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Pharmacology Exam 4 > Psychotropic Medications > Flashcards

Psychotropic Medications Flashcards

1
Q

What can be altered by sedative and hypnotic agents?

A

CNS, autonomic responsiveness, cardiac conduction, bleeding, seizure potential, endocrine response to stress

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2
Q

What is one of the greatest threats of psychopharmacologic drugs?

A

abuse

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3
Q

What are the 6 major categories of Psychiatric Disorders?

A

Neurosis, Psychosis, Depression, Schizophrenia, Tourette’s Syndrome, Dementia.

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4
Q

What metabolism pathway do psychopharmacologic drugs often affect?

A

alter P450

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5
Q

Define Neurosis.

A

broad category of psychological disturbances, mild forms of mental disorders including anxiety, hysteria, hypochondria, phobias, OCD, panic disorders, and PTSD.

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6
Q

Define Psychosis.

A

loss of contact with reality, wide variety of diseases of CNS, characterized by impaired behavior, inability to think coherently and comprehend reality, inability to understand disturbance

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7
Q

What are some S/S of psychoses?

A

S/S: hallucinations, delusions, thought disorders

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8
Q

What are some examples of psychoses?

A

schizophrenia/schizoaffective disorder, organic psychoses (delirium, dementia), bipolar disorder, psychotic depression, drug-induced

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9
Q

Define depression/depressive disorders.

A

reflects a sad/irritable mood exceeding normal sadness or grief. Characterized by greater intensity, duration, and more severe symptoms/functional disabilities

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10
Q

What can depression increase risk of?

A

developing CAD, HIV, asthma, other

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11
Q

What are the major types of depression?

A

Major depression, Dysthymia, Bipolar/Manic Depression

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12
Q

Describe the 2 types of bipolar?

A

Bipolar 1: longer swings, Bipolar 2: less mini highs

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13
Q

Describe schizophrenia.

A

mental disorders characterized by abnormal perceptions/expressions of reality. paranoia, auditory hallucinations. usually adult diagnosis

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14
Q

Describe tourette’s syndrome.

A

associated with exclamation of obscene or inappropriate or derogatory remarks. may be accompanied by motor tics. mostly inherited with some environmental factors involved.

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15
Q

What are the 3 categories of symptoms of schizophrenia?

A

Positive, Negative & Cognitive.

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16
Q

Describe positive schizophrenia symptoms.

A

delusion, hallucinations, disorganized speech/thinking, grossly disorganized behaviors/catatonic.

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17
Q

Describe negative schizophrenia symptoms.

A

lack of emotion, lack of interest/low motivation, flat affect, alogia, inappropriate socialization or social isolation

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18
Q

Describe cognitive schizophrenia symptoms.

A

disorganized thinking, slow thinking, difficulty understanding, poor concentration, poor memory, difficulty expressing thoughts, difficulty integrating thoughts/feelings/behaviors.

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19
Q

What is the dopamine hypothesis for schizophrenia?

A

brain produces more dopamine than normal brains and the increased dopamine is responsible for the symptoms. Due to a disturbed and hyperactive dopaminergic system with increased activity at the D2 receptor subtype.

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20
Q

What are the 4 DA pathways?

A

mesolimbic, mesocortical, nigrostriatal, tuberoinfundibular

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21
Q

Describe mesolimbic pathway

A

runs from tegmentum (midbrains) to nucleus accumbens (limbic system). mediates positive symptoms of schiz. blocking D2 receptors lead to decrease in positive symptoms

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22
Q

Describe mesocortical pathway.

A

tegmentum (midbrain) to frontal and limbic cortex. Mediates negative symptoms of schiz. Decreasing DA levels may produce or worsen negative symptoms likely due to increase in 5-HT which inhibits DA release. Explains why negative sx are unaffected or worsened by antipsychotics

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23
Q

Describe the nigrostriatal pathway.

A

runs from substantia nigra (midbrain) to basal nuclei. regulates posture and voluntary movements. first gen antipsychotics block DA receptors and cause EPS. This pathway is where side effects happen, not necessarily to treat psychoses.

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24
Q

Describe tuberoinfundibular pathway.

A

from hypothalamus to anterior pituitary. also where side effect happen, not treatment. prolactin release is inhibited by DA. females may experience galactorrhea amenorrhea, and sexual dysfunction

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25
Q

What drugs have primarily serotonergic activity?

A

SSRIs, TCAs, MAOIs, buspirone, lithium.

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26
Q

What is the goal of treatment of antidepressants?

A

remission of symptoms

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27
Q

Whats the MOA of serotonergic drugs?

A

unknown, but increases amount of serotonin in synapses to alter receptor signaling. (5HT receptors)

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28
Q

What are serotonin receptors responsible for?

A

GI motility, genital arousal, vascular tone, hematopoiesis, platelet aggregation, aspects of inflammatory response. also release broad array of NT and peptide hormones affecting mood, sleep, aggression, appetite, sex, memory

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29
Q

What are serotonergic drugs used for?

A

major depressive disorder, bipolar depressive episodes, panic disorder, social phobia, PTSD, OCD, bulimia, neuropathic pain, migraine prophylaxis

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30
Q

What do serotonin reuptake inhibitors do?

A

bind and inhibit transporter protein SERT, blocks reuptake of serotonin from synaptic cleft into presynaptic neuron enhancing serotonergic neurotransmisison. Most widely kind of meds for psychiatric conditions

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31
Q

What has more side effects? SSRIs or TCAs?

A

TCAs, SSRIs are safer, hard to OD

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32
Q

What is the onset for SSRIs/

A

1-4 weeks up to 12 for full effect

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33
Q

What are some common SSRIs?

A

Fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram

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34
Q

What are some side effects of SSRIs?

A

decreased sex drive, increased bleeding, hyponatremia, withdrawal if stopped suddenly (most common with paroxetine, least with fluoxetine)

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35
Q

What do serotonin norepinephrine reuptake inhibitors do?

A

inhibit NE transporter (NET) as well as SERT. lack affinity for adrenergic, histaminergic and cholinergic receptors

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36
Q

When are SNRIs preferred?

A

patients with heart disease

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37
Q

What are the side effects of SNRIs?

A

nausea, dry mouth, somnolence, headaches, sexual dysfunction.

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38
Q

What should you not take when on SNRIs?

A

SSRIs

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39
Q

What are some examples of SNRIs?

A

Pristiq, duloxetine (cymbalta), venlafaxine (effexor)

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40
Q

When are SNRIs better than SSRIs?

A

treating chronic pain

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41
Q

How does buspirone work?

A

serotonin agonist, for short-term treatment of GAD, partial agonist at serotonin receptors particularly 5-HT resulting in decreased serotonin turnover and anxiolytic effects

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42
Q

Why does buspirone not react with benzos, barbs, or alcohol?

A

no direct effects at GABA receptors

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43
Q

Does buspirone cause dependence?

A

No, but highly toxic in OD

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44
Q

When are TCAs C/I?

A

recent MI, long QT, dysrhythmias, CHF.

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45
Q

How do TCAs work?

A

inhibiting synaptic reuptake of NE and serotonin at presynaptic terminals increasing their availabilities but also affect histaminergic and cholinergic systems so lots of side effects.

46
Q

What are some common side effects of TCAs?

A

postural hypotension, dysrhythmias, urinary retention

47
Q

What is the prototype of TCAs?

A

amitryptiline, used as adjunct for neuropathic and somatic chronic pain

48
Q

What are examples of TCAs?

A

amitriptyline, imipramine, protriptyline, doxepin

49
Q

What are symptoms of TCA OD?

A

seizures, ventricular dysrhythmias, heart block hypotension

50
Q

How do MAOIs work?

A

classed as serotonin, NE, and DA enzyme inhibitors or multimodal drugs. block enzyme that metabolizes biogenic amines, increasing bioavailability of these NT in CNS and peripheral ANS.

51
Q

Are MAOIs 1st line treatment?

A

no, 2-3rd line because complicated SE and can be hazardous. hypotension, insomnia. 1st line for patients with atypical depression.

52
Q

What are common MAOIs?

A

phenelzine, tranylcypromine

53
Q

How do you treat the profound hypotension with MAOIs?

A

phenylephrine

54
Q

What NT are with MAO-A and what are with MAO-B?

A

A: serotonin, dopamine, NE (60% of people);
B: Tyramine, phenethylamine

55
Q

What’s the MOA of MAOIs?

A

form stable IRREVERSIBLE complex MAO enzyme so amount of NT available for release in CNS neurons is increased.

56
Q

Why the profound hypotension with MAOIs?

A

accumulation of false NT octopamine in cytoplasm of postganglionic nerve endings. most prominent in elderly

57
Q

Describe hypertensive crisis with MAOIs.

A

acute, severe rise in BP resulting in organ impairment. due to combination of MAOIs and certain drinks/foods rich in indirectly acting sympathomimetics.

58
Q

What are the dietary restrictions while on MAOIs?

A

aged cheese, cured or processed meats, preserved or pickled fish, liver, fermented soy products, yeast extracts, broad beans, dried or overripe fruits, red wine, draft beer.

59
Q

What are the drug restrictions while on MAOIs?

A

SSRIs, SNRIs, TCAs, cold/allergy meds, nasal decongestants, sympathomimetic drugs, opioids.

60
Q

How do FGAs work?

A

all block D2 receptors in limbic system, most effective against positive symptoms. blocks DA receptors everywhere in brain causing EPS and other adverse effects

61
Q

What’s the most and least potent FGA?

A

haloperidol and chlorpromazine

62
Q

What is clozapine used for?

A

effective for positive and negative symptoms

63
Q

Does clozapine cause EPS?

A

No

64
Q

What is the life threatening adverse effect of clozapine?

A

agranulocytosis

65
Q

What receptors do SGA block?

A

D2 and 5-HT receptors

66
Q

What are the side effects of SGAs?

A

sedation, weight gain, orthostatic hypotension, and hyperglycemia

67
Q

What are examples of SGAs?

A

quetipaine, risperidone, aripiprazole, olanzapine, ziprasidone

68
Q

What happens when you activate 5-HT2 receptors and block them?

A

activate=block release of DA, block-increase release of DA

69
Q

Is tardive dyskinesia reversible?

A

may be irreversible or may take years to vanish.

70
Q

What is the incidence of TD?

A

53% in elderly with FGAs, 5% in elderly with SGAs, 0 with clozapine

71
Q

What is the drug of choice in schizophrenics with moderate to severe dyskinesia?

A

Clozapine

72
Q

What types of drugs are commonly used to treat bipolar and antimanic/mood stabilization?

A

glutamate antagonist and channel blockers: anticonvulsants valproate and carbamazepine

73
Q

What is lamotrigine?

A

channel-blocking anticonvlusant that impacts glutamanergic signaling

74
Q

What do gabapentin and pregabalin do?

A

anticonvulsant calcium channel subunit blocking drugs that decrease synaptic glutamate release.

75
Q

What type of drug is ketamine?

A

NMDA glutamate receptor antagonist

76
Q

What are the s/s of parkinsonism and what causes them?

A

tremor, rigidity, akinesia/bradykinesia. due to degeneration of inhibitory DA pathway projecting from substantia nigra to caudate nucleus in striatum…causing deficiency in DA in specific area of brain

77
Q

What is the treatment for parkinsons?

A

replacement therapy but cannot just give DA b/c it doesn’t cross the BBB. Levodopa is drug of choice. it’s a precursor to DA so can cross BBB

78
Q

What does levodopa do?

A

decrease akinesia and tremor, most effective in early therapy, life expectancy increases in duration and quality.

79
Q

Are large or small doses of levodopa required?

A

large because 95% metabolized in gut and doesn’t get to brain but should keep daily dose as low as possible (<600mg)

80
Q

What are the short term side effects of levodopa?

A

GI–n/v, loss appetite, CV–postural hypotension, Sleep–somnolence, insomnia, vivid dreams/nightmares, inversion of sleep-wake cycle

81
Q

What are long term side effects of levodopa?

A

involuntary movements–peak dose dyskinesia, diphasic dyskinesia, dystonia, response fluctuations–wearing off, unpredictable on/off, psychiatric–confusion, visual hallucinations, delusions/illusions.

82
Q

What reverses the therapeutic effects of levodopa by increasing the peripheral metabolism of levodopa to DA?

A

pyridoxine (vit B6)

83
Q

What med increases the effectiveness of levodopa?

A

Carbidopa, a peripheral decarboxylase inhibitor, decreases peripheral metabolism of levodopa to DA

84
Q

What is the most effective med for parkinsons?

A

Sinemet 1:10 or 1:4 carbidopa:levodopa

85
Q

What are other parkinsons disease drugs?

A

DDC inhibitors, COMT inhibitors, MAO-B inhibitors, dopamine agonists

86
Q

What are the anesthetic implications with antiparkinsonian drugs?

A

patients prone to hemodynamic instability, gastric aspiration, laryngospasm, postop cognitive dysfunction, upper airway obstruction. Avoid drugs that exacerbate parkinsonism like phenothiazines, butyrophenones, reglan, and MAOIs. very sensitive to CV and resp depressant effects of anesthetic agents.

87
Q

What meds should you take caution with in the OR when on antiparkinsonian drugs?

A

fentanyl and neostigmine.

88
Q

Should the patient continue their meds the morning of surgery?

A

yes! may need dose intraop as well.

89
Q

What is lithium used for?

A

mood-stabilizer used most often with rapid cycling bipolar disorder.

90
Q

What is the MOA of lithium?

A

effects most likely related to actions on 2nd messenger systems based on phosphatidylinositol turnover, also affects transmembrane ion pumps and has inhibitory effects on adenylate cyclase

91
Q

What are the general symptoms of lithium toxicity?

A

skeletal muscle weakness, ataxia, sedation, widening of QRS complex, AV heart block, hypotension, seizures.

92
Q

What are some drugs that interact with lithium?

A

thiazide diuretics, furosemide, NSAIDs, aminophylline, ACE-I, dopamine antagonists, anticonvulsants, beta adrenergic antagonists, NMBDs

93
Q

What are the s/s of mild lithium toxicity?

A

level 1-1.5, lethargy, irritability, skeletal muscle weakness, tremor, slurred speech, nausea

94
Q

What are the s/s of moderate lithium toxicity?

A

confusion, drowsiness, restlessness, unsteady gait, coarse tremor, dysarthria, skeletal muscle fasciculations, vomiting

95
Q

What are the s/s of severe lithium toxicity?

A

impaired consciousness, delirium, ataxia, EPS, seizures, impaired renal function

96
Q

What is the most psychotropically active cannabinoid?

A

D9THC

97
Q

Do cannabinoids undergo 1st pass metabolism?

A

yes, substantial. only 10-20% ingested reaches systemic circulation

98
Q

What are toxicity symptoms of cannabinoids?

A

euphoria, relaxation, perceptual alterations, distortion of time, intensification of senses, decreased reaction time, increased appetite

99
Q

When does Neuroleptic Malignant Syndrome occur?

A

rare, related to rapid increase or over admin of high doses of antipsychotics especially HALDOL

100
Q

What are the 4 main Extrapyramidal Syndromes?

A

acute dystonia, akathisia, parkinsonism, TD

101
Q

Why do discontinuation syndromes occur?

A

after stopping of med, include n/v, anorexia, somatic distress, insomnia, anxiety, agitation.

102
Q

What are the typical symptoms of serotonin syndrome?

A

agitation, delirium, autonomic hyperactivity, hyperreflexia, clonus, and hyperthermia.

103
Q

What does serotonin syndrome resemble?

A

MH, also consider autonomic instability, excess muscle activity, and hyperthermia.

104
Q

What causes mortality with serotonin syndrome?

A

results from rhabdomyolysis–renal failure, hyperK, DIC and/or acute RDS

105
Q

What can you treat the agitation and tremor of serotonin syndrome with?

A

benzos

106
Q

What do tranquilizers block?

A

alpha adrenergic blockade=decreased PVR and hypotension

107
Q

What effect does lithium have on NDMR?

A

potentiates action

108
Q

Do patients receiving TCAs have increased or decreased anesthetic requirements?

A

increased due to elevation of NT in CNS.

109
Q

What type of side effects do TCAs have?

A

anticholinergic, coadmin of admin of tertiary amine antichoinergics may lead to postop delirium and confusion

110
Q

What are the most common antidepressants used for pain??

A

TCAs, SSRIs, SNRIs by blocking reuptake of serotonin and NE in CNS

Pharmacology Exam 4 (7 decks)

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