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Cardiovascular and Haematology (PHAR1017 ) year 1 > Biochemical principles of pharmacology > Flashcards

Biochemical principles of pharmacology Flashcards

1
Q

what are ACE inhibitors an example of?

A

enzyme inhibitors

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2
Q

what are the proteins targeted by drugs?

A

enzymes
ion channels
transport proteins

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3
Q

what are the most common targets of drugs?

A

receptors because they can stimulate or stop an action

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4
Q

what inhibitors are used in the hospitals for cardiovascular?

A

ACE inhibitors
statins
aspirin

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5
Q

what inhibitors are used in the hospitals as blood thinners?

A

Warfarin
Rivaroxaban
Dabigatran

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6
Q

what inhibitors are used in the hospitals as Analgesic/pain?

A

paracetamol
ibuprofen

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7
Q

what inhibitors are used in the hospitals as antibiotics?

A

Amoxicillin

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8
Q

what is ACE an example of?

A

protease which catalyses peptide bonds

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9
Q

where are ACE taken from and inspired by?

A

taken from venom of snakes inspired by carboxypeptidase A

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10
Q

what do ACE inhibitors do?

A

reduce the formation of Angiotensin ll causing decrease in blood pressure
decrease breakdown of Bradykinin causing coughing

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11
Q

what is Angiotensin ll?

A

signalling hormone

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12
Q

what is Angiotensin l?

A

precursor peptide

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13
Q

what is angiotensinogen?

A

precursor protein

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14
Q

what are At1 receptors for?

A

vasoconstriction and aldosterone release

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15
Q

what are the two kinds of inhibtion?

A

reversible (non-covalent)
irreversible (covalent)
competitive
uncompetitive
mixed

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16
Q

how can the mode of action of an enzyme inhibitor be determined?

A

enzyme kinetics

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17
Q

what is the Michaelis-Menten constant Km?

A

‘Concentration of substrate [S] at which the initial velocity V0 of catalysis is half maximal.’

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18
Q

how do you determine Km?

A

carry experiments where:
enzyme concentration remains constant
substrate concentrations is varied
initial velocity is determined over time

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19
Q

why is Lineweaver-Burk plot used?

A

‘because hyperbola is difficult to fit so 1/[S] (x-axis) vs 1/V0 (y-axis) is used’

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20
Q

what are the effects of calcium blocker?

A

stop uptake of Ca2+ ions by smooth muscle cells
causing smooth muscle relaxation: vasodilation
decreases muscle contractions which decreases heart rate

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21
Q

what are the adverse effects of calcium blockers?

A

arteries dilate
veins are unaffected
swollen ankles because excess fluid remains

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22
Q

what are examples of membrane transport proteins?

A

ion channels
ion pumps
solute transporters
ABC transporters

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23
Q

what are pharmaceutically important types of proteins?

A

drug targets
drug uptake and secretion

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24
Q

what are the two types of ion channels?

A

voltage gated
ligand gated

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25
Q

how do particles pass ion channels?

A

diffusion which is passive process

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26
Q

what is the structure of ion channels?

A

integral membrane proteins
multimetric proteins

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27
Q

what is a selectivity filter?

A

negatively charged amino acids only allow certain ions through

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28
Q

what is the selective filter for calcium ion channels?

A

four aspartates

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29
Q

what causes asymmetry in selectivity filter?

A

‘binding of calcium-channel blocker amlodipine therefore Ca2+ is unable to pass through’

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30
Q

how is the potency of inhibitors determined?

A

comparing concentration at 50% of inhibition (IC50)

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31
Q

what is potency?

A

‘a measure of drug activity expressed in terms of the amount required to produce an effect’

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32
Q

what is selectivity?

A

comparing the action of two inhibitors to each other

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33
Q

what are other classes of proteins in membrane transport?

A

Solute transporters
Thiazide diuretics

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34
Q

what are Thiazide diuretics?

A

inhibit activity of a transporter
involves active transport
Na+, Cl- symporter on kidney
increased water and slat excretion
reduced blood volume and cardiac output
reduced blood pressure

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35
Q

what is vasoconstriction?

A

narrowing blood vessels increasing blood pressure

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36
Q

what does aldosterone do?

A

salt and water control

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37
Q

what is Km a measure of?

A

how well enzyme binds to substrate

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38
Q

what does a Michaelis-Menten plot and Lineweaver-Burk plot for competitive inhibitor look like?

A

slide 23
lecture 1 Biochem Pharmacology

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39
Q

what does a Michaelis-Menten plot and Lineweaver-Burk plot for uncompetitive inhibitor look like?

A

slide 24
lecture 1 Biochem Pharmacology

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40
Q

what does a Michaelis-Menten plot and Lineweaver-Burk plot for mixed inhibitor look like?

A

slide 25
lecture 1 Biochem Pharmacology

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41
Q

what is the sodium/potassium pump inhibited by?

A

cardiac glycosides

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42
Q

what does the sodium/potassium pump result in?

A

reduced heart rate while increases force of contraction of heart muscle so used for heart failure treatment

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43
Q

what does inhibition of Na+/K+-ATPase lead to?

A

increase in intracellular Na+
and then increase in intracellular Ca2+

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44
Q

what happens when a bioassay increases in complexity?

A

better representation of pateint

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45
Q

what happens when bioassay decreases in complexity?

A

better understanding of mechanism

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46
Q

what is the central nervous system?

A

brain and spinal chord

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47
Q

what is the peripheral nervous system?

A

somatic nervous system
autonomic nervous system

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48
Q

what does the somatic nervous system consist of?

A

voluntary response of skeletal muscles
motor control- efferent nerves
sensory control-afferent nerves
an axon connecting from CNS to effector

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49
Q

what does the autonomic NS?

A

sympathetic and parasympathetic NS
subconscious control
smooth muscle, glands
two neurones from CNS to ganglion and then to effector

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50
Q

what is sympathetic NS?

A

fight or flight
body prepared for activity
increases heart rate
vasoconstriction

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51
Q

what is parasympathetic NS?

A

rest and digest
encourages restorative functions
slows heart rate
movement and secretion by GI tract

52
Q

what is ganglion?

A

cluster of peripheral autonomic neurones

53
Q

what is the neurotransmitter used?

A

acetylcholine

54
Q

what are the receptors for noradrenaline and adrenaline?

A

adrenergic receptors

55
Q

what are adrenergic receptors?

A

similar 3D shape
similar amino acid sequence
different genes
different expression pattern

56
Q

what are the receptors for acetylcholine?

A

muscarinic receptors

57
Q

what are muscarinic receptors?

A

similar 3D shape
similar amino acid sequence
different genes
different expression pattern

58
Q

what does SNAP stand for?

A

sympathetic/noradrenaline
acetylcholine/parasympathetic

59
Q

signals for sympathetic and parasympathetic?

A

antagonistic
cooperative
complimentary

60
Q

adrenergic and muscarinic receptors?

A

‘Members of the largest group of receptors: G protein-coupled receptors (GPCRs)
Characteristic: seven trans-membrane -helices (7-TM)’

61
Q

what do beta blockers do?

A

compete for adrenergic receptors with noradrenaline and adrenaline

62
Q

relationship between beta blockers and B1 receptors?

A

antagonistic pairs

63
Q

what are beta blockers used to treat?

A

angina
heart failure
heart attack
atrial fibrillation
high blood pressure

64
Q

what are the types of receptors?

A

ligand-gated ions channels-nicotinic acetylcholine receptors
G protein-coupled receptors-Adrenergic and cholinergic receptors
Kinase-linked receptors
Nuclear receptors

65
Q

what do drugs do to receptors?

A

they can stimulate or oppose receptors

66
Q

what kind of drug is an adrenaline and beta blocker?

A

adrenaline is an agonist
beta blocker is an antagonist

67
Q

what is the role of a receptor?

A

protein that recognises a chemical signal then brings about a response

68
Q

what is ligand?

A

chemical that forms complex with receptor

69
Q

what are examples of receptors?

A

adrenergic receptors
cholinergic receptors

70
Q

what is the process of G protein-coupled receptor signalling?

A

noradrenaline binds to B1 receptor
ligand-receptor complex causes GDP bound to GSa to change into GTP
then GTP bound-Gsa dissociates from GsBy protein then binding to adenylyl cyclase
converting ATP to cAMP
GTP hydrolysed by GSa
cAMP converted to PKA

71
Q

what membrane proteins are linked to GPCR singalling?

A

integral membrane protein
lipid-modified membrane protein
accesory membrane protein

72
Q

when is a G protein-coupled receptor active?

A

a-helix structure of the receptor
Gsa
GTP converted to GDP
acts as an agonsit

73
Q

when is a G-protein-coupled receptor inactive?

A

loop structure
Gsa cannot bind
antagonist

74
Q
A

receptors signalling use interchangeable parts

75
Q

example of interchangeable parts used?

A

B1 and B2 both use Gs proteins and adenylyl cyclase.

76
Q

what is principle 4 of signalling?

A

desensitisation
once receptor activated then feedback loop is triggered inactivating the receptor

77
Q

what is the process of desensitisation of B1 receptor?

A

‘decrease in noradrenaline, reducing binding and activation, Ga not activated further
GTP hydrolysed by Ga protein, Adenylyl cyclase isn’t stimulated anymore
cAMP degraded to AMP
Internalisation of β1 receptor upon continued activation’

78
Q

what is the 5 principle of singalling?

A

integration of singalling

79
Q

what is integration signalling?

A

‘activation of two receptors that leads to a response that integrates both signals’

80
Q

how does a ligand binding assay work?

A

tissue is extracted
Incubated with [3H]-compound
separate bound from unbound ligands
Detect bound [3H]-compound

81
Q

what is Bmax in Scatchard analysis?

A

total number of possible binding sites of receptor-ligand interactions

82
Q

what is the two state receptor response?

A

there is a resting state R and an activated state R*

83
Q

what is the binding and stabilising during R?

A

during resting state R there is a high affinity binding by antagonist and stabilising by antagonist

84
Q

what is the binding and stabilising during R*?

A

during activated state R* there is a high affinity binding by agonist and stabilising by agonist

85
Q

what is the tow state receptor model?

A

lecture 5
slide 3

86
Q

in the presence of an antagonist what is the shift of equilibrium?

A

to resting state

87
Q

in presence of an agonist what is the shift of equilibrium?

A

to activated state

88
Q

what is potency?

A

‘a measure of drug activity expressed in terms of the amount required to produce an effect’

89
Q

what is E50?

A

effective concentration at 50% of maximal response

90
Q

what is receptor occupancy?

A

the amount of drug bound by ligand

91
Q

what is the graph of [Agonist] against response % show?

A

relationship between receptor occupancy and response
relationship between EC50 and Kd

92
Q

what is the equation for a simple system?

A

𝑅 =𝑅_𝑚𝑎𝑥× ( [𝐷])/([𝐷]+𝐸𝐶50) )

93
Q

what is the definition of efficacy?

A

‘the ability of a drug to produce and effect’

94
Q

what is a partial agonist?

A

can’t produce a full response even with full receptor occupancy

95
Q

what is Kd?

A

affinity- the ability of ligand to bind to receptor

96
Q

what is the efficacy of a ligand-receptor interaction?

A

intrinsic ability of ligand to induce an activated state of the receptor

97
Q

what do different agonists differ in?

A

different agonists have different efficacy and affinity

98
Q

what are the features of a reversible inhibtor?

A

non-covalent ligand
competitive, non-competitive, other
an example: binding of propranolol to 1 adrenergic receptor

99
Q

what are the feature of a irreversible inhibtor?

A

covalent ligand
example:: phenoxybenzamine binding to a1 and a2 adrenergic receptors

100
Q

what is pure antagonists effect?

A

no change in receptor activity

101
Q

what is inverse agonist?

A

inhibits constitutive activity

102
Q

features of Receptor antagonists – competitive binding?

A

in antagonist prescence the potency of agonisst is reduced
no change in efficacy
inverse agonist behave similarly to pure antagonist
antagonists have affinity no efficacy

102
Q

how can partial agonists can act as antagonists – competitive binding?

A

in the presence of an agonist a partial agonist has antagonistic activity

102
Q

what is constitutive activity?

A

receptors showing noticeable activity in the absence of an agonist

103
Q

what is the potency and efficacy of agonist in the presence of partial agonist?

A

Potency and efficacy of agonist are reduced in presence of partial agonist

104
Q

what is a treatment for bradycardia?

A

Adrenaline β1 receptor agonist and Atropine M2 receptor antagonist stimulate myocyte contraction

105
Q

what is adrenaline an example of?

A

sympathomimetric drug

106
Q

what is Atropine M2 receptor antagonist an example of?

A

parasympatholytic drug

107
Q

what is the effect of adrenaline?

A

increases sympathetic signal

108
Q

what is the effect of atropine?

A

decreases parasympathetic signals

109
Q

what does noradrenaline do?

A

promotes smooth muscle relaxation

110
Q

what does acetylcholine do?

A

promotes smooth muscle contraction

111
Q

what receptor promotes muscle relaxation?

A

B2 receptor agonist

112
Q

what drug promotes muscle relaxation?

A

anticholinergic drugs

113
Q

what are the adverse effects of B2 receptor agonist?

A

Fine tremor, feeling shaky, anxiety

114
Q

what are the adverse effects of antimuscarinics?

A

Dry mouth and/or throat irritation

115
Q

why is it difficult to make a drug specific to a receptor?

A

B1 and B2 adrenergic receptors are similar

116
Q

why are beta blockers no used for asthma patients?

A

ins’t recommended because it can be harmful

117
Q

what are the drugs in treatment of asthma?

A

Salmeterol and Salbutamol

118
Q

what is therapeutic index?

A

ratio of the dose of drug that causes toxic effect vs the effective dose
𝑇ℎ𝑒𝑟𝑎𝑝𝑒𝑢𝑡𝑖𝑐 𝑖𝑛𝑑𝑒𝑥 𝑇𝐼 = TD50/ ED50
TD50 is toxic dose for 50% of population
ED50: effective dose for 50% of population

119
Q

what is a narrow therapeutic index?

A

therapeutic index <10

120
Q

what are teh main targets of drugs?

A

enzymes
ion channels
transport proteins
receptors

121
Q

examples of drugs that target enzymes, ion channels, transport proteins?

A

Proton-pump inhibitors
ibuprofen, paracetamol

122
Q

examples of drugs for receptors?

A

Histamine H1 antagonists
Histamine H2 antagonists

123
Q

what are the features of Receptor antagonists – irreversible binding?

A

In the presence of an irreversible antagonist, the efficacy of an agonist is reduced
There is no change in potency

124
Q

what are antagonists binding at different site than agonist?

A

unsurmountable antagonists

125
Q

what are spare receptors?

A

the fraction of receptors that is not occupied at Rmax

Cardiovascular and Haematology (PHAR1017 ) year 1 (14 decks)

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