CRNA 844 Exam 3 - Part 3 2024/2025 EXAM QUESTIONS AND
CORRECT ANSWERS ALREADY GRADED A+ PROFESSOR
VERIFIED
1. What are common SSRIs?: Fluoxetine, Sertraline, & Paroxetine
2. What are first-line agents of choice for depression?: SSRIs - large
percentage of the population on these medications
3. What does serotonin play a crucial role in?: Neurotransmitter that helps
transmit signals between the brain & nerve cells - plays a crucial role in
regulating mood, emotions, & overall wellbeing
4. How do SSRIs work?: Inhibit the reuptake of serotonin by binding to and
blocking serotonin transporters on the neuron's surface
5. Do SSRIs have anticholinergic activity? Do the affect cardiac function?:
No
6. What are side effects of SSRIs?: headache, agitation, insomnia
7. What can SSRIs do to the cytochrome P450 system? What does this
mean?-
: Inhibit
May need higher doses of prodrugs but lower doses of everything else
8. What does inhibition of CYP 2D6 cause?: Prevents conversion of codeine
to morphine and reduces the metabolism of oxycodone & hydrocodone
,9. What does inhibition of CYP 3A4 cause?: Prevents metabolism of opioids,
benzos, & local anesthetics - need to decrease dose
10. What are anesthetic considerations of SSRIs?: Hypotension, arrhythmias,
impaired thermoregulation, & shivering
11. How do SNRIs work? What are they used for?: Block reuptake of both
serotonin & norepinephrine Chronic pain - fibromyalgia
12. What are examples of SNRIs? What are the side effects similar to?:
Duloxetine (Cymbalta) & venlafaxine (Effexor)
SSRIs
13. What are tricyclic antidepressants (TCAs) used for?: Depression & chronic
pain syndrome
14. When did the use of TCAs begin? SSRIs?: 1950s
1980s
15. How do TCAs work?: Work at nerve synapses by blocking neuronal reuptake
of catecholamines, serotonin, or both
16. What are side effects of TCAs?: Anticholinergic (antimuscarinic) actions: dry
mouth, blurred vision, prolonged gastric emptying, & urinary retention
Quinidine-like cardiac effects: tachycardia, T-wave flattening or inversion, and
prolongation of the PR, QRS, & QT intervals
17. What are anesthetic considerations of TCAs?: Exaggerated response to
both indirect-acting vasopressors & sympathetic stimulation
18. Why is an OD of TCAs more dangerous than SSRIs?: More receptor types
effects
19. What are special characteristics of desipramine & nortiptyline?: Less
sedating
Fewer side effects
20. What do amitriptyline, imipramine, protriptyline, amoxapine, doxepin, &
trimipramine have in common?: Most sedative properties
21. What is clomipramine used for?: OCD
, 22. What does amitriptyline have?: Most profound anticholinergic effects
23. What does doxepin have?: Fewest cardiac effects
24. What to MAOIs block?: oxidative deamination of naturally occurring amines
25. What are the 2 types of MAO isoenzymes? What is each selective for?: -
MAO-A: serotonin, dopamine, & norepinephrine
MAO-B: dopamine & phenylephrine
26. What were MAOIs the first to treat? Are they still used?: Depression
No longer considered first or second line agents d/t side effects - used infrequently
today
27. What are side effects of MAOIs?: Orthostatic hypotension, agitation, tremor,
seizures, muscle spasms, urinary retention, paresthesia, jaundice, &
hypertensive crisis
28. What causes hypertensive crisis in patients on MAOIs? How?: Eating
tyramine containing foods (cheeses & red wines)
Tyramine is used to generate norepinephrine - normally dietary tyramine is broken
down by intestinal MAO during absorption & hepatic MAO during initial circulation
through the liver - when on MAO this is blocked and tyramine is not broken down
and builds up to excessive levels in the body
29. What are examples of MAOIs?: Isocarboxazid (Marplan)
Phenelzine (Nardil)
Selegiline (Emsam)
Tranylcypromine (Parnate)
30. What can Phenelzine (Nardil) cause?: Decreased plasma cholinesterase &
prolong DOA of succinylcholine
31. What should be used in caution in patients on MAOI? What should not
be administered? Why?: Opioids
CORRECT ANSWERS ALREADY GRADED A+ PROFESSOR
VERIFIED
1. What are common SSRIs?: Fluoxetine, Sertraline, & Paroxetine
2. What are first-line agents of choice for depression?: SSRIs - large
percentage of the population on these medications
3. What does serotonin play a crucial role in?: Neurotransmitter that helps
transmit signals between the brain & nerve cells - plays a crucial role in
regulating mood, emotions, & overall wellbeing
4. How do SSRIs work?: Inhibit the reuptake of serotonin by binding to and
blocking serotonin transporters on the neuron's surface
5. Do SSRIs have anticholinergic activity? Do the affect cardiac function?:
No
6. What are side effects of SSRIs?: headache, agitation, insomnia
7. What can SSRIs do to the cytochrome P450 system? What does this
mean?-
: Inhibit
May need higher doses of prodrugs but lower doses of everything else
8. What does inhibition of CYP 2D6 cause?: Prevents conversion of codeine
to morphine and reduces the metabolism of oxycodone & hydrocodone
,9. What does inhibition of CYP 3A4 cause?: Prevents metabolism of opioids,
benzos, & local anesthetics - need to decrease dose
10. What are anesthetic considerations of SSRIs?: Hypotension, arrhythmias,
impaired thermoregulation, & shivering
11. How do SNRIs work? What are they used for?: Block reuptake of both
serotonin & norepinephrine Chronic pain - fibromyalgia
12. What are examples of SNRIs? What are the side effects similar to?:
Duloxetine (Cymbalta) & venlafaxine (Effexor)
SSRIs
13. What are tricyclic antidepressants (TCAs) used for?: Depression & chronic
pain syndrome
14. When did the use of TCAs begin? SSRIs?: 1950s
1980s
15. How do TCAs work?: Work at nerve synapses by blocking neuronal reuptake
of catecholamines, serotonin, or both
16. What are side effects of TCAs?: Anticholinergic (antimuscarinic) actions: dry
mouth, blurred vision, prolonged gastric emptying, & urinary retention
Quinidine-like cardiac effects: tachycardia, T-wave flattening or inversion, and
prolongation of the PR, QRS, & QT intervals
17. What are anesthetic considerations of TCAs?: Exaggerated response to
both indirect-acting vasopressors & sympathetic stimulation
18. Why is an OD of TCAs more dangerous than SSRIs?: More receptor types
effects
19. What are special characteristics of desipramine & nortiptyline?: Less
sedating
Fewer side effects
20. What do amitriptyline, imipramine, protriptyline, amoxapine, doxepin, &
trimipramine have in common?: Most sedative properties
21. What is clomipramine used for?: OCD
, 22. What does amitriptyline have?: Most profound anticholinergic effects
23. What does doxepin have?: Fewest cardiac effects
24. What to MAOIs block?: oxidative deamination of naturally occurring amines
25. What are the 2 types of MAO isoenzymes? What is each selective for?: -
MAO-A: serotonin, dopamine, & norepinephrine
MAO-B: dopamine & phenylephrine
26. What were MAOIs the first to treat? Are they still used?: Depression
No longer considered first or second line agents d/t side effects - used infrequently
today
27. What are side effects of MAOIs?: Orthostatic hypotension, agitation, tremor,
seizures, muscle spasms, urinary retention, paresthesia, jaundice, &
hypertensive crisis
28. What causes hypertensive crisis in patients on MAOIs? How?: Eating
tyramine containing foods (cheeses & red wines)
Tyramine is used to generate norepinephrine - normally dietary tyramine is broken
down by intestinal MAO during absorption & hepatic MAO during initial circulation
through the liver - when on MAO this is blocked and tyramine is not broken down
and builds up to excessive levels in the body
29. What are examples of MAOIs?: Isocarboxazid (Marplan)
Phenelzine (Nardil)
Selegiline (Emsam)
Tranylcypromine (Parnate)
30. What can Phenelzine (Nardil) cause?: Decreased plasma cholinesterase &
prolong DOA of succinylcholine
31. What should be used in caution in patients on MAOI? What should not
be administered? Why?: Opioids
