Pharmacology-Treatments for Substance Abuse Flashcards Preview

Multisystems II > Pharmacology-Treatments for Substance Abuse > Flashcards

Flashcards in Pharmacology-Treatments for Substance Abuse Deck (17)

Detox treatments for heroin addiction

Cold turkey - not recommended. METHADONE - replaces heroin and has a longer, slower, more mild withdraw. CLONIDINE - alpha-2 receptor agonist suppresses locus ceruleus firing and reduces pain from opioid withdrawal from spinal cord receptors. NALOXONE - accelerated withdraw used with anesthetics


Maintenance therapy for heroin addiction (to prevent relapse)

METHADONE - high dose induces tolerance to other opiates (including street heroin) and prevents “high”, once patient is stable, detox w/slow methadone withdraw. *Must go to the clinic everyday. NALTREXONE - give after detox to block effects of self-administered opiate, limited success. BUPRENORPHINE - blocks opiate effects, induces a mild high, no respiratory depression and reduces incidence of relapse. *Note that there is an emerging black market for buprenorphine. BUPRENORPHINE/NALOXONE (suboxone) - combination of sublingual tablet. When taken orally, the naloxone is metabolized in the liver and is not effective. When ground up and injected IV, naloxone is bioavailable and blocks the “high” from buprenorphine. *Only need to go to the clinic 1x a week.


Side effects of methadone

Long QT syndrome and arrhythmias


Pregnancy maintenance therapy for heroin abuse.

Buprenorphine mono therapy, naloxone has not been studied in pregnancy


Treating stimulant abuse

No tx for chronic abuse. Tx anxiety and seizures with benzodiazepines


Pharmacologic Tx for nicotine addiction? Risks?

Varenicline is a partial nicotinic receptor agonist and reduces CNS stimulation of neurons by nicotine and indirectly reduces DA release so there is no reward for taking it. Risks include liver injury, depression and suicide.


Tx for acute ethanol poisoning

Gastric lavage to prevent further alcohol absorption. Maintain cardiac function, temperature, acid-base and fluids. Reduce gastric acid secretion with ranitidine (H2 antagonist) or omeprazole (PPI).


Tx for a kid who drank antifreeze

Ethylene glycol is metabolized to glycoaldehyde which is toxic to the kidney, glycol acid which causes metabolic acidosis and oxalic acid which causes crystals to form in the urine. Tx by delaying metabolism of ethylene glycol with ethanol (saturates alcohol dehydrogenase) or fomepizole (inhibits alcohol dehydrogenase)


Tx for alcohol withdraw

Diazepam for seizures, haloperidol for hallucinations and PPI/ranitidine for gastric acid secretion


Tx for maintaining alcohol abstinence

Disulfiram: inhibits aldehyde dehydrogenase and makes the patient very sick if they drink alcohol while on it. Naltrexone: opioid receptor antagonist reduces reward effect of ethanol. Acamprosate: blocks glutamate neurotransmission. 


Alcohol harm is closely related to what?

Consumption, note that the majority of alcohol is consumed by a minority of people (15% of drinkers become alcoholics)…meaning that alcoholism is also related.


What works as far as alcohol-related harm goes?

Tax, drunk-driving legislation, banning advertising, limit availability, providing help for hazardous drinking. Industry-favored school-base programs don’t work, are expensive and are being used more than other cheaper, more effective methods.


Criteria for Alcohol Use Disorder

Repeated failures to curb intake, inability to cut down use despite desire, time consuming seeking, cravings, failure to fulfill major obligations, continued use despite problems, reduction of activities, hazardous use, continued use despite knowledge of psychological problems, tolerance, withdrawal.


Alcoholism relapse rate 

Usually 60% within one year


Main triggers of relapse

Small priming dose of drug, associated stimuli and stress


What pushes someone into alcoholism if they have low vs. high genetic risk?

High genetic risk needs less strong environmental push into alcoholism


How does the brain reward system get activated by alcohol?

Alcohol consumption -> endogenous opioid release from VTA -> Disinhibition of DA pathway -> Reward. This is why naltrexone is somewhat effective, it blocks opioid receptor activation and prevents the reward pathway.