Mechanisms of drug interaction can be classified as: pharmacodynamic, pharmacokinetic, and pharmaceutic.
T/F the interaction between nitrous oxide and sevoflurane is an example of synergism because the combined effect is greater than would be predicted by simple addition
T/F the interaction between propofol and remifentanil can be represented by a linear isobologram
T/F in a patient using buprenorphine patches, morphine can have a reduced effect because buprenorphine is a partial antagonist
T/F in a patient who has been reversed with neostigmine, but then needs to be urgently reintubated, suxamethonium would have a significantly reduced effect
T/F cigarette smoking inhibits many of the cytochrome P450 enzymes, thereby slowing the metabolism of many drugs
T/F competition for plasma protein binding sites between drugs, is a common reason for adverse drug effects in anaesthesia
T/F if suxamethonium is injected into an IV port immediately after thiopentone, a precipitate will form in the line
Hemmings & Hopkins, Chapter 9 (Anesthetic drug interactions)
The law of mass action states that the rate of a reaction is proportional to the concentration of the reacting substrates T/F
The affinity constant (Ka) is a measure strength of drug-receptor binding T/F
The dissociation constant (Kd) is a measure of the the tendency for the drug-receptor complex to split T/F
Ka is the molar concentration of the drug at which 50% of receptors are bound at equilibrium T/F
Kd is the molar concentration of the drug at which 50% of receptors are bound at equilibrium T/F
All drug receptors are proteins T/F
In general, drugs binding to receptors cause a conformational change T/F
Physiologic response is directly proportional to the number of receptors bound by drug T/F
An enzyme is a biological catalyst that increases the speed of a reaction without being consumed in the reaction itself T/F
A zero-order reaction is one whose rate is independent of the concentration of the reacting components and is, therefore, constant T/F
The Michaelis-Menten equation can model the velocity of both zero-order and first order reactions T/F
The following is an (incomplete) list of a few ‘types’ of receptors I could think of or find in a few textbooks I perused. I am sure you can add to this list.
Can you provide a definition of a ‘receptor’ that covers the list above?
Which of these would not fit with the usual idea of a ligand/receptor interaction?
There was a time when the concept of a receptor did not exist but now we use the word almost every day.
How did we get from then to now, i.e. what is the evidence for the existence of receptors?
There are six LO’s relevant to receptor theory. A number have been covered before and there are two that will be covered is the next two posts.
BT_GS 1.1 Explain the concept of drug action with respect to: Receptor theory, Enzyme interactions, Physico-chemical interactions
BT_GS 1.5 Explain the law of mass action and describe affinity and dissociation constants
I know BT_GS 1.21 does not mention receptors but it is related to the main question of this post. Can you explain how?
These two eBooks on the ANZCA Library website have comprehensive sections on receptor theory:
Rang & Dale’s Pharmacology 8e Ch 2 How drugs act: general principles. (Probably the better of the two)
Goodman & Gilman The Pharmacological Basis of Therapeutics 13e Ch 3
If you think the CICM syllabus seems similar to the ANZCA Primary Exam LO’s (Appendix Two) – you would be right – the CICM syllabus was created from the old ANZCA Primary Exam Syllabus.
Which one do you prefer?