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Principles (Y1) > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is distribution

A

the process by which a drug leaves the circulation and enters tissues perfused by blood

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2
Q

what is metabolism

A

the process by which tissue enzymes catalyse the chemial conversion of a drug to a more polar form that is more readily excreted from the body

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3
Q

what is excretion

A

the process by which the drug is removed from the body

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4
Q

what is pharmacodynamics

A

what a drug does to the body

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5
Q

what is pharmacokinetics

A

what the body does to a drug

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6
Q

what is an agonist

A

a drug that binds to a receptor to produce a cellular response

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7
Q

what is affinity

A

strength of assoiation between a ligand and a receptor, as affinity increases dissociation rate decreases

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8
Q

what is efficacy

A

ability of an agonist to evoke a cellular response, as efficacy increases the response rate also increases

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9
Q

what is an antagonist

A

drug that blocks the action of an agonist, possess affinity but not effcacy

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10
Q

competitive antagonism

A

binding of an agonist and antagonist occur at the same site and is therefore competitive- reduced potency of agonist, does nothing to efficacy of agonist. causes parallel right shift of angoist concentration with no depression in maximal response

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11
Q

non-competitive antagonism

A

agonist and antagonist do not bind at the same site, does not effect the potency of the agonist but decreases the efficacy of the agonist and the depresses the slope and maximum response curve.

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12
Q

factors controlling drug absorption

A
  1. solubility
  2. chemical stability
  3. lipid to water partition coefficient- the relatice solubility of a drug in lipid compared to water and rate of diffusion of drug increases with lpid solubility
  4. degree of ionisation- most drugs exist in equilibrium, on unionised forms readily diffuse across the lipid bilayer
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13
Q

5 factors for drug absorption in the gut

A
  • GI motility
  • pH at the absorptive site
  • blood flow
  • the way in which the drug is manufactured ie is it slow released
  • physiochemical interactions
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14
Q

enteral route of administration

A

oral (convienent, non-sterile, good absorption generally, not good for some drugs due stomach acid and enzymes, first pass metabolism and GI irritation)
sublingual (by passes portal system so avoids first pass metabolism, avoids gastric acid)
rectal (by passes portal system, so avoids first pass metabolism, avoids gastric acid and variable absorption)

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15
Q

parenteral route of administration

A

IV (100% systemic availability, rapid onset, continuous infusion, can be used for drugs that cuases local tissue damage, sterile, risk of sepsis, high drug level at heart)
IM (rapid onset of lipid soluble drugs, slow prolonged release, painful, tissure damage and absorption variable)
inhalation (lungs have higher surface area, good for volitle agents, good for local effect)
topical (ideal for local effect)

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16
Q

First order kinetics

A

rate of elimination is directly proportional to drug concentration. Half life is inversely proportional to elimination rate constant

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17
Q

First order kinetics

A

rate of elimination is directly proportional to drug concentration. Half life is inversely proportional to elimination rate constant

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18
Q

rate of elimination=

A

clearance x plasma conc

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19
Q

what is volume of distribution

A

volume into which a drug appears to be distributed with a conc equal to that of the plasma

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20
Q

factors which affect drug disposition

A

ADME- absorption, distribution, metabolism and excretion

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21
Q

Phase 1 of drug metabolism:

A

oxidation, reduction and hydrolysis (making a drug more polar, adds a chemically reactive gorup permitting conjugation)

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22
Q

Phase 2 of drug metabolism:

A

conjugation, adds endogenous compound increasin polarity

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23
Q

renal excretion of drugs:

A
  1. glomerular filtration (occurs freely for most drugs)
  2. active tubular secretion (organic anion transporter- handles acidic drugs and organic cation transporter- handles basic drugs)
  3. passive reabsorption
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24
Q

what is depolarisation

A

the membrane potential has become less negative or even positive

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25
Q

what is Hyperpolarisation

A

the membrane potential becomes even more negative

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26
Q

sodium channels

A

Na+ flows inwards
concentration of 140mm outside cell and 10-15mm inside cell
negative driving force- inward movement of sodium

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27
Q

Potassium channels

A

K flows outwardly

positive driving force- outward movement of K

28
Q

Ion channels

A

protein complexes spanning lipid bilayer, form a central pathway to allow rapid flow of selected ions

29
Q

ion channels responsibe for action potentials in neurones:

A

voltage activated Na channels- depolarising

voltage activated K channels- hyperpolarising

30
Q

how are voltage activated Na and K channels activated

A

by membrane depolarisation

Na rapidly activted, K slightly delayed

31
Q

activation of Na channels self-reinforcing, opening of a few channels causes further depolarisation

A

positive feedback (upstoke of graph)

32
Q

Activation of K channels is self-limiting, outward movement of K causes repolarisation which turns off the stimulus

A

negative feedback (downstroke of graph)

33
Q

what is absolute refreactory period?

A
  • No stimulus, however strong, can elicit a second action potential
  • All Na channels inactivated
34
Q

what is relative refractory period?

A

-Stronger than normal stimulus may elicit a second action potential

35
Q

Oligodendrocytes

A

produce myelinated Cells in the CNS

36
Q

myelinated cells

A

Myelin is a fatty white substance that surrounds the axon of some nerve cells, forming an electrically insulating layer. It is essential for the proper functioning of the nervous system

37
Q

Astrocytes

A

star shaped, support homeostasis and maintain BBB

38
Q

Microglia

A

immune surveillance, amrcophages of CNS

39
Q

functions of the autonomic NS

A
  • Carries output from the CNS to the whole of the body other than skeletal muscle
  • Regulates visceral functions that are largely involuntary
40
Q

sympathetic nervous system:

A

orchestrates the stress response and energy consumption associated with ‘fight or flight’ reactions, but also has very important ongoing activity

41
Q

parasympathetic nervous system:

A

regulates many functions, some of which are restorative and energy conserving ‘rest and digest’

42
Q

Sympathetic facts:

A

Pre ganglionic neurone=Ach
post ganglionic neurone=noradrenaline
outflow at T1-L2

43
Q

effects of sympathetic nervous system:

A
  • increases HR and force of contraction
  • relaxes bronchi and decreases mucus production
  • Reduces GI motility and constricts sphincters
  • Vasoconstriction but relaxation in skeletal muscle
  • Release of adrenaline from adrenal gland
  • Ejaculation
44
Q

parasympathetic facts

A

both pre and post ganlionic neurones are Ach

cranial nerves 3/7/9/10

45
Q

effects of parasympathetic nervous system:

A
  • Decreases HR
  • Bronchoconstriction, stimulates mucus production
  • Increases GI motility and relaxes sphincters
  • No effect on blood vessels or adrenal glands
  • Erection
46
Q

what is Neurochemical Transmission

A
  • Precursor taken up
  • Transmitter synthesised and stored
  • Action potential depolarises
  • Calcium influx through voltage-activated channels
  • Calcium induced release of transmitter
  • Receptor activation
  • Enzyme-mediated inactivation of transmitter or reuptake of transmitter
47
Q

what is sympathetic chemical transmission

A

action pot from CNS
travels to presynaptic terminal of preganglionic neurone triggering ca entry and release Ach
Ach opens ligand gated ion channels in the post ganlionic neurone causing depolarisation and generation of an AP that travels to presynaptic terminal of neurone, triggering ca entry and release of noradrenaline
Noradrenaline activates G protein coupled receptors - adrenoceptors

48
Q

what is parasympathetic chemical transmission

A

Pretty much the same as sympathetic BUT
ACh always the transmitter used by postganglionic neurones
ACh activates G protein coupled muscarinic acetylcholine receptors in target cell membrane

49
Q

Ligand gated channels

A
  • Consist of separate glycoprotein subunits forming a central, ion conducting channel
  • Allow rapid changes in the permeability of membrane to certain ions
  • Rapidly alter membrane potential
50
Q

G-protein Coupled Receptors - Muscarinic ACh receptors

A
  • Receptor, G-protein and effector are separate proteins
  • G protein couples receptor activation to effector modulation
  • Signalling slow in comparison to transmitter-gated ion channels
51
Q

G protein

A

oPeripheral membrane protein
o3 polypeptide subunits (alpha = binding site)
oContains guanine nucleotide binding site which can hold GTP

52
Q

depolarisation

A

the membrane pot becomes positive

53
Q

for voltage activated Ca2+channels to open the membrane pot must be…

A

positive

54
Q

Nicotinic Acetlycholine Receptors (Ligand-gated)

A
  • Consist of 5 glycoprotein subunits forming a central, cation conducting, channel
  • Diverse range of subunits
  • Alpha 1-10, beta 1-4, gamma, delta, epsilon
  • Binding of transmitter opens gate
55
Q

what are the 2 types of Ach receptors?

A

nitcotinic

muscarinic

56
Q

nicotine acts as an agonist- mimic the action of Ach

A

..

57
Q

G proteins coupled Muscarinic Ach receptor subtypes at parasymapthetic neuroeffector junctions

A

M1 - Gq - stimulates phospholipase C - increased stomach acid secretion

M2 - Gi - inhibition of adenylyl cyclase, opening of K+ channels - deacreased HR

M3 - Gq - stimulates phospholipase C - increased saliva secretion and bronchoconstriction

58
Q

Cholinergic transmission at parasympathetic neuroeffector junctions

A
  • Synthesis and storage of ACh
  • Depolarisation by action potential
  • Calcium influx through voltage-activated calcium channels
  • Calcium induced release of ACh
  • Activation of muscarinic ACh receptor subtypes (M1-M3) causing cellular response
  • Degradation of ACh to choline and acetate by AChE - terminates transmission
  • Reuptake and reuse of choline
59
Q

G protein coupled adrenoceptor subtypes at sympathetic neuroeffector junctions

A
  • B1 - Gs - stimulation of adenylyl cyclase - Increased HR and force
  • B2 - Gs - stimulation of adenylyl cyclase - Relaxation of bronchial and vascular smooth muscle
  • A1 - Gq - stimulation of phospholipase C - contraction of vascular smooth muscle
  • A2 - Gi - inhibition of adenylyl cyclase - inhibition of NA release
60
Q

Noradrenergic Transmission at Sympathetic Neuroeffector Junctions

A
  • NA synthesis and storage
  • Depolarisation by action potential
  • Calcium influx through voltage activated calcium channels
  • Calcium induced release of NA
  • Activation of adrenoceptor subtypes causing cellular response
  • Reuptake of NA by transporters U1/U2
  • Metabolism of NA by MAO and COMT
61
Q

Amphetamine

A
  • U1 substrate
  • Inhibits MAO
  • Displaces NA into cytoplasm
  • NA accumulates in synaptic cleft causing increased adrenoceptor stimulation
62
Q

Prazosin

A
  • Selective, competitive antagonist of a1

- Vasodilator used as anti-hypertensive

63
Q

Atenolol

A
  • Selective, competitive antagonist of B1

- Used as an anti-anginal and anti-hypertensive agent

64
Q

Salbutamol

A
  • Selective agonist at B2

- Used as bronchodilator in asthma

65
Q

Atropine

A
  • Competitive antagonist of Muscarinic ACh receptors, does not block nicotinic ACh receptors
  • Blocks parasympathetic division of ANS
  • Used to reverse bradycardia post MI and in AChE poisoning

Principles (Y1) (9 decks)

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