P: Summary Resource Table [Study] Flashcards
[lec1/2] Name the 4 components for pharmacokinetics, and an anagram for it
ADME: Absorption, Distribution, Metabolism, Excretion
[lec1/2] Name the 4 components for pharmacodynamics, and an anagram for it
RICE: Receptor, Ion channel, Carrier, Enzyme
[lec1/2] Define the following terms: A: Absorption B: Distribution C: Metabolism D: Excretion
A: drug entering circulation
B: drug spreading throughout body
C: biotransformation of drug
D: removal of drug from body
[lec1/2] Define pharmacological efficacy
The ability of a drug to activate a receptor
[lec1/2] Define clinical efficacy
The strength of the beneficial effect to make the patient feel better
[lec1/2] Define affinity. Give a formula for this
ability of the drug to bind. Affinity = [A]/Ka
[lec1/2] Define potency. Describe high vs low potency
How much of a drug is needed to elicit an action
High potency = only low dose needed
Low potency = higher dose needed
[lec1/2] How does the therapeutic ratio correlate to drug safety
The bigger the ratio, the better the drug since the range of safe dosage is large
[lec1/2] How can agonists differ from each other? (4)
can be selective or non-selective
full agonists will have spare receptors
partial agonists do not have spare receptors
full agonists desensitizes more than partial agonists
[lec1/2] How do non-competitive antagonists act? (2)
stops and slows down system by releasing agonist in opposite direction OR
turn off enzyme that is upstream or downstream
[lec1/2] How do competitive antagonists act? (1)
competes with agonists for receptors
[lec1/2] How can non-competitive antagonists chemically antagonise?
can add chemicals to bind to ligands to stop it binding to a receptor
[lec1/2] How can non-competitive antagonists act on the receptor? (2)
Allosteric modulations
Bind to receptor but not reduce affinity of agonist receptor
[lec1/2] What 2 things can you do to make a competitive antagonist?
Decrease efficacy
Increase affinity
[lec1/2] Why does low affinity make a drug dangerous?
Because you need a higher dosage to get the same effect
[lec3/4] Name 4 factors to consider when administering a drug
Convenience
Cost
Bioavailability
Local vs systemic
[lec3/4] How can you help ensure a drug stays in local circulation?
use a poorly absorbed drug
also occlude your puncta if it’s a topical eye drop
[lec3/4] Why feature of oral administration helps drug absorption?
intestine has large surface area and provides maximum opportunity for absorption
(note: however, direct IV has the best absorption obviously)
[lec3/4] What type of metabolism do drugs taken orally go through? Explain the process
1st-pass hepatic metabolism: drug enters hepatic portal vein and is transferred directly to the liver
[lec3/4] Why must bioavailability be taken into account in orally administered drugs?
If low bioavailability, effect will be very minor since the drug will be going through 1st-pass hepatic metabolism
If low, consider alternative pathway
[lec3/4] In regards to RAPID IV administration:
A: Describe the peak drug concentration reached in the blood
B: Describe the rate of drug elimination
C: Describe the rate of excretion
A: High
B: Most drugs eliminated at a rate proportional to concentration in the plasma
C: Quick excretion
[lec3/4] In regards to SHORT-TERM IV administration:
A: Describe the peak drug concentration reached in the blood
B: What is this useful for?
C: What happens to the rate of accumulation of drug in relation to drug concentration
D: What happens to the drug when you stop infusion?
A: Not as high as rapid:
B: Drugs that show toxicity at high concentrations
C: rate of accumulation decreases as concentration increases
D: You get elimination only
[lec3/4] What does drug distribution rely on? (1)
The binding to cells/uptake into cells
[lec3/4] Provide the formula for volume of distribution
Vd = X/C
X = amount of drug in body, C = concentration of drug in blood
If C is big, need more X to get same amount distributed
[lec3/4] How are drugs excreted? (2) Describe the processes
Glomerular filtration: limited by GFR; cannot remove bound protein
Tubular secretion: active carrier - can remove bound protein
(note: tubular reabsorption doesn’t count because that’s not excretion now is it)
[lec3/4] What is lipid solubility affected by that affects drug diffusion?
pH
[lec3/4] Define Phase I and II metabolism
Phase I: add functional group
Phase II: conjugate with water
[lec3/4] what type of metabolism is cytochrome p450 involved in?
Phase I
[lec6] Name the major sites/targets for pharmacological manipulation of synapses (8)
- conduction of action potential down axon to nerve terminal
- synthesis of the N.T
- storage of the N.T
- metabolism of the N.T
- release of the N.T
- uptake of the N.T
- degradation of the N.T
- Receptor for the N.T
[lec6] Name 4 receptor families activated by N.Ts
ligand-gated ion channels (ionotropic receptors)
G-protein coupled receptors
Kinase-linked receptors
Nuclear receptors
[lec6] Describe the length of the pre-ganglionic fibre vs post-ganglionic fibre for sympathetic neruons
pre-ganglionic = short post-ganglionic = long
[lec6] Describe the length of the pre-ganglionic fibre vs post-ganglionic fibre for PARASYMPATHETIC neruons
pre-ganglionic = long post-ganglionic = short
[lec6] What N.T is released by sympathetic neurons? and what receptor is there for it?
Noradrenaline. Alpha/beta adrenoceptors
[lec6] What N.T is released by parasympathetic neurons? and what receptor is there for it?
ACh. Muscarinic receptors.
[lec 7] How is ACh synthesized and transported? (3)
- Choline enters blood stream via choline carrier
- Choline + acetylCoA –> acetylcholine + CoA
- Acetylcholine (i.e. ACh) transported to vescile by ACh carrier
[lec 7] How does botox affect ACh? Explain the mechanism and outcome
blocks the release mechanism by which the vesicle (containing ACh) fuses and releases its contents into the synapse – leads to reduced levels of ACh released in the synapse
[lec 7] What do acetycholinesterases do? What do anticholinesterases do?
Breaks up ACh into acetate and choline. Therefore anticholinesterases will stop this, allowing more ACh to accumulate at the synapse
[lec 7] Name 2 anticholinesterases and state what they are each selective for and what they each treat
Physostigmine: selective for parasympathetic junctions - treat glaucoma
Neostigmine: selective for NMJ - treats Myaesthenia Gravis
[lec 7] Describe Myaesthenia Gravis and state what it leads to (3)
is where the nicotinic cholinergic receptors are seen as foreign. Antibodies bind them and attack them, degrading them
Leads to muscle paralysis
[lec 7] In regards to Muscarinic Receptors:
A: What type of N.T do they respond to?
B: What are their agonist effects? (4)
A: cholinergic N.T
B: SLUD: salivation, lacrimation, urination, defectation (note: therefore antagonists to this receptor would have anti-slud effects)
[lec 7] Give 2 examples of drugs that act on muscarinic receptors
Pilocarpine (agonist, SLUD, pupil constriction)
Atropine (antagonist, ANTI-SLUD, pupil dilation)
