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CSC1005 - Integrated Human Physiology > Pharmocology > Flashcards

Pharmocology Flashcards

1
Q

What is absorption?

A

The movement of a drug from its site of administration into the systemic circulation

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2
Q

What is adverse effect?

A

General term for an undesirable and potentially harmful drug effect

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3
Q

What does ADME stand for?

A

Absorption
Distribution
Metabolism
Elimination

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4
Q

What is affinity?

A

The ability of thedrugto bind to a receptor

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5
Q

What is Kd?

A

Attraction with which a drug binds to the receptor and it is the concentration at which half of all the receptors are occupied by the drug

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6
Q

Is the affinity greater or lower with a low Kd?

A

Greater

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7
Q

What is a full agonist?

A

A drug capable of eliciting a maximal response as it displays full efficacy at that drug receptor

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8
Q

What is inverse agonist?

A

A drug capable of eliciting a maximal response as it displays full efficacy at that drug receptor.

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9
Q

What is partial agonsist?

A

Drugs that bind to and activate a given receptor, but only have partial efficacy at the receptor relative to the agonist

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10
Q

What is antagonist?

A

A receptor ligand or drug that blocks, dampens or inhibits an agonist-
mediated response rather than provoking a biological response itself upon binding to a receptor

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11
Q

What is a competitive antagonist?

A

A receptor ligand or drug that binds to the same
binding site as an endogenous ligand or agonist but without activating the
receptor. Agonists and antagonists effectively ‘compete’ for the binding site on the receptor

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12
Q

What is a non-competitive antagonist?

A

A receptor ligand or drug that binds to an allosteric (non-agonist) site on a receptor to prevent the activation of that receptor

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13
Q

What is an allosteric modulator?

A

A substance which indirectly influences (modulates) the effects of an agonist or inverse agonist at a target protein

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14
Q

What is Bmax?

A

The maximum amount of drug which can bind specifically to receptors in a
membrane preparation. If one drug molecule binds to each receptor it acts as an indication of the concentration of receptors in the tissue

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15
Q

What is EC50?

A

The molar concentration (EC 50 ) of an agonist that produces a 50% response of the maximum possible response for that agonist

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16
Q

What is ED50?

A

Dose (ED 50 ) of drug that produces 50% of its maximum response or effect.

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17
Q

What is efficacy?

A

Used to describe agonist responses in relation to receptor occupation

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18
Q

What is the first pass effect?

A

-Orally administered drugs that are
absorbed into the circulation, must pass the liver first prior to becoming
available to the rest of the body.

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19
Q

What is LD50?

A

The dose of a drug that causes death in 50% of the animals tested.

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20
Q

What is a ligand?

A

Chemical compound, endogenous or exogenous, that binds to

a pharmacologically relevant binding site.

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21
Q

What is pharmacodynamics?

A

The biochemical and physiological effects of drugs, particularly those that define the drugs mechanism of action on the body.

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22
Q

What is pharmacokinetics?

A

The absorption, distribution, metabolism, and excretion (ADME) of
bioactive drugs following their administration to higher organisms

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23
Q

What is potency?

A

Compares the ability of drugs to produce a

given effect.

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24
Q

What is prodrug?

A

A drug administered in an inactive form that is metabolised in the body to an active form

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25
Q

What is a drug?

A

Chemical substance of known structure, when administrated to a living organism produces a biological effect

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26
Q

What are categories of drugs?

A
  • Physiological system
  • Therapeutic group
  • Chemical properties
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27
Q

What is the most prescribed drug in USA 2017?

A

Lisoprinal

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28
Q

What is the most prescribed drug in UK 2017?

A

Atorvastatins

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29
Q

What is the biggest man-made medical disaster ever?

A

Thalidomide

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30
Q

What are relentlessly incurable diseases?

A
  • Alzheimers disease
  • Glioblastoma
  • Common cold
  • Rabies
  • Diabetes
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31
Q

Why are Alzheimers disease/Glioblastoma/common cold/Rabies/Diabetes so difficult to treat?

A
  • Genetic requirement for increased hormone production
  • Once established, virus is unstoppable
  • Disease mechanism undetermined
  • Pathogen mutates too quickly
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32
Q

What are the routes of drug administration?

A
  • Oral
  • Rectal
  • Intravenous
  • Intramuscular
  • Perecutaneous
  • Nasal
  • Inhalation
  • Sublingal
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33
Q

What are contributing physiological to absorption of oral drugs?

A
  • Gut content
  • GI motility
  • Splanchnic blood flow
  • Drug formation
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34
Q

How do drugs pass membranes?

A
  • Simple diffusion
  • Facilitated diffusion through aqueous channels
  • Carrier-mediated transport
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35
Q

What are different types of carrier-mediated transport?

A
  • ATP-dependent: active

- ATP-independent: passive

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36
Q

What helps the movement of drugs across a membrane?

A
  • High concentration gradient
  • Low molecular weight
  • Low degree of ionisation
  • Lipid solubility
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37
Q

What is bioavailability?

A

Describe how much of the orally given drug makes it into circulation in its active form

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38
Q

What must happen to a dose when converting from intravenous to oral route from with a bioavailability of 50%?

A

Double the dose

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39
Q

What is pro of the route of oral administration?

A

Easy to administer

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40
Q

What is con of the route of oral administration?

A

Subject to first pass effect

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41
Q

What is pro of the route of intravenous administration?

A

100% Bioavailability

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42
Q

What is con of the route of intravenous administration?

A

Enters tissues rich in blood vessels first

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43
Q

What is pro of the route of rectal administration?

A

Can be used in vomiting patients

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44
Q

What is con of the route of rectal administration?

A

Bioavailability varies depending on blood supply

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45
Q

What is pro of the route of intrathecal administration?

A

Cross the blood brain barrier

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46
Q

What is con of the route of intrathecal administration?

A

Difficult to administer

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47
Q

What is pro of the route of inhalation administration?

A

Local effect, very fast

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48
Q

What is con of the route of inhalation administration?

A

Not suitable for large molecules, can leak into systemic blood

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49
Q

What is pro of the route of percutaneous administration?

A

Not subject to first pass effect

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50
Q

What is con of the route of percutaneous administration?

A

Bioavailability varies depending on subcutaneous muscle and fat

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51
Q

Describe alcohol absorption on an empty stomach:

A
  • Some absorbed in stomach

- Most absorbed rapidly in small intestine

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52
Q

Describe alcohol absorption on a full stomach:

A
  • Fatty meal reduce blood alcohol concentration up to 50%
  • Pyloric sphincter is closed
  • Alcohol absorbed more slowly in stomach
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53
Q

What is ethanol?

A

Small molecules with both hydrophobic and hydrophilic properties

54
Q

Can ethanol readily cross cell membrane?

55
Q

How does ethanol distribute around the body?

A

Passively down its concentration gradient

56
Q

Does drug distribute itself evenly between tissues?

57
Q

What is the distribution dependent on?

A
  • Blood flow for speed delivery

- Lipid solubility for tissue accumulation

58
Q

What is pattern of distribution determined by?

A

How rapidly the drug is administered

59
Q

What does fenestra make it easier for large cells to do?

A

Move between cells

60
Q

Where do you find more poorly lipid soluble in blood or fat?

61
Q

Where do you find more highly lipid soluble in blood or fat?

62
Q

What is the distribution of alcohol limited to?

A

Total body water

63
Q

What tissue does alcohol not enter?

A

Adipose tissue

64
Q

Does the total body water difference between males and females?

65
Q

What is the total body of water in males?

66
Q

What is the total body of water in females?

67
Q

Do females have a higher or lower blood alcohol concentration?

68
Q

Can alcohol cross the blood brain barrier?

69
Q

What happens if alcohol crosses blood brain barrier?

A

Leading to cognitive and motor impairment

70
Q

What happens in phase I metabolism?

A

Drug to primary product via expose or add functional group (Oxidation/Reduction/Hydrolysis)

71
Q

What happens in phase II metabolism?

A

Primary product to secondary product to be secreted via conjugation (glucuronyl/suplhate/methyl/glutathione)

72
Q

Describe the metabolism of alcohol in the liver:

A

-Metabolised by oxidation reaction to acetaldehyde to be oxidised to acetic acid to be excreted

73
Q

What is acetaldehyde?

A
  • Toxic metabolite

- Causes: flushing/increases heart rate/headaches/nausea

74
Q

What does alcohol elimination follow?

A

Zero order kinetics

75
Q

Describe alcohol elimination:

A

More than one drink of alcohol, metabolism proceeds at a constant rate because ADH molecules are fully saturated with alcohol, alcohol accumulates in the blood stream

76
Q

What is zero-order elimination kinetics?

A

Elimination of a constant quantity per time unit of the drug present in organism.
Elimination rate is not proportional to amount of drug present

77
Q

What is first order elimination kinetics?

A

Elimination of constant fraction per time of the drug present in the organism.
The elimination is proportional to the drug concentration

78
Q

What is clearance?

A

Volume of plasma cleared of drug per uni time by the processes of metabolism and excretion

79
Q

What is pharmacology?

A

Science that studies the interaction between substances and living organisms

80
Q

What do drugs generally bind to?

A

Regulatory proteins

81
Q

What are types of regulatory proteins?

A
  • Enzymes
  • Carrier proteins
  • Ion channels
  • Receptors
82
Q

What can drugs target?

A

DNA
RNA
Lipids
Ion

83
Q

What is an enzyme?

A

Proteins that regulate chemical reaction in the body

84
Q

How can drugs act on enzymes?

A
  • Enzyme inhibitors
  • False substrates
  • Prodrugs
85
Q

What are enzyme inhibitor drugs?

A

Drugs that inhibit enzyme activity in a reversible or irreversible

86
Q

What are false substrates drug?

A

The drug is converted by enzymes to an abnormal product that disrupts normal metabolic pathway

87
Q

What are prodrug?

A

Inactive precursors that are converted to active dugs by action of an enzyme

88
Q

What are carrier proteins?

A

Transport non-lipid soluble ions and small molecules across cell membrane

89
Q

How do drugs the function of carrier proteins?

A

Drugs affect the transport process by binding to their binding sites

90
Q

What are ion channels?

A

Transmembrane proteins that facilitate the diffusion of ions across the cell membrane

91
Q

How do drugs block ion activity?

A
  1. Enter the channel and bind to recognition site
    or
  2. Diffuse across the cell membrane and bind to a n intracellular recognition site
92
Q

What are receptors?

A

Transmembrane proteins involved in cell signalling

93
Q

How do drugs affect receptors?

A
  • Act on ligand binding domain of the receptor
  • Conformational change activates an intracellular effector domain
  • Triggers transduction mechanism
94
Q

Wha are the different types of receptors?

A
  1. Ligand-gated ion channels (inotropic receptors)
  2. G-protein coupled receptors
  3. Kinase-linked receptors
  4. Nuclear receptors
95
Q

What are ionotropic receptors?

A

Membrane receptors directly coupled to an ion channel

96
Q

What do ionotropic receptors posses?

A

A binding site on the extracellular domain

97
Q

How long does it take for a tissue response from an ionotropic receptor?

A

Milliseconds

98
Q

What are G protein coupled receptors?

A

Membrane receptors coupled to an intracellular effector via G protein

99
Q

What can effectors be in G protein coupled receptors?

A

Enzyme

Ion channel

100
Q

How long does it take for a tissue response from a G protein coupled receptors?

A

100ms to seconds

101
Q

What are kinase-linked receptors?

A

Receptors with an extracellular binding domain and an intracellular catalytic domain

102
Q

What is an intracellular catalytic domain?

A

Binding-domain is occupied

103
Q

What ligands can be included in kinase-linked receptors?

A

Insulin

Growth factors

104
Q

How long does it take for a tissue response from a kinase-linked receptors?

A

Occurs in minutes

105
Q

What are intracellular receptors?

A

act on DNA and modulate gene expression

106
Q

Where are intracellular receptors located?

A

In nucleus or cytoplasm

107
Q

How long does it take for a tissue response from an intracellular receptor?

A

hours - days

108
Q

What are the proteins expressed in cell
membranes that interact with drugs to initiate an
intracellular response?

A.Enzymes
B.Hormones
C.Ligands
D.Receptors

109
Q 
What of the following is not a drug target
A.Enzymes
B.Hormones
C.Ions
D.DNA
110
Q

What are agonists?

A

Ligands that bind to a receptor and induce a conformational change that initiates an intracellular signal

111
Q

What is affinity?

A

Chemical forces that cause the drug to bind to its receptor

112
Q

What is efficacy?

A

Drug ability to activate the receptors once it has bound to it

113
Q

What governs the interaction of an agonist to its binding site on the receptors?

A

Affinity and efficacy

114
Q

Is the drug effect proportional or non-proportional to drug concentration?

A

Proportional

115
Q

What does dose-response curve show?

A

Biological response in relation to drug concentration

116
Q

What is a therapeutic index?

A

Relative safety of the drug

117
Q

What factors are involved in the potency
agonist drugs?

A.Affinity
B.Efficacy
C.Affinity and efficacy
D.Specificity

118
Q

The therapeutic index is…

A. A measure of how effective a drug is to
treat a disease.
B. A measure of the relative safety of the
drug.
C. The amount of drug needed to exert a
therapeutic effect.
D. The effective dose of the drug in the
population.
119
Q

What is antagonist?

A

A drug that binds to a receptor, but does not induce a conformation change
No biological response

120
Q

What are the types of antagonists?

A
  • Receptor antagonists

- Non-receptor antagonists

121
Q

What are different types of receptor antagonists?

A
  • Competive

- Non-competitive

122
Q

What are different types of non-receptor antagonists?

A
  • Chemical
  • Physiological
  • Pharmacokinetic
123
Q

What is a reversible competitive antagonism?

A

Effect of the antagonist can be reversed by increasing the concentration of the agonist

124
Q

What is an irreversible competitive antagonism?

A

Antagonist dissociates very slowly or not at all from the receptor
Synthesis of new receptors may be needed for the agonist to induce a response

125
Q

What is a non-competitive antagonism?

A
  • Binds to an allosteric site the receptor
  • Prevents receptor activation
  • Inhibits the response of the agonist
126
Q

What is a chemical antagonism?

A

Two drugs combine in solution to produce an inactive product

127
Q

What is a physiological antagonism?

A

Two drugs have opposing actions via different receptors on the same tissue

128
Q

What is pharmacokinetic antagonism?

A

Antagonist alters the pharmacokinetics of the agonist

  • Increasing excretion or metabolism
  • Reducing rate of absorption
129
Q

What factors are involved in antagonist drugs
potency?

A.Affinity
B.Efficacy
C.Affinity and efficacy
D.Specificity

130
Q

Non-competitive antagonists…

A. Bind to the agonist site of the
receptor.
B. Prevents receptor activation.
C. Inhibits the response of the
agonist.
D. B and C

CSC1005 - Integrated Human Physiology (18 decks)

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