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Pharmacology Exam 4 > Psychotropic Medications > Flashcards

Psychotropic Medications Flashcards

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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
What drugs have primarily serotonergic activity?
SSRIs, TCAs, MAOIs, buspirone, lithium.
26
What is the goal of treatment of antidepressants?
remission of symptoms
27
Whats the MOA of serotonergic drugs?
unknown, but increases amount of serotonin in synapses to alter receptor signaling. (5HT receptors)
28
What are serotonin receptors responsible for?
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
29
What are serotonergic drugs used for?
major depressive disorder, bipolar depressive episodes, panic disorder, social phobia, PTSD, OCD, bulimia, neuropathic pain, migraine prophylaxis
30
What do serotonin reuptake inhibitors do?
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
31
What has more side effects? SSRIs or TCAs?
TCAs, SSRIs are safer, hard to OD
32
What is the onset for SSRIs/
1-4 weeks up to 12 for full effect
33
What are some common SSRIs?
Fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram
34
What are some side effects of SSRIs?
decreased sex drive, increased bleeding, hyponatremia, withdrawal if stopped suddenly (most common with paroxetine, least with fluoxetine)
35
What do serotonin norepinephrine reuptake inhibitors do?
inhibit NE transporter (NET) as well as SERT. lack affinity for adrenergic, histaminergic and cholinergic receptors
36
When are SNRIs preferred?
patients with heart disease
37
What are the side effects of SNRIs?
nausea, dry mouth, somnolence, headaches, sexual dysfunction.
38
What should you not take when on SNRIs?
SSRIs
39
What are some examples of SNRIs?
Pristiq, duloxetine (cymbalta), venlafaxine (effexor)
40
When are SNRIs better than SSRIs?
treating chronic pain
41
How does buspirone work?
serotonin agonist, for short-term treatment of GAD, partial agonist at serotonin receptors particularly 5-HT resulting in decreased serotonin turnover and anxiolytic effects
42
Why does buspirone not react with benzos, barbs, or alcohol?
no direct effects at GABA receptors
43
Does buspirone cause dependence?
No, but highly toxic in OD
44
When are TCAs C/I?
recent MI, long QT, dysrhythmias, CHF.
45
How do TCAs work?
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
What are some common side effects of TCAs?
postural hypotension, dysrhythmias, urinary retention
47
What is the prototype of TCAs?
amitryptiline, used as adjunct for neuropathic and somatic chronic pain
48
What are examples of TCAs?
amitriptyline, imipramine, protriptyline, doxepin
49
What are symptoms of TCA OD?
seizures, ventricular dysrhythmias, heart block hypotension
50
How do MAOIs work?
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
Are MAOIs 1st line treatment?
no, 2-3rd line because complicated SE and can be hazardous. hypotension, insomnia. 1st line for patients with atypical depression.
52
What are common MAOIs?
phenelzine, tranylcypromine
53
How do you treat the profound hypotension with MAOIs?
phenylephrine
54
What NT are with MAO-A and what are with MAO-B?
A: serotonin, dopamine, NE (60% of people); B: Tyramine, phenethylamine
55
What's the MOA of MAOIs?
form stable IRREVERSIBLE complex MAO enzyme so amount of NT available for release in CNS neurons is increased.
56
Why the profound hypotension with MAOIs?
accumulation of false NT octopamine in cytoplasm of postganglionic nerve endings. most prominent in elderly
57
Describe hypertensive crisis with MAOIs.
acute, severe rise in BP resulting in organ impairment. due to combination of MAOIs and certain drinks/foods rich in indirectly acting sympathomimetics.
58
What are the dietary restrictions while on MAOIs?
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
What are the drug restrictions while on MAOIs?
SSRIs, SNRIs, TCAs, cold/allergy meds, nasal decongestants, sympathomimetic drugs, opioids.
60
How do FGAs work?
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
What's the most and least potent FGA?
haloperidol and chlorpromazine
62
What is clozapine used for?
effective for positive and negative symptoms
63
Does clozapine cause EPS?
No
64
What is the life threatening adverse effect of clozapine?
agranulocytosis
65
What receptors do SGA block?
D2 and 5-HT receptors
66
What are the side effects of SGAs?
sedation, weight gain, orthostatic hypotension, and hyperglycemia
67
What are examples of SGAs?
quetipaine, risperidone, aripiprazole, olanzapine, ziprasidone
68
What happens when you activate 5-HT2 receptors and block them?
activate=block release of DA, block-increase release of DA
69
Is tardive dyskinesia reversible?
may be irreversible or may take years to vanish.
70
What is the incidence of TD?
53% in elderly with FGAs, 5% in elderly with SGAs, 0 with clozapine
71
What is the drug of choice in schizophrenics with moderate to severe dyskinesia?
Clozapine
72
What types of drugs are commonly used to treat bipolar and antimanic/mood stabilization?
glutamate antagonist and channel blockers: anticonvulsants valproate and carbamazepine
73
What is lamotrigine?
channel-blocking anticonvlusant that impacts glutamanergic signaling
74
What do gabapentin and pregabalin do?
anticonvulsant calcium channel subunit blocking drugs that decrease synaptic glutamate release.
75
What type of drug is ketamine?
NMDA glutamate receptor antagonist
76
What are the s/s of parkinsonism and what causes them?
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
What is the treatment for parkinsons?
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
What does levodopa do?
decrease akinesia and tremor, most effective in early therapy, life expectancy increases in duration and quality.
79
Are large or small doses of levodopa required?
large because 95% metabolized in gut and doesn't get to brain but should keep daily dose as low as possible (<600mg)
80
What are the short term side effects of levodopa?
GI--n/v, loss appetite, CV--postural hypotension, Sleep--somnolence, insomnia, vivid dreams/nightmares, inversion of sleep-wake cycle
81
What are long term side effects of levodopa?
involuntary movements--peak dose dyskinesia, diphasic dyskinesia, dystonia, response fluctuations--wearing off, unpredictable on/off, psychiatric--confusion, visual hallucinations, delusions/illusions.
82
What reverses the therapeutic effects of levodopa by increasing the peripheral metabolism of levodopa to DA?
pyridoxine (vit B6)
83
What med increases the effectiveness of levodopa?
Carbidopa, a peripheral decarboxylase inhibitor, decreases peripheral metabolism of levodopa to DA
84
What is the most effective med for parkinsons?
Sinemet 1:10 or 1:4 carbidopa:levodopa
85
What are other parkinsons disease drugs?
DDC inhibitors, COMT inhibitors, MAO-B inhibitors, dopamine agonists
86
What are the anesthetic implications with antiparkinsonian drugs?
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
What meds should you take caution with in the OR when on antiparkinsonian drugs?
fentanyl and neostigmine.
88
Should the patient continue their meds the morning of surgery?
yes! may need dose intraop as well.
89
What is lithium used for?
mood-stabilizer used most often with rapid cycling bipolar disorder.
90
What is the MOA of lithium?
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
What are the general symptoms of lithium toxicity?
skeletal muscle weakness, ataxia, sedation, widening of QRS complex, AV heart block, hypotension, seizures.
92
What are some drugs that interact with lithium?
thiazide diuretics, furosemide, NSAIDs, aminophylline, ACE-I, dopamine antagonists, anticonvulsants, beta adrenergic antagonists, NMBDs
93
What are the s/s of mild lithium toxicity?
level 1-1.5, lethargy, irritability, skeletal muscle weakness, tremor, slurred speech, nausea
94
What are the s/s of moderate lithium toxicity?
confusion, drowsiness, restlessness, unsteady gait, coarse tremor, dysarthria, skeletal muscle fasciculations, vomiting
95
What are the s/s of severe lithium toxicity?
impaired consciousness, delirium, ataxia, EPS, seizures, impaired renal function
96
What is the most psychotropically active cannabinoid?
D9THC
97
Do cannabinoids undergo 1st pass metabolism?
yes, substantial. only 10-20% ingested reaches systemic circulation
98
What are toxicity symptoms of cannabinoids?
euphoria, relaxation, perceptual alterations, distortion of time, intensification of senses, decreased reaction time, increased appetite
99
When does Neuroleptic Malignant Syndrome occur?
rare, related to rapid increase or over admin of high doses of antipsychotics especially HALDOL
100
What are the 4 main Extrapyramidal Syndromes?
acute dystonia, akathisia, parkinsonism, TD
101
Why do discontinuation syndromes occur?
after stopping of med, include n/v, anorexia, somatic distress, insomnia, anxiety, agitation.
102
What are the typical symptoms of serotonin syndrome?
agitation, delirium, autonomic hyperactivity, hyperreflexia, clonus, and hyperthermia.
103
What does serotonin syndrome resemble?
MH, also consider autonomic instability, excess muscle activity, and hyperthermia.
104
What causes mortality with serotonin syndrome?
results from rhabdomyolysis--renal failure, hyperK, DIC and/or acute RDS
105
What can you treat the agitation and tremor of serotonin syndrome with?
benzos
106
What do tranquilizers block?
alpha adrenergic blockade=decreased PVR and hypotension
107
What effect does lithium have on NDMR?
potentiates action
108
Do patients receiving TCAs have increased or decreased anesthetic requirements?
increased due to elevation of NT in CNS.
109
What type of side effects do TCAs have?
anticholinergic, coadmin of admin of tertiary amine antichoinergics may lead to postop delirium and confusion
110
What are the most common antidepressants used for pain??
TCAs, SSRIs, SNRIs by blocking reuptake of serotonin and NE in CNS

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