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Pharmacology > Module 1 > Flashcards

Module 1 Flashcards

1
Q

Science of substances used to prevent, diagnose, and treat disease.

A

Medical pharmacology

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2
Q

Ancient Hindu text describes 760 medicinal herbs.

A

Susruta

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3
Q

Wrote “Kitab Al Shifa “ which considered 760 drugs and is the chief guide to medical sciences from the 12th century to the 16th century.

A

Avicenna/ Abu Ali Al Hussain Ibn Sina (980-1037)

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4
Q

The science of drug preparation and the medical use of drugs - developed as the precursor to pharmacology.

A

Materia Medica

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5
Q

Developed methods of experimental physiology and pharmacology.

A

Francois Magendie

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6
Q

Investigated the plant extract Curare(muscle relaxant) and proposed site of action of this agent.

A

Claude Bernard

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7
Q

Proposed: Corpora non agunt nisi fixate = “Agents do not act unless they are bound” (drug-receptor binding)

A

Paul Ehrlich

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8
Q

Any substance that produces a change in biologic function through its chemical actions.

A

Drugs

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9
Q

Single, active chemical entity that is used for diagnosis, prevention and treatment of diseases.

A

Drug

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10
Q

Drug that acts as an activator

A

Agonist

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11
Q

Drug that acts as an inhibitor

A

Antagonist

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12
Q

A specific molecule in the biologic system that plays a regulatory role. Drug molecules interact with this molecule.

A

Receptor

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13
Q

Drugs synthesized within the body

A

Hormones

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14
Q

Chemicals not synthesized in the body

A

Xenobiotic (Greek: Xenos = stranger)

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15
Q

Drugs that are exclusively harmful

A

Poison

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16
Q

Defined as poisons of biologic origin,ie, synthesized by plants or animals, in contrast to inorganic poisons such as lead and arsenic

A

Toxins

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17
Q

Nature of drug that determines the best route of administration

A

Physical nature: solid, liquid, gas

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18
Q

Nature of drug that determines specificity of action

A

Drug size: MW 100 - MW 1000

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19
Q

Bond that is very strong and in many cases not reversible under biologic conditions

A

Covalent bond

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20
Q

Bonds that are usually quite weak and are probably important in the interactions of highly lipid-soluble drugs.

A

Hydrophobic bond

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21
Q

The actions of the drug on the body

A

Pharmacodynamics

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22
Q

The actions the body on the drug

A

Pharmacokinetics

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23
Q

When drugs bind to the same receptor molecule but do not prevent binding of the agonist.

A

Allosteric inhibition

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24
Q

Effect in which even in the absence of any agonist, some receptor pool must exist in the activated form some of the time and may produce the same physiologic effect as agonist-induced activity

A

Constitutive activity

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25
Q

The study of substances that interact with living systems through chemical processes, especially by binding to regulatory molecules and activating or inhibiting normal body process.

A

Pharmacology

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26
Q

Largely determine the quantitative relations between dose or concentration of drug and pharmacologic effects

A

Receptor

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27
Q

The specific binding region of the receptor macromolecule has a relatively high and selective affinity for the drug molecule

A

Receptor site

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28
Q

Molecules that translate the drug-receptor interaction into a change in cellular activity. This include your secondary messenger system, protein kinases, etc.

A

Effector

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29
Q

Graph of the response versus the drug concentration. Response of a particular receptor-effector system is measured against increasing concentrations of a drug

A

Graded dose-response relationship

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30
Q

Concentration of drug required to bind 50% of the receptor sites. Useful measure of the affinity of a drug molecule for its binding site on the receptor molecule.

A

Kd

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31
Q

A maximum amount of drug or radiology do which can bind specifically to the receptors in a membrane preparation. Can be used to measure density of the receptors in a particular preparation

A

Bmax

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32
Q

Ability of drug to bind to receptor

A

Affinity

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33
Q

Greatest effect an agonist can produce if the dose is taken to the highest tolerated level

A

Emax

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34
Q

Emax is determined mainly by:

A

Nature of the drug
Receptor
Associated effector

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35
Q

Amount of drug needed to produce a given effect

A

Potency

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36
Q

Effective concentration in specific person

A

EC50

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37
Q

Effective dose in the population

A

ED50

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38
Q

Potency is determined mainly by:

A

Affinity of the receptor to the drug

Number of receptors available

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39
Q

Defined as the minimum dose required to produce a specified response determined in each member of the population.

A

Quantal - dose response

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40
Q

The dose that produces a quantal effect (all or nothing) in 50% of the population that takes it

A

Median effective dose (ED50)

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41
Q

Dosage of the drug where side effects starts to manifest

A

Median toxic dose (TD50)

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42
Q

Dosage there there is death of the population

A

Median lethal dose (LD50)

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43
Q

Exist if the maximal drug response (Emax) is obtained at less than 100% occupation of the receptors (Bmax)

A

Spare receptor

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44
Q

A drug capable of fully activating the effector system when it binds to the receptor conformation

A

Full agonist

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45
Q

Drug that produces less than the full effect, even when it has saturated the receptors. In the presence of a full agonist, it acts as an inhibitor

A

Partial agonist

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46
Q

Bind with equal affinity of the activated and inactivated states. Prevents deviation from the level of constitutive activity

A

Neutral agonist

47
Q

Have a much higher affinity for the inactive state than for the active state. It decreases or abolishes any constitutive activity

A

Inverse agonist

48
Q

The property of increasing doses of a given medication to have progressively smaller incremental effect. The phenomenon in which a drug reaches a maximum effect, so that increasing the drug dosage does not increase its effectiveness

A

Ceiling effect

49
Q

Drugs that bind to, or very close to, the agonist receptor site. Does exactly not activate the effector system for that receptor

A

Competitive antagonist

50
Q

Bind the receptor without shifting the activated and inactivated equilibrium. Retains the status quo

A

Neutral antagonists

51
Q

Appear to decrease the efficacy of the agonist. It causes a downward shift of the maximum

A

Irreversible antagonist

52
Q

Drugs that act at the aldosterone site of the receptor may bind reversible or irreversibly. They do not compete with agonists for binding at the active site

A

Non-competitive antagnonist

53
Q

Binds to a different receptor molecule. Produces an effect opposite to that produced by the drug it antagonizes

A

Physiologic antagonists

54
Q

Determined from quantal-dose response curve. It represents an estimate of the safety of a drug

A

Therapeutic index

55
Q

Measure the clinical drug effectiveness for a patient. Describes the dosage range between the minimum effective therapeutic concentration or dose and the minimum toxic concentration or dose.

A

Therapeutic window

56
Q

5 tea of signaling mechanism

A 
Transmembrane diffusion 
Transmembrane enzyme receptor
JAK-STAT
Gated transmembrane channels
G-protein coupled receptors
57
Q

Complexes translocate to the nucleus, where they interact with response elements in spacer DNA. slower in onset but longer in duration. (e.g steroid hormones)

A

Intracellular receptors

58
Q

Mimic or antagonize the actions of endogenous Logan’s. Regulate flow of ions through excitable membranes. (e.g nicotine, ach)

A

Membrane receptors directly coupled to ion channels

59
Q

Typically serpentine. Seven transmembrane spanning domains, the third of which is coupled to the G-protein effector mechanism

A

Receptors linked via coupling proteins to intravenous are effectors

60
Q

Binding of agonists to receptors linked to this protein increases cAMP production

A

Gs protein

61
Q

Binding to receptors linked with this protein decreases cAMP production

A

Gi protein

62
Q

Activates phospholipids C. Releases the second messengers IP3 and DAG

A

Gq protein

63
Q

Receptors for cytokines

A

Janus kinases (JAKs)

64
Q

Frequent or continuous exposure to agonists often results in short term diminution of the receptor response

A

Tachyphylaxis

65
Q

The rate at which a drug reaches its site of action depends on two rates:

A

Absorption and distribution

66
Q

Passage of the drug from its site of administration into the blood

A

Absorption

67
Q

Delivery of the drug to the tissues

A

Distribution

68
Q

Most important transport mechanism for foreign molecules. It passes from a region of higher to lower concentration

A

Passive diffusion

69
Q

Passage to different pores of membrane (i.e via fenestrations)

A

Filtration

70
Q

Mechanism of drug transfer against a concentration gradient. It is energy-dependent, saturable and selective-carrier mediated

A

Active transport

71
Q

Mechanism of drug transfer down a concentration gradient. It does not require energy, it is saturable and selective-carrier mediated

A

Facilitated diffusion

72
Q

Four parameters that influence the rate of diffusion of drugs

A

Concentration gradient
Surface area
Permeability coefficient
Thickness

73
Q

Expression of the ability of a drug to diffuse across membranes. Ratio of concentration of a drug in two phases: oil and water

A

Lipid-water partition coefficient

74
Q

In this area of absorption, weak bases will be ionized resulting to poor absorption while weak acids will be un-ionized and are absorbed well

A

Gastric absorption

75
Q

In this area of absorption, weak acids will be ionized resulting to poor absorption while weak bases will be un-ionized and are absorbed well

A

Intestinal absorption

76
Q

Fraction of the drug which is available in the systemic circulation and obtained by comparing the area under the curve of drugs with dose that of IV

A

Bioavailability

77
Q

Rate and availability of two products after administration are similar in the same doses.

A

Bioequivalence

78
Q

Implies the same amount of same active substance, in the same dosage for. For that same route of administration and is identical in strength and concentration

A

Pharmaceutical equivalence

79
Q

Criteria for both bioequivalence and pharmaceutical equivalence are met

A

Therapeutic equivalence

80
Q

General principle: speed of effect of the different routes of drug administration

A

IV > IM > SC > Oral

81
Q

The extent of distribution of a drug is quantified by this parameter. The volume of fluid required to dissolve the amount of drug in the body to give the same concentration as that in the plasma at the same time.

A

Apparent volume of distribution (Vd)

82
Q

Factors affecting the rate of distribution

A

Lipids solubility
Degree of ionization
Molecular weight
Blood flow

83
Q

Factors affecting the extent of distribution

A

Lipid solubility
Protein binding
Tissue binding

84
Q

What are the processes involved in pharmacokinetics?

A

Absorption
Distribution
Metabolism
Excretion

85
Q

What are the phases of metabolism?

A

Phase I - REDOX

Phase II - CONJUGATION

86
Q

Examples of phase I reactions

A 
Hydrolysis
Methylation
Dealkylation
Hydroxylation 
Desulfuration 
Reduction
Oxidation
 Deamination
87
Q

Reactions that are hallmarks of Phase II metabolism

A

Glucoronidation
Sulfation
Methylation
Acetylation

88
Q

Most important of phase II conjugation reactions. Requires the activated form of glucoronic acid - glucoronic acid uridine diphosphate

A

Glucoronidation

89
Q

This antibiotic should not be given to infants as this can lead to Grey Baby Syndrome

A

Chloramphenicol

90
Q

Site of cellular metabolism

A

Endoplasmic reticulum, specifically smooth ER

91
Q

Primary phase I enzyme system

A

Cytochrome P450 family

92
Q

Most abundantly expressed cytochrome

A

CYP3A4

93
Q

Cytochrome expressed only in the fetus

A

CYP3A7

94
Q

Second most common cytochrome. Known for its propensity to exhibit polymorphisms

A

CYP2D6

95
Q

Metabolizes several clinically important drugs with narrow T.I (eg Phenytoin, Warfarin)

A

CYP2C9

96
Q

Inhibitor of CYP2C19

A

Cimetidine, Ketaconazole

97
Q

Inducer of CYP2A6

A

Phenobarbital, dexamethasone

98
Q

Primary organ of removal of most drugs

A

Kidney

99
Q

3 principal processes that determine the urinary excretion of a drug

A

Glomerular filtration
Tubular secretion
Tubular reabsorption

100
Q

True or False: Almost all drugs that a mother take can be expressed in the milk

A

True

101
Q

Which of the following is true about the drug concentration time profiles of a drug X when given PO and SL?

A. PO formulation would have a faster rate of absorption.
B. SL formulation would have a longer Tmax
C. Bioavailability of PO > SL

A

D.

102
Q

Time needed to reach Cmax

A

Tmax

103
Q

Maximum concentration achieved in the blood

A

Cmax

104
Q

Used to asses the person’s overall exposure to a drug. Also useful in calculating clearance

A

Area under the Curve (AUC)

105
Q

The time it takes for the drug to be eliminated from the body.

A

Half-life

106
Q

When the rate of drug entering the body is equal to the rate of drug leaving the body

A

Steady state

107
Q

How many half-lives does it take to remove 97% of the drug from the body?

A

Five

108
Q

How many half-lives does it take to reach a steady state?

A

Five

109
Q

Fraction of administered drug that reaches the systemic circulation

A

Bioavailability

110
Q

This mechanism limits the efficacy of many drugs when orally taken.

A

First-pass hepatic metabolism

111
Q

Kinetics resulting from saturable drug transfer, leading to variation of the standard kinetic parameters with drug concentration

A

Michaelis-Menten kinetics

112
Q

The rate of elimination is independent of the concentration of the drug.

A

Zero order kinetics

113
Q

The rate of elimination is directly proportional to the drug concentration.

A

First order kinetic

114
Q

Examples of drugs that undergo zero order kinetic

A

“PPWHEATS”

Phenytoin
Phenylbutazone
Warfarin
Heparin
Ethanol
Aspirin
Theophylline
Salicylates

Pharmacology (12 decks)

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