Neural Sciences & Psychopharmacology Prescribing Principles

MOD 1 Neural Sciences & Psychopharmacology Prescribing Principles

1. -Review how the amygdala part of the brain is involved in involved in production of
anxiety.
The AMYGDALA produces anxiety when identifying any threats .

2. Review neurotransmitters associated with depression
a. Too little norepinephrine has been associated with depression
b. Too little serotonin is associated with depression
c. Too little dopamine is associated with some forms of depression
d. Others mentioned, not likely to be on the exam IMO because there was little focus on
them this term:
i. Too much acetylcholine is associated with depression
ii. High levels of glutamate contribute to depression
3. -Review neurotransmitters associated with antipsychotic medications
Dopamine for FGA’s; Dopamine and Serotonin for SGA’s
4. -Review over Chapter 29 “General principles of psychopharm treatment”
▫ Pharmacokinetics – what the body does to the drug
▫ Pharmacodynamics = what the drug does to the body
▫ Inducers – speed up the metabolism (breakdown) of the drug, thereby lowering serum levels
1. A common one that is mentioned often – Tegretol and birth control
(Tegretol induces birth control, can lower level and lead to an unwanted
pregnancy)
▫ Inhibitors – slow down the metabolism of the drug, thereby increasing serum levels

5. -What is a common mistake leading to an unsuccessful antidepressant drug trial?
▫ Too low a dosage for too short a time. Unless adverse events prevent it, the dosage of an
antidepressant should be raised to the maximum recommended level and maintained at that
level for at least 4 or 5 weeks before a drug trial is considered unsuccessful.


Module 2 – Antidepressants

1. What role does Serotonin have in in the different aspects of depression?
▫ Diffuse serotonin dysfunction drives the increase in negative affect (depressed mood, guilt,
disgust, fear, anxiety, hostility, irritability and loneliness).

▫ Enhancing serotonin function may improve information processing in the circuits that
hypothetically mediate this cluster of symptoms.

2. Which neurotransmitters have been implicated in depression?
a. Serotonin (SSRI’s)
b. Norepinephrine (SNRI’s, NDRIs)
c. Dopamine (NDRIs)
3. General information or education you would provide a patient about starting any
antidepressant medication
a. Give it 4-6 weeks to take effect
b. Common adverse effects:
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i. Headache/Dizziness
ii. Dry Mouth
iii. QT prolongation
iv. Nausea
v. Possible insomnia/hypersomnia
vi. Agitation/anxiety
vii. Sedation
viii. GI distress (Diarrhea or constipation)
ix. Sexual dysfunction
c. S/S serotonin syndrome
1. 🡪
4. Which of the SSRIs has an indication for the treatment of bulimia to decrease binging
patterns?
a. Fluoxetine/Prozac
i. “flu-blu”
5. Mechanism of action of SSRIs & SNRIs
a. Inhibits reuptake of the neurotransmitter, leaving more behind in the synaptic cleft.

6. Review over discontinuation syndrome
a. SSRI Withdrawal – Don’t stop abruptly, taper slowly. Discontinuation sx: flu-like sx,
fatigue & lethargy, weakness, decreased concentration, N/V, impaired memory, shock-
like sensations (aka “brain-
zaps“, acute return of major depressive episode, return of
anxiety if that’s what was being treated, irritability, anxiety, insomnia, crying w/o
provocation, dizziness & vertigo
b. Paroxetine (Paxil) is the most common SSRI with venlafaxine (Effexor) being the next
most likely to cause this syndrome with abrupt discontinuation.
c. Fluoxetine (Prozac) is least likely.
d. The withdrawal symptoms are typically flu-like or neurologic. For patients with
compliance issues, a SSRI such as Fluoxetine (Prozac) is likely a good choice to avoid
recurrent discontinuation syndrome symptoms.

7. Sexual side effects to SSRIs—Possible interventions for decreased sex drive?
a. For a reduction in sexual side effects which are common with SSRIs, SNRIs and TCAs,
bupropion

8. Which of the SSRIs is highest risk of drug drug interactions due to CYP enzymes?
a. SSRIs who have the most significant enzyme inhibitors are fluoxetine (Prozac),
fluvoxamine (Luvox) and paroxetine (Paxil).
b. Duloxetine (Cymbalta) has the greatest potential for inhibition of metabolism of other
drugs among the SNRIs. St. John’s Wart can also decrease the efficacy of some
medications.

9. Mechanism of action of TCAs
▫ Blocks NE and 5-HT, thus increasing synaptic concentrations of these NT’s.

10. Side effects you would be most concerned about related to the TCAs
▫ Anticholinergic effects – dry mouth, constipation, blurred vision, urinary retention, delirium.
Also cardiac issues and sexual dysfuction.
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11. Risks with patients being on a TCA?
▫ Not used for treatment of depression very much anymore. Too many anticholinergic side
effects, and too sedating. You might use them if a patient has failed SSRIs, or has had several
several med trials.

▫ Amitriptyline (Elavi)l – don’t give to a pt who is suicidal

12. Mechanism of action of MAOIs
▫ Primarily metabolizes NE, 5-HT, epinephrine, DA, and tyramine. So it prevents the breakdown
of tyramine. Unfortunately, it also blocks the ability of foods with tyramine to be broken down.
If you can’t break down tyramine, you can develop a toxic level of it, which causes the
hypertensive crisis.

13. Side effects you would be most concerned about with the MAOIs
▫ Orthostatic HoTN; Insomnia; weight gain; edema; sexual dysfunction; several drug interactions
(serotonin syndrome risk)

▫ Tyramine-induced HTN crisis (with tyramine containing foods)

14. Patient education that is important related to the MAOIs
▫ Avoid tyramine-containing foods: Sauerkraut; Alcohol (beer, wine); Cured meats (sausage,
salami, pepperoni, hot dog, bologna, smoked fish); bananas; avocados; pickled foods; figs,
raisins; chocolate; yeast; aged cheese (aged cheddar, swiss, parmesan, blue cheese).

▫ Serotonin syndrome is most severe when a SSRI is combined with a MAOI. Typically seen in
combination.

15. Treatment considerations before starting an MAOI with regard to other
medications/risks
▫ WASH OUT: You have to wait a period of time, a few days with other antidepressant types to
make sure they have cleared, before starting an MAOI;

Module 3 – Anxiolytics & Hypnotics

16. Review generalized anxiety, social anxiety, panic disorder, OCD & PTSD (generally be
able to identify each)

a. GAD
i. Excessive anxiety and worry, occurring more days than not, for at least 6
months, about multiple events/activities
ii. The individual finds it difficult to control the worry.
iii. The anxiety and worry are associated with three or more of the following 6 sx (1
for kids):
1. Restlessness or feeling keyed up or on edge
2. Being easily fatigued
3. Difficulty concentrating, or mind going blank
4. Irritability
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5. Muscle tension
6. Sleep disturbance (can’t fall asleep or stay asleep, or restless unsatisfying
sleep).
iv. The anxiety interferes with daily functioning (this makes it pathological).
b. Social Anxiety
i. Individuals with social anxiety d/o often have anticipatory anxiety that is focused
on upcoming social situations in which they must perform or be evaluated by
others, whereas individuals with generalized anxiety disorder worry, whether or
not they are being evaluated.
c. Panic d/o
i. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense
fear or intense discomfort that reaches a peak within minutes, and during which
time 4 or more sx occur:
1. Palpitations, pounding heart, or accelerated heart rate
2. Sweating
3. Trembling or shaking
4. Sensations of SOB or smothering
5. Feelings of choking
6. Chest pain or discomfort
7. Nausea or abdominal distress
8. Feeling dizzy, unsteady, light-headed, or faint
9. Chills or heat sensations
10. Paresthesias (numbness or tingling sensations)
11. Derealization (feelings of unreality) or depersonalization (being detached
from one-self)
12. Fear of losing control or “going crazy”
13. Fear of dying
ii. At least one of the attacks has been followed by 1 month (or more) of one or both
of the following:
1. Persistent concern or worry about additional panic attacks
2. A significant maladaptive change in behavior r/t the attacks (behaviors
designed to avoid having panic attacks)

d. OCD
i. Obsessive-compulsive disorders are set apart by an array of recurrent obsessive
ideas or compulsive actions that significantly interfere with daily functioning.
ii. Obsessions are persistent thoughts, images or impulses experienced as alien
intrusions that must be neutralized or suppressed, e.g., obscene or blasphemous
thoughts, repugnant sexual images, unrealistic doubts about whether something
has been done correctly.
iii. Compulsions are repetitive, purposeful behaviors performed in response to an
obsession or according to certain rules.
iv. Researchers using neuroimaging have discovered abnormal brain structure and
activity in patients with OCD. The abnormality apparently lies mainly in a pathway
that links the frontal lobes of the cerebral cortex with the basal ganglia. MRI
suggests a loss of tissue in the caudate nuclei, areas in the basal ganglia that
filter messages, fails to dampen the obsessional thinking.
e. PTSD
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Post-traumatic stress disorder (PTSD) is the injury that results from a traumatic event
that overwhelms a person’s coping mechanisms.

17. Review which medications are used to treat each of these types of anxiety disorders,
OCD, and PTSD.
f. GAD
i. Venlafaxine is approved by the FDA for treatment of generalized anxiety disorder
and may be useful in panic disorder combined with depression.
ii. FDA approved meds (from Stahl index): alprazolam, duloxetine, escitalopram,
paroxetine, venlafaxine
iii.
g. Social Anxiety
i. FDA approved meds: fluvoxamine, paroxetine, sertraline, venlafaxine
ii. Clonidine has an off-label use for social anxiety d/o.
h. Panic d/o
i. Treatment of panic disorder combines cognitive-behavioral therapy, self-
management techniques, and medications, including antidepressants and
anxiolytic agents.
1. The clinician needs to address the patient’s catastrophic misinterpretation
of panic symptoms, such as their beliefs that they may die or that the
attacks produce physical harm. They need to be taught appropriate
cognitive interventions.
ii. Alprazolam (Xanax) and paroxetine (Paxil) are the two drugs approved by the US
Food and Drug Administration (FDA) for the treatment of panic disorder.
iii. In general, experience is showing superiority of the selective serotonin reuptake
inhibitors (SSRIs) and clomipramine (Anafranil) over the benzodiazepines,
monoamine oxidase inhibitors (MAOIs), and tricyclic and tetracyclic drugs in
terms of effectiveness and tolerance of adverse effects.
iv. Some reports have suggested a role for venlafaxine (Effexor), and buspirone
(BuSpar) has been suggested as an additive medication in some cases.
v. Venlafaxine is approved by the FDA for treatment of generalized anxiety disorder
and may be useful in panic disorder combined with depression.
vi. FDA approved meds: alprazolam, clonazepam, fluoxetine, paroxetine, sertraline
i. OCD
i. The standard treatments for obsessive-compulsive disorder are behavior therapy
and medications.
ii. Therapists may train the patient in “thought stopping” therapy (when the
obsessive thought encroaches, the patient says “stop”) or saturation therapy (in
which the client concentrates so intensely on the obsessive thought that it loses
its compelling quality).
iii. The standard approach is to start treatment with a SSRI or clomipramine and
then move to other pharmacological strategies if the serotonin-specific drugs are
not effective.
iv. The serotonergic drugs have increased the percentage of patients with OCD who
are likely to respond to treatment to the range of 50 to 70 percent.
v. Generally speaking meds you will see used in treating OCD usually are the
SSRIs, chiefly fluoxetine/Prozac, fluvoxamine/Luvox, sertraline/Zoloft or
paroxetine/Paxil.
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1. These inhibit the reuptake (reabsorption) of the neurotransmitter
serotonin.
vi. Unfortunately, patients usually relapse unless they go on taking the drug
indefinitely. Compliance by patients can be a problem in that many patients with
OCD are also reluctant to take drugs.
vii. FDA approved meds: clomipramine, fluoxetine, fluvoxamine, paroxetine,
sertraline
j. PTSD
i. Selective serotonin reuptake inhibitors (SSRIs), such as sertraline (Zoloft) and
paroxetine (Paxil), are considered first-line treatments for PTSD, due to their
efficacy, tolerability, and safety ratings.
ii. SSRIs reduce symptoms from all PTSD symptom clusters and are effective in
improving symptoms unique to PTSD, not just symptoms similar to those of
depression or other anxiety disorders.
iii. Buspirone (BuSpar) is serotonergic and may also be of use.
iv. The efficacy of imipramine (Tofranil) and amitriptyline (Elavil), two tricyclic drugs,
in the treatment of PTSD is supported by a number of well-controlled clinical
trials.
1. Although some trials of the two drugs have had negative findings, most of
these trials had serious design flaws, including too short a duration.
2. Dosages of imipramine and amitriptyline should be the same as those
used to treat depressive disorders, and an adequate trial should last at
least 8 weeks.
v. Although you will see antipsychotics used in practice for the treatment of PTSD
there are almost no positive data concerning the use of antipsychotic drugs in the
disorder.
vi. FDA approved meds: paroxetine, sertraline

18. Possible treatment for test anxiety—What patient education would you include about
this medication?
Propanolol-take 1 hr before test

19. Treatment for PTSD nightmares
k. Prazosin
2. “non-addictive” medication choices to assist with anxiety treatment
a. Buspar
3. Review over the general prescribing guidelines for benzodiazepines.
a. In pre-anesthetic doses, decreases blood pressure and increases heart rate
b. Tolerance occurs with all benzodiazepines
c. Benzodiazepines vary greatly in duration of action
d. Short acting – better hypnotics with reduced hang-over effect upon wakening
e. Long acting – better anxiolytics and anticonvulsant drugs
f. Withdrawal symptoms typically mimic those of anxiety disorders
g. Gradually taper to d/c, esp if on med x6 months. Work with your patient, make a plan,
know that it can take awhile, go off of it slowly.
i. When used for short periods (1-2 weeks) in moderate dosages, they usually have
no significant tolerance, dependence, or WDL effects.
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1. Short acting benzos may be exception to the rule; some persons may
have increased aneity 1 day after stopping a single dose.
ii. When the med is d/c’d, the drug must be tapered slowly (25%/week), otherwise
reoccurrence or rebound sx are likely.
4. Review over the patient education you would provide for benzodiazepines.
a. High potential for abuse; psychological and physical dependence. –
i. WDL sx
b. Gradually taper to d/c, esp if on med x6 months.
c. CNS Effects: -drowsiness, -ataxia, -fatigue, -confusion.
d. Geriatric patients: High fall risk.
e. This is a tough one, because I feel like you could teach everything to the pt, from MOA,
to how some stay in the body longer than others, risk for abuse/dependence, d2d
interactions, s/s withdrawal, need to discuss with provider before they stop so we can
create a taper plan, etc. Hard to narrow down.
f. Kaplan pgs 949-953 has a fantastic overview. Benzos are lipid-soluble; benzos and
their active metabolites bind to plasma proteins; the extend of this binding is
proportional to their lipid solubility. Distribution, onset, and termination of action after a
single dose are largely determined by benzodiazepine lipid solubility, not elimination
half-life.
5. Risk of discontinuation of long term use of a benzodiazepine
a. Seizures r/t withdrawal

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