T/F naloxone is a competitive opioid antagonist, which binds covalently to opioid receptors
T/F in the presence of an agonist, a competitive antagonist has the effect of making the agonist less potent
T/F the structure of naloxone is almost identical to morphine
T/F naloxone has zero efficacy, and low receptor affinity
T/F using small titrated doses of naloxone, it is possible to reverse respiratory depression without reversing analgesia
T/F especially at high doses, the partial agonist buprenorphine can act as an antagonist to other opioids
T/F Suboxone™ contains a mixture of buprenorphine and naloxone, and is used in the management of opioid abuse (can you explain why the naloxone is added?)
- any decent pharmacology book will contain the answers to the above
- general information about agonists and antagonists would be found in the chapter(s) on pharmacodynamics
Write brief notes on the pharmacology of tramadol.
A question like this is a gift because it requires little more than reproducing what is on one of your summary cards! This question requires no higher order application or integration of knowledge, but it is still important for core drugs like tramadol, to be able to recall pharmacological data in significant detail. This is what you should be doing when you draw up the drug!!
T / F tramadol is a racemic mixture of 2 enantiomers – the (-) isomer inhibits noradrenaline reuptake and the (+) isomer inhibits serotonin reuptake
T / F tramadol is metabolised by CYP2D6 to O-desmethyltramadol, which is responsible for most of the opioid effect
T / F patients who are ultra-rapid codeine metabolisers, are also ultra-rapid tramadol metabolisers
T / F tramadol is 90% renally excreted, with 30% being excreted as unchanged drug
T / F tramadol has low potential for dependence and abuse
T / F tramadol does not cause respiratory depression or constipation
T / F some anaesthetists describe tramadol as a weak analgesic that reliably causes nausea and vomiting
Describe the clinical effects of non-steroidal anti-inflammatory drugs including the mechanisms through which they exert these effects.
Anaesthetists prescribe NSAIDS frequently. These drugs are very effective analgesics, but have significant potential adverse effects. Obviously, an in depth pharmacological knowledge is required.
T / F NSAIDS produce analgesia by inhibiting the synthesis of prostaglandins in injured tissue. Prostaglandins act directly on free nerve endings to produce pain.
T / F inhibiting prostaglandin synthesis decreases renal blood flow because PGE2 maintains efferent arteriolar dilation
T / F an advantage of COX-2 selective agents is that there is less inhibition of PGE2 and therefore less reduction in renal blood flow
T / F NSAIDS produce gastric mucosal ulceration via a direct irritant effect – therefore, they should not be taken on an empty stomach
T / F NSAIDS provide an overall reduction in the risk of acute coronary events because they inhibit platelet thromboxane
T / F inhibition of either COX-1 or COX-2 promotes the production of leukotrienes from arachidonic acid, which can precipitate asthma in some patients
Ok this is a bit of a weird one for the primary syllabus in my books. It could be asked in an MCQ but I don’t think it would be asked in a viva, because we all know it is virtually impossible to do mental arithmetic under pressure!
It is of practical consideration for us though and is something we do all the time, when managing patients in the post operative period.
There are various opioid conversion tables out there, including an app produced by the FPM. If you look the app, I would suggest that you look at the “practical considerations” in the information section (it is a bit hidden at the bottom of the Opioid Dose Equivalence page)
I think this poor patient needs more of whichever opioid he has received…. Taken at the Legend of Hong Kong Toys exhibition. I hate to think what happens when you turn that toy on…..
BT_PM 1.16 Outline the dose conversion between commonly used opioids
No change in tramadol dose is required when switching from oral to s/c dosing TRUE/FALSE
Twice as much oral compared with intravenous morphine is required to produce the same analgesic effect TRUE/FALSE
It is easy to calculate an equipotent dose of morphine for a patient taking methadone TRUE/FALSE
When switching a patient between one opioid and another, equipotent doses of the two drugs tend to underestimate the amount of the new opioid that will be required TRUE/FALSE
A buprenophine patch 20mcg/hr is equipotent to a 12.5mcg/hr fentanyl patch TRUE/FALSE
Outline the genetic variations in the cytochrome P450 2D6 enzyme and discuss the clinical relevance for drugs used in the perioperative period.
This enzyme is responsible for much of the variation in efficacy and toxicity of some commonly used drugs.
This enzyme metabolises tramadol into a more active metabolite TRUE/FALSE
Ondansetron may be ineffective with poor metabolisers TRUE/FALSE
Patients from the middle east are more likely to be ultrarapid metabolisers TRUE/FALSE
Approximately 90% of caucasians are poor metabolisers TRUE/FALSE
This enzyme metabolises codeine into a more active metabolite TRUE/FALSE
Sticking with neuraxial opioids…
Intrathecal fentanyl has fewer adverse effects than intrathecal morphine TRUE/FALSE
Intrathecal morphine produces better postoperative analgesia than intrathecal fentanyl after LSCS TRUE/FALSE
Doses of intrathecal morphine greater than 50mcg have no greater benefits in terms of analgesia but carry a higher incidence of respiratory depression TRUE/FALSE
100 mcg of morphine is 0.1ml of morphine 10mg/ml TRUE/FALSE
extended-release epidural morphine is associated with less respiratory depression than IVPCA morphine TRUE/FALSE
This has been a popular topic in vivas (and the occasional SAQ) for ages. It’s an important and relevant topic that is not always well-covered in the basic texts.
BT_PM 1.18 Describe the pharmacology of opioids deposited in the epidural space or cerebrospinal fluid
With regard to epidural fentanyl (1 mcg.kg-1)
plasma concentrations of fentanyl are similar to the same dose given intramuscularly TRUE/FALSE
the duration of analgesia is 1 hour TRUE/FALSE
the CSF concentrations of fentanyl are maximal at 50 minutes TRUE/FALSE
the incidence of pruritis is greater than following an equi-analgesic dose of epidural morphine TRUE/FALSE
the onset of analgesia is around 2-5 minutes because fentanyl is highly lipid soluble TRUE/FALSE
It’s such fun being able to use so many different routes to administer drugs in our jobs. So many doctors out there don’t get our opportunities.
BT_PM 1.15 Discuss the pharmacokinetic and clinical implications of different routes of administration for commonly used opioids, including the oral, transdermal, subcutaneous, intramuscular and intravenous routes, and with particular reference to fentanyl, morphine, methadone, tramadol and codeine
Fentanyl undergoes significant first pass pulmonary uptake and metabolism. TRUE/FALSE
The cytochrome P450 3A4 (CYP3A4) is predominantly responsible for the metabolism of Alfentanil. TRUE/FALSE
Alfentanil undergoes extensive hepatic metabolism that demonstrates extensive interindividual variability TRUE/FALSE
The bioavailability of sublingual buprenorphine is similar to that of parenteral buprenorphine TRUE/FALSE
Epidural fentanyl undergoes a biphasic absorption pattern TRUE/FALSE
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