Psychopharmocology

Question 1

What are the FDA indications for Modafinil?

Answer 1

daytime sleepiness associated with narcolepsy, shift work sleep disorder, and obstructive sleep apnea/hypopnea syndrome

Question 2

What are the side effects of Modafinil?

Answer 2

Headache, nervousness, diarrhea, insomnia, anxiety, dizziness

Question 3

What are contraindications to Modafinil?

Answer 3

Severe hypertension or cardiac arrythmias

Question 4

What are the FDA indications for Fluvoxamine?

Answer 4

OCD, also used off label for social anxiety/mdd/gad/ptsd

Question 5

What are the side effects of Fluvoxamine

Answer 5

Nausea, Diarrhea, Xerostomia,Headache, Drowsiness, Dizziness, ejaculatory disorder, weakness

Question 6

What is the MOA for Fluvoxamine

Answer 6

SSRI and sigma 1 antagonism

Question 7

What is the CYP interactions for Fluvoxamine

Answer 7

Inhibits 1A2, 2C19, 2D6

Question 8

What is the FDA approval for Atomoxetine?

Answer 8

ADHD (Non-stimulant)

Question 9

What is the MoA of Atomoxetine

Answer 9

SNRI

Question 10

What are the adverse effects of Atomoxetine

Answer 10

The serious medication adverse events that have been reported are psychosis, mania, aggressive behavior, suicidal ideation, depression, orthostatic hypotension, syncope, hypertension, tachycardia, QT prolongation, myocardial infarction, stroke, sudden death, seizures, hepatotoxicity, priapism, Raynaud phenomenon, hypersensitivity reaction, angioedema, anaphylaxis, and rhabdomyolysis.

Question 11

What are adverse effects of desipramine

Answer 11

Common side effects are blurred vision, constipation, increased appetite, nausea, diarrhea, weakness, fatigue, sexual dysfunction and headache. Similar to other tricyclics, desipramine has life threatening side effects such as hyperthermia, lowered seizure threshold, orthostatic hypotension, arrhythmias, tachycardias, QTc prolongation, blood dyscrasias, rare activation of mania, suicidal ideation and it can be potentially lethal in overdose

Question 12

What is the MOA of Desipramine

Answer 12

tricyclic antidepressant, impacts norepi more so than serotonin. It notably has the least amount of M1 and H1 receptor affinity compared to other TCA. Remember this is the metabolite of Imipramine

Question 13

What is the MOA of Deutetrabenazine?

Answer 13

VMAT2 inhibitor

Question 14

What are potential side effects of Deutetrabenazine

Answer 14

somnolence, diarrhea, xerostomia, fatigue, UTI, insomnia, anxiety, constipation, confusion, nasopharyngitis, akathisia, and dysthymic disorder and QT prolongation

Question 15

What are the pharmacokinetics of Pramipexole?

Answer 15

The bioavailability following absorption exceeds 90%. The peak plasma time of the IR formulation is 2 hours and is 6 hours for ER. Pramipexole is 15% protein bound. Less than 10% of pramipexole is metabolized. The majority of the drug is excreted in the urine (90%), with a renal clearance of 400 mL/min. The elimination half-life is 8.5 hours. As most of pramipexole is not metabolized, 70% is not metabolized in the liver, and multiple cytochromes are not involved in its metabolism.

Question 16

What is the MoA of Pyridiostigmine

Answer 16

Cholinesterase Inhibitor

Question 17

What are the pharmacokinetics of pyridiostigmine

Answer 17

It reversibly binds to and inactivates acetylcholinesterase (cholinesterase inhibitor). Pyridostigmine metabolism is both via plasma and the liver. It is metabolized by the CYP450 pathway. It is excreted in the urine, primarily unchanged. The half-life of pyridostigmine is 3 hours. Pyridostigmine is dosed at 60–120 mg PO Q3–8 hours.

Question 18

What are side effects of pyridiostigmine?

Answer 18

Sweating
Diarrhea
Nausea
Vomiting
Abdominal cramps
Increased salivation
Tearing
Increased bronchial secretions
Constricted pupils
Facial flushing due to vasodilation
Erectile dysfunction

Question 19

What is the only medication to be FDA approved for Seasonal Affective Disorder?

Answer 19

Buproprion

Question 20

What are some contraindications/potential side effects of Hydroxizine

Answer 20

have QT prolongation; a congenital long QT syndrome; a family history of QT prolongation; a history of torsades de pointes; electrolyte abnormalities; ventricular arrhythmias; bradycardia; history of a recent MI; history of congestive heart failure; or if the environmental temperature is hot; or if the patient has asthma.

Question 21

What are the dose related side effects of Lithium?

Answer 21

Dose-related side effects include polyuria, polydipsia as (nephrogenic diabetes insipidus), weight gain, cognitive slowing, confusion, impaired memory, poor concentration, confusion, tremor, sedation, gastrointestinal distress, leukocytosis, acne, and edema.

Question 22

What are mild symptoms of lithium toxicity?

Answer 22

mild symptoms of toxicity, such as increased tremor, slurred speech, and mild lethargy, generally occur when the serum lithium concentration falls between 1.5 to 2.5 mEq/L.

Question 23

What are the moderate/severe symptoms of lithium toxicity?

Answer 23

worsening lethargy, coarse tremors, and clonus, can be seen when lithium levels are between 2.5 to 3.5 mEq/L.

Question 24

What is the treatment for Lithium Toxicity?

Answer 24

The general approach lithium toxicity begins with assessment and stabilization of the airway, breathing, and circulation. The treatment for lithium toxicity includes intravenous fluids to maintain the glomerular filtration rate and replace losses, gastrointestinal decontamination in selected circumstances, and, hemodialysis in cases of severe toxicity. Hemodialysis criteria are not firmly established but generally when levels are below 2.5 mEq/L hemodialysis is not necessary. Hemodialysis is generally required with serum levels between 6 to 8 mEq/L however it may be necessary for those on long term lithium treatment at levels as low as 4 mEq/L. Regardless of level, hemodialysis is indicated in those with coma, convulsions, cardiovascular symptoms, or respiratory failure. Serum levels of lithium may rebound as intracellular stores of lithium enter the bloodstream and repeat dialysis may be needed.

Question 25

In patients with PD, what medications can worsen iatrogenic psychosis?

Answer 25

Amantadine, anticholinergics, COMT inhibitors, and dopamine agonists.

Question 26

What is the MOA of Dihydoregotamine? (DHE)

Answer 26

DHE is an alpha-adrenergic blocking agent with a direct stimulating effect on smooth muscle of peripheral and cranial blood vessels. It depresses central vasomotor centers.

Question 27

What are the pharmakokinetics of Dihydoregotamine? (DHE)

Answer 27

The pharmacokinetics of DHE are as follows: it has an onset of action of 15–20 minutes IM, less than 5 minutes IV, and 30 minutes intranasal. The duration of action for IM is 3–4 hours, and for IV/SQ, 8 hours. DHE has a half-life of 28 hours. It is 93% protein bound, is metabolized by the liver via CYP3A4, and is excreted mainly in the feces, with less than 10% of excretion via the urine.