Flashcards in Cognitive Enhancers: Lichtblau Deck (19):
Describe Methylphenidate. MOA and immediate vs. sustained release.
Enhances DA release and inhibits re-uptake. Immediate release is Ritalin and sustained release is Concerta.
Describe the amphetamines. MOA, enantiomers, and different forms of release.
They enhance DA release and block re-uptake. If you give both d and l amphetamine, it will also enhance NE release.
Sustained release form is Adderall. It has good compliance because it can be administered in the morning and removes the burden on schools to administer drugs.
What is the only 1st line ADHD medication that has no abuse potential? and why?
Atomoxetine. It doesn't elevate DA in the nucleus accumbens.
Describe the MOA of Atomexetine.
It is a NE re-uptake inhibitor. It elevates DA in the prefrontal cortex. These two things lead to an increase in Ach levels.
There is a gal down by the river who stuck a tac in my memory
Mnemonic: Alzheimer Disease Drugs
It inhibits AChE and stimulates cholinergic neurons to release more stored Ach.
What is the site of earliest damage in AD?
Nucleus basalis of Meynert.
What are some drugs patients should not take while on Galanatamine? And what should they use with caution due to increased risk of stomach ulcers?
They should not take the anti-depressants: paroxitine, amitryptiline, fluoxetine, and fluvoxamine.
They should take NSAIDs with caution!
Descirbe MOA of Rivastigmine and its side effects.
Inhibits AChE and BuChE. Take 2x daily (better compliance). It can cause GI issues and muscle weakness moreso than other cholinesterase inhibitors.
What 2nd line AD drug needs to be given multiple times per day (poor compliance), has a short half-life, has drug interactions with NSAIDs and may cause liver damage?
What drug is used for moderate to severe AD and how does it work?
Memantine. it is an antagonist of the NMDA Glutamate receptor.
What drug is popular with students to enhance performance?
Signature symptom of AD.
What neurons are destroyed in AD?
What are adverse effects of increasing ACh throughout the brain in AD patients?
Nausea, anorexia, vomiting, diarrhea. (limits the max dose clinically)
Describe drug tolerance in ADHD patients vs. non-ADHD patients. and describe what can happen in people who abuse amphetamine and cocaine.
Drug tolerance develops at a slower pace in ADHD patients than in non-ADHD patients.
People who abuse amphetamine and cocaine may see "reverse tolerance": psychosis with chronic use even without dose escalation. This doesn't occur in ADHD patients.
Describe why using a psychostimulant works to improve ADHD symptoms.
They turn on inhibitory centers so you don't notice outside things anymore. Kids with ADHD have inhibitory areas that are not working. At low therapeutic doses, areas of prefrontal and limbic cortex involved with maintaining attention are ACTIVATED!
What is a nootropic?
drugs that "bend the mind": cognitive enhancers, intelligence enhancers, "smart drugs"