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pharmacology > Psychological > Flashcards

Psychological Flashcards

1
Q

What is acute pain?

A

sudden onset, usually subsides when treated. 6 weeks or less

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2
Q

what is chronic pain?

A

persistent/recurring, more difficult to treat. 3-6 months, OR longer than 1 months after healing from an acute injury

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3
Q

what are analgesics?

A

medications that relieve pain without causing a loss of consciousness

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4
Q

what is tolerance?

A

effectiveness of a drug is significantly reduced after prolonged use

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5
Q

what is withdrawal?

A

unpleasant physical/mental symptoms when a drug is suddenly stopped or decreased in dosage

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6
Q

what is physical dependence?

A

a need to continue taking a drug to avoid unwanted side effects

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7
Q

what is addiction?

A

chronic neurobiological disease in which genetic, psychosocial, environmental factors induce changes in behavior to compulsively use drugs

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8
Q

what are opioid analgesics?

A

synthetic drugs that bind to the opiate receptors in the brain and relieve pain. Strong, can alleviate pain of any origin, known to cause tolerance and dependence

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9
Q

what are nonopioid analgesics?

A

do NOT work on opiate receptors. Examples are NSAIDs. This is a large, chemically diverse group of drugs that also have anti-inflammatory and antipyretic activity.

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10
Q

what is neuropathic pain?

A

pain resulting from a damaged nervous system or damaged nerve cells. Does not usually respond to NSAIDs or opioids. Extremely difficult to treat

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11
Q

what drug classes can help with neuropathic pain?

A

antiseizure, antidepressants

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12
Q

what is fibromyalgia?

A

one of the most common neuropathic conditions. Widespread musculoskeletal pain accompanied by fatigue as well as sleep, memory, and mood issues. Amplifies painful sensations by affecting the way your brain processes pain signals

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13
Q

what are the 3 classes of opioid drugs?

A

morphine-like
meperidine-like
methadone-like

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14
Q

how do opioids work?

A

bind to opioid receptor in the brain, causing an analgesic response. Most are known as opioid agonists

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15
Q

what are 3 types of opioid receptors?

A

mu, kappa, delta

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16
Q

what are 4 adverse events of opioid use?

A

potential for abuse
histamine release
CNS depression => respiratory depression
GI tract - nausea/vomiting, constipation

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17
Q

what class of opioid causes the most histamine release?

A

morphine-like

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18
Q

what class of opioid causes the least histamine release?

A

meperidine-like

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19
Q

what are 2 opioid antagonists?

A

naloxone
naltrexone

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20
Q

what is the main drug interaction concern for opioids?

A

added respiratory depression with other CNS depressants like barbiturates, benzodiazepines, alcohol

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21
Q

what schedule are most opioids, and what is the exception?

A

II
Codeine is III if combined with other drugs

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22
Q

what class are morphine-like drugs?

A

phenanthrenes

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23
Q

what class are meperidine-like drugs?

A

phenylpiperidines

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24
Q

what class are methadone-like drugs?

A

phenylheptanes

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25
Q

Name 3 morphine-like (phenanthrene) drugs

A

Morphine
Hydromorphone
Oxymorphone
Codeine
Hydrocodone
Oxycodone

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26
Q

Name 2 meperidine-like (phenylpiperidine) drugs

A

meperidine
fentanyl

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27
Q

Name one methadone-like (phenylheptane) drug

A

methadone

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28
Q

what 3 drugs are stronger than morphine?

A

hydromorphone
oxymorphone
fentanyl

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29
Q

what 3 drugs are the same strength as morphine?

A

oxycodone
meperidine
methadone

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30
Q

what 2 drugs are weaker than morphine?

A

codeine
hydrocodone

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31
Q

what is inflammation?

A

localized protective response stimulated by injury to tissues that destroy, dilute, or wall off both the injurious agent and the injured tissue. Due to increased blood flow

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32
Q

what chemical is released from phospholipids in the first response of inflammation?

A

arachidonic acid

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33
Q

what are the 2 routes for arachidonic acid to be metabolized?

A

prostaglandin pathway
leukotriene pathway

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34
Q

what chemical is involved in the prostaglandin pathway and what does it do?

A

cyclooxygenase (COX) converts arachidonic acid into prostaglandins that cause vasodilation and vasopermeability, increasing action of histamine and bradykinin

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35
Q

what chemical is involved in the leukotriene pathway and what does it do?

A

lipoxygenase converts arachidonic acid into leukotrienes and increases the inflammatory response

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36
Q

what is the method of action of NSAIDs?

A

they inhibit the prostaglandin or leukotriene pathway, or both

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37
Q

what does COX-1 do and what’s wrong with inhibiting this too much?

A

many effects including maintaining intact GI tract. Inhibiting this makes NSAIDs ulcerogenic and risky for bleeds.

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38
Q

what does COX-2 do?

A

more of a primary role in converting inflammatory prostaglandins

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39
Q

what are adverse effects of NSAIDs?

A

GI tract - heartburn to GI bleeds
Acute renal failure
Increased heart attack or stroke risk - especially COX-2

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40
Q

what happens when you mix NSAIDs with anticoagulants?

A

increased bleeding risk

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41
Q

what happens when you mix NSAIDs with aspirin/salicylate?

A

increased GI toxicity

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42
Q

what happens when you mix NSAIDs with corticosteroids?

A

increased risk of ulcers

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43
Q

what happens when you mix NSAIDs with ACE inhibitors?

A

reduced antihypertensive effects due to inhibited renal prostaglandins synthesis

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44
Q

which NSAID is offered as a topical gel?

A

diclofenac sodium

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45
Q

which NSAID is used for gout?

A

indomethacin

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46
Q

which NSAID is used for kidney failure?

A

ketorolac

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47
Q

what is the name of a COX-2 inhibitor?

A

celecoxib

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48
Q

what are the names of 2 propionic acid derivatives?

A

ibuprofen
naproxen

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49
Q

what are the 5 classes of NSAIDs?

A

salicylate
acetic acid derivative
cyclooxygenase-2 inhibitor
enolic acid derivative
propionic acid derivative

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50
Q

what happens when you mix NSAIDs with diuretics?

A

reduced diuretic effects due to inhibited renal prostaglandins synthesis

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51
Q

what 2 antiseizure medications can be used for neuropathic pain?

A

gabapentin
pregabalin

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52
Q

how does gabapentin work for neuropathic pain?

A

not well understood. Chemically related to GABA, a neurotransmitter that inhibits brain activity. It’s thought to build up GABA

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53
Q

how does pregabalin work?

A

not well understood. Chemically related to gabapentin but binds to alpha2-delta receptor sites instead of GABA. This affects calcium channels in CNS tissue

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54
Q

what are adverse events of gabapentin and pregabalin?

A

dizziness
drowsiness
nausea
edema

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55
Q

what is a third drug that can be used for neuropathic pain and what class is it?

A

milnacipran, SNRI

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56
Q

what disease is milnacipran indicated for?

A

fibromyalgia

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57
Q

what happens when milnacipran is mixed with digoxin?

A

adverse hemodynamic events like postural hypotension and tachycardia

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58
Q

what happens when milnacipran is mixed with clonidine?

A

inhibited antihypertensive effect due to blocking of norepinephrine uptake

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59
Q

what are adverse events of milnacipran?

A

Nausea
Headache
Constipation
Dizziness
Insomnia
Hot flush
Excessive sweating
Vomiting
Palpitations
Increased HR
Dry mouth
Hypertension

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60
Q

what is anxiety?

A

an unpleasant state of mind in which real or imagined dangers are anticipated and/or exaggerated

61
Q

what is bipolar disorder?

A

characterized by both mania and depression and is defined as a psychological disorder characterized by episodes of mania or hypomania cycling with depression. Formerly called manic depressive illness.

62
Q

what is depression?

A

an abnormal emotional state characterized by exaggerated feelings of sadness, melancholy, dejection, worthlessness, emptiness, and hopelessness. Signs include withdrawal from social contact, loss of appetite, and insomnia

63
Q

what is mania?

A

an acute illness characterized by an expansive emotional state including extreme excitement, elation, hyperactivity, agitation, talkativeness, flight of ideas, reduced attention span, increased psychomotor activity, impulsivity, insomnia, anorexia, and sometimes violent destructive and self-destructive behavior.

64
Q

what is psychosis?

A

A type of serious mental illness that is associated with being out of touch with reality where the individual is unable to distinguish imaginary from real circumstances and events

65
Q

what is schizophrenia?

A

a major form of psychosis where behavior is inappropriate. Symptoms include bizarre behavior, auditory and visual hallucinations, lack of motivation and emotional expression, and diminished speech and thought processes.

66
Q

what are 2 classes of anxiolytics?

A

benzodiazepine
buspirone

67
Q

what schedule are benzodiazepines?

A

IV

68
Q

what are 3 intermediate acting benzo’s?

A

alprazolam
clonazepam
lorazepam

69
Q

what are 2 long acting benzo’s?

A

diazepam
chlordiazepoxide

70
Q

how do benzo’s work?

A

reduce overactivity in the brain that causes unwanted anxiety, by increasing the inhibitory neurotransmitter GABA (gamma aminobutyric acid)

71
Q

what are adverse events of benzo’s?

A

Excessive CNS depression: sedation, lethargy, fatigue, confusion, drowsiness, dizziness
Hypotension
Can be habit-forming; schedule IV controlled substance

72
Q

what are drug interactions of benzo’s?

A

additive depression when combined with other CNS depressants, including alcohol. Can lead to death

73
Q

what is the typical onset of action for benzo’s?

A

15-30 minutes

74
Q

how does buspirone work?

A

not completely understood. Thought to work on dopamine and serotonin receptors. Takes about 2-3 weeks to exert its full effect

75
Q

what are adverse events for buspirone?

A

dizziness, blurred vision, headache, nausea

76
Q

what are drug interactions for buspirone?

A

Increased levels when taken with CYP3A4 inhibitors like ketoconazole, verapamil, and diltiazem
Should not be taken with MAOI
Increases risk of serotonin syndrome when combined with other drugs that increase serotonin, like antidepressants

77
Q

what drug is the only one use uniquely as mood stabilizer specifically for acute mania?

A

lithium

78
Q

how does lithium work?

A

not completely understood. Lithium ions are thought to alter sodium ion transport, altering the metabolism of dopamine and norepinephrine. Therapeutic level is very close to the toxic level (narrow therapeutic index), so patients must be closely monitored

79
Q

what are adverse events of lithium?

A

GI discomfort
tremor
confusion
somnolence
slurred speech
muscle coordination disturbances
seizure
death due to cardiac dysrhythmia

80
Q

what are drug interactions for lithium?

A

thiazide diuretics, ACE inhibitors, and NSAIDs can increase the risk of lithium toxicity

81
Q

what is the drug class of choice for bipolar disorder?

A

antiepileptics

82
Q

how do antiepileptics work for bipolar disorder?

A

not fully understood. They stabilize neurons to keep them from getting hyperexcited and generating excess nerve impulses.

83
Q

name 4 antiepileptics

A

valproic acid
oxcarbazepine
lamotrigine
topiramate

84
Q

what are adverse events of valproic acid?

A

hepatotoxicity, pancreatitis
Dizziness, drowsiness, GI upset, weight gain

85
Q

what are adverse events of topiramate?

A

ataxia
Dizziness, drowsiness, GI upset

86
Q

what are adverse events of lamotrigine?

A

Stevens Johnson syndrome
Drowsiness, ataxia, headache, nausea, blurred vision

87
Q

what are adverse events of oxcarbazepine?

A

unusual eye movements, visual changes, behavioral changes
nausea, headache, dizziness, abdominal pain, GI upset

88
Q

why are there so many drug interactions within the antiepileptics?

A

due to being metabolized in the cytochrome P450 system.

89
Q

which neurotransmitters are thought to be involved in depression?

A

serotonin
dopamine
norepinephrine

90
Q

what is the acute phase of depression?

A

6-8 weeks

91
Q

how long should depression treatment continue after remission?

A

8-14 months

92
Q

what increases the chances of depression recovery?

A

early aggressive treatment

93
Q

what needs to be considered when selecting depression drug therapy?

A

psychotropic drug history
family history
side effects

94
Q

what 3 classes are in the first generation antidepressants?

A

tricyclic
monoamine oxidase inhibitors (MAOIs)
tetracycline

95
Q

what antidepressant drug class is used for Parkinson’s?

A

monoamine oxidase inhibitor (MAOI)

96
Q

name an antidepressant drug and class that is used for neuropathic pain

A

amitriptyline, tricyclic

97
Q

name an antidepressant drug and class that is used for OCD

A

clomipramine, tricyclic

98
Q

name an antidepressant drug and class that is used for bedwetting

A

imipramine, tricyclic

99
Q

what classes are in the second generation of antidepressants?

A

selective serotonin reuptake inhibitor
selective norepinephrine reuptake inhibitor
miscellaneous

100
Q

what was the first SSRI to be approved?

A

fluoxetine / prozac

101
Q

name 3 MAOIs

A

Isocarboxazid
Phenelzine
Tranylcypromine

102
Q

name 2 tetracyclines

A

Maprotiline
Mirtazapine

103
Q

which neurotransmitters do tricyclics work on?

A

serotonin and norepinephrine

104
Q

what 4 general ways can tricyclic adverse events show up?

A

anticholinergic receptor blockage
adrenergic/dopaminergic receptor blockage
histamine blockage
serotonergic blockage

105
Q

what does anticholinergic receptor blockage look like?

A

urinary retention
constipation

106
Q

what does adrenergic/dopaminergic receptor blockage look like?

A

cardiac issues

107
Q

what does histamine blockage look like?

A

sedation

108
Q

what does serotonergic blockage look like?

A

lower seizure threshold
sexual dysfunction

109
Q

what is serotonin syndrome?

A

too much serotonin leads to confusion, agitation, tachycardia, sweating, headache, muscle rigidity, fever. In severe cases, seizures, irregular heartbeat, unconsciousness

110
Q

how do tricyclics work?

A

Correct imbalance of serotonin and norepinephrine in the nerve endings of CNS blocking reuptake

111
Q

what should tricyclics NOT be used with, due to risk of serotonin syndrome?

A

MAOI

112
Q

how do MAOIs work?

A

inhibit monoamine oxidase, an enzyme that breaks down neurotransmitters

113
Q

what are adverse events of MAOIs?

A

Dry mouth, urinary retention, constipation, blurred vision, hypotension, weight gain, sexual dysfunction
CNS disturbances: restlessness, dizziness, insomnia, tremors, seizures
Potentially fatal liver damage
Hypertensive crisis (>180/110) when combined with stimulants or tyramine-containing foods

114
Q

how do SSRIs work?

A

block reuptake of serotonin

115
Q

how do SNRIs work?

A

block reuptake of both serotonin and norepinephrine

116
Q

what are some uses for SSRIs and SNRIs besides depression?

A

but also bipolar (not monotherapy), obesity, eating disorders, OCD, panic attacks, social anxiety, PTSD

117
Q

what are adverse events of SSRI and SNRI?

A

although side effects are better than TCAs and MAOIs, they can be problematic and cause people to stop taking them. Also, insomnia, weight gain, sexual dysfunction. Serotonin syndrome when combined with other drugs that increase serotonin

118
Q

what are drug interactions of SSRI and SNRI?

A

Serotonin syndrome when combined with MAOIs, lithium, buspirone, triptans, and/or the other
Benzodiazepine toxicity when used in combination
Increase warfarin and phenytoin levels
Bleeding risk with warfarin and NSAIDs

119
Q

what are 3 miscellaneous antidepressants?

A

bupropion
trazadone
vilazodone

120
Q

how does bupropion work?

A

seems to exert its effect on dopamine and norepinephrine

121
Q

what is bupropion used for?

A

originally depression, but good for smoking cessation

122
Q

what are adverse events of bupropion?

A

Lowers seizure threshold, should not be used in those with a seizure disorder
Dizziness, confusion, tachycardia, agitation, tremor, dry mouth

123
Q

how does trazadone work?

A

selectively inhibits serotonin reuptake without affecting norepinephrine

124
Q

what is the dopamine hypothesis of psychosis?

A

patients have excessive dopaminergic activity in the brain

125
Q

what are positive symptoms of psychosis?

A

delusions, hallucinations, confusion

126
Q

what are negative symptoms of psychosis?

A

apathy, social withdrawal, blunted affect, monotone speech. These symptoms are more impactful in everyday life

127
Q

how do antipsychotics work?

A

block dopamine receptors in the brain. This results in both the therapeutic and the toxic effects. However, the newer drugs selectively block D2 and some 5-HT2A receptors, making them safer and more effective

128
Q

what are the 4 first generation antipsychotics?

A

Phenothiazine
Thioxanthene
Phenylbutylpiperidine
Dihydroindolone

129
Q

what are the 3 second generation antipsychocics?

A

Dibenzodiazepine
Quinolinone
Benzisoxazole

130
Q

what was the first antipsychotic developed, which class, and when?

A

chlorpromazine in the 1950s, in the phenothiazine class

131
Q

what 2 phenothiazine antipsychotics are used as antiemetics?

A

Perphenazine
Prochlorperazine

132
Q

what antipsychotic drug is used for more resistant schizophrenia, and its class?

A

clozapine, dibenzodiazepine

133
Q

what antipsychotic drug is extra sedating, and its class?

A

quetiapine, dibenzodiazepine

134
Q

what antipsychotic is popular, and also used as an adjunct for depression, and its class?

A

aripiprazole, quinolinone

135
Q

what 2 antipsychotics are offered as monthly long-acting injections, and their class?

A

Paliperidone and Risperidone, benzisoxazole

136
Q

what are 3 main adverse events of antipsychotics?

A

extrapyramidal symptoms
tardive dyskinesia
neuroleptic malignant syndrome

137
Q

what are extrapyramidal symptoms?

A

pathological changes to the pyramidal portions of the brain
Motion disorders similar to Parkinson’s disease
Akathisia - motor restlessness
Dystonia - painful muscle spasms

138
Q

what is tardive dyskinesia?

A

drug-induced involuntary movements of the lips, jaw, tongue, and extremities

139
Q

what is neuroleptic malignant syndrome?

A

uncommon but serious. Fever, cardiovascular instability, muscle breakdown

140
Q

what are alpha adrenergic adverse effects of antipsychotics?

A

hypotension, lightheadedness, tachycardia

141
Q

what are endocrine adverse effects of antipsychotics?

A

gynecomastia, menstrual changes, sexual dysfunction

142
Q

what are histamine adverse effects of antipsychotics?

A

sedation, drowsiness, hypotension, weight gain

143
Q

what are cholinergic adverse effects of antipsychotics?

A

blurred vision, dry mouth, tachycardia, constipation, urinary retention, decreased sweating

144
Q

what are unique adverse effects of second generation antipsychotics?

A

also have other effect due to their effect on the endocrine system. This is not seen in first generation - Metabolic syndrome

145
Q

what is metabolic syndrome?

A

insulin resistance, weight gain, lipid changes

146
Q

what are drug interactions of antipsychotics?

A

Other drugs that act on the CNS - additive CNS depressant effects
Antihypertensives - additional antihypertensive effects

147
Q

what is another term for the first generation antipsychotics?

A

conventional

148
Q

what is another term for the second generation antipsychotics?

A

atypical

149
Q

what is non-response to depression treatment and what is done to manage it?

A

failure to respond after at least 6 weeks. First step: dose optimization. Then consider different drug

pharmacology (6 decks)

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