#2

Question 1

MOA of naltrexone?

Clinical use and effect?

Answer 1

Mu opioid receptor antagonist
Alcohol and opioid dependence
Reduces the craving and relapse to drink
NEED TO BE OPIOD FREE TO START

Question 2

MOA of acamprosate?

Clinical use?

Answer 2

Weak NMDA receptor blocker and GABA a agonist

Alcohol dependence

Question 3

MOA of Disulfiram?
Clinical use?
Should not be administered with any what?

Answer 3

Irreversibly inhibits aldehyde DH and makes anyone who drinks incredibly uncomfortable and sick because of aldehyde build up.

Alcohol dependence

Any med or anything with alcohol

Question 4

Problem with Wernickes?
Triad of the disease?
What will the patient usually do to compensate?
What 2 things may be seen on PE?
MRI might show?

Answer 4

Thiamine deficiency (can be because of alcohol)
Mental confusion, amnesia, and impaired short term memory
Make up stuff because of their memory
Skin changes and a red beefy tongue
Shrunken mammillary bodies

Question 5

What is the dopamine hypothesis of addition and what is the effect of addictive drugs on dopamine?

Answer 5

Dopamine activity, both NT and the neurons themselves, is reduced in the brain because of addictive substances. Currently, it is believed that low DA function results in less interest of a person in non drug (or whatever they are addicted to) related stimuli.

Question 6

Why are ACHE blockers indicated for dementia?

Answer 6

Patients with dementia have a deficiency of intact cholinergic neurons

Question 7

How do we best treat toxication by ACHE blockers?
What is it ineffective against?
What is the best combo to regenerate ACHE?

Answer 7

Atropine
Ineffective against peripheral neuromuscular stimulation
Atropine, pralidoxime and benzo

Question 8

MOA of memantine?

Clinical use?

Answer 8

NMDA type glutamate receptors. Binds to the magnesium site

Dementia