Pharmacology- Mental Health Flashcards
1
Q
The CNS can be divided grossly into
A
the brain and the spinal cord
2
Q
The highest order of conscious function and integration in the CNS
A
Cerebral cortex
3
Q
The largest and most rostral aspect of the brain
A
cerebrm
4
Q
Most CNS therapeutic medications affect cortical function __________ by altering the function of lower brain and spinal cord structures
A
indirectly
5
Q
Drugs used to treat epilepsy often target what region of the brain?
A
cerebrum
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
7
Q
Area of the brain primarily involved in the control of motor activities
A
basal ganglia
8
Q
Medications that treat movement disorders often exert their effects where?
A
basal ganglia
9
Q
The diencephalon consists of what structures?
A
thalamus & hypothalamus
10
Q
Temperature, appetite, water balance, and certain emotions are all controlled by what?
A
hypothalamus
11
Q
Drugs that target the HPA axis are
A
opiates, ethanol, cannabinoids, nicotine, cocaine, amphetamine, growth hormone, gonadotropins,
12
Q
The brainstem includes what structures?
A
pons, medulla oblongata
13
Q
The midbrain and brainstem are responsible for controlling what?
A
respiration and cardiovascular function
14
Q
What structure monitors and controls consciousness and is important in regulating alertness or arousal of the cerebral cortex?
A
Reticular formation
15
Q
Stimulants will most likely _______ the reticular formation, while depressants will likely _____ the reticular formation.
A
increase activity, decrease activity
16
Q
True or False: Therapeutic medications are not usually targeting the cerebellum directly.
A
True
17
Q
What is does the limbic system accomplish and what structures are included?
A
Involved in behavior and emotional control; amygdala, hippocampus, hypothalamus
18
Q
Drugs that affect the limbic system are often associated with what class of meds?
A
anti-anxiety, antipsychotics
19
Q
Gray matter vs. white matter
A
Gray: serves as an area for synaptic connections
White: myelinated axons of neurons grouped into tracts
20
Q
Local anesthetics work where? Narcotic analgesics?
A
Local –> white matter
narcotics –> gray matter
21
Q
The blood brain barrier is comprised of what?
A
Tight junctions
22
Q
What substance is most likely to cross the BBB?
A
non-polar, lipid-soluble drugs; lipophilic, hydrophobic
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
24
Q
Discuss Acetylcholine
A
- Found in many areas of CNS
- Likely involved in cognition and memory
- Excitatory
25
Discuss Monamines
- include: dopamine, NE, serotonin
- Dopamine --> inhibitory
- NE --> Disinhibition
- Serotonin --> inhibitor
26
Discuss amino acids
- GABA --> primary inhibitory NT
27
Discuss peptides
- Substance P, endogenous opioids
- Excitatory neurotransmitters
28
The majority of CNS drugs act by what mechanism?
modifying synaptic transmissions
29
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
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
30
What is the difference between an anxiolytic and a sedative-hypnotic?
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.
31
Insomnia may effect approx. what percentage of people? What can trigger it?
10-15%
Illness, injury, recent relocation to unfamiliar environment
32
What are the two categories of sedative-hypnotics?
Benzos
Non-benzos (z-hypnotics, barbiturates, +)
33
What is the primary indication for benzodiazepines?
anxiety
34
True or false: Benzos are no longer frequently recommended for insomnia d/t their side effect profile
True
35
Prolonged use of benzos is associated with what?
tolerance, dependence
36
How do benzos work?
Increase inhibitory effects of GABA
(GABAA is the main therapeutic target)
37
Differentiate tolerance and dependence
38
Who is most likely to experience sedation w/ use of benzos?
elderly
39
ADRs of benzos include
- Tolerance, dependence
- Sedation
- Disinhibition
40
What suffix is generally associated with benzos?
-lam
-pam
41
Discuss: alprazolam (xanax)
-Benzodiazepine
42
Clonazepam (klonopin)
Benzodiazepine
43
Diazepam (valium)
Benzodiazepine
44
Flurazepam (Dalmane)
Benzodiazepine
45
Lorazepam (ativan)
Benzo
46
Midazolam (versed)
Benzo
47
Triazolam (halcyon)
bento
48
Discuss the therapeutic index of barbituates
Narrow therapeutic range --> dangerous
49
What is the suffix that denotes barbiturates?
-barbital
50
AMobarbital (amytal)
barbituate
51
Pentobarbital
barbituate
52
Phenobarbital
Luminal, solfoton, ancalixir
53
Secobarbital
novosecobarb, seconal
54
How do barbiturates work?
Unsure, but may potentiate GABA
55
Regardless of their MOA, barbiturates are specific for neurons in the ______ of the _______ and some ____ structures.
midbrain portion of the reticular formation and some limbic system structures.
56
Discuss Z-hypnotics
- Non-benzos
- Still affect GABAA
57
What is the benefit of Z-hypnotics?
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
58
Discuss Ramelteon
- Similar in structure/function to melatonin
- Sleep onset and sleep maintenance improvement
59
Discuss antihistamines
- 1st gen antihistamines are associated w/ drowsiness as a side effect, which may be applied to sleep
60
Discuss antidepressants
_specifically trazadon,
61
Discuss the ADRs of sedative hypnotics
- Residual effects (drowsiness, motor performance decreases)
- Anterograde amnesia
- Tolerance/dependence
62
Discuss BZDs use as anxiolytics
- 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
63
Discuss Buspirone (buspar)
- 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
64
Antidepressant classes
SSRIs, SNRIs, TCAs
65
Antidepressants frequently used in the treatment of anxiety
Duloxetine (cymbalta)
Excitalopram (lexapro)
Paroxetine (paxil)
Sertraline (zoloft)
Venlafaxine (effexor XR)
66
In companies w/ benzos, antidepressants for anxiety
- have fewer side effects and low risk of dependence/addiction
67
Discuss Gabapentin and pregabalin
- neuropathic pain, anticonvulsant
- increase GABA concentrations in the brain
68
Discuss propranolol
Stage fright drug
Decrease sympathetic nervous system activity
69
Discuss the ADRs of anxiolytics
- Dependency on BZDs can create rebound anxiety
- sedation and drowsiness
-
70
Discuss the ADRs of anxiolytics
- Dependency on BZDs can create rebound anxiety
- sedation and drowsiness
-
71
Affective disorders may incldue
depression, bipolar syndrome, +++
72
Fluctuations between periods of depression and periods of excessive excitation and elation (mania) are characteristic of what?
Bipolar disorder
73
The most prevalent mental illness in the United States
Depression
74
Who is more likely to struggle with depression?
Young adult females
75
True or False: treating depression cannot help improve other health outcomes
False
76
Discuss the signs/symptoms of major depressive disorder
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
Discuss the proposed pathophysiology of depression
- disturbance in CNS neurotransmission involving amine NTs (serotonin, dopamine, norepinephrine)
78
Discuss the following hypotheses:
- Monoamine hypothesis
- Monamine Receptor hypothesis
- Neurotrophic hypothesis
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
Discuss the realities of depression treatment
- Lag time of 2-4 weeks
- Symptoms often get worse before getting better
80
Discuss the classes of antidepressants
SSRIs
SNRIs
TCAs
MAOIs
81
Citalopram (celexa)
SSRI
82
Escitalopram (lexapro)
SSRI
83
Fluoxetine (prozac)
SSRI
84
Fluvoxamine (luvox)
SSRI
85
Paroxetine (paxil)
SSRI
86
Sertraline (Zoloft)
SSRI
87
Desvenlafaxine (pristiq)
SNRI
88
Duloxetine (cymbalta)
SNRI
89
Venlafaxine (effexor)
SNRI
90
Amitriptyline (elavil, endep, others)
TCA
91
Doxepin (sinequan)
TCA
92
Nortriptyline (aventyl, pamelor)
TCA
93
Bupropion (welbutrin)
Other
94
Mirtazapine (remeron)
Other
95
Trazadone (desire)
other
96
MOI: Selective Serotonin Reuptake Inhibitors
SSRIs work by blocking the reuptake of serotonin into the presynaptic terminal, making more serotonin present in the cleft for transmission
97
MOA: Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)
Work on both serotonin and NE reuptake w/ little appreciable effect on dopamine
98
Discuss SNRIs
Comparable efficacy and side effect profile to SSRIs
Duloxetine, venlafaxine, desvenlafaxine
Have received attention for benefits w/ chronic pain, peripheral neuropathies, & fibromyalgia
99
MAO: Tricyclic antidepressants (TCAs)
- Block the reuptake of amine neurotransmitters
- Very poorly selective, which increases their side effect profile
- e.g. amitriptyline, nortriptyline
- Historically very popular
100
What side effects are uniquely associated with TCAs?
Anticholinergic side effects (can't see, can't pee, can't spit, can't ___)
101
TCAs are generally reserved for individuals who
have failed to respond to first-line agents
102
MOA: Monamine Oxidase Inhibitors (MAOis)
- Blocks enzyme destruction of neurotransmitters by blocking monamine oxidase enzyme
103
Discuss MAOIs
- e.g. selegiline, rasagiline
- Rather non-specific --> more side effects
- Tyramine food interactions (no cheese & wine)
104
Antidepressants must generally be ________ upon initial introduction
titrated
105
Antidepressants are metabolized where?
Liver
106
Discuss the adverse effects associated with SSRIs and SNRIs
- Some GI effects
- Some sedation
- Serotonin syndrome
- Rarely CV problems and anticholinergic effects
107
Symptoms of serotonin syndrome include
sweating, agitation, restlessness, tachycardia, shivering, tremor, seizures, coma, death
108
Discus adverse effects of TCAs
- Significant anticholinergic effects
- More sedating than SSRIs/SNRIs
- More common CV effects: arrhythmia, orthostatic hypotension (highest risk of overdose)
- Increased seizure risk
109
Discuss the adverse effects of MAOis
- CNS excitation: restlessness, irritability, agitation, sleep loss, anticholinergic effects, tyramine interactions can lead to increased catecholamines and hypertensive crisis
110
Suicide hotline
1-800-273-TALK
111
3-digit suicide hotline
988
112
Signs of suicide
IS PATH WARM
Ideation, substance use, purposelessness, anxiety, trapped, hopelessness, withdrawal, anger, recklessness, mood changes
113
Bipolar disorder is associated with what primary symptoms?
Mood swings from depression to mania
114
Differentiate Bipolar I and Bipolar II
BP I: mania + major depression
BP II: hypomania + major depression
115
What causes bipolar disorder?
- 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
Treatment of bipolar disorder focuses on what?
prevention of pendulum-like mood swings (i.e. mood stabilization)
117
The front-line treatment for bipolar disorder is what?
Lithium
118
MOA: Lithium
- 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
Discuss adverse effects of lithium
- 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
Signs/symptoms of lithium toxicity
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
What other medications besides lithium may be used to treat bipolar disorder?
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
Impaired perception of reality refers to what?
Psychosis
123
Historically, what treatments were utilized for patients presenting with psychosis?
Strong, sedative-type drugs were the primary method of treatment patients with psychosis (i.e. tranquilizers)
124
True or False: antipsychotic medications do not cure schizophrenia
True
125
Antipsychotics may also be utilized in the treatment of what conditions
depression, bipolar disorder, alzheimers disease, agitation in dementia, anxiety, Tourette's ++++
126
Both ____ and ____ factors have been associated with the development of schizophrenia
genetic & epigenetic
Genetic: altered expression of neurotransmitter receptors
Epigenetic: without a change in gene sequence, methylation of DNA
127
Factors that put a patient at higher risk for developign psychosis when combined with environmental triggers include
brain injury in youth, social stresses, etc.
128
The primary cause of schizophrenia is thought to be what?
overactivity of dopamine pathways in the brain, particularly within the limbic system --> most antipsychotics block dopamine receptors to some extent
129
Increased dopamine transmission in what area seem to be the primary neurochemical change associate with schizophrenia
limbic system
130
What NT may also play a role in schizophrenia?
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
First-get antipsychotics do what?
antagonists of specific dopamine receptors in mesolimbic pathways; also known as "traditional"
132
First gen antipsychotics have an affinity for which receptors?
D2 receptors (appears to be most important in mediating psychosis)
133
Discuss atypical or second-generation antipsychotics
- Generally only weak D2 receptor antagonists
- Strong blockers of serotonin receptors
- Capable of producing antipsychotic effects with a lower risk of side effects
134
Chlorpromazine (thorazine)
Traditional antipsychotic
135
Fluphenazine (permit, prolix)
Traditional antipsychotic
136
Haloperidol (haldol)
1st gen antipsychotic
137
Prochlorperazine (compazine)
1st gen antipsychotic
138
Aripiprazole (abilify)
2nd gen/atypical antipsychotic
139
Clozapine (clozaril)
2nd gen/atypical antipsychotic
140
Olanzapine (zyprexa)
2nd gen/atypical antipsychotic
141
Paliperidone
2nd gen/atypical antipsychotic
142
Quetiapine
2nd gen/atypical antipsychotic
143
Risperidone
2nd gen/atypical antipsychotic
144
Ziprasidone
2nd gen/atypical antipsychotic
145
Discuss 1st gen antipsychotics
- 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
Discuss atypical antipsychotics
- 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
Discuss the choice of antipsychotic therapy
- Varying first-line recommendations
- Based primarily off of side effects
- No clear choice based on efficacy
148
Discuss depot administration and give one example
long-acting injection given every few weeks
e.g. risperidone, paliperidone
149
Metabolism of antipsychotic medications takes place where?
Liver; prolonged use is associated with some degree of enzyme induction, leading to an increased rate of metabolism with use
150
At worst, extrapyramidal symptoms can progress to what?
Tardive dyskinesia
151
Risk factors for the development of adverse effects of antipsychotic meds incldue
age, alcohol abuse, diabetes, continual drug use (6+ months)
152
Facial grimacing, involuntary upward eye movement, muscles spasms of the tongue/face/neck/back, and laryngeal spasms are all associated primarily with
acute dystonia
153
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?
154
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?
Tardive dyskinesia
155
Restlessness, trouble standing still, pacing, and feet in constant motion rocking back and forth are primarily assoicated with what?
akathisia
156
True or False: Tardive dyskinesia is always reversible
FALSE
157
The key to tardive dyskinesia is what
prevention and early identification
158
____ _______ is thought to be the cause of tardive dyskinesia
disuse supersensitivity; blockade of postsynaptic dopamine receptors may cause upregulation and therefore increased sensitivity of the receptors
159
Movement disorders are generally managed how?
lowering drug dosage, different antipsychotic
160
Pseudoparkinsonism is considered ___________ reversible and ______ are more at risk/
quickly reversible; the elderly
161
What should not be used to treat pseudoparkinsonism
PArkinson's meds
162
What drug may be used to help manage akathisia
propranolol (beta blocker)
163
Dyskinesias and dystonias may also be managed with what type of medciations
benzos
164
discuss neuroleptic malignant syndrome
- 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
Atypical antipsychotics are associated with substantial _______ side effects
metabolic; e.g. weight gain, increased lipids, diabetes
pines and ones: olanzipine, quetiapine, risperidone, paliperiodne
166
the atypical antipsychotic with the highest risk of metabolic side effects is
olanzapine
167
atypical antipsychotics with a moderate risk of metabolic side effects include
quetiapine, risperiodone, paliperidone
168
True or false: sedation does not enhance the efficacy of antipsychotics
TRUE
169
Discuss non-motor side effects of antipsychotics
anticholinergic effects --> usually self-limiting
orthostatic hypotention --> especially initially
nausea/vomiting --> associated priamrily w/ withdrawal, meds should be tapered
170
True or false, antipsychotics are recommended for agitation in dementia patients
False --> should only be used as a last resport for patients who are a danger to themselves and others
171
Which antipsychotic is used frequently in bipolar disordeR?
abilify (aripiprazole)
172
What antipsychotics might be used in patients to reduce nausea/vomiting?
haloperidol (haldol), prochlorperazine (compazine) because they can block dopamine receptors in the brainstem responsible for those reflexes
