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Fall 2022 > Pharmacology- Mental Health > Flashcards

Pharmacology- Mental Health Flashcards

1
Q

The CNS can be divided grossly into

A

the brain and the spinal cord

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2
Q

The highest order of conscious function and integration in the CNS

A

Cerebral cortex

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3
Q

The largest and most rostral aspect of the brain

A

cerebrm

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4
Q

Most CNS therapeutic medications affect cortical function __________ by altering the function of lower brain and spinal cord structures

A

indirectly

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5
Q

Drugs used to treat epilepsy often target what region of the brain?

A

cerebrum

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6
Q

Drugs used in the attempt to enhance cognitive function in Alzheimer’s are likely to exert their effects in what region of the brain?

A

cerebrum

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7
Q

Area of the brain primarily involved in the control of motor activities

A

basal ganglia

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8
Q

Medications that treat movement disorders often exert their effects where?

A

basal ganglia

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9
Q

The diencephalon consists of what structures?

A

thalamus & hypothalamus

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10
Q

Temperature, appetite, water balance, and certain emotions are all controlled by what?

A

hypothalamus

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11
Q

Drugs that target the HPA axis are

A

opiates, ethanol, cannabinoids, nicotine, cocaine, amphetamine, growth hormone, gonadotropins,

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12
Q

The brainstem includes what structures?

A

pons, medulla oblongata

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13
Q

The midbrain and brainstem are responsible for controlling what?

A

respiration and cardiovascular function

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14
Q

What structure monitors and controls consciousness and is important in regulating alertness or arousal of the cerebral cortex?

A

Reticular formation

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15
Q

Stimulants will most likely _______ the reticular formation, while depressants will likely _____ the reticular formation.

A

increase activity, decrease activity

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16
Q

True or False: Therapeutic medications are not usually targeting the cerebellum directly.

A

True

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17
Q

What is does the limbic system accomplish and what structures are included?

A

Involved in behavior and emotional control; amygdala, hippocampus, hypothalamus

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18
Q

Drugs that affect the limbic system are often associated with what class of meds?

A

anti-anxiety, antipsychotics

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19
Q

Gray matter vs. white matter

A

Gray: serves as an area for synaptic connections
White: myelinated axons of neurons grouped into tracts

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20
Q

Local anesthetics work where? Narcotic analgesics?

A

Local –> white matter
narcotics –> gray matter

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21
Q

The blood brain barrier is comprised of what?

A

Tight junctions

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22
Q

What substance is most likely to cross the BBB?

A

non-polar, lipid-soluble drugs; lipophilic, hydrophobic

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23
Q

Is the NT excitatory or inhibitory generally?
Acetylcholine
NE
Dopamine
Serotonin
GABA
Glycine
Glutamate, aspartate
Substance P
Enkephalins

A

Excitatory
Inhibitory
Inhibitory
Inhibitory
Inhibitory
Inhibitory
Excitation
Excitation
Excitation

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24
Q

Discuss Acetylcholine

A
  • Found in many areas of CNS
  • Likely involved in cognition and memory
  • Excitatory
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25
Q

Discuss Monamines

A
  • include: dopamine, NE, serotonin
  • Dopamine –> inhibitory
  • NE –> Disinhibition
  • Serotonin –> inhibitor
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26
Q

Discuss amino acids

A
  • GABA –> primary inhibitory NT
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27
Q

Discuss peptides

A
  • Substance P, endogenous opioids
  • Excitatory neurotransmitters
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28
Q

The majority of CNS drugs act by what mechanism?

A

modifying synaptic transmissions

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29
Q

Discuss the following sites of drug action:
1. Action potential
2. Synthesis
3. Storage
4. Release
5. Reuptake
6. Degradation
7. Post-synaptic receptors
8. Presynaptic autoreceptors
9. Membrane effects

A
  1. block propagation
  2. block the synthesis
  3. Impair vesicle storage of NTs
  4. Change the release rate
  5. Impair reuptake to increase NT in synapse
  6. Inhibition of enzymes
  7. blocking postsynaptic receptors
  8. negative feedback to control NT release
  9. Affect membrane organization/fluidity
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30
Q

What is the difference between an anxiolytic and a sedative-hypnotic?

A

An anxiolytic is generally a sedative-hypnotic with a mechanism that does not have an overt sedative effect, though they are still capable of producing said effect.

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31
Q

Insomnia may effect approx. what percentage of people? What can trigger it?

A

10-15%
Illness, injury, recent relocation to unfamiliar environment

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32
Q

What are the two categories of sedative-hypnotics?

A

Benzos
Non-benzos (z-hypnotics, barbiturates, +)

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33
Q

What is the primary indication for benzodiazepines?

A

anxiety

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34
Q

True or false: Benzos are no longer frequently recommended for insomnia d/t their side effect profile

A

True

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35
Q

Prolonged use of benzos is associated with what?

A

tolerance, dependence

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36
Q

How do benzos work?

A

Increase inhibitory effects of GABA
(GABAA is the main therapeutic target)

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37
Q

Differentiate tolerance and dependence

A
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38
Q

Who is most likely to experience sedation w/ use of benzos?

A

elderly

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39
Q

ADRs of benzos include

A
  • Tolerance, dependence
  • Sedation
  • Disinhibition
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40
Q

What suffix is generally associated with benzos?

A

-lam
-pam

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41
Q

Discuss: alprazolam (xanax)

A

-Benzodiazepine

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42
Q

Clonazepam (klonopin)

A

Benzodiazepine

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43
Q

Diazepam (valium)

A

Benzodiazepine

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44
Q

Flurazepam (Dalmane)

A

Benzodiazepine

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45
Q

Lorazepam (ativan)

A

Benzo

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46
Q

Midazolam (versed)

A

Benzo

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47
Q

Triazolam (halcyon)

A

bento

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48
Q

Discuss the therapeutic index of barbituates

A

Narrow therapeutic range –> dangerous

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49
Q

What is the suffix that denotes barbiturates?

A

-barbital

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50
Q

AMobarbital (amytal)

A

barbituate

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51
Q

Pentobarbital

A

barbituate

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52
Q

Phenobarbital

A

Luminal, solfoton, ancalixir

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53
Q

Secobarbital

A

novosecobarb, seconal

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54
Q

How do barbiturates work?

A

Unsure, but may potentiate GABA

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55
Q

Regardless of their MOA, barbiturates are specific for neurons in the ______ of the _______ and some ____ structures.

A

midbrain portion of the reticular formation and some limbic system structures.

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56
Q

Discuss Z-hypnotics

A
  • Non-benzos
  • Still affect GABAA
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57
Q

What is the benefit of Z-hypnotics?

A

As effective in promoting sleep as BZDs w/ a lower risk of certain side effects
i.e. fewer hangover effects
- Associated w/ vivid dreams/hallucinations
- Disorientation, confusion, depression

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58
Q

Discuss Ramelteon

A
  • Similar in structure/function to melatonin
  • Sleep onset and sleep maintenance improvement
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59
Q

Discuss antihistamines

A
  • 1st gen antihistamines are associated w/ drowsiness as a side effect, which may be applied to sleep
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60
Q

Discuss antidepressants

A

_specifically trazadon,

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61
Q

Discuss the ADRs of sedative hypnotics

A
  • Residual effects (drowsiness, motor performance decreases)
  • Anterograde amnesia
  • Tolerance/dependence
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62
Q

Discuss BZDs use as anxiolytics

A
  • Still used quite often
  • Prescribed PRN or in acute agitation/attacks
  • Should not be used for extended periods of time d/t dependency
  • Dangerous for patients at risk of falls
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63
Q

Discuss Buspirone (buspar)

A
  • in its own class called azapirone
  • Increases effects of serotonin in regions of the brain (“serotonin agonist”)
  • Milder side-effect provide w/ low abuse potential
  • slower acting & less potent
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64
Q

Antidepressant classes

A

SSRIs, SNRIs, TCAs

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65
Q

Antidepressants frequently used in the treatment of anxiety

A

Duloxetine (cymbalta)
Excitalopram (lexapro)
Paroxetine (paxil)
Sertraline (zoloft)
Venlafaxine (effexor XR)

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66
Q

In companies w/ benzos, antidepressants for anxiety

A
  • have fewer side effects and low risk of dependence/addiction
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67
Q

Discuss Gabapentin and pregabalin

A
  • neuropathic pain, anticonvulsant
  • increase GABA concentrations in the brain
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68
Q

Discuss propranolol

A

Stage fright drug
Decrease sympathetic nervous system activity

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69
Q

Discuss the ADRs of anxiolytics

A
  • Dependency on BZDs can create rebound anxiety
  • ## sedation and drowsiness
70
Q

Discuss the ADRs of anxiolytics

A
  • Dependency on BZDs can create rebound anxiety
  • ## sedation and drowsiness
71
Q

Affective disorders may incldue

A

depression, bipolar syndrome, +++

72
Q

Fluctuations between periods of depression and periods of excessive excitation and elation (mania) are characteristic of what?

A

Bipolar disorder

73
Q

The most prevalent mental illness in the United States

A

Depression

74
Q

Who is more likely to struggle with depression?

A

Young adult females

75
Q

True or False: treating depression cannot help improve other health outcomes

A

False

76
Q

Discuss the signs/symptoms of major depressive disorder

A

At least 1: depressed mood, apathy/loss of interest
Other: weight/appetite changes, sleep disturbances, agitation/retardation, fatigue, worthlessness, guilt, executive dysfunction, suicidal ideation

77
Q

Discuss the proposed pathophysiology of depression

A
  • disturbance in CNS neurotransmission involving amine NTs (serotonin, dopamine, norepinephrine)
78
Q

Discuss the following hypotheses:
- Monoamine hypothesis
- Monamine Receptor hypothesis
- Neurotrophic hypothesis

A

Monamine: patient is deficient in amine transmitters

Monoamine receptor: post-synaptic receptors become more sensitive or person becomes deficient in them; presynaptic auto receptors become more sensitive, limiting amount of NT released into the cleft

Neurotrophic hypothesis: based in neurogenesis; stress, trauma, environment inhibit neurogenesis in the hippocampus (i.e. cortisol impairs neurogenesis)

79
Q

Discuss the realities of depression treatment

A
  • Lag time of 2-4 weeks
  • Symptoms often get worse before getting better
80
Q

Discuss the classes of antidepressants

A

SSRIs
SNRIs
TCAs
MAOIs

81
Q

Citalopram (celexa)

A

SSRI

82
Q

Escitalopram (lexapro)

A

SSRI

83
Q

Fluoxetine (prozac)

A

SSRI

84
Q

Fluvoxamine (luvox)

A

SSRI

85
Q

Paroxetine (paxil)

A

SSRI

86
Q

Sertraline (Zoloft)

A

SSRI

87
Q

Desvenlafaxine (pristiq)

A

SNRI

88
Q

Duloxetine (cymbalta)

A

SNRI

89
Q

Venlafaxine (effexor)

A

SNRI

90
Q

Amitriptyline (elavil, endep, others)

A

TCA

91
Q

Doxepin (sinequan)

A

TCA

92
Q

Nortriptyline (aventyl, pamelor)

A

TCA

93
Q

Bupropion (welbutrin)

A

Other

94
Q

Mirtazapine (remeron)

A

Other

95
Q

Trazadone (desire)

A

other

96
Q

MOI: Selective Serotonin Reuptake Inhibitors

A

SSRIs work by blocking the reuptake of serotonin into the presynaptic terminal, making more serotonin present in the cleft for transmission

97
Q

MOA: Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)

A

Work on both serotonin and NE reuptake w/ little appreciable effect on dopamine

98
Q

Discuss SNRIs

A

Comparable efficacy and side effect profile to SSRIs

Duloxetine, venlafaxine, desvenlafaxine

Have received attention for benefits w/ chronic pain, peripheral neuropathies, & fibromyalgia

99
Q

MAO: Tricyclic antidepressants (TCAs)

A
  • Block the reuptake of amine neurotransmitters
  • Very poorly selective, which increases their side effect profile
  • e.g. amitriptyline, nortriptyline
  • Historically very popular
100
Q

What side effects are uniquely associated with TCAs?

A

Anticholinergic side effects (can’t see, can’t pee, can’t spit, can’t ___)

101
Q

TCAs are generally reserved for individuals who

A

have failed to respond to first-line agents

102
Q

MOA: Monamine Oxidase Inhibitors (MAOis)

A
  • Blocks enzyme destruction of neurotransmitters by blocking monamine oxidase enzyme
103
Q

Discuss MAOIs

A
  • e.g. selegiline, rasagiline
  • Rather non-specific –> more side effects
  • Tyramine food interactions (no cheese & wine)
104
Q

Antidepressants must generally be ________ upon initial introduction

A

titrated

105
Q

Antidepressants are metabolized where?

A

Liver

106
Q

Discuss the adverse effects associated with SSRIs and SNRIs

A
  • Some GI effects
  • Some sedation
  • Serotonin syndrome
  • Rarely CV problems and anticholinergic effects
107
Q

Symptoms of serotonin syndrome include

A

sweating, agitation, restlessness, tachycardia, shivering, tremor, seizures, coma, death

108
Q

Discus adverse effects of TCAs

A
  • Significant anticholinergic effects
  • More sedating than SSRIs/SNRIs
  • More common CV effects: arrhythmia, orthostatic hypotension (highest risk of overdose)
  • Increased seizure risk
109
Q

Discuss the adverse effects of MAOis

A
  • CNS excitation: restlessness, irritability, agitation, sleep loss, anticholinergic effects, tyramine interactions can lead to increased catecholamines and hypertensive crisis
110
Q

Suicide hotline

A

1-800-273-TALK

111
Q

3-digit suicide hotline

A

988

112
Q

Signs of suicide

A

IS PATH WARM
Ideation, substance use, purposelessness, anxiety, trapped, hopelessness, withdrawal, anger, recklessness, mood changes

113
Q

Bipolar disorder is associated with what primary symptoms?

A

Mood swings from depression to mania

114
Q

Differentiate Bipolar I and Bipolar II

A

BP I: mania + major depression
BP II: hypomania + major depression

115
Q

What causes bipolar disorder?

A
  • Cause is unknown
  • Exactly which neurotransmitters are most influential remains TBD
  • Likely caused by some imbalance between inhibitory neurotransmitters (serotonin, GABA) and excitatory (NE, dopamine, glutamate, aspartate)
116
Q

Treatment of bipolar disorder focuses on what?

A

prevention of pendulum-like mood swings (i.e. mood stabilization)

117
Q

The front-line treatment for bipolar disorder is what?

A

Lithium

118
Q

MOA: Lithium

A
  • Influences neural excitation by competing with other cations, such as sodium, potassium, and calcium
    -May also prevent neuronal degeneration ‘
  • May also effect release of serotonin, NE, dopamine
119
Q

Discuss adverse effects of lithium

A
  • Lithium accumulates in the body as it is not metabolized and must be excreted in urine
  • Signs of toxicity depend on amount present in blood stream
120
Q

Signs/symptoms of lithium toxicity

A

CNS: fine hand tremors, fatigue, dizziness, blurred vision, slurred speech, ataxia, fasciculations, nystagmus, confusion, stupor, seizures, coma

CV: ECG changes, syncope, bradycardia, AV block, artial/ventricular arrhythmias

121
Q

What other medications besides lithium may be used to treat bipolar disorder?

A

Antiseizure meds: carbamazepine, lamotrigine (lamictal)

antipsychotic meds: aripiprazole, risperidone

Used to stable mood in patients getting started on lithium, but may be used adjunct to it long-term or in place if lithium is not tolerated

122
Q

Impaired perception of reality refers to what?

A

Psychosis

123
Q

Historically, what treatments were utilized for patients presenting with psychosis?

A

Strong, sedative-type drugs were the primary method of treatment patients with psychosis (i.e. tranquilizers)

124
Q

True or False: antipsychotic medications do not cure schizophrenia

A

True

125
Q

Antipsychotics may also be utilized in the treatment of what conditions

A

depression, bipolar disorder, alzheimers disease, agitation in dementia, anxiety, Tourette’s ++++

126
Q

Both ____ and ____ factors have been associated with the development of schizophrenia

A

genetic & epigenetic
Genetic: altered expression of neurotransmitter receptors
Epigenetic: without a change in gene sequence, methylation of DNA

127
Q

Factors that put a patient at higher risk for developign psychosis when combined with environmental triggers include

A

brain injury in youth, social stresses, etc.

128
Q

The primary cause of schizophrenia is thought to be what?

A

overactivity of dopamine pathways in the brain, particularly within the limbic system –> most antipsychotics block dopamine receptors to some extent

129
Q

Increased dopamine transmission in what area seem to be the primary neurochemical change associate with schizophrenia

A

limbic system

130
Q

What NT may also play a role in schizophrenia?

A

increased serotonin activity
Defect in activity of GABA to control glutamate
Decreased sensitivity to acetylcholine

–> Overall still caused by the influence of excessive dopamine

131
Q

First-get antipsychotics do what?

A

antagonists of specific dopamine receptors in mesolimbic pathways; also known as “traditional”

132
Q

First gen antipsychotics have an affinity for which receptors?

A

D2 receptors (appears to be most important in mediating psychosis)

133
Q

Discuss atypical or second-generation antipsychotics

A
  • Generally only weak D2 receptor antagonists
  • Strong blockers of serotonin receptors
  • Capable of producing antipsychotic effects with a lower risk of side effects
134
Q

Chlorpromazine (thorazine)

A

Traditional antipsychotic

135
Q

Fluphenazine (permit, prolix)

A

Traditional antipsychotic

136
Q

Haloperidol (haldol)

A

1st gen antipsychotic

137
Q

Prochlorperazine (compazine)

A

1st gen antipsychotic

138
Q

Aripiprazole (abilify)

A

2nd gen/atypical antipsychotic

139
Q

Clozapine (clozaril)

A

2nd gen/atypical antipsychotic

140
Q

Olanzapine (zyprexa)

A

2nd gen/atypical antipsychotic

141
Q

Paliperidone

A

2nd gen/atypical antipsychotic

142
Q

Quetiapine

A

2nd gen/atypical antipsychotic

143
Q

Risperidone

A

2nd gen/atypical antipsychotic

144
Q

Ziprasidone

A

2nd gen/atypical antipsychotic

145
Q

Discuss 1st gen antipsychotics

A
  • associated w/ more side effects
  • Extrapyrimidal side effects (movement) affected because of effect on dopamine receptors
  • high potency: haloperidol, fluphenazine
  • low potency: chlorpromazine; have an increased incidence of sedation/anticholinergic effects fewer motor side effects
  • Typically less predictable
146
Q

Discuss atypical antipsychotics

A
  • Unifying feature = less side effects; decreased risk of movement disorder/side effects
  • Work on 5-Ht2 serotonin receptors in limbic system
  • Associated w/ a lower risk of relapse, possibly due to better tolerability
147
Q

Discuss the choice of antipsychotic therapy

A
  • Varying first-line recommendations
  • Based primarily off of side effects
  • No clear choice based on efficacy
148
Q

Discuss depot administration and give one example

A

long-acting injection given every few weeks
e.g. risperidone, paliperidone

149
Q

Metabolism of antipsychotic medications takes place where?

A

Liver; prolonged use is associated with some degree of enzyme induction, leading to an increased rate of metabolism with use

150
Q

At worst, extrapyramidal symptoms can progress to what?

A

Tardive dyskinesia

151
Q

Risk factors for the development of adverse effects of antipsychotic meds incldue

A

age, alcohol abuse, diabetes, continual drug use (6+ months)

152
Q

Facial grimacing, involuntary upward eye movement, muscles spasms of the tongue/face/neck/back, and laryngeal spasms are all associated primarily with

A

acute dystonia

153
Q

Protrusion and rolling of the tongue
sucking and smacking movements of the lips
chewing motion
Facial dyskinesias
Involuntary movements of the body and extremities

are also primarily associated with what?

A
154
Q

Protrusion and rolling of the tongue
sucking and smacking movements of the lips
chewing motion
Facial dyskinesias
Involuntary movements of the body and extremities

are also primarily associated with what?

A

Tardive dyskinesia

155
Q

Restlessness, trouble standing still, pacing, and feet in constant motion rocking back and forth are primarily assoicated with what?

A

akathisia

156
Q

True or False: Tardive dyskinesia is always reversible

A

FALSE

157
Q

The key to tardive dyskinesia is what

A

prevention and early identification

158
Q

____ _______ is thought to be the cause of tardive dyskinesia

A

disuse supersensitivity; blockade of postsynaptic dopamine receptors may cause upregulation and therefore increased sensitivity of the receptors

159
Q

Movement disorders are generally managed how?

A

lowering drug dosage, different antipsychotic

160
Q

Pseudoparkinsonism is considered ___________ reversible and ______ are more at risk/

A

quickly reversible; the elderly

161
Q

What should not be used to treat pseudoparkinsonism

A

PArkinson’s meds

162
Q

What drug may be used to help manage akathisia

A

propranolol (beta blocker)

163
Q

Dyskinesias and dystonias may also be managed with what type of medciations

A

benzos

164
Q

discuss neuroleptic malignant syndrome

A
  • occur on high doses of potent antipsychotics
  • particularly w/ large injections
  • fever, tremors, stupor, rigidity, catatonia
  • Treatment is supportive care and discontinuation of the offending antipsychotics
165
Q

Atypical antipsychotics are associated with substantial _______ side effects

A

metabolic; e.g. weight gain, increased lipids, diabetes

pines and ones: olanzipine, quetiapine, risperidone, paliperiodne

166
Q

the atypical antipsychotic with the highest risk of metabolic side effects is

A

olanzapine

167
Q

atypical antipsychotics with a moderate risk of metabolic side effects include

A

quetiapine, risperiodone, paliperidone

168
Q

True or false: sedation does not enhance the efficacy of antipsychotics

A

TRUE

169
Q

Discuss non-motor side effects of antipsychotics

A

anticholinergic effects –> usually self-limiting
orthostatic hypotention –> especially initially
nausea/vomiting –> associated priamrily w/ withdrawal, meds should be tapered

170
Q

True or false, antipsychotics are recommended for agitation in dementia patients

A

False –> should only be used as a last resport for patients who are a danger to themselves and others

171
Q

Which antipsychotic is used frequently in bipolar disordeR?

A

abilify (aripiprazole)

172
Q

What antipsychotics might be used in patients to reduce nausea/vomiting?

A

haloperidol (haldol), prochlorperazine (compazine) because they can block dopamine receptors in the brainstem responsible for those reflexes

Fall 2022 (3 decks)

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