CNS DEPRESSION PSYCHOTICS

1. LP is a 24 yo nursing student recently diagnosed with depression. Her family asks how long should it take for
the medication to reach its maximally beneficial effect. What should they be told? Any CNS drug is going to
take 4-6 weeks to see maximal effects.

2. What are the 4 major classes of antidepressants? What is the mechanism of action for each class in treating
depression? Please list 2-3 medications in each class.
a. Tricyclic Antidepressants (FIRST GENERATION): correct imbalance in the NT concentrations of serotonin
& NE at the nerve endings in the CNS BY blocking the presynaptic reuptake- which makes it available for
transmission of nerve impulses to adjacent neurons in the brain; also affect histamine receptors;
AMITRIPTYLINE (ELAVILE), IMIPRAMINE
b. Monoamine Oxidase Inhibitors (FIRST GENERATION): These drugs inhibit the MAO enzyme system in the
CNS so amines (dopamine, serotonin, NE) are not broken down, resulting in higher levels in the brain.
ISOCARBOXAZID (MARPLAN), PHENELZINE (NARDIL), TRANYLCYPROMINE (PARNATE), SELEGILINE
(ENSAM)
c. Selective Serotonin Reuptake Inhibitors (SSRI’s): Selectively inhibit serotonin reuptake, have little or no
effect of NE or dopamine. No effect on histamine receptor; FLUOXETONE (PROZAC), PAROXETINE
(PAXIL), SERTRALINE (ZOLOFT), FLUVOXAMINE (LUVOX), CITALOPRAM (CELEXA), ESCITALOPRAM
(LEXAPRO)
d. Serotonin-norepinephrine reuptake Inhibitors: Inhibit reuptake of serotonin & NE; VENLAFAXINE
(EFFEXOR), DULOXETINE (CYMBALTA)

3. LP is started on an antidepressant. 2 weeks after starting she complains of dry mouth, dry eyes, sedation and
tachycardia. Which class was she most likely given and why are those side effects seen? LP was on first
generation drugs because these cause anticholinergic effects which include dry mouth & eyes, sedation, ↑ HR.
He was most likely taking a TCA- AMITRIPTYLINE (ELAVILE), IMIPRAMINE

4. One month into therapy LP OD’d on Amitriptyline. What side effects may be seen and what should be
monitored? Side effects of this TCA are anticholinergic effects, sedation, seizures, & CV effects, ortho
hypotension, impotence, etc. These prolong QRS waves (the longer these, the higher risk to arrhythmias)
therefore these need to be monitored.

5. PL is a 42 yo dentist recently diagnosed with depression. His family asks how long should it take for the
medication to reach its maximally beneficial effect. What should they be told? Any anti-depressant medication
takes about 4-6 weeks to see effects.

6. Why are TCAs no longer first line therapy for depression? Due to their side effects (anticholinergic effects,
sedation) & interactions- OD higher risk of death

7. TY is to be started on fluoxetine or citalopram. How does each work compare to a TCA? What is the best time
to take these medications and why? These are both SSRI’s. TCA’s work by blocking the presynaptic reuptake of
the NTs which makes it available for transmission of nerve impulses to adjacent neurons in the brain while SSRI’s
only inhibit serotonin reuptake with little or no effect of NE or dopamine. TCA’s at night (sedation), SSRI’s in the
am (activation feeling).
8. What side effects will you educate TY about with respect to taking fluoxetine or citalopram? These LACK
anticholinergic effects, cause an ‘activated feeling’, headaches, dizziness, tremor, nervousness, insomnia,
fatigue, nausea, diarrhea, constipation, dry mouth, sexual dysfunction, wt gain, wt loss, sweating, & bloating;
also make sure to take in the am

9. MAO is a 57 yo that has been receiving sertraline with little benefit. She has failed other medication in the
past. A decision is made to start her on Parnate (Tranylcypromine) or Nardil (Phenelzine), how do these
 medications work and why are they often last line? These inhibit the MAO enzyme system in the CNS so
amines (dopamine, serotonin, NE) are not broken down, resulting in higher levels in the brain. Rarely used
because they have a potential to cause hypertensive crisis when taken with tyramine and serotonin syndrome
when taken with other serotonergic meds. – need about a 14 day wash out. Also, cannot abruptly stop the SSRI
cause withdrawal will be experienced

10. What should MAO be educated about with respect to diet and use of other medications? Why? They need to
avoid anything with TYRAMINE (aged cheeses, smoke/pickled meats, yeast extracts, bananas, red wines, Italian
broad beans, ripe avocado, soy sauce, yogurt, fava beans, sour cream, etc) because there is a potential for a
hypertensive crises. Also serotonin syndrome may be a risk with other meds

11. STS is a 19 yo male that comes into the ED with myoclonus and a temp of 105. He is diagnosed with serotonin
syndrome. What are the S/S of it, what is the cause of it and how is it treated? Serotonin syndrome is a rare
collection of sxs from elevated levels of serotonin; it may occur with the use of any psychotropic drug that
enhances brain serotonin activity, if multiple drugs are taken at the same time. Sxs include: delirium, agitation,
tachycardia, sweating, myoclonus (muscle spasms), hyperreflexia, shivering, coarse, tremors, extensor plantar
muscle responses. In extreme cases: hyperthermia, seizures, rhabdomyolysis, renal failure, cardiac
dysrhythmias, disseminated intravascular coagulation. Treatment: benzos, IV fluids, cool pt down

12. AP is a 32 yo prescribed an Antipsychotic. What are the diff between “conventional” antipsychotics and
atypical ones? Please list several agents in each class. What is the mechanism of action for each class? They
both have the ↓same mechanism: blocking dopamine receptors in the brain which ↓dopamine concentration
in the CNS.
a. Conventional drugs aka typical: block dopamine receptors post-synaptically in certain areas such as
limbic system & basal ganglia- positive sxs
i. Phenothiazines: chlorpromazine
ii. Thioxanthene: thiothixine (Navane)
iii. Phenylbutylpieridines: Haloperdol (Haldol)- for long term treatment of psychosis
iv. Dihydroindolone: Molindone (Moban)
b. Atypical drugs: block dopamine 2 receptors & specific serotonin 2 (5-HT2); these are just newer with
fewer side effects. - positive & neg signs
i. Clozapine (Clozaril), Olanzapine (Zyprexa), Quetiapine (Seroquel), paliperidone (Invega),
risperidone (Risperdal), Ziprasidone (Geodon), aripiprazole (Abilify)

13. LP is a 45 yo in the ED out of control. He has a history of psychosis. Haloperidol IM is ordered. What side
effects may be seen with that? It can cause Neuroleptic malignant syndrome, EPS & tardive dyskinesia. NMS:
fever, unstable BP, myoglobinemia. EPS: common with atypicals, involuntary muscle sxs similar to those of
Parkinson’s, akathisia (distressing muscle restlessness), acute dystonia (painful muscle spasms). TD: involuntary
contractions of oral & facial muscles, choreoathetosis (wavelike movement of extremities), occurs with lon-term
therapy of antipsychotics. Along with sedation, delirium, ortho htn, syncope, dizziness, ecg changes, skin rash,
photosensitivy, dry mouth, constipation, agranulocytosis, etc.

14. DM is a 32 yo with a history of psychosis since childhood. He currently takes olanzapine. What side effects
may be seen with this medication? Olanzapine (Zyprexa) is an atypical antipsychotic. These can get these
effects but there is less risk than if taking a typical med: sedation, delirium, ortho htn, su=yncope, dizziness, ecg
changes, photosensitivity, skin rash, hyperpigmentation, pruritus, dry mouth, constipation, Urinary
hesitancy or retention, impaired erection, Leukopenia and agranulocytosis, Galactorrhea, irregular
menses, increased appetite, polydipsia, ↑ glucose & wt gain, NMS, EPS, TD

15. Why is clozapine considered a “last line” antipsychotic? This drug has agranulocytosis (wipe out of WBCs) as a
side effect