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2-Pharm Final > Antidepressant drugs and Serotonin receptors > Flashcards

Antidepressant drugs and Serotonin receptors Flashcards

1
Q

What is the components of most “antidepressants”?

A

Most drugs classified as “antidepressants” impact either serotonergic neurotransmission or noradrenergic (norepinephrine) neurotransmission

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2
Q

What do serotonin drugs do?

A

increase amount of serotonin in CNS synapses or by altering serotonin receptor signaling

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3
Q

What do serotonin signalling mediate?

A

by large family of serotonin receptors located within the CNS (6 of these receptor-types signal via excitatory or inhibitory G proteins and 1 [5-HT3] is ligand-gated ion channel)

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4
Q

Define serotonin?

A

a neurotransmitter; within the CNS, influences mood, sleep, aggression, appetite, sex, and memory

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5
Q

What is the components of serotonin reuptake inhibitors?

A

consist of several classes of medications which bind and inhibit the serotonin transporter protein (SERT) which blocks reuptake of serotonin from synaptic cleft into the presynaptic neuron – leads to enhanced serotonergic neurotransmission

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6
Q

Define the drug classes involved in serotonin reuptake inhibitors.

A

selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic-serotonin reuptake inhibitors

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7
Q

What are adverse effects of serotonin reuptake inhibitors?

A

insomnia, agitation, headache, nausea, diarrhea

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8
Q

What are serios adverse effects of serotonin reuptake inhibitors?

A

increased suicidality; sudden discontinuation may precipitate withdrawal symptoms – dizziness, increased irritability, insomnia, visual disturbances, paresthesias/”brain zaps”: shock-like sensations in the head; withdrawal symptoms resolve with reintroduction of SRI medication; increased bleeding risk, hyponatremia

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9
Q

What is important about the discontinuation of serotonin reuptake inhibitors?

A

Outpatient SRI medications should be continued in acute care settings & not discontinued abruptly; must be tapered if discontinued

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10
Q

Define Serotonin syndrome.

A

attributed to toxic levels of synaptic & extracellular serotonin; presents with classic triad: neuromuscular excitability, autonomic nervous system excitability, & mental status changes

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11
Q

What are the neuromuscular components of Serotonin syndrome?

A

Neuromuscular excitability: hyperreflexia, clonus, myoclonus, rigidity

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12
Q

What are the autonomic components of Serotonin syndrome?

A

diarrhea, tachycardia, hypertension, fever, diaphoresis, flushing, mydriasis

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13
Q

What are the Mental status components of Serotonin syndrome?

A

insomnia, agitation, anxiety, confusion, coma

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14
Q

What are the Severe cases components of Serotonin syndrome?

A

life-threatening hyperpyrexia, rigidity leading to rhabdomyolysis, multiorgan failure, DIC

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15
Q

What is the cause of Serotonin syndrome?

A

Serotonin syndrome typically results from combo of different classes of serotonergic medications; most dangerous combo: SRI w/MAO inhibitor drug; rarely results from single serotonergic medication at therapeutic dose

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16
Q

What other drugs can trigger Serotonin syndrome?

A

nonpsychiatric/nonserotonergic, may trigger serotonin syndrome in conjunction with SRI or other serotonergic drugs: linezolid; methylene blue; lithium; opioids (tramadol, fentanyl, dextromethorphan); stimulants (amphetamine, methamphetamine, methylphenidate, phentermine); muscle relaxants (cyclobenzaprine); recreational drugs (ecstasy)

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17
Q

What is true about drug interactions that can lead to Serotonin syndrome?

A

Drugs that cause rapid elevation in serum level of SRI medications via drug interaction (ciprofloxacin, fluconazole, ritonavir, & erythromycin) may lead to serotonin syndrome

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18
Q

Where is Serotonin syndrome a concern?

A

Serotonin syndrome is of particular concern in the PACU or ICU as serotonergic agonists (known or unknown) may have been administered during surgery & used during anesthesia

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19
Q

When do symptoms for Serotonin syndrome develop?

A

Symptoms typically develop acutely within hours after introduction of causative medication

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20
Q

What do the symptoms of Serotonin syndrome resemble?

A

Symptoms can resemble alcohol withdrawal, encephalitis, & neuroleptic malignant syndrome

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21
Q

What is the treatment for Serotonin syndrome?

A

discontinue serotonergic drug (s), initiate supportive care, benzodiazepine, IV fluids, cooling; life-threatening cases may require paralysis, intubation, & ventilation

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22
Q

What are examples of Selective serotonin reuptake inhibitors?

A

fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram, & escitalopram

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23
Q

What do Selective serotonin reuptake inhibitors (fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram, & escitalopram) block?

A

Selectively block neuronal reuptake of serotonin

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24
Q

What is the first line therapy for majority of depressive and anxiety disorders?

A

Selective serotonin reuptake inhibitors (fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram, & escitalopram)

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25
Q

How do various SSRIs differ?

A

differ from each other on basis of anticholinergic effects, elimination half-time, & pharmacokinetic interactions – some are potent inhibitors of CYP450 enzymes which can lead to significant risk of drug-drug interactions

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26
Q

What are specific side effects of Citalopram?

A

may cause dose-dependent QT interval prolongation, increases risk for torsades de pointes; escitalopram also can cause prolonged QT interval, but to less degree

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27
Q

What are Tricyclic antidepressant drugs examples?

A

desipramine, nortriptyline, amitriptyline, imipramine, clomipramine

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28
Q

What do Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) do?

A

These drugs block reuptake of serotonin and/or norepinephrine at presynaptic terminals – increases availability of these neurotransmitters within the CNS

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29
Q

What is the clinical use of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine)?

A

Highly effective antidepressant medications but are no longer considered 1st line d/t unfavorable side effect profile resulting from anticholinergic & antihistamine properties

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30
Q

What are side effects groups of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine)?

A

Side effect groups: anticholinergic effects, cardiovascular effects, & CNS effects

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31
Q

What are the anticholinergic side effects of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine)?

A

dry mouth, blurred vision, tachycardia, urinary retention, slowed gastric emptying, ileus; elderly more sensitive to effects;

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32
Q

How does anticholinergic toxicity occur?

A

; anticholinergic toxicity can result from polypharmacy with more than one anticholinergic drug (TCA + OTC drug w/anticholinergic effects [tx of diarrhea or insomnia])

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33
Q

What are the cardiovascular effects of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine)?

A

orthostatic hypotension, modest increases in heart rate

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34
Q

What are the CNS effects of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine)?

A

sedation, weakness, fatigue; TCAs lower seizure threshold; TCAs may enhance the CNS-stimulating effects of enflurane

35
Q

How are Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) metabolized?

A

CYP450 IA2 enzymes

36
Q

What drugs can increase Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) concentrations?

A

Drugs that inhibit CYP450 IA2: verapamil, cimetidine

37
Q

What drugs could reduce & duration of action Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine)?

A

Drugs that induce CYP450 IA2: rifampin, omeprazole, insulin, barbiturates, & carbamazepine

38
Q

What is the relationship between Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) and sympathomimetics?

A

Patients recently started on TCAs may demonstrate exaggerated pressor response to direct-acting or indirect-acting sympathomimetics (phenylephrine/ephedrin)

39
Q

Pressor response may be more pronounced ________

A

w/indirect-acting drug (ephedrine)

40
Q

Titrating smaller-than-usual doses of _______ recommended

A

direct-acting sympathomimetic

41
Q

What is the dose of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) and sympathomimetics for chronic use ?

A

Pts chronically tx w/TCAs >6 weeks, can administer either direct or indirect-acting sympathomimetic, decrease dose to 1/3 usual dose

42
Q

What may not be effected with chronic use of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) and sympathomimetics?

A

Pts chronically tx w/TCAs: conventional sympathomimetics (phenylephrine, ephedrine) may not be effective in tx hypotension d/t catecholamine depletion, may require potent direct-acting sympathomimetic (norepinephrine)

43
Q

What is the interaction of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) and anticholinergics?

A

Pts receiving TCA + an anticholinergic drug preop are more susceptible to postop delirium & confusion (central anticholinergic syndrome) – less likely w/glycopyrrolate

44
Q

What is the interaction of Tricyclic antihypertensives drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) and anticholinergics?

A

rebound HTN from sudden DC of clonidine can be more intense in pts taking TCA

45
Q

What is the interaction of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) and MAOIs?

A

Combination of a TCA & MAOI may result in fatal serotonin syndrome; combining TCAs & MAOIs are relatively contraindicated

46
Q

What is a life threatening situation with Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine)?

A

TCA overdose

47
Q

What is the s/s of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine) overdose?

A

CNS & cardiac toxicity; can cause intractable myocardial depression & ventricular arrhythmias; may initially see agitation, seizures, hypoventilation, hypotension, QRS prolongation

48
Q

What is the treatment for CNS symptoms of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine?

A

Airway support, benzodiazepine, possibly phenytoin for seizures

49
Q

What is the treatment for cardiotoxicity symptoms of Tricyclic antidepressant drugs (desipramine, nortriptyline, amitriptyline, imipramine, clomipramine?

A
  • Alkalinize plasma – sodium bicarbonate, hyperventilation
  • lidocaine, phenytoin for ventricular arrhythmias
  • atropine, sympathomimetics, inotropic drugs may still be used if slow cardiac rhythm & hypotensive despite fluid administration
50
Q

What are MOA inhibitors?

A

phenelzine (Nardil), isocarboxazid (Marplan), tranylcypromine (Parnate) moclobemide, selegiline (Eldepryl/Zelapar),

51
Q

What is the function of Monoamine oxidase inhibitors (phenelzine (Nardil), isocarboxazid (Marplan), tranylcypromine (Parnate) moclobemide, selegiline (Eldepryl/Zelapar)?

A

block the enzyme monoamine oxidase (MAO) – especially cerebral neuronal MAO, which metabolizes amines: serotonin, epinephrine, norepinephrine, dopamine

52
Q

What are the two forms of MAO?

A

MAO-A deaminates serotonin, epinephrine, norepinephrine, dopamine

53
Q

What do MAOIs result in?

A

increased amounts of neurotransmitter available for release from CNS neurons and also within the sympathetic nervous system

54
Q

What re the adverse effects of MAOIs (phenelzine (Nardil), isocarboxazid (Marplan), tranylcypromine (Parnate) moclobemide, selegiline (Eldepryl/Zelapar)?

A

orthostatic hypotension (elderly); pts taking MAOIs may require dietary tyramine restriction b/c MAO inhibition prevents dietary tyramine metabolism & produce indirect sympathomimetic response & HTN (dietary tyramine can then enter systemic circulation & be taken up by sympathetic nervous system nerve endings resulting in release of endogenous catecholamines and result in HTN, hyperpyrexia, poss CVA)

55
Q

What medications do MAOIs (MAOIs (phenelzine (Nardil), isocarboxazid (Marplan), tranylcypromine (Parnate) moclobemide, selegiline (Eldepryl/Zelapar)) adverse interact wtih?

A

opioids, ephedrine, TCAs, & SSRIs: HTN crisis, serotonin syndrome

56
Q

What is imperative to recognize about MAOIs?

A

***it is imperative to identify MAOI medications on the patient medication list during the preanesthetic evaluation to incorporate this data into the patient’s anesthetic plan

57
Q

What is the FDA warning with Opioids?

A

FDA warning – risk of serotonin syndrome for all opioid medications administered w/serotonergic drugs

58
Q

What can happen withh MAOIs and meperidine?

A

MAOIs & meperidine can result in an excitatory response (agitation, HA, skeletal muscle rigidity) or depressive response (hypotension, hypoventilation, coma);

59
Q

adverse rxns of MAOIs can also occur w/ _____________, __________, _________

A

fentanyl, sufentanil, alfentanil but incidence less than meperidine

60
Q

What is the response of Monoamine oxidase inhibitor drug interactions given with ephedrine?

A

Potential for exaggerated hypertensive response to indirect-acting pressor (ephedrine) administration d/t increased release of norepinephrine from neuronal nerve endings

61
Q

What symmpathomimetic is okay to treat hypotension for a patient with MAIOs?

A

Direct-acting sympathomimetic preferred (phenylephrine); receptor hypersensitivity may result in exaggerated pressor response to phenylephrine

62
Q

What is the recommended dose of phenylephrine when given with MAOIs?

A

Decrease dose of phenylephrine to 1/3 of normal dose, titrate additional doses to cardiovascular response

63
Q

What is the S/S of MAOIs overdose?

A

reflected in signs of excessive SNS activity (tachycardia, hyperthermia, mydriasis, seizures, coma)

64
Q

What is the treatment for MAOIs overdose?

A

tx supportive; Dantrolene has possible role in treatment of hypermetabolic signs asso/w MAOI overdose

65
Q

What is the recommendation for MAOIs during the preop phase?

A

No longer recommended to hold MAOIs preoperatively; recommendation is to continue these meds preoperatively & avoid administration of drugs w/interactions, especially meperidine

66
Q

What is important to know about the anesthetic technique for MAOIs?

A

minimize SNS stimulation or drug-induced hypotension; regional anesthesia acceptable

67
Q

What should be avoided for hypotension treatment with MAOIs?

A

avoid ephedrine in tx hypotension)

68
Q

What is the indication for Lithium?

A

Current use: bipolar disorders, treatment-resistant depressive disorder

69
Q

What is the history of Lithium use?

A

Used in treatment of mood disorders since the 1890s

70
Q

What is the pk of Lithium?

A

Has narrow therapeutic index & significant potential for toxicity & drug interactions

71
Q

What is true about the plasma concentrations of Lithium?

A

Safe & effective use can be achieved only by monitoring lithium plasma concentrations

72
Q

How often do blood levels need to be monitored with Lithium?

A

Lithium blood levels, electrolytes, BUN/creatinine, & TSH should be measured every 6 months

73
Q

What are renal effects of Lithium?

A

nephrogenic diabetes insipidus (polyuria) resulting in hypovolemia, hypernatremia, hyperchloremic metabolic acidosis, distal renal tubular acidosis; chronic kidney disease can develop with chronic lithium therapy

74
Q

What endocrine dx can Lithium cause?

A

hypothyroidism

75
Q

Lithium May cause serotonin syndrome when combined with ____ or ______

A

SRIs or MAOIs

76
Q

What is the anesthetic requirements with lithium?

A

Anesthetic requirements for injected & inhaled drugs could be decreased (sedation w/lithium therapy)

77
Q

What can lithium prolong?

A

prolonged responses to depolarizing & nondepolarizing neuromuscular blocking drugs with lithium therapy

78
Q

What is lithium toxicity?

A

may occur with increased plasma concentrations (diuretic therapy, NSAIDs, sodium restriction or sodium wasting)

79
Q

What occurs with lithium levels of Mild (lithium level 1.0-1.5)?

A

sedation, skeletal muscle weakness, widened QRS complex on ECG, slurred speech, nausea

80
Q

What occurs with lithium levels of Moderate (lithium level 1.6-2.5?

A

confusion, drowsiness, tremor, skeletal muscle fasciculations

81
Q

What occurs with lithium levels of Moderate Severe (lithium level >2.5)?

A

impaired consciousness, coma, delirium, ataxia, extrapyramidal symptoms, seizures, impaired renal function

82
Q

What lithium level can cause cardiac effects?

A

AV heart block, hypotension, cardiac dysrhythmias may occur at lithium levels > 2mEq/L

83
Q

What is the treatment of lithium toxicity?

A

Treatment: hemodialysis; if adequate renal function, lithium excretion accelerated by osmotic diuresis & IV sodium bicarbonate

2-Pharm Final (10 decks)

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