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Psychopharmacology > Intro and Anti-psychotics > Flashcards

Intro and Anti-psychotics Flashcards

1
Q

Pharmacokinetics

A

How a drug is absorbed, distributed, metabolized, excreted. What the body does to a drug. Liberation, Absorption, Distribution, Metabolism, Excretion.

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2
Q

Pharmacodynamics

A

Mechanism of action of a drug. What the drug does to the body.

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3
Q

Enteral/Oral administration

A

via the GI tract: safest, easiest route; must pass through the GI tract (w/stomach acid, enzymes) and enter portal circulation for 1st pass metabolism (1st pass effect)

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4
Q

1st-pass metabolism

A

absorbed in GI tract, enters portal vein to liver, metabolized, then enters general circulation. eventually sent back to liver by arterial circulation for more metabolism. PO takes 1-3 hours for 75% of dose of most psychoactive drugs to enter blood, depending on lipid solubility.

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5
Q

Parenteral/Inhalation

A

Avoids GI tract, 1st-pass metabolism, inhaled to lungs. Fastest drug effects (8-10 seconds) b/c lungs have largest surface area, avoids most of 1st-pass metabolism, blood goes from lungs to left side of heart and pumped out to arterial system (to brain very fast).

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6
Q

Why are smoking drugs of abuse (when inhaled) very reinforcing?

A

Partially due to very fast effects.

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7
Q

Transmucosal

A

Across mucous membranes, directly into bloodstream. Sprayed into nose/snorted. Drug effects in 2-3 minutes for cocaine.

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8
Q

Buccal (sublabial)

A

Between cheek and gums (nicotine gum)

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9
Q

Sublingual (SL)

A

Under tongue (nitroglycerine-for heart pt; alprazolam-xanax)

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10
Q

Intravenous (IV)/Injected

A

Very fast drug effects (15-30 seconds)

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11
Q

Intramuscular (IM)

A

Drug effects in 10-20 minutes.

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12
Q

Depot form

A

Intramuscular (IM): allows slow, controlled release over weeks (e.g., Risperdal Consta, Haldol Decanoate)

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13
Q

Intravenous/IV Advantages

A

Emergency; Dose titration; Irritating substances when diluted

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14
Q

Intravenous/IV Disadvantages

A

Risk of adverse drug reactions (ADRs); Cannot give highly lipid drugs; Vein collapse with frequent repetitions.

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15
Q

Subcutaneous (SC, SQ, subcut)

A

Injected just under skin, not into the vein: Drug effects in 15-30 minutes, or hours to months. Examples: vaccines, insulin, TB skin test.

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16
Q

Subcutaneous Advantages

A

Better for highly lipid drugs, implantation of solid pellets

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17
Q

Subcutaneous Disadvantages

A

Possible pain, tissue damage from irritating substances

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18
Q

Transdermal

A

Through skin by patch

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19
Q

Transdermal Advantages

A

Slow, controlled release over hours to days

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20
Q

Transdermal Disadvantages

A

May get irritation, sometimes inconsistent absorption, must avoid heat and rubbing

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21
Q

Transdermal Examples

A

nicotine patch for addiction, hormonal patches, methylphenidate (daytrana) for ADHD, rivastigmine (exelon) for dementia, selegiline (emsam) for depression, scopolomine for motion sickness

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22
Q

Liberation

A

release of drug from its dosage form

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23
Q

Absorption

A

movement of drug from administration site into the blood

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24
Q

Distribution

A

movement of drug from intravascular to extra-vascular space

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25
Q

Metabolism

A

transformation of drug into compounds that are easier to eliminate

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26
Q

Excretion

A

elimination of drug or metabolite via renal, biliary, or pulmonary processes

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27
Q

Absorption in the stomach considerations

A

many drugs are absorbed better in the stomach than in intestines (and vice versa). You can reach a desired concentration level faster when taken on an empty stomach. Some pills are enteric-coated to decrease irritation of the stomach lining, and may delay absorption until intestine for those drugs that are better absorbed in intestine. Bottom line: take drugs as instructed.

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28
Q

Immediate release (IR)

A

drug is released with no time lapse

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29
Q

Controlling release, absorption

A

Sustained-release (SR); Sustained-action (SA); Extended-release (ER, XR, XL); Controlled-release (CR); and Time release technology (TR)

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30
Q

Benefits of Delayed Release

A

Decreases side effects, (possibly) improves therapeutic effects by smoothing out peaks, troughs. Often may be sprinkled on applesauce (in insert says so).

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31
Q

Caution with Delayed Release

A

Should not be chewed or crushed (unless insert states otherwise)

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32
Q

Metabolism

A

Drugs are metabolized by enzymes primarily in the liver, but also intestines. The drug is usually inactivated, easier to excrete.

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33
Q

Prodrug

A

A drug that is initially inactive, but becomes active when absorbed or metabolized.

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34
Q

Excretion

A

Mainly in urine, but also in feces, sweat, mammary milk, or exhaled air.

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35
Q

What happens if a drug is delayed in its metabolism or elimination, or is ineffective?

A

It can reach toxic levels, or can cause GI, liver, kidney, or lung disease.

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36
Q

Cytochrome P450 (CYP)

A

System in the liver that is main system of enzymes that inactivate drugs. Different in every individual (ex: poor, extensive (normal), ultra rapid, or rapid metabolizers).

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37
Q

Variability in Cytochrome system (different metabolizers) - Elderly

A

Age-elderly may have decreased hepatic (liver), renal (kidney) function. They may get toxic levels, particularly if liver or kidney dysfunction. Dose usually halved. Polypharmacy often leads to many drug-drug interactions.

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38
Q

Variability in Cytochrome system (different metabolizers) - Supersensitivity (allergic)

A

Rash is most common reaction. Discontinue (D/C) drug immediately. Take antihistamine, topical corticosteroid. Call doctor. Some can become fatal. Must not try drug again.

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39
Q

Variability in Cytochrome system (different metabolizers) - General susceptibility factors

A

Less effective barriers to absorption (GI, blood-brain barrier); Increased body fat (keeps fat-soluble drugs in body longer); More sensitive receptors.

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40
Q

Impact of drug-drug interactions

A

Significant side effects (ex: excessive drowsiness with xanax and ambien)

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41
Q

What are the most common type of drug-drug interactions?

A

Those of addictive drugs.

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42
Q

Synergistic effects of drug-drug interactions

A

Two drugs are adding to one another or having an impact on one another for an additive effect. Ex: thyroid hormone added to antidepressant.

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43
Q

Antagonistic drug effects of drug-drug interactions

A

two drugs doing opposite things cancel one another out. Can lead to decreased therapeutic effect.

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44
Q

Drug-drug interactions: inhibition

A

a drug can inhibit an enzyme that metabolizes itself or other drugs

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45
Q

Drug-drug interactions: induce

A

a drug can induce an enzyme that metabolizes itself or other drugs

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46
Q

CYP enzymes

A

main system which inactivates drugs, found in liver and some in the intestines. Involved in drug-drug interactions by inhibiting or inducing metabolization of a drug. Psychotropics are infamous for being effected by, or effecting other drugs.

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47
Q

Drug Inhibition process

A

Drug A (a CYP-substrate) usually binds to CYP enzyme and is metabolized. Drug B (a CYP inhibitor) blocks the site and does not allow A to be metabolized. Increases level of “un-metabolized” drug A in blood plasma, which may increase side effects and toxicity.

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48
Q

Timeframe for Drug-drug interactions

A

occurs immediately, within hours to days. It doesn’t matter which drug is added first.

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49
Q

Drug Induction process

A

Drug A (a CYP-substrate) usually binds to CYP enzyme and is metabolized. Drug C (a CYP-inducer) induces a cell that makes the enzyme to make more. Increases metabolism of A, decreases plasma levels of A, and decreases drug effects. Can take days to weeks to develop if drug C is added second. Will occur immediately if drug C is already present for several days.

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50
Q

Effects of diet on drug metabolism

A

Grapefruit juice: inhibits 3A4, causing increased levels of 3A4-metabolized drugs. (85 drugs affected by DDIs- ex: ability, celexa). May cause death. One glass may have an effect for greater than 3 days.
Herbs: St. John’s wort induces 3A4. As a result, drugs like seroquel will had less effect.

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51
Q

How can you warn your patients?

A

instruct patients to ask their doctor or pharmacist about potential DDIs, including food, OTC drugs, herbs, supplements

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52
Q

Peak level

A

drug concentration at it’s highest

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53
Q

Trough level

A

drug concentration at it’s lowest

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54
Q

Half-life (T1/2)

A

Time required for plasma concentration to decline by 50% after 1 dose. After 1T1/2, 50% of drug is eliminated. After 2 T1/2, 75% is eliminated. After 3 T1/2, 87.5% is eliminated. Etc.

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55
Q

How long does it take for most of a drug to be entirely eliminated?

A

About 6 half-lives.

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56
Q

First-order kinetics

A

How a drug is eliminated slowly in the body (half-lives). The metabolism rate is a constant fraction of the remaining drug.

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57
Q

What drug does not follow the half-life rule?

A

Alcohol - zero-order kinetics: an absolute amount is eliminated per hour, regardless of the amount in the blood.

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58
Q

Steady state (SS)

A

Plasma drug concentration does not change with repeated (or continuous) same dose administration. Drug in rate = drug out rate. After 6 half lives, 98.4% of steady state is achieved - SS concentration is reached with regular-interval (or continuous) dosing after 6 half-lives.

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59
Q

How many half-lives does it take to reach Steady State concentration?

A

6 half-lives

60
Q

Maintenance dose

A

matching the rate of drug excretion with the drug dosing. The typical regime would be to take the drug at the end of each half-life. For example, if T1/2 is 24 hours, take 1 dose each day, and expect a steady state (SS) after 6 days.

61
Q

LD50

A

lethal dose in 50% of animal test subjects

62
Q

ED50

A

dose that produces desired effect in 50%

63
Q

Therapeutic Index (TI)

A

relative safety

64
Q

What do the results of this equation mean? TI=LD50/ED50

A

a High TI indicates that a client will be safer after an overdose; a Low TI indicates that they will be less safe and that it could possibly be fatal.

65
Q

TD50

A

toxic dose in 50% of human subjects (Safety Index TD50/ED50 indicates the relative safety from toxicity)

66
Q

Therapeutic window

A

Range between minimum effective concentrations for desired and adverse effects.

67
Q

Therapeutic drug monitoring (TDM)

A

Correlating plasma concentration with effects in a specific patient. As the therapist, you can encourage client to get regular blood tests, which may help to increase therapeutic effects and avoid toxic side effects.

68
Q

Tolerance

A

Increased dose required for a response. Receptors decrease in number/sensitivity (down-regulation).

69
Q

Physical Dependence

A

Physical, psychological withdrawal symptoms occur when discontinuing the drug. This can occur without tolerance, abuse, or “addiction.” Frequently occurs with many psychotropics. Should generally never D/C psychotropics or drugs in general abruptly. Should titrate off slowly.

70
Q

Direct agonist

A

Activates receptor just as natural neurotransmitter does.

71
Q

Direct antagonist

A

Blocks action of natural neurotransmitter by binding to receptor, thereby preventing natural neurotransmitter from binding, and from doing what it would normally do. Has no effect on the receptor.

72
Q

Partial agonist

A

Exerts same but weaker effect as full agonist (same thing the natural neurotransmitter does, but weaker effect).

73
Q

Inverse agonist

A

Exerts opposite effect as full agonist (opposite what the natural neurotransmitter normally does).

74
Q

Mesolimbic dopamine pathway

A

Goes from ventral segmental area (VTA) to limbic brain, particularly nucleus accumbens

75
Q

What causes the positive symptoms of psychosis?

A

Hyperactivity of D2 receptors in the mesolimbic dopamine pathway.

76
Q

What do antipsychotic drugs (APs) do in the mesolimbic pathway?

A

antagonize D2 receptors and decrease positive symptoms.

77
Q

What is the primary effect of “conventional”/”typical”/”first generation” anti-psychotics?

A

D2 antagonism

78
Q

What is the down-side to using “conventional” anti-psychotics?

A

Pure D2 antagonism (what they do) may cause side effects when it occurs in other pathways. Occurring in the mesolimbic pathway, they successfully reduce/eliminate positive symptoms of psychosis. However, other pathways lead to side effects.

79
Q

Mesocortical dopamine pathway

A

Goes from VTA to prefrontal cortices. When conventional antipsychotics lead to deficient dopamine in this pathway, it results in cognitive, negative, and affective symptoms. (Side Effects)

80
Q

Nigrostriatal dopamine pathway

A

Goes from substantial nigra to the dorsal part of the striatum of the basal ganglia (part of the extrapyramidal system). Decreased dopamine activation in this pathway causes Parkinson’s disease, extrapyramidal symptoms (EPS). Also rigidity, tremor, akathisia, and dystonia occur due to excessive ACh activity, because dopamine normally blocks this being released into the basal ganglia. Also, D2 antagonists may cause such EPS.

81
Q

Extrapyramidal system

A

Controls automatic functions of movement in the body (movement that didn’t occur because you consciously told it to)

82
Q

Pyramidal system

A

Controls movement that occurs as part of the conscious motor system (think of picking up your arm and do it)

83
Q

EPS (Extrapyramidal symptoms)

A

Dystonia, akathisia, pseudoparkinonism, Acute dystonia= painful muscle spasms of: tongue, face, jaw [facial grimacing], neck [spasmodic torticollis], back, eyes [oculogyric crisis], larynx [laryngospasm], hand [writer’s cramp], foot.

84
Q

What symptom of EPS is fatal?

A

Larynx muscle spasms (laryngospasm). Must get the client an anticholinergic shot immediately.

85
Q

Akathisia

A

Symptom of EPS involving restlessness, pacing, anxiety, agitation. Patients often don’t tell their doctors about this, and it frequently leads to suicide.

86
Q

Pseudoparkinsonism

A

Symptom of EPS involving mask-like faces, blank stare (decreased blink), bradykinesia, shuffling gait, muscular rigidity (bent over, “cogwheel rigidity”, resting tremor, pill-rolling, drooling.

87
Q

Tardive dyskinesia (TD)

A

Side effect of antipsychotics (conventionals) - darting, twisting, protruding of tongue; lip licking, smacking, puckering; chewing and lateral jaw movements; puffing cheeks; face and eye movements (facial grimacing, tics, blinking, brow arching; upward deviation of eyes); athetoid (warlike) or choreiform (rapid, jerky) movement of extremities (finger, wrist arms); and trunk movements (twisting, swaying). This is one of the most serious side effects. It sometimes improves with D/C of AP. Temporarily worse on withdrawal. Caused by up-regulation of DA2 receptors after prolonged use of APs. May avoid by using atypical APs at lowest effective dose. Switch to closapine (Clozaril) if necessary.

88
Q

Tuberoinfundibular dopamine pathway

A

Goes from hypothalamus to anterior pituitary gland. DA normally blocks prolactin (creates milk for breast feeding) release from pituitary gland, but fails to do so if blocked by D2 blockers. AKA prolactin-releasing cells are disinhibited, causing hyperprolactinemia. This leads to gynecomastia, galactorrhea, anovulation (not ovulating), amenorrhea (irregular/absent menstrual cycles), decreased testosterone/libido/orgasmic dysfunction, decreased estrogen/fertility/demineralization of bones in women (leads to osteoporosis).

89
Q

Conventional APs (Conventionals)

A

First generation of anti-psychotics (FGAs) - AKA typical APs, or neuroleptics. Antagonize D2 receptors, but cause many side effects in other pathways due to antagonism of other receptors (M1, a1, H1).

90
Q

Psychopharmacologic dilemma regarding anti-psychotic medications.

A

How to: antagonize mesolimbic D2 receptors to treat positive symptoms of psychosis, increase mesocortical dopamine to treat cognitive, negative, and affective symptoms, and avoid affecting stratal, tuberoinfundibular dopamine. = Atypicals, AKA second-generation of APs (SGAs)

91
Q

What do atypical anti-psychotics generally do in the body?

A

Treat positive sx and (less effectively) treat negative sx. Have low EPS, tar dive dyskinesia, prolactinemia (side effects of conventionals). Primary do this by blocking D2 and 5-HT2a receptors (SDA).

92
Q

What do 5-HT2a receptors typically do?

A

Inhibit dopamine release in the 4 pathways. Antagonizing 5-HT2a reverses D2 inhibition (what atypicals do), allowing dopamine to increase and avoiding the increase of cognitive, negative, and affective symptoms that occurs with conventionals. Reverses side effects while still allowing for therapeutic effects of drug. This occurs while still antagonizing D2 receptors to decrease positive symptoms. Sum: atypicals antagonize 5-HT2a and D2 receptors.

93
Q

What is sufficient to reverse the side effects of D2 blockade in stratal, mesocortical, and tuberoinfundibular pathways, while being insufficient to reverse therapeutic effects against positive symptoms (D2 blockade in mesolimbic pathway)?

A

Antagonism of 5-HT2a receptors enhancing dopamine release caused by atypical anti-psychotics.

94
Q

What percentage of D2 receptors are blocked in all brain areas by conventional anti-psychotics?

A

greater than 80%

95
Q

What percentage of blockage of D2 receptors must be blocked in the mesolimbic pathway to decrease positive symptoms of psychosis?

A

80%

96
Q

Does the blockage of D2 and 5-HT2a receptors occur in the to the same degree in all brain areas?

A

No.

97
Q

Atypicals effect in the dorsal striatum

A

5-HT2a antagonism causes dopamine to compete with D2 binding to a degree sufficient to reduce percentage of blocked D2 receptors to about 60%. This is sufficient to reduce EPA & TD side effects.

98
Q

Atypicals effect in the pituitary gland

A

Similar to in the dorsal striatum, 5-HT2a antagonism causes dopamine to compete with D2 binding to a degree sufficient to reduce percentage of blocked D2 receptors to about 60%. This is sufficient to reduce hyperprolactinemia.

99
Q

Atypicals effect in the mesolimbic pathway.

A

the percentage of D2 blockage remains greater than 80%, successfully treating positive symptoms just as well as conventionals.

100
Q

Therapeutic Window

A

D2 antagonism occurs in the striatum and pituitary at the same dosage that leads these drugs to have successful antipsychotic effects, because atypicals have an affinity for 5-HT2a receptors that is greater than their affinity for D2 receptors.

101
Q

What two receptors have opposite effects on DA release?

A

5-HT1a and 5-HT2a

102
Q

What do 5-HT2a receptors do?

A

Decrease DA release.

103
Q

What does blocking 5-HT2a receptors do?

A

Increases DA release.

104
Q

What do 5-HT1a receptors do?

A

Increase DA release.

105
Q

What do 5-HT1a partial agonists do?

A

Increase DA release, causes less EPS in striatum, and has antidepressant effect and improves cognition in prefrontal cortex.

106
Q

What atypical drug is most potent in its -HT1a partial agonist property?

A

aripiprazole (Abilify)

107
Q

What do D2 parital agonists do?

A

“stabilize” DA transmission between “silent” antagonism and full stimulation. It takes only a very small degree of partial agonist effect in striatum to avoid EPS.

108
Q

Goldilocks drugs

A

Ideal drug with antipsychotics actions without EPS at higher doses, antidepressant and precognitive effects at lower doses. Abilify is as close as we’ve gotten to this.

109
Q

Cardiometabolic effects

A

Common side effects of atypicals: weight gain, abnormal BMI, may be greater in adolescents

110
Q

Dyslipidemia

A

cardiometabolic side effect of atypicals: high levels of triglycerides (lipids), can result in heart attack. Resting triglycerides may return to normal if AP is D/C.

111
Q

Hyperclycemia

A

cardiometabolic side effect of atypicals: high blood sugar, risk of type 2 diabetes

112
Q

When administrating an AP (atypical), what should physicians do?

A

Obtain family history, and monitor weight, resting level of triglycerides, fasting glucose level, and blood pressure.

113
Q

What can psychologists do if a client is taking an AP (atypical) to assist physician and client in monitoring side effects?

A

Encourage/educate client on why it is important to adhere to required lab work, change diet, increase exercise, stop smoking.

114
Q

Rashes, photosensitivity, temperature deregulation, liver effects, seizures (mostly with clozapine/clozaril) are side effects of what?

A

Atypical antipsychotics

115
Q

Agranulocytosis

A

side effect of atypicals - fever, sore throat, mouth sores, infections, unusual bleeding/bruising due to not making enough white blood cells. develops very rapidly and can be fatal in 3 days. most with clozapine/clozaril. requires weekly CBC for 1st 6 months, biweekly for months 6-12, every 4 weeks thereafter.

116
Q

Can antagonism of D2 receptors cause EPS, TD, and hyperprolactinemia with atypical anti-psychotics?

A

Yes. EPS & TD max incidences with conventionals, and minimum incidences with atypicals. There is a low incidence of hyperprolactinemia with atypicals.

117
Q

Antagonism of H1, M1 and a1 can cause:

A

sedation - most sedating= clozapine(Clozaril), quetiapine(Seroquel), olanzapine(Zyprexa), and of conventionals=low potency types such as chlorpromazine

118
Q

Antagonism of H1 (histamine 1) receptor can cause:

A

weight gain, especially if 5-HT2c is also blocked.

119
Q

Antagonism of ACh-M1 (cholinergic, muscarinic) receptor can cause:

A

anticholinergic side effects: memory problems, delirium (disturbed consciousness; perception; cognition; mood-perplexed, excitable, labile; motor functions, autonomic functions, sleep), blurred vision, dry mouth (cotton mouth), constipation, urinary hesitation/retention, reflex tachycardia (increased heart rate), and difficulty with sexual arousal (ACh released from parasympathetic nervous system binds to M1 receptors). In sum: “Mad as a hatter, blind as a bat, dry as a bone, red as a beet.”

120
Q

Antagonism of a1 receptor (alpha adrenergic) can cause:

A

low blood pressure, orthostasis (postural hypotension-can result in falls), dizziness, increased heart rate (compensatory)

121
Q

What does hyperprolactinemia cause?

A

Hyperprolactinemia is a side effect of atypical anti-psychotics, and it causes loss of libido.

122
Q

Black Box Warning

A

all APs may increase risk of death in elderly patients with dementia, primarily from cardiovascular or infectious events (usually pneumonia). APs are not FDA-approved for dementia-related psychosis.

123
Q

QTc prolongation

A

QT interval is a portion of the ETC (electrocardiogram) that shows the time between two points. If the time is off, it lets the doctor know that there is an arrhythmia (heart pulses are going slower than they normally should, which impacts several parts of the body reliant on that blood). This can be fatal. A drug that causes QTc prolongation indicates to the doctor that the client is at increased risk of heart problems.

124
Q

Neuroleptic malignant syndrome (NMS)

A

side effects of atypical anti-psychotics: lead-pipe rigidity, altered consciousness, autonomic instability (BP, HR), diaphoresis (sweating), fever. client should refer to the emergency room or prescribing provider for immediately D/C of AP (can be fatal).

125
Q

What is one of the main determining factors for choosing a specific drug for a particular patient?

A

the many different specific side effects

126
Q

What other purposes can anti-psychotics be used for, other than to treat symptoms of psychosis?

A

as a “mood stabilizer”, may be useful for bipolar disorder, unipolar depression, anxiety, and behavioral disruption

127
Q

When determining the choice of drug for a particular person, consider:

A

Diagnose properly, then go beyond diagnosis and treat symptoms, and problems of that unique person.

128
Q

Consideration of different drugs for treating schizophrenia:

A

treatment of positive symptoms is similar for conventionals and atypicals; treatment of negative, cognitive, affective symptoms are usually better with atypicals

129
Q

Are conventionals or atypicals (anti-psychotics) typically prescribed first?

A

atypicals, due primarily to lower EPS and TD compared to conventionals.

130
Q

Cons of prescribing atypicals

A

generally more expensive, may increase cardiometabolic risk, death in patients with dementia, and require periodic physiologic monitoring

131
Q

Considerations of side effects when prescribing specific anti-psychotic drugs:

A

usually start a client at the lowest dose and titrate up to avoid/minimize side effects. Because pharmacodynamics differ somewhat for every AP (different receptors affected by different types, in addition to D2 or 5HT2a), one AP may be preferred over another for a specific symptom profile of a specific patient. Closest thing we have so far to “Personalized Medicine”.

132
Q

Which type of anti-psychotic is better for agitated patients?

A

more sedating drugs

133
Q

Which type of anti-psychotic is better for patients with psychomotor retardation and pronounced withdrawal?

A

less sedating drugs

134
Q

What percentage of symptoms decrease in general when someone take anti-psychotics?

A

20-50%

135
Q

How long does it take for a decrease in positive symptoms after beginning to take anti-psychotics?

A

a few days

136
Q

How long does it take for a decrease in negative, mood, and cognitive symptoms after beginning to take anti-psychotics?

A

may take months, if at all.

137
Q

If a client comes in having just had their third psychotic episode, how long would a doctor usually treat them with medication?

A

for life. (first episode=1 year; second episode=5 years)

138
Q

What are some reasons that a person taking anti-psychotics would experience only partial responses to the meds?

A

poor adherence (compliance) to drug regimen is the most common reason, but could also be poor absorption, “ultra-rapid metabolizer”, patient skipping doses, drug-drug interactions, and different brains just may respond differently.

139
Q

What are some reasons that people do not adhere, or have poor adherence to anti-psychotic regime?

A

side effects

140
Q

Storing anti-psychotic drugs

A

avoid high temperatures and sunlight

141
Q

What can a client do to assist themselves in maintaining adherence to drug regime?

A

involve significant others to help with adherence

142
Q

Different treatment options for anti-psychotic prescriptions

A

Optimize (check adherence, check DDIs including drug abuse, increase dose perhaps beyond those used in studies, or increase time for therapeutic effects); Augment (add a non-antipsychotic such as anti-depressant, anxiolytic, mood stabilizer, hypnotic for sleep, or another AP); or Switch (to another AP)

143
Q

How can psychotherapy help? And what type?

A

CBT - improve adherence, increase normal thinking & self-observation, examine bases for delusions & hallucinations, cope with residual positive symptoms, and improve social, vocational, occupational functions. Family therapy may help with outside support (improve relationships, decrease delusions, encouragement for adherence, recognize side effects early, or signs of relapse, educate family members on illness and reduce their emotional reactions so that they don’t trigger acting out by client)

144
Q

Treatment-resistant psychosis

A

mainly positive symptoms persist

145
Q

Psychotic aggression

A

hostility, impulsivity, violence with mainly positive symptoms

146
Q

Treatment options for treatment resistant or psychotic aggression

A

switch to clozapine (clorazil) 30% of drug resistant clients respond to it, augment or add clozapine, 2 APs, augment with mood stabilizer, very high dose monotherapy (may cause intolerable side effects of sedation, EPS, cognitive impairment, metabolic sxs), give drugs longer time to work, or aggression related to sociopathy may require bx tx.. Very high-dose monotherapy, polypharmacy are used as last resorts.

Psychopharmacology (2 decks)

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