P: Summary Resource Table [Study]

Question 1

[lec1/2] Name the 4 components for pharmacokinetics, and an anagram for it

Answer 1

ADME: Absorption, Distribution, Metabolism, Excretion

Question 2

[lec1/2] Name the 4 components for pharmacodynamics, and an anagram for it

Answer 2

RICE: Receptor, Ion channel, Carrier, Enzyme

Question 3

[lec1/2] Define the following terms:
A: Absorption
B: Distribution
C: Metabolism
D: Excretion

Answer 3

A: drug entering circulation
B: drug spreading throughout body
C: biotransformation of drug
D: removal of drug from body

Question 4

[lec1/2] Define pharmacological efficacy

Answer 4

The ability of a drug to activate a receptor

Question 5

[lec1/2] Define clinical efficacy

Answer 5

The strength of the beneficial effect to make the patient feel better

Question 6

[lec1/2] Define affinity. Give a formula for this

Answer 6

ability of the drug to bind. Affinity = [A]/Ka

Question 7

[lec1/2] Define potency. Describe high vs low potency

Answer 7

How much of a drug is needed to elicit an action
High potency = only low dose needed
Low potency = higher dose needed

Question 8

[lec1/2] How does the therapeutic ratio correlate to drug safety

Answer 8

The bigger the ratio, the better the drug since the range of safe dosage is large

Question 9

[lec1/2] How can agonists differ from each other? (4)

Answer 9

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

Question 10

[lec1/2] How do non-competitive antagonists act? (2)

Answer 10

stops and slows down system by releasing agonist in opposite direction OR
turn off enzyme that is upstream or downstream

Question 11

[lec1/2] How do competitive antagonists act? (1)

Answer 11

competes with agonists for receptors

Question 12

[lec1/2] How can non-competitive antagonists chemically antagonise?

Answer 12

can add chemicals to bind to ligands to stop it binding to a receptor

Question 13

[lec1/2] How can non-competitive antagonists act on the receptor? (2)

Answer 13

Allosteric modulations
Bind to receptor but not reduce affinity of agonist receptor

Question 14

[lec1/2] What 2 things can you do to make a competitive antagonist?

Answer 14

Decrease efficacy
Increase affinity

Question 15

[lec1/2] Why does low affinity make a drug dangerous?

Answer 15

Because you need a higher dosage to get the same effect

Question 16

[lec3/4] Name 4 factors to consider when administering a drug

Answer 16

Convenience
Cost
Bioavailability
Local vs systemic

Question 17

[lec3/4] How can you help ensure a drug stays in local circulation?

Answer 17

use a poorly absorbed drug

(also occlude your puncta if it’s a topical eye drop)

Question 18

[lec3/4] Why feature of oral administration helps drug absorption?

Answer 18

intestine has large surface area and provides maximum opportunity for absorption

(note: however, direct IV has the best absorption obviously)

Question 19

[lec3/4] What type of metabolism do drugs taken orally go through? Explain the process

Answer 19

1st-pass hepatic metabolism: drug enters hepatic portal vein and is transferred directly to the liver

Question 20

[lec3/4] Why must bioavailability be taken into account in orally administered drugs?

Answer 20

If low bioavailability, effect will be very minor since the drug will be going through 1st-pass hepatic metabolism

If low, consider alternative pathway

Question 21

[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

Answer 21

A: High
B: Most drugs eliminated at a rate proportional to concentration in the plasma
C: Quick excretion

Question 22

[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?

Answer 22

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

Question 23

[lec3/4] What does drug distribution rely on? (1)

Answer 23

The binding to cells/uptake into cells

Question 24

[lec3/4] Provide the formula for volume of distribution

Answer 24

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

Question 25

[lec3/4] How are drugs excreted? (2) Describe the processes

Answer 25

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)

Question 26

[lec3/4] What is lipid solubility affected by that affects drug diffusion?

Answer 26

pH

Question 27

[lec3/4] Define Phase I and II metabolism

Answer 27

Phase I: add functional group Phase II: conjugate with water

Question 28

[lec3/4] what type of metabolism is cytochrome p450 involved in?

Answer 28

Phase I

Question 29

[lec6] Name the major sites/targets for pharmacological manipulation of synapses (8)

Answer 29

1. conduction of action potential down axon to nerve terminal 2. synthesis of the N.T 3. storage of the N.T 4. metabolism of the N.T 5. release of the N.T 6. uptake of the N.T 7. degradation of the N.T 8. Receptor for the N.T

Question 30

[lec6] Name 4 receptor families activated by N.Ts

Answer 30

ligand-gated ion channels (ionotropic receptors) G-protein coupled receptors Kinase-linked receptors Nuclear receptors

Question 31

[lec6] Describe the length of the pre-ganglionic fibre vs post-ganglionic fibre for sympathetic neruons

Answer 31

pre-ganglionic = short post-ganglionic = long

Question 32

[lec6] Describe the length of the pre-ganglionic fibre vs post-ganglionic fibre for PARASYMPATHETIC neruons

Answer 32

pre-ganglionic = long post-ganglionic = short

Question 33

[lec6] What N.T is released by sympathetic neurons? and what receptor is there for it?

Answer 33

Noradrenaline. Alpha/beta adrenoceptors

Question 34

[lec6] What N.T is released by parasympathetic neurons? and what receptor is there for it?

Answer 34

ACh. Muscarinic receptors.

Question 35

[lec 7] How is ACh synthesized and transported? (3)

Answer 35

1. Choline enters blood stream via choline carrier 2. Choline + acetylCoA --> acetylcholine + CoA 3. Acetylcholine (i.e. ACh) transported to vescile by ACh carrier

Question 36

[lec 7] How does botox affect ACh? Explain the mechanism and outcome

Answer 36

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

Question 37

[lec 7] What do acetycholinesterases do? What do anticholinesterases do?

Answer 37

Breaks up ACh into acetate and choline. Therefore anticholinesterases will stop this, allowing more ACh to accumulate at the synapse

Question 38

[lec 7] Name 2 anticholinesterases and state what they are each selective for and what they each treat

Answer 38

Physostigmine: selective for parasympathetic junctions - treat glaucoma Neostigmine: selective for NMJ - treats Myaesthenia Gravis

Question 39

[lec 7] Describe Myaesthenia Gravis and state what it leads to (3)

Answer 39

is where the nicotinic cholinergic receptors are seen as foreign. Antibodies bind them and attack them, degrading them Leads to muscle paralysis

Question 40

[lec 7] In regards to Muscarinic Receptors: A: What type of N.T do they respond to? B: What are their agonist effects? (4)

Answer 40

A: cholinergic N.T B: SLUD: salivation, lacrimation, urination, defectation (note: therefore antagonists to this receptor would have anti-slud effects)

Question 41

[lec 7] Give 2 examples of drugs that act on muscarinic receptors

Answer 41

Pilocarpine (agonist, SLUD, pupil constriction) Atropine (antagonist, ANTI-SLUD, pupil dilation)