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.
2
Q
Sedative drugs binding site:
A
GABA (w/ a variety of subtype receptors)
3
Q
Benzodiazepines facilitate the
A
binding of GABA
4
Q
Benzodiazepines act on __ and bind at __ and __.
A
amygdala; insula and orbital-frontal cortex
5
Q
What is the amygdala responsible for?
A
anxiety
6
Q
What are the insula and orbital-frontal cortex responsible for, respectively?
A
behavior and fear related responses
7
Q
What is the difference between anxiety and panic?
A
duration and intesity
8
Q
Are Benzodiazepines GABA agonist?
A
yes
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
10
Q
GABAergic
A
any chemical that modifies the effects of GABA in the body or brain
11
Q
Benzodiazepines chemically block:
A
GABA-A
12
Q
True or False: Benzodiazepines are low in toxicity.
A
true
13
Q
About how many benzodiazepines are available in the US?
A
15 to 20
14
Q
What are the most commonly used benzodiazepines?
A
- Ativan
- Volume
- Xanax
15
Q
When does benzodiazepine peak concentration?
A
1 hour
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
17
Q
What are benzodiazepines metabolized into?
A
nordiazepam, oxazepam, and temazepam
18
Q
What is considered a low dose of benzodiazepines?
A
5 to 10 mg
19
Q
Buspar/Buspirone
A
-antianxiety
-serotonin drug
-5HT1AA agonist
-treats anxiety and depression
-used to treat GAD
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
21
Q
About what percent of Buspar/Buspirone makes it into the bloodstream?
A
~5%
22
Q
How can the efficacy of Buspar/Buspirone be improved?
A
by drinking grapefruit juice
23
Q
What are the 4 main antidepressants?
A
- MAO inhibitors
- tricyclics
- SSRI
- SNRI
24
Q
What are the 2 different types of depression?
A
- major depressive disorder
- dysthymic disorder/persistent depressive disorder
25
What are the major differences between major depressive disorder and dysthymic disorder/persistent depressive disorder?
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
26
MAO
monoamine oxidate
-works really well
-monoamines are inhibited
-the only antidepressant meds that work inside the membrane
27
__ is the only antidepressant that works inside the membrane. What is their location? Why is this an issue?
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)
28
MAO inhibitors: Neurotransmitters make it to the membrane in a __ quantity meaning __.
large; brain fires better
29
MAO inhibitors are very well tolerated as long as __.
patients watch what they eat and other meds aren't crossed
30
What types of foods should be avoided when taking MAO inhibitors? Why?
Cheese, nuts, and alcohol should be avoided because the body will be unable to break it down.
31
In MAO inhibitors, the covalent bond is easily breakable or unbreakable? What does this bond look like?
The bond is unbreakable;
MAO---covalent bond---drug
32
MAO inhibitors prevent
monoamine oxidase from removing the neurotransmitters norepinephrine, serotonin, and dopamine from the brain
33
Tricyclics
-3 ring structure
-"dirty drugs"
34
Why are tricyclics called "dirty" drugs?
they attach to different neurotransmitters all over the brain
35
What are the main neurotransmitters that tricyclics bind to?
acetylcholine, serotonin, and muscarinic receptors
36
What is the major issue with tricyclics?
side effects
37
What are some side effects of taking tricyclics?
-Drowsiness
-Blurred vision
-Constipation
-Dry mouth
-Drop in blood pressure
-Urine retention
38
How long does it take for tricyclics to show effects?
about 3 weeks
39
SSRIs
-only target serotonin
-weight loss frequently reported
-selectively blocks serotonin
40
Why are SSRIs a better treatment option?
They're cheaper and safer to use, and people are more likely to stay on these drugs.
41
SNRIs
-only block norepinephrine
42
When are SNRIs more likely to be used?
When there is no response to SSRIs or they do not work for the patient.
43
What are the major symptoms of depression?
1. behavior
2. emotional
3. physical
4. cognitive
5. motivational
44
What symptom of depression are we more likely to associate with?
emotional
45
When one is experiencing physical depression symptoms, what is the best approach?
medication
46
When one is experiencing cognitive depression symptoms, what is the best approach?
psychotherapy
47
What is the overall best approach to treating depression?
a combination of medication and psychotherapy
48
What are you looking for when diagnosing depression?
-issues with sex
-cognitive symptoms (what they think/how they think)
-issues with substance
49
What is first assessed when diagnosing/treating depression?
duration and trigger
50
Endogenous Depression
-the person "always kind of felt this way"
-responds better to medication
-persistent depression
-assumed to be within
51
Reactive Depression
-response to something
-trigger
-very common
-produces very serious depressive episodes
52
What causes depression?
The exact cause of depression is unknown but we know that there are issues with serotonin, dopamine, and norepinephrine
53
We're not sure how drugs that are used to treat depression work, but we know that __.
the drugs provide more of a neurotransmitter longer in the synapse
54
The delay in drugs that treat depression has to do with what?
change at the receptor (up or down)
55
What triggers the 2nd messanger inside the cell?
inotropic receptors and metabotropic receptors
56
The first messenger is
serotonin
57
Neurogenic depression causes issues with the
2nd messenger
58
neurogenic depression
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.
59
About __% of people diagnosed with depression have some kind of hippocampal damage in response to stress.
50
60
CREB cAMP response element-binding protein controls
BDNF (brain-derived neurotrophic factor)
61
What does BDNF do in the brain?
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
62
Antidepressants work at the __ level.
cellular
63
Antidepressants promote __ and __.
repair and neuron survival
64
What is the first thing that antidepressants do?
modulate neurotransmitters
65
What is the second and most important thing that antidepressants do?
targets intracellular molecules that are responsible for maintaining neural health
66
Tricyclics work well for
major depression
67
Tricyclics have __ effects.
analgesic
68
What causes the sedative and/or memory/cognitive issues with tricyclics and other medications?
histamine
69
Tricyclics block
pre-synaptic norepinephrine and serotonin; post-synaptic acetylcholine and histamine
70
Tricyclics are metabolized by the __ into __.
liver; active intermediates and then inactive
71
What are some other characteristics of tricyclics?
-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
72
What happens when norepinephrine is blocked/reuptake is blocked?
-trimers
-tachycardia
-ED and ejaculation issue
-
73
What happens when serotonin receptor is blocked?
-GI issues
-anxiety (dose-dependent)
-sexual dysfunction
-EPS
74
What happens when dopamine receptor is blocked?
-psychomotor disturbances
-psychosis possible
-male sexual dysfunction
-EP
75
What happens when norepinephrine receptor receptors are blocked?
-memory issues
-exasperates issues
76
What happens when histamine receptor is blocked?
-weight gain
-sedation
-hypotension
77
What happens when ACH receptor is blocked is blocked?
-blurred vision
-urinary retention
78
Antidepressants seem to be really effective when high in __.
dopamine
79
What are the 4 different types of anxiety disorders?
1. GAD
2. OCD
3. panic disorder
4. PTSD
80
When are MAOs typically used?
when other drugs do not work (probably more effective)
81
MAOs form irreversible covalent bonds with
monoamine oxidase
82
Heterocyclics are __ typical.
a
83
What is the function of SSRIs?
treat depression by increasing levels of serotonin in the brain
-they make more serotonin available (5HT1A)
84
Side effects of SSRIs are related to?
5HT2A and 5HT3
85
Clinical effects of SSRIs are related to?
5HT1A
86
What are the side effects of 5HT2A?
-insomnia
-restlessness
-sexual dysfunction
87
What are the side effects of 5HT3?
-GI issues
-nasea
88
How are SSRIs used for those who are treatment resistant?
general approach, increase the dose
89
What can occur as a result of using SSRIs?
serotonin disorder
90
What is serotonin disorder?
when serotonin accumulates/clusters and the medication stops working
91
What are some symptoms of serotonin disorder?
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
92
SSRI discontinuation syndrome
happens when you quit clod turkey
93
Which SSRI is most likely to cause discontinuation syndrome?
Paroxetine
94
What are some symptoms of SSRI discontinuation syndrome?
flu-like symptoms, insomnia, nausea, imbalance, sensory disturbances, and hyperarousal
95
About _% of people that take SSRIs experience sexual dysfunction. How is this treated?
70; psychotherapy and discontinue use of medication
96
What is the half-life of prozac?
2 to 3 days
97
What is the active metabolite of Prozac?
norfluoxetine
98
How long does Prozac take to leave the system and see effects?
about 3 months
99
What is often the first prescribed/first response SSRI?
Prozac
100
Zoloft is an SSRI that is more effective than __.
Prozac
101
How long is the steady state of Zoloft?
1 week
102
Zolof is also known as
Sertraline
103
What is the active metabolite of Zoloft?
Desmethylsertraline
104
How long does it take Zoloft to reach its peak?
8 to 10 hours
105
Paxil is an SSRI used to treat
OCD
106
Paxil has the __ half-life of the other SSRIs mentioned.
shortest
107
Bipolar disorder has the __ med compliance rate.
lowest
108
What are the two stages of bipolar disorder?
1. bipolar 1
2. bipolar 2
109
Bipolar 1
"frank mania", more serious/more severe symptoms
110
Bipolar 2
tend not to have psychotic episodes
111
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.
65; X
112
How is bipolar 1 disorder treated?
with antipsychotics but only works for a little, doesn't treat bipolarism
113
Does bipolar 1 or 2 look more like schizophrenia?
bipolar 1
114
What is rapid cycling disorder?
four or more manic, hypomanic, or depressive episodes have taken place within a twelve-month period
115
What are some treatment options for bipolar disorder?
The first option is lithium and has been the standard of care for years. Mood stabilizers and anti-convulscents will be used after.
116
If mood stabilizers and anti-convalescence don't work, __ antipsychotics will be used.
a-typical
117
Why are people bipolar?
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
What are the 4 theories/explanations as to why bipolar disorder occurs?
1. dysregulation theory
2. permissive theory
3. chaotic theory
4. neurotransmitter theory
119
Explain the permissive theory:
decrease in norepinephrine + decrease in serotonin= depression
decrease in norepinephrine + increase in serotonin= bipolar
120
Explain the chaotic theory:
the brain is not making neurotransmitters like it should
121
Explain the neurotransmitter theory:
dysregulation in cell membrane
122
How do you explain bipolar disorder?
up one day, down the next
123
What are some bipolar comorbidities?
-anxiety
-substance use/abuse
-sometimes these are treated but bipolar can make them worse
124
About how many medications are there to treat bipolar disorder?
~16
125
What are some things you have to address when finding a drug to treat bipolar?
How well does the drug treat acute depression episodes? Mania? Stabilize?
126
What is the overall problem with bipolar medications?
symptoms
127
What are the 4 categories of pharmacotherapy for bipolar?
1. lithium
2. anti-convalescents
3. 2nd generation antipsychotics/A-typical
4. omega 3 fatty acids
128
The approaches to bipolar treatment depend on what?
the severity of the mania and depression
129
If mood swings are __, lithium does not work as well for the depression symptom of bipolar.
balanced
130
When is lithium combined with a typical for bipolar treatment?
when mood swings are severe
131
What happens if bipolar is left untreated?
bipolar can worsen and the brain can become damaged
132
What did the Step BD study find?
-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
Lithium shares characteristics with
sodium
134
_ has been the treatment of choice for bipolar since the 1950s.
lithium
135
Lithium makes you feel __ making it hard for people to stay on.
"zombied out"
136
Lithium is effective up to __% of the time.
80
137
Lithium can damage which organs if too much is used?
the liver and the kidney
138
What is the dosage issue with lithium?
too much can be toxic and too little will have no effect
139
What has to happen in order for lithium to be effective?
In order for it to be effective, it has to function in low blood content.
140
Lithium is __, therefore, it causes issues with fetal development.
teratogenic
141
How long does it take for lithium to reach its peak?
about 3 hours
142
What is the usual dose range for lithium?
200 to 900 mg
143
Is lithium metabolized? If so, what is the metabolite?
No, lithium is not metabolized
144
Lithium has no __ properties.
reward
145
Lithium inhibits __ which increases levels of the protein __.
GSK3; beta-catenin
146
Beta-catenin promotes what?
cell survival and axon growth
147
The side effects of lithium depend on what?
blood content levels
148
What are some symptoms of taking lithium?
-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
What drugs are now being combined with lithium?
carbamazepine (Tegretol) and 2nd gen (when mania is bad)
150
what did the "Balance Study" find?
lithium combined with another drug showed better outcomes than just taking anti-convalescents
151
Anticonvulsants are usually used to treat what?
seizures
152
How do the effects of anticonvulsants occur?
by blocking sodium channels
153
Valproic acid works at __.
Gabba-b
154
Valproic acid is used to treat
aggression, BPD, antisocial disorder, acute mania, rapid cycling
155
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?
Valproic acid; ~75%
156
What are some side effects of taking Valproic acid?
-GI issues
-sedative
-hair loss
-decrease in cognitive function
157
Valproic acid can inhibit __.
other drugs, especially lamotrigine
158
Valproic acid has the best effects when combined with
olanzapine, but especially lithium
159
What is one serious disease that Valproic acid can cause?
pancreatitis
160
Lamotrigine is most effective for which disorder?
rapid cycling disorder
161
Lamotrigine is better at preventing
recurrence of bipolar symptoms
162
Lamotrigine is not as effective for treating
manic
163
Is Lamotrigine a better choice for Bipolar 1 or 2?
2
164
Lamotrigine is currently the drug of choice for
bipolar-depression
165
What are some symptoms of taking Lamotrigine?
-dizziness
-nausea
-rash (most serious and can be fatal)
166
Lamotrigine half-life is doubled by __ and halved by __.
Valproic acid; carbamazepine
167
Lamotrigine is FDA approved for
long-term maintenance
168
Lamotrigine doesn't help when in a manic episode, but it helps by __.
keeping one from heading into one
169
Gabapentin inhibits
the release of glutamate
170
Gabapentin is excreted
unchanged
171
Gabapentin is not as effective by itself and should therefore be taken with __ as it would be more effective.
lithium
172
Pregabalin is used for
-pain disorders
173
Pregabalin is used for
-pain disorders
-fibromyalgia
-anxiety
-bipolar
-GAD
174
Pregabalin is excreted
unchanged
175
Pregabalin is __ times as potent as gabapentin.
3 times
176
Which has a longer half-life, pregabalin or gabapentin?
pregabalin
177
Topamax can produce what effects?
anxiety, depression, and cognitive deficits
178
What are first-generation antipsychotics?
reduce dopaminergic neurotransmission in the four dopamine pathways by blocking D2 receptors; they differ in potency but not effectiveness
179
1st generation antipsychotics are not really used for
bipolar
180
What are the most common 1st generation antipsychotics?
risperidone and olanzapine
181
Risperidone
used by itself to prevent relapse
-"keeps people in the middle"
182
Is Olanzapineis effective for bipolar 1 or 2?
both
183
What are some risks of olanzapine use?
-have to avoid MAOs
-have to be careful/monitor use of serotonin drugs
-weight gain
-glucose intolerance
184
What is the primary difference between bipolar disorder and schizophrenia?
bipolar disorder primarily causes extreme mood shifts, whereas schizophrenia causes delusions and hallucinations
185
Schizophrenia is connected to what other disorders?
ADHD and major depressive disorder
186
Schizophrenia has a __ component that has not yet been isolated.
genetic
187
Why does schizophrenia occur?
We are not really sure why it occurs, but we know that it has something to do with overactivity of dopamine.
188
What drug shifted us more into medical psychology?
Thorazine
189
What are the diagnoses/characterizations of Schizophrenia?
1. Positive Symptoms/Type I
2. Negative Symptoms/Type II
190
Positive Symptoms/Type I
over-the-top symptoms/out-of-the-ordinary hallucinations (paranoid to the max)
191
Negative Symptoms/Type II
subtractions from normal behavior; loner/withdrawn; human contact is uncomfortable
-under symptoms
-disordered speech
-frontal lobe issues
192
Why are there two types of Schizophrenia?
Because Type I is related to overactive dopamine while type II is related to physiological abnormalities of the brain
193
What neurotransmitters are involved with Schizophrenia?
dopamine, serotonin, and glutamate
194
Long-term/chronic use of Schizophrenia medications can produce
long-term motor symptoms
195
What is an important benefit of a-typical drugs?
the antagonistic effect at 5HT
196
Nuplazid
5HT drug agonist
-treats parkinson's
197
What are some characteristics of first-generation antipsychotics?
-lipid soluble
-mostly taken orally but can be taken intramuscularly
-long half-life
198
How long is the half-life of first-generation antipsychotics?
up to 2 days
199
First-generation antipsychotics are metabolized by
the liver.
200
What is the efficacy of first-generation antipsychotics?
70%
201
First-generation antipsychotics' effectiveness is best when they block ~__% of the __ receptor in the brain.
70; D2
202
First-generation antipsychotics block
D2 receptors, acetylcholine, histamine, and norepinephrine
203
What are the two categories of first-generation antipsychotic symptoms?
low potency and high potency
204
Low-potency first-generation antipsychotics symptom requires
high dose (~100+ mg)
205
High-potency first-generation antipsychotics require
small dose (~10+ mg)
206
What are the first-generation antipsychotics' low-potency effects?
-sedation
-anticholinergic
-skin issues
-sexual dysfunction
207
What are the first-generation antipsychotics' high-potency effects?
-toxicity
208
First-generation antipsychotics work if __. Explain.
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
Second-generation antipsychotics are better for treating which symptoms?
negative symptoms
210
What is the pharmacological difference between 1st generation and 2nd generation antipsychotics?
1st gen: D2 antagonist
2nd gen: 5HT2A/D2 antagonist
211
What are some of the most common causes of sleep issues?
-diet
-hormone issues
-blue light
-stress
212
Agoraphobia
"fear of the marketplace"
213
Hyperpolarization of the cell results in
decrease in GABA
214
Benzos stimulate the __ levels of the brain.
chlorine
215
Benzodiazepines may be prescribed to treat
severe anxiety, severe insomnia, or even panic disorder
216
Chemically blocking GABA may produce an intense __ response.
anxiety
217
Hypofunctioning GABA receptors lower the
threshold of anxiety-related stimuli
218
Why is diazepam a long-lasting benzo?
because it is metabolized into multiple active metabolites
219
Diazepam can cause what kind of issues?
-can disrupt sleep patterns (long-term cycling)
-can cause paranoia
-suicidal ideations
-impair memory
220
When do withdrawal symptoms from benzos typically appear?
after 1 month of consistent use
221
BZRA's
benzodiazepine receptor agonist
222
Why does it take so long for SSRIs to work?
They provide an immediate increase in serotonin, yet it doesn't get used. Time may indicate that the issue is with synaptic membranes.
223
Neurogenic Theory of Depression
-intercellular issues
-issue with second messenger system
-metabotropic issues
224
Kreb protein
-cAMP cycle
-cAMP response
-brain-derived neurotrophic factor (bdmf)
225
SSRIs may increase the production of __, thus causing the neurogenitive effect.
brain-derived neurotrophic factor (bdmf)
226
SSRIs are associated with what effects?
analgesic and anxiolytic effects
227
Tricyclics block
serotonin and norepinephrine presynaptically
228
Histamines and acetylcholine are associated with a __ block.
postsynaptic
229
What are some clinical limitations of tricyclics?
-slow uptake
-side effects
- can overdose
