PHARM Y1 S1: Intro to pharm

Question 1

good resources for looking up drugs

Answer 1

• MIMS
• Aus medicines handbook
• Cochrane library
• PBS website
• Monash ePharm (Moodle)

Question 2

selectivity vs specificity for receptors

Answer 2

• selectivity is better for tissues because they only display specificity within a particular dose range
• specificity is better for a receptor
• not all keys fit all locks

Question 3

4 types of targets for drug action (usually proteins)

Answer 3

• receptors (agonist/antagonist)
• ion channels (blockers/modulators)
• enzymes (inhibitor, false substrate, pro-drug)
• carriers/transporters (normal transport, inhibitor, false substrate)

Question 4

pharmacokinetics vs pharmacodynamics

Answer 4

• kinetics: what the body does to a drug (absorption, distribution, metabolism, excretion)
• dynamics: what the drug does to the body (how drug binds and what happens after)

Question 5

agonist vs antagonist

Answer 5

• agonist: binds to receptor and activates it
• antagonist: binds to receptor and doesn’t activate it but blocks actions of agonists

Question 6

3 phases of drug action

Answer 6

• pharmaceutical (released from capsule/tablet)
• pharmokinetic (absorption, distribution, metabolism, excretion)
• pharmacodynamic (binding to target site, stimulus, effect)

Question 7

law of mass action

Answer 7

the more drug (key) you have, the more chance you have of interacting w/ the receptor (lock) and having desired effect

Question 8

criteria for a neurotransmitter

Answer 8

• synthesised and released from nerve
• post-synaptic receptor specific to NT
• has a competitive antagonist
• must be an active mechanism to terminate activity of NT

Question 9

types of nerves + their receptors

Answer 9

• adrenergic nerves: release NA (a/B receptors)
• cholinergic nerves: release ACh (nicotinic (ionotropic) /muscarinic (metabotropic) receptors)

Question 10

sympathetic and parasympathetic nerves

Answer 10

• pre-ganglionic: cholinergic (N receptor)
• post-ganglionic: parasympathetic is cholinergic (M receptor) and sympathetic is adrenergic (a/B receptor)

Question 11

somatic nerves

Answer 11

• just one cholinergic nerve (N receptor)

Question 12

3 types of B-receptors

Answer 12

• β1: increased HR and contraction force (we have 1 heart)
• β2: vasodilation to lungs + pupil dilation (we have 2 lungs)
• β3: lipolysis in adipose tissue

Question 13

2 types of a-receptors

Answer 13

• a1: vasodilation to muscle (constriction to GIT) + pupil dilation
• a2: noradrenaline -ve feedback + vasoconstriction of vascular smooth muscle

Question 14

how is Ach synthesised

Answer 14

• choline + acetyl-coA > acetylcholine
• uses enzyme choline acetyltransferase

Question 15

how is noradrenaline synthesised

Answer 15

• precursor tyrosine (AA)
• -ve feedback system of inhibiting tyrosine hydroxylase

Question 16

how is noradrenaline removed

Answer 16

• reuptake into pre and post synaptic nerves
• then broken down by 2 enzymes: monoamine oxidase (MOA) and catechol-O-methyltransferase (COMT)

Question 17

how is Ach removed?

Answer 17

• must be removed almost immediately @ NMJ otherwise depolarising block
• mainly done by enzymatic breakdown by acetylcholinesterase

Question 18

how do amphetamines work?

Answer 18

• increased NA into synaptic cleft
• sympathetic effects

Question 19

how does cocaine work?

Answer 19

• inhibits pumping of NA back into neuron > more left in synaptic cleft
• excitatory effect on post-synaptic neuron

Question 20

2 types of drugs which block NMJ

Answer 20

• non-depolarising blockers
• depolarising blockers

Question 21

non-depolarising blockers

Answer 21

• competitive antagonists @ N receptors
• overcome by increasing [Ach]
• e.g. rocuronium (synthetic derivative of tubocurarine - can’t be used b/c side effects)

Question 22

depolarising blockers

Answer 22

• agonist @ N receptors
• keep in depolarised state instead of allowing for depol/repol cycle which is needed for contraction
• inactivate Na+ channel > receptors unresponsive to Ach
• action made worse by increasing Ach
• e.g. suxamethonium (succinylcholine)

Question 23

why does suxamethonium have a short effect?

Answer 23

• hydrolysed rapidly in body by plasma cholinesterase
• this enzyme is absent in some people > causes paralysis
• no clinically suitable drugs to reverse depolarising blockers

Question 24

when do we use non-depolarising blockers

Answer 24

• e.g. surgery when we want to produce paralysis, stop breathing
• muscle relaxation, facilitate tracheal intubation + mechanical ventilation
• Pt is conscious but can feel pain

Question 25

myasthenia gravis

Answer 25

- autoantibodies reduce action of nicotinic receptors > Ach can't bind to transmit AP - AP only generated in a small proportion of muscle fibres, contraction not sustained > muscle weakness

Question 26

how do we treat myasthenia gravis

Answer 26

- give ANTIcholinesterase (pyridostigmine) to reduce breakdown of Ach > increased chance of binding to an available nicotinic receptor - need atropine to act as a competitive antagonist @ M receptors (prevent parasympathetic side effects of excess ACh) - don't just give Ach b/c it won't get into the NMJ

Question 27

what does pralidoxime do

Answer 27

reactivates acetylcholinesterase to promote breaking down of ACh

Question 28

how do orthodontic surgeries achieve delayed absorption, promoting local drug impact and stopping systemic entrance?

Answer 28

- co-administration of the drug with epinephrine

Question 29

absorption vs penetration

Answer 29

- absorption: travel from site of administration to action - penetration: ability for drug to disperse in the body