causes depression?

A

The exact cause of depression is unknown but we know that there are issues with serotonin, dopamine, and norepinephrine

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53
Q

We’re not sure how drugs that are used to treat depression work, but we know that __.

A

the drugs provide more of a neurotransmitter longer in the synapse

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54
Q

The delay in drugs that treat depression has to do with what?

A

change at the receptor (up or down)

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55
Q

What triggers the 2nd messanger inside the cell?

A

inotropic receptors and metabotropic receptors

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56
Q

The first messenger is

A

serotonin

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57
Q

Neurogenic depression causes issues with the

A

2nd messenger

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58
Q

neurogenic depression

A

depression that is associated with a reduction in the birth of new neurons in the hippocampus, an area of the brain important to stress regulation, cognition, and mood.

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59
Q

About __% of people diagnosed with depression have some kind of hippocampal damage in response to stress.

A

50

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60
Q

CREB cAMP response element-binding protein controls

A

BDNF (brain-derived neurotrophic factor)

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61
Q

What does BDNF do in the brain?

A

promotes the survival of neurons by playing a role in the growth, differentiation, and maintenance of cells
-it is the healing part of brain development
-intracellular

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62
Q

Antidepressants work at the __ level.

A

cellular

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63
Q

Antidepressants promote __ and __.

A

repair and neuron survival

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64
Q

What is the first thing that antidepressants do?

A

modulate neurotransmitters

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65
Q

What is the second and most important thing that antidepressants do?

A

targets intracellular molecules that are responsible for maintaining neural health

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66
Q

Tricyclics work well for

A

major depression

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67
Q

Tricyclics have __ effects.

A

analgesic

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68
Q

What causes the sedative and/or memory/cognitive issues with tricyclics and other medications?

A

histamine

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69
Q

Tricyclics block

A

pre-synaptic norepinephrine and serotonin; post-synaptic acetylcholine and histamine

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70
Q

Tricyclics are metabolized by the __ into __.

A

liver; active intermediates and then inactive

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71
Q

What are some other characteristics of tricyclics?

A

-long half-life
-crosses blood-brain barrier and placental barrier
-not addictive
-well absorbed
-slow onset
-fatal in overdose (cardiotoxic)
-wide variety of side effects

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72
Q

What happens when norepinephrine is blocked/reuptake is blocked?

A

-trimers
-tachycardia
-ED and ejaculation issue
-

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73
Q

What happens when serotonin receptor is blocked?

A

-GI issues
-anxiety (dose-dependent)
-sexual dysfunction
-EPS

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74
Q

What happens when dopamine receptor is blocked?

A

-psychomotor disturbances
-psychosis possible
-male sexual dysfunction
-EP

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75
Q

What happens when norepinephrine receptor receptors are blocked?

A

-memory issues
-exasperates issues

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76
Q

What happens when histamine receptor is blocked?

A

-weight gain
-sedation
-hypotension

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77
Q

What happens when ACH receptor is blocked is blocked?

A

-blurred vision
-urinary retention

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78
Q

Antidepressants seem to be really effective when high in __.

A

dopamine

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79
Q

What are the 4 different types of anxiety disorders?

A
  1. GAD
  2. OCD
  3. panic disorder
  4. PTSD
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80
Q

When are MAOs typically used?

A

when other drugs do not work (probably more effective)

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81
Q

MAOs form irreversible covalent bonds with

A

monoamine oxidase

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82
Q

Heterocyclics are __ typical.

A

a

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83
Q

What is the function of SSRIs?

A

treat depression by increasing levels of serotonin in the brain
-they make more serotonin available (5HT1A)

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84
Q

Side effects of SSRIs are related to?

A

5HT2A and 5HT3

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85
Q

Clinical effects of SSRIs are related to?

A

5HT1A

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86
Q

What are the side effects of 5HT2A?

A

-insomnia
-restlessness
-sexual dysfunction

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87
Q

What are the side effects of 5HT3?

A

-GI issues
-nasea

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88
Q

How are SSRIs used for those who are treatment resistant?

A

general approach, increase the dose

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89
Q

What can occur as a result of using SSRIs?

A

serotonin disorder

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90
Q

What is serotonin disorder?

A

when serotonin accumulates/clusters and the medication stops working

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91
Q

What are some symptoms of serotonin disorder?

A

can range from mild (shivering and diarrhea) to severe (muscle rigidity, fever, and seizures)
-can result in death if not treated
-can sometimes resolve on its own

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92
Q

SSRI discontinuation syndrome

A

happens when you quit clod turkey

93
Q

Which SSRI is most likely to cause discontinuation syndrome?

A

Paroxetine

94
Q

What are some symptoms of SSRI discontinuation syndrome?

A

flu-like symptoms, insomnia, nausea, imbalance, sensory disturbances, and hyperarousal

95
Q

About _% of people that take SSRIs experience sexual dysfunction. How is this treated?

A

70; psychotherapy and discontinue use of medication

96
Q

What is the half-life of prozac?

A

2 to 3 days

97
Q

What is the active metabolite of Prozac?

A

norfluoxetine

98
Q

How long does Prozac take to leave the system and see effects?

A

about 3 months

99
Q

What is often the first prescribed/first response SSRI?

A

Prozac

100
Q

Zoloft is an SSRI that is more effective than __.

A

Prozac

101
Q

How long is the steady state of Zoloft?

A

1 week

102
Q

Zolof is also known as

A

Sertraline

103
Q

What is the active metabolite of Zoloft?

A

Desmethylsertraline

104
Q

How long does it take Zoloft to reach its peak?

A

8 to 10 hours

105
Q

Paxil is an SSRI used to treat

A

OCD

106
Q

Paxil has the __ half-life of the other SSRIs mentioned.

A

shortest

107
Q

Bipolar disorder has the __ med compliance rate.

A

lowest

108
Q

What are the two stages of bipolar disorder?

A
  1. bipolar 1
  2. bipolar 2
109
Q

Bipolar 1

A

“frank mania”, more serious/more severe symptoms

110
Q

Bipolar 2

A

tend not to have psychotic episodes

111
Q

It is thought that bipolar disorder may be genetic as about __% of people who have parents with bipolar disorder also experience this illness. Bipolar disorder may be connected to the _ chromosome.

A

65; X

112
Q

How is bipolar 1 disorder treated?

A

with antipsychotics but only works for a little, doesn’t treat bipolarism

113
Q

Does bipolar 1 or 2 look more like schizophrenia?

A

bipolar 1

114
Q

What is rapid cycling disorder?

A

four or more manic, hypomanic, or depressive episodes have taken place within a twelve-month period

115
Q

What are some treatment options for bipolar disorder?

A

The first option is lithium and has been the standard of care for years. Mood stabilizers and anti-convulscents will be used after.

116
Q

If mood stabilizers and anti-convalescence don’t work, __ antipsychotics will be used.

A

a-typical

117
Q

Why are people bipolar?

A

While we don’t really know why people are bipolar, we know that there is a lack of chemical activity and underfunctioning of the brain. Patients are found on opposite sides of the spectrum, with their brains experiencing hypoactivity.

118
Q

What are the 4 theories/explanations as to why bipolar disorder occurs?

A
  1. dysregulation theory
  2. permissive theory
  3. chaotic theory
  4. neurotransmitter theory
119
Q

Explain the permissive theory:

A

decrease in norepinephrine + decrease in serotonin= depression

decrease in norepinephrine + increase in serotonin= bipolar

120
Q

Explain the chaotic theory:

A

the brain is not making neurotransmitters like it should

121
Q

Explain the neurotransmitter theory:

A

dysregulation in cell membrane

122
Q

How do you explain bipolar disorder?

A

up one day, down the next

123
Q

What are some bipolar comorbidities?

A

-anxiety
-substance use/abuse
-sometimes these are treated but bipolar can make them worse

124
Q

About how many medications are there to treat bipolar disorder?

A

~16

125
Q

What are some things you have to address when finding a drug to treat bipolar?

A

How well does the drug treat acute depression episodes? Mania? Stabilize?

126
Q

What is the overall problem with bipolar medications?

A

symptoms

127
Q

What are the 4 categories of pharmacotherapy for bipolar?

A
  1. lithium
  2. anti-convalescents
  3. 2nd generation antipsychotics/A-typical
  4. omega 3 fatty acids
128
Q

The approaches to bipolar treatment depend on what?

A

the severity of the mania and depression

129
Q

If mood swings are __, lithium does not work as well for the depression symptom of bipolar.

A

balanced

130
Q

When is lithium combined with a typical for bipolar treatment?

A

when mood swings are severe

131
Q

What happens if bipolar is left untreated?

A

bipolar can worsen and the brain can become damaged

132
Q

What did the Step BD study find?

A

-anti-depressants don’t help with mood stabilizers
-anti-depressants don’t increase manic episodes
-overall, anti-depressants aren’t very helpful for treating bipolar

133
Q

Lithium shares characteristics with

A

sodium

134
Q

_ has been the treatment of choice for bipolar since the 1950s.

A

lithium

135
Q

Lithium makes you feel __ making it hard for people to stay on.

A

“zombied out”

136
Q

Lithium is effective up to __% of the time.

A

80

137
Q

Lithium can damage which organs if too much is used?

A

the liver and the kidney

138
Q

What is the dosage issue with lithium?

A

too much can be toxic and too little will have no effect

139
Q

What has to happen in order for lithium to be effective?

A

In order for it to be effective, it has to function in low blood content.

140
Q

Lithium is __, therefore, it causes issues with fetal development.

A

teratogenic

141
Q

How long does it take for lithium to reach its peak?

A

about 3 hours

142
Q

What is the usual dose range for lithium?

A

200 to 900 mg

143
Q

Is lithium metabolized? If so, what is the metabolite?

A

No, lithium is not metabolized

144
Q

Lithium has no __ properties.

A

reward

145
Q

Lithium inhibits __ which increases levels of the protein __.

A

GSK3; beta-catenin

146
Q

Beta-catenin promotes what?

A

cell survival and axon growth

147
Q

The side effects of lithium depend on what?

A

blood content levels

148
Q

What are some symptoms of taking lithium?

A

-rash
-heart, liver, and kidney issues
-trimers
-cognitive impairment
-weight gain
-nausea
-increase in urination frequency
-hypothyroidism
-lack of coordination/ataxia
-alterations in consciousness

149
Q

What drugs are now being combined with lithium?

A

carbamazepine (Tegretol) and 2nd gen (when mania is bad)

150
Q

what did the “Balance Study” find?

A

lithium combined with another drug showed better outcomes than just taking anti-convalescents

151
Q

Anticonvulsants are usually used to treat what?

A

seizures

152
Q

How do the effects of anticonvulsants occur?

A

by blocking sodium channels

153
Q

Valproic acid works at __.

A

Gabba-b

154
Q

Valproic acid is used to treat

A

aggression, BPD, antisocial disorder, acute mania, rapid cycling

155
Q

What drug has a good response rate for lithium-resistant people? What percentage of lithium-resistant people show the benefits of using this drug as an alternative?

A

Valproic acid; ~75%

156
Q

What are some side effects of taking Valproic acid?

A

-GI issues
-sedative
-hair loss
-decrease in cognitive function

157
Q

Valproic acid can inhibit __.

A

other drugs, especially lamotrigine

158
Q

Valproic acid has the best effects when combined with

A

olanzapine, but especially lithium

159
Q

What is one serious disease that Valproic acid can cause?

A

pancreatitis

160
Q

Lamotrigine is most effective for which disorder?

A

rapid cycling disorder

161
Q

Lamotrigine is better at preventing

A

recurrence of bipolar symptoms

162
Q

Lamotrigine is not as effective for treating

A

manic

163
Q

Is Lamotrigine a better choice for Bipolar 1 or 2?

A

2

164
Q

Lamotrigine is currently the drug of choice for

A

bipolar-depression

165
Q

What are some symptoms of taking Lamotrigine?

A

-dizziness
-nausea
-rash (most serious and can be fatal)

166
Q

Lamotrigine half-life is doubled by __ and halved by __.

A

Valproic acid; carbamazepine

167
Q

Lamotrigine is FDA approved for

A

long-term maintenance

168
Q

Lamotrigine doesn’t help when in a manic episode, but it helps by __.

A

keeping one from heading into one

169
Q

Gabapentin inhibits

A

the release of glutamate

170
Q

Gabapentin is excreted

A

unchanged

171
Q

Gabapentin is not as effective by itself and should therefore be taken with __ as it would be more effective.

A

lithium

172
Q

Pregabalin is used for

A

-pain disorders

173
Q

Pregabalin is used for

A

-pain disorders
-fibromyalgia
-anxiety
-bipolar
-GAD

174
Q

Pregabalin is excreted

A

unchanged

175
Q

Pregabalin is __ times as potent as gabapentin.

A

3 times

176
Q

Which has a longer half-life, pregabalin or gabapentin?

A

pregabalin

177
Q

Topamax can produce what effects?

A

anxiety, depression, and cognitive deficits

178
Q

What are first-generation antipsychotics?

A

reduce dopaminergic neurotransmission in the four dopamine pathways by blocking D2 receptors; they differ in potency but not effectiveness

179
Q

1st generation antipsychotics are not really used for

A

bipolar

180
Q

What are the most common 1st generation antipsychotics?

A

risperidone and olanzapine

181
Q

Risperidone

A

used by itself to prevent relapse
-“keeps people in the middle”

182
Q

Is Olanzapineis effective for bipolar 1 or 2?

A

both

183
Q

What are some risks of olanzapine use?

A

-have to avoid MAOs
-have to be careful/monitor use of serotonin drugs
-weight gain
-glucose intolerance

184
Q

What is the primary difference between bipolar disorder and schizophrenia?

A

bipolar disorder primarily causes extreme mood shifts, whereas schizophrenia causes delusions and hallucinations

185
Q

Schizophrenia is connected to what other disorders?

A

ADHD and major depressive disorder

186
Q

Schizophrenia has a __ component that has not yet been isolated.

A

genetic

187
Q

Why does schizophrenia occur?

A

We are not really sure why it occurs, but we know that it has something to do with overactivity of dopamine.

188
Q

What drug shifted us more into medical psychology?

A

Thorazine

189
Q

What are the diagnoses/characterizations of Schizophrenia?

A
  1. Positive Symptoms/Type I
  2. Negative Symptoms/Type II
190
Q

Positive Symptoms/Type I

A

over-the-top symptoms/out-of-the-ordinary hallucinations (paranoid to the max)

191
Q

Negative Symptoms/Type II

A

subtractions from normal behavior; loner/withdrawn; human contact is uncomfortable
-under symptoms
-disordered speech
-frontal lobe issues

192
Q

Why are there two types of Schizophrenia?

A

Because Type I is related to overactive dopamine while type II is related to physiological abnormalities of the brain

193
Q

What neurotransmitters are involved with Schizophrenia?

A

dopamine, serotonin, and glutamate

194
Q

Long-term/chronic use of Schizophrenia medications can produce

A

long-term motor symptoms

195
Q

What is an important benefit of a-typical drugs?

A

the antagonistic effect at 5HT

196
Q

Nuplazid

A

5HT drug agonist
-treats parkinson’s

197
Q

What are some characteristics of first-generation antipsychotics?

A

-lipid soluble
-mostly taken orally but can be taken intramuscularly
-long half-life

198
Q

How long is the half-life of first-generation antipsychotics?

A

up to 2 days

199
Q

First-generation antipsychotics are metabolized by

A

the liver.

200
Q

What is the efficacy of first-generation antipsychotics?

A

70%

201
Q

First-generation antipsychotics’ effectiveness is best when they block ~__% of the __ receptor in the brain.

A

70; D2

202
Q

First-generation antipsychotics block

A

D2 receptors, acetylcholine, histamine, and norepinephrine

203
Q

What are the two categories of first-generation antipsychotic symptoms?

A

low potency and high potency

204
Q

Low-potency first-generation antipsychotics symptom requires

A

high dose (~100+ mg)

205
Q

High-potency first-generation antipsychotics require

A

small dose (~10+ mg)

206
Q

What are the first-generation antipsychotics’ low-potency effects?

A

-sedation
-anticholinergic
-skin issues
-sexual dysfunction

207
Q

What are the first-generation antipsychotics’ high-potency effects?

A

-toxicity

208
Q

First-generation antipsychotics work if __. Explain.

A

the diagnosis is correct. Schizophrenia can sometimes be mistaken for bipolar disorder, some people are treatment resistant, and positive symptoms are easier to treat than negative symptoms.

209
Q

Second-generation antipsychotics are better for treating which symptoms?

A

negative symptoms

210
Q

What is the pharmacological difference between 1st generation and 2nd generation antipsychotics?

A

1st gen: D2 antagonist
2nd gen: 5HT2A/D2 antagonist

211
Q

What are some of the most common causes of sleep issues?

A

-diet
-hormone issues
-blue light
-stress

212
Q

Agoraphobia

A

“fear of the marketplace”

213
Q

Hyperpolarization of the cell results in

A

decrease in GABA

214
Q

Benzos stimulate the __ levels of the brain.

A

chlorine

215
Q

Benzodiazepines may be prescribed to treat

A

severe anxiety, severe insomnia, or even panic disorder

216
Q

Chemically blocking GABA may produce an intense __ response.

A

anxiety

217
Q

Hypofunctioning GABA receptors lower the

A

threshold of anxiety-related stimuli

218
Q

Why is diazepam a long-lasting benzo?

A

because it is metabolized into multiple active metabolites

219
Q

Diazepam can cause what kind of issues?

A

-can disrupt sleep patterns (long-term cycling)
-can cause paranoia
-suicidal ideations
-impair memory

220
Q

When do withdrawal symptoms from benzos typically appear?

A

after 1 month of consistent use

221
Q

BZRA’s

A

benzodiazepine receptor agonist

222
Q

Why does it take so long for SSRIs to work?

A

They provide an immediate increase in serotonin, yet it doesn’t get used. Time may indicate that the issue is with synaptic membranes.

223
Q

Neurogenic Theory of Depression

A

-intercellular issues
-issue with second messenger system
-metabotropic issues

224
Q

Kreb protein

A

-cAMP cycle
-cAMP response
-brain-derived neurotrophic factor (bdmf)

225
Q

SSRIs may increase the production of __, thus causing the neurogenitive effect.

A

brain-derived neurotrophic factor (bdmf)

226
Q

SSRIs are associated with what effects?

A

analgesic and anxiolytic effects

227
Q

Tricyclics block

A

serotonin and norepinephrine presynaptically

228
Q

Histamines and acetylcholine are associated with a __ block.

A

postsynaptic

229
Q

What are some clinical limitations of tricyclics?

A

-slow uptake
-side effects
- can overdose

Drugs and Psychopharmacology (3 decks)

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