DRUUUUUUUGS Flashcards
what are some risk factors for alcohol withdrawal?
level of alcohol consumption use of other depressants previous episodes of withdrawal/seizures duration of drinking early morning drinking increasing age coexisting med disorders (infection, metabolic disturbances, hypoxia) recent trauma or surgery highly stimulating and threatening external environment
what is the classic triad of Wernicke Korsakoff syndrome?
the mnemonic is EGO
Encephalopathy Gait ataxia (particularly truncal) Oculomotor dysfunction
How does naltrexone work?
how does acamprosate work?
how well do these agents work?
Naltrexone is a pure myu opioid recept antagonist. It blocks the reinforcing effects of alcohol mediated by beta-endorphin.
- Must have normal LFTs and not be on opioids.
- SE: gut, sleep disturbance, depression
- NOT THE SAME AS NALOXONE
Acamprosate is an agonist at GABAa-receptor and antagonist at NMDA glutamate receptor. Overall, it potentiates the inhibitory effects
Together, these agents are particularly good. They have a reasonably weak effect, but some patients do find it useful. NNT = 9 to reduce drinking by 10-20%.
What is disulfiram?
this is an aldehyde dehydrogenase inhibitor.
it leads to an increase in the unpleasant metabolite, acetylaldehyde
what is the classic triad of serotonin toxicity?
neuromuscular changes (clonus and hyper-reflexia)
autonomic hyperactivity (hyperthermia, tachycardia, diaphoresis, flushing)
altered level of consciousness
particularly hyperreflexia, clonus, hyperthermia and confusion
what types of medications have been associated with serotonin toxicity?
SSRIs,
MAOI
opioids - pethidine, tramadol, FENTANYL
linezolid!
MDMA, amphetamines
Lithium!
dextromethorphan (cough suppressant in OTC medications)
how might one differentiate between NMS and serotonin toxicity?
neuroleptic malignant syndrome should NOT have hyperreflexia, clonus or myoclonus. In fact, these patients typically have bradykinesia. They will have lead-pipe rigidity and EPSE
BOTH conditions have high temp
how do we manage serotonin toxicity?
about supportive care
cease any serotonergic medications
benzos can be used for agitation and muscle hyperactivity
cyproheptadine (5HT2a antag) can be used, but only if diagnosis is clear
how do we treat amphetamine dependence?
there isn’t any good pharmaceutical treatment
behavioural therapies are the best we have
what is the pharmacology of buprenorphine?
this is a synthetic opioid
it is given by the sublingual route with approx 40% absorption
it is a partial agonist at the myu receptor. It has a low intrinsic activity and also has a ceiling effect
there is a high affinity for this receptor and, in fact, displaces other opioids
it also has a long half life
because it displaces opioids, it can induce withdrawal! you have to ensure patient is in withdrawal before giving
which drug has a very long period of being positive in a urine drug screen? why?
cannabis is distributed to the fat. it takes many weeks after exposure for the body to completely excrete it (as it continues to be held in fat and slowly released)
what are the 3 pharmacological modalities for tobacco cessation?
- NRT - roughly double chances of cessation
- buproprion: dopamine/noradrenaline reuptake inhibitor (2D6 inhibitor) - DO NOT PRESCRIBE IN SEIZURE DISORDER - roughly 2.12x of quitting
- varenicline: nicotinic acetylcholine partial agonist A4 B2 subreceptor - mimics the effect of nicotine and blocks subsequent nicotine and also causes a dopamine release - strongest effect at about 2.55 x more likely
Which one of the following best summarises the effect of naltrexone in the management of opiate-dependent individuals? Naltrexone:
A. prevents the euphoric effect of opiates.
B. blocks withdrawal symptoms.
C. produces unpleasant adverse effects when opiates are taken. D. reduces opiate craving.
E. increases opiate tolerance.
Naltrexone is an opioid antagonist, thus it blocks the euphoric (analgaesic) and other actions of opioid agonists, it will also precipitate withdrawal (ie give unpleasant adverse effects) if given to someone with opioid dependence when under the influence of opioids. Disulfiram produces unpleasant adverse effects when alcohol is taken; naltrexone has little effect on opioid craving and if anything it reduces tolerance, hence the risk of opioid overdose for individuals who relapse to opioid use after naltrexone treatment. Naloxone is a short acting parenteral preparation given to reverse the effects of opioids
in patients with overdose and respiratory depression leading to hypoxia.
A 56-year-old man with alcoholic cirrhosis has a long history of alcohol dependence. He is brought to hospital after being disruptive at his home, where he lives alone. He has been accusing his neighbours of “spying” on him. He is found to have been experiencing persistent auditory hallucinations for two months. He has no previous history of these symptoms. He has continued his intake of over 300 g of alcohol/day.
The most likely cause of these hallucinations is:
A. delirium tremens.
B. alcohol-related hallucinosis.
C. hepatic encephalopathy.
D. Wernicke-Korsakoff syndrome. E. schizophrenia
Delirium Tremens lies at the most severe end of the spectrum of alcohol withdrawal, Answer B fits best with the scenario, auditory hallucinations are not
a typical feature of hepatic encephalopathy, the full WKS (seen in only a minority of cases, while many cases are not diagnosed in life) involves
ophthalmoplegia, truncal ataxia and confusional state. Schizophrenia is the other possibility, however alcohol is clearly the most probable organic cause,
thus takes precedence.
A patient with cirrhosis is being treated with normal doses of chlormethiazole for alcohol withdrawal. Chlormethiazole has an hepatic extraction ratio of 0.9, hepatic clearance of 100 L/h, protein binding of 64% and volume of distribution of 12 L/kg.
The much higher concentrations and greater effect of chlormethiazole in people with cirrhosis is mostly due to:
A. decreased protein binding.
B. decreased clearance.
C. decreased volume of distribution.
D. increased bioavailability.
E. increased absorption.
Chlormethiazole is an acidic, water-soluble, thiazole derivative with hynotic and anti-convulsant properties. It is well absorbed orally, however there is a

major first pass effect (85%) which leads to low oral bioavailability. In cirrhosis oral bioavailability may be increased ~10 fold. It is little used
currently, diazepam or lorazepam being the preferred treatments (plus thiamine) for alcohol withdrawal.
