Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Principles (Y1) > Pharmacology > Flashcards

Pharmacology Flashcards

(65 cards)

Start Studying
1
Q

what is distribution

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is excretion

A

the process by which the drug is removed from the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is pharmacodynamics

A

what a drug does to the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is pharmacokinetics

A

what the body does to a drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is an agonist

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is affinity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is efficacy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is an antagonist

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

First order kinetics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

First order kinetics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

rate of elimination=

A

clearance x plasma conc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

factors which affect drug disposition

A

ADME- absorption, distribution, metabolism and excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Phase 1 of drug metabolism:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Phase 2 of drug metabolism:

A

conjugation, adds endogenous compound increasin polarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is depolarisation

A

the membrane potential has become less negative or even positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what is Hyperpolarisation
the membrane potential becomes even more negative
26
sodium channels
Na+ flows inwards concentration of 140mm outside cell and 10-15mm inside cell negative driving force- inward movement of sodium
27
Potassium channels
K flows outwardly | positive driving force- outward movement of K
28
Ion channels
protein complexes spanning lipid bilayer, form a central pathway to allow rapid flow of selected ions
29
ion channels responsibe for action potentials in neurones:
voltage activated Na channels- depolarising | voltage activated K channels- hyperpolarising
30
how are voltage activated Na and K channels activated
by membrane depolarisation | Na rapidly activted, K slightly delayed
31
activation of Na channels self-reinforcing, opening of a few channels causes further depolarisation
positive feedback (upstoke of graph)
32
Activation of K channels is self-limiting, outward movement of K causes repolarisation which turns off the stimulus
negative feedback (downstroke of graph)
33
what is absolute refreactory period?
- No stimulus, however strong, can elicit a second action potential - All Na channels inactivated
34
what is relative refractory period?
-Stronger than normal stimulus may elicit a second action potential
35
Oligodendrocytes
produce myelinated Cells in the CNS
36
myelinated cells
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
Astrocytes
star shaped, support homeostasis and maintain BBB
38
Microglia
immune surveillance, amrcophages of CNS
39
functions of the autonomic NS
- Carries output from the CNS to the whole of the body other than skeletal muscle - Regulates visceral functions that are largely involuntary
40
sympathetic nervous system:
orchestrates the stress response and energy consumption associated with 'fight or flight' reactions, but also has very important ongoing activity
41
parasympathetic nervous system:
regulates many functions, some of which are restorative and energy conserving 'rest and digest'
42
Sympathetic facts:
Pre ganglionic neurone=Ach post ganglionic neurone=noradrenaline outflow at T1-L2
43
effects of sympathetic nervous system:
- 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
parasympathetic facts
both pre and post ganlionic neurones are Ach | cranial nerves 3/7/9/10
45
effects of parasympathetic nervous system:
- Decreases HR - Bronchoconstriction, stimulates mucus production - Increases GI motility and relaxes sphincters - No effect on blood vessels or adrenal glands - Erection
46
what is Neurochemical Transmission
- 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
what is sympathetic chemical transmission
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
what is parasympathetic chemical transmission
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
Ligand gated channels
- 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
G-protein Coupled Receptors - Muscarinic ACh receptors
- 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
G protein
oPeripheral membrane protein o3 polypeptide subunits (alpha = binding site) oContains guanine nucleotide binding site which can hold GTP
52
depolarisation
the membrane pot becomes positive
53
for voltage activated Ca2+channels to open the membrane pot must be...
positive
54
Nicotinic Acetlycholine Receptors (Ligand-gated)
- 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
what are the 2 types of Ach receptors?
nitcotinic | muscarinic
56
nicotine acts as an agonist- mimic the action of Ach
..
57
G proteins coupled Muscarinic Ach receptor subtypes at parasymapthetic neuroeffector junctions
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
Cholinergic transmission at parasympathetic neuroeffector junctions
- 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
G protein coupled adrenoceptor subtypes at sympathetic neuroeffector junctions
- 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
Noradrenergic Transmission at Sympathetic Neuroeffector Junctions
- 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
Amphetamine
- U1 substrate - Inhibits MAO - Displaces NA into cytoplasm - NA accumulates in synaptic cleft causing increased adrenoceptor stimulation
62
Prazosin
- Selective, competitive antagonist of a1 | - Vasodilator used as anti-hypertensive
63
Atenolol
- Selective, competitive antagonist of B1 | - Used as an anti-anginal and anti-hypertensive agent
64
Salbutamol
- Selective agonist at B2 | - Used as bronchodilator in asthma
65
Atropine
- 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions