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Phase 2a Introductory Clinical Science > Pharmacology > Flashcards

Pharmacology Flashcards

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1
Q

what is a drug?

A

chemical substance of known structure which, when administered to a living organism, produces a biological effect

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2
Q

what is pharmacology?

A

branch of medicine concerned with uses, effects and modes of action of drugs

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3
Q

what is pharmacodynamic?

A

how the drug affects the body

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4
Q

what is druggability/ligandability?

A

the ability of a protein target to bind to a small molecule with high affinity.

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5
Q

what is the estimated number of human genes that are druggable?

A

10-15%

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6
Q

what are four types of drug targets?

A

receptors
enzymes
transporters
ion channels

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7
Q

what is a receptor?

A

component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligand’s observed effects which could be an intracellular response

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8
Q

what kind of susbtance can ligands be? (2) give examples

A

exogenous (e.g. drug)

endogenous (e.g. hormones, neurotransmitter)

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9
Q

what is a ligand?

A

a molecule that binds to another (usually larger) molecule

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10
Q

what is an agonist?

A

compound that binds to a receptor and activates it

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11
Q

what is an antagonist?

A

a compound that reduces the effect of an agonist, do not activate receptors

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12
Q

what are the two types of antagonists?

A

competitive antagonist

non-competitive antagonist

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13
Q

what is another name of competitive antagonist?

A

selective antagonist

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14
Q

what is another name of non-competitive antagonist?

A

allosteric antagonist

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15
Q

where do competitive antagonists bind?

A

same site as agonist (orthosteric site)

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16
Q

where do non-competitive antagonists bind?

A

other site to agonist binding site (called allosteric site)

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17
Q

what can a competitive antagonist do?

A

reverse effects of agonist

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18
Q

what does a non-competitive antagonist do to the site of an agonist?

A

conformation changes so agonist can’t bind to it

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19
Q

what are the three types of chemicals that communicate with receptors? give examples

A
  1. neurotransmitters (acetylcholine, serotonin)
  2. autacoids (cytokines, histamine)
  3. hormones (testosterone, oestrogen)
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20
Q

what are the four types of receptors?

A
  1. ligand-gated ion channels
  2. G protein coupled receptors
  3. Kinase-linked receptors
  4. cytosolic/nuclear receptors
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21
Q

typically, what type of chemical work on ligand-gated ion channels? give an example

A

neurotransmitters e.g. nicotinic acetylcholine

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22
Q

how fast do ligand-gated ion channels work?

A

milliseconds

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23
Q

how does the effects of the receptor initiate an effect?

A

ligand binds to receptor -> receptor channel opens (coupling between receptor and ion channel so ion channel opens)

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24
Q

give two examples of G protein coupled receptors

A

beta-adrenoceptors

muscarinic ACh receptors

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25
Q

how fast do G protein coupled receptors work?

A

within seconds

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26
Q

what are G protein coupled receptors?

A

membrane receptor coupled to intracellular effector system via G protein

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27
Q

how do the G protein coupled receptors lead to a change in the cell?

A

ligand binds to receptor causing changes in receptor causing changes with G protein which lead to activation of intracellular signalling pathway

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28
Q

how does a G protein shape change with the receptor?

A

GTPase is part of receptor, changes to receptor lead to GTPase changing G protein. G protein in GTP format will keep signalling off, and in GDP format will make signalling on. GTPase causes changes from GTP to GDP etc.

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29
Q

give three examples of uses of kinase-linked receptors

A
  1. cytokine receptors
  2. for insulin
  3. for growth factors
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30
Q

how fast do kinase receptors work?

A

hours

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31
Q

describe the structure of kinase-linked receptors

A

extracellular binding domain linked to intracellular domain by single transmembrane helix

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32
Q

what molecules are the most common ligands for kinase-linked receptors?

A

peptide molecules

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33
Q

how do kinase-linked receptors lead to changes in the cell?

A

ligand binds to receptor leading to phosphorylation of intracellular domain of receptor leading to cellular signalling cascade usually leading to gene transcription

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34
Q

what is common about ligand-gated receptors, G protein coupled receptors, kinase-linked receptors that is not common to cytosolic/nuclear receptors?

A

the first three work by transducing a signal from outside of cell leading to changes in receptor which initiates signalling cascade

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35
Q

give 3 example of cytosolic/nuclear receptors

A

steroid hormone, thyroid hormone, oestrogen hormone receptors

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36
Q

how fast do cytosolic/nuclear receptors work?

A

hours

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37
Q

where are cytosolic/nuclear receptors found?

A

soluble phase of cell
some in cytosol then move to nucleus when ligand activated
others already in nucleus

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38
Q

what do cytosolic/nuclear receptors do?

A

transcription regulators (activators usually)

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39
Q

what is the structure of cytosolic/nuclear receptors?

A

DNA binding domain and Ligand binding domain:
DNA binding domain made of two zinc fingers which can interact directly with DNA and recognise different parts of DNA
Ligand binding domain can directly interact with ligand protein, leading to changes in receptor which changes zinc fingers so that they can access DNA.
(zinc fingers can’t interact or recognise DNA without ligand)

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40
Q

describe the zinc fingers in DNA binding domain

A

two cysteine rich loops in amino acid change held together in formation by zinc ions

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41
Q

how do cytosol/nuclear receptors lead to changes in cell?

A

ligand bound to receptor -> receptor bound to DNA -> transcription occurs

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42
Q

give an example of a receptor that has subtypes? give the subtypes and their jobs

A 
histamine receptors
H1: allergic responses
H2: gastric acid secretion and contraction of ileum
H3: CNS disorders e.g Alzheimer's
H4: immunity and inflammatory
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43
Q

what is potency?

A

can be measure of effective concentration at 50% (EC50) which is the concentration of agonist needed to reach half the maximum response. having a lower concentration to reach a higher response means higher potency

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44
Q

what is efficacy?

A

maximum response achievable from a dose, can be referred to as Intrinsic Activity referring to ability of drug-receptor complex to produce maximum functional response

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45
Q

what is a partial agonist?

A

those that can never get a total full response from a receptor. their efficacy is lower than that of the ability of the receptor. a full agonist has more efficacy than a partial agonist

46
Q

give an example of a non-selective agonist

A

isopernaline non-selective to beta-adrenoceptor because can bind to beta1 and beta2 receptors

47
Q

what is isopernaline used for?

A

bradycardia (to slow heart rate) and heart block

48
Q

give an example of a selective agonst

A

salbutamol selective to beta2-adrenoceptor

49
Q

what is salbutamol used for?

A

open medium and large airways for COPD and asthma

50
Q

what are the four factors that govern drug action with receptors?

A

affinity
efficacy
receptor number
signal amplification

51
Q

what is affinity

A

how well a ligand binds to the receptor

52
Q

what is efficacy

A

how well a ligand activates the receptor

53
Q

which out of affinity and efficacy is shown by both antagonists and agonists

A

affinity

54
Q

how does receptor number effect drug interaction with a receptor

A

number of receptors present on cell surface varies. cells have receptor reserves but the reserves are not for partial agonists

55
Q

what is meant by signal amplification in the context of drugs interacting with receptors

A

some tissues are better at signal amplification than others, two tissues may have same receptor and same agonist but one tissue will have a larger response because it has more signal amplification ability

56
Q

what is tolerance?

A

reduction in the drug/agonist effects over time, occurring due to continuously, repeated, high concentrations of agonist

57
Q

what is desensitisation?

A

occurs if uncoupling, internalisation, degradation of receptor occurs

58
Q

what is an enzyme inhibitor?

A

molecule that binds to an enzyme and decreases (normally) its activity. prevents the substrate from entering the enzyme’s active site thus preventing the enzyme from catalysing the reaction

59
Q

what are the two types of enzyme inhibitors?

A

irreversible and reversible inhibitors

60
Q

how do irreversible inhibitors work?

A

react with enzyme and change it chemically e.g. via covalent bonds

61
Q

what is a reversible inhibitor?

A

those that bind non-covalently to enzyme

62
Q

give two examples of drugs that are enzyme inhibitors

A

statins

angiotensin converting enzyme inhibitors

63
Q

what enzyme do statins inhibit?

A

HMG-CoA reductase in cholesterol production pathway

64
Q

what do statins reduce and why are they taken?

A

they reduce bad cholesterol and they reduce the risk of cardiovascular disease and mortality in those with high risk

65
Q

what enzyme do ACE inhibitors work on?

A

angiotensin converting enzyme

66
Q

what is the renin-angiotensin-aldosterone system for?

A

blood pressure regulator, increases blood pressure by increasing salt and water retention

67
Q

what do ACE inhibitors reduce and why do people take them?

A

reduce angiotensin 2 (because ACE inhibited so less angiotensin 1 -> 2) reduce blood pressure

68
Q

what is wrong in Parkinson’s disease?

A

abnormal low dopamine in brain.

69
Q

how is LDOPA linked to dopamine?

A

LDOPA is a precursor to dopamine but has to cross the blood brain barrier to become dopamine

70
Q

name four inhibitors used to treat parkinson’s disease

A
  1. peripheral DDC inhibitor
  2. peripheral COMT inhibitor
  3. central COMT inhibitor
  4. Monoamine oxidase B inhibitor
71
Q

what does peripheral DDC inhibtor do?

A

inhibits DDC enzyme outside of brain from converting LDOPA to dopamine outside of brain so more LDOPA enters brain to make dopamine in brain

72
Q

what does peripheral COMT inhibitor do?

A

inhibits COMT enzyme in periphery so prevents breakdown of LDOPA so more LDOPA enters brain

73
Q

what does central COMT inhibitors do?

A

block central COMT which convert dopamine to another substance, therefore the inhibition means that there is more dopamine to activate D1 and D2 receptors

74
Q

what do monoamine oxidase B inhibitors do?

A

prevent dopamine breakdown in brain

75
Q

what do we mean by transport when referring to cells?

A

transport: molecules moving across cell membrane allowing cells to get what they need e.g. ions, glucose

76
Q

give three examples of channels that use passive transport

A
  • ENaC (epithelium sodium channels)
  • voltage gated channels
  • receptor activated channels
77
Q

describe ENaC

A

selectively permeable to Na ions and cause absorption of Na ions in some areas.

78
Q

where are ENaC found?

A

kindey- collecting ducts
colon
lungs
sweat glands

79
Q

what endogenous substance blocks ENaC

A

atrial natriuretic peptide

80
Q

what exogenous substance blocks ENaC

A

amiloride

thaizide

81
Q

where are voltage gated channels found?

A

excitable cells membrane e.g. muscle, neurons

82
Q

when are voltage gated channels closed and open?

A

resting membrane potential- closed

depolarised membrane potential- activated and opened

83
Q

give four ions that can use voltage gated channels to pass

A

calcium
sodium
potassium

84
Q

what does activation of voltage gated calcium channels lead to?

A

calcium enters cell and activated calcium-sensitive potassium channels leading to muscle contraction/ excitation of neurons etc.

85
Q

what is a drug that blocks calcium channels?

A

amlodipine

86
Q

what does amlodipine do to calcium channels?

A

stops calcium ions entering vascular smooth and cardiac muscle

87
Q

what is amlodipine used for?

A

reduce blood pressure because causes vasodilation and less peripheral vascular resistance

88
Q

what does lidocaine do in relation to voltage gated channels?

A

blocks transmission of action potential so does not allow voltage gated channels to open

89
Q

what is lidocaine used for?

A

anaesthetic

90
Q

how does increased glucose affect potassium channels?

A

increased glucose leads to voltage gated potassium channels being locked in pancreas beta cells so lots of repetitive firing of of action potential leading to lots of calcium entry triggering insulin release

91
Q

name a drug that lowers blood glucose by blocking voltage gated K channels?

A

nateglinide

92
Q

give a example of receptor activated channel

A

receptor activated chloride channels

93
Q

what is another two names for receptor activated channels

A

ligand gated ion channel

ionotropic channel

94
Q

what opens receptor activated channels

A

ligand binding to receptor

95
Q

describe GABA-A receptors and how they are involved to receptor activated chloride channels

A

chloride channel attached that opens when GABA (ligand) (inhibitory neurotransmitter) binds to GABA-A receptor on post-synaptic membrane

96
Q

what does the opening of GABA-A receptor activated chloride channels do

A

lots of Cl- enter cell so hyperpolarisation occurs

97
Q

give a drug that can enhance the GABA-A receptor activated chloride channel and how it does so

A

phenobarbitone by increasing permeability of channel to chloride

98
Q

what are the names of the three main protein ports in the cell membrane?

A

uniporters
symporters
antiporters

99
Q

what are uniporters?

A

use energy to pull molecules into cell

100
Q

what is a symporter

A

co-transporter
use movement into cell of one molecule to pull in another molecule against its concentration gradient (molecule so not always ions)

101
Q

give an example of a symporter

A

Na-K-Cl cotransporter (NKCC) moves those ions into cell in same direction. found in organs that secrete fluids

102
Q

give a drug that inhibits NKCC

A

furosemide

binds to NKCC so Na, Cl, K lost in urine (inhibits NKCC at thick ascending limb of loop of henle)

103
Q

what is an antiporter

A

cotransporter
uses energy from one substance moving down its gradient (mostly Na/K/H) to move another substance against its concentration gradient

104
Q

give two examples of antiporters

A

na/k ATPase

k/H ATPase

105
Q

what does Na/K ATPase do

A

pumps 3Na out and 2K into cell against their concentration gradient using ATP

106
Q

give a drug that inhibits Na/K ATPase and why it is used

A

Digoxin

atrial fibrillation, atrial flutter, heart failure

107
Q

how does digoxin reduce heart rate

A

inhibits Na/K ATPase so more intracellular Na so less activity from Na-Ca exchanger so more Ca intracellular which lengthens cardiac action potential leading to a decreased heart rate

108
Q

where is K/H ATPase used and what does it do

A

in stomach
proton pump
exchanges K from intestinal lumen with cytoplasmic H so acidifies stomach and activates pepsin enzymes

109
Q

what blocks K/H ATPase

A

proton pump inhibitors

inhibit acid secretion

110
Q

give an example of a drug that use irreversible inhibition

A

Omeprazole

Phase 2a Introductory Clinical Science (7 decks)

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