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PCOL > INTRO TO PHARMACOLOGY (1) > Flashcards

INTRO TO PHARMACOLOGY (1) Flashcards

1
Q

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

A

Pharmacology

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2
Q

General Areas of Pharmacology

A

Pharmacodynamics, Pharmacokinetics, Pharmacotherapeutics, Toxicology

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3
Q

describes the adverse effects of therapeutic agents on the human body

A

Toxicology

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4
Q

describes the clinical applications, C/Is & drug interactions useful for the diagnosis, prevention & treatment of disease

A

Pharmacotherapeutics

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5
Q

prescribed chemically defined substances with such success that professional enemies had him prosecuted as a poisoner

A

Theophrastus von Hohenheim

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6
Q

first attempted to consider the theoretical background of pharmacology

A

Claudius Galen

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7
Q

began to question doctrines handed down from antiquity, demanding knowledge of the active ingredient(s) in prescribed remedies, while rejecting the irrational concoctions and mixtures of medieval medicine

A

Theophrastus von Hohenheim

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8
Q

whole name of theophrastus von hohenheim

A

Philippus Theophrastus Aureolus Bombastus von Hohenheim (PTABH)

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9
Q

first to verify by animal experimentation assertions about pharmacological or toxicological actions

A

Johann Jakob Wepfer

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10
Q

study of the effects and MOAs of drugs

A

Pharmacodynamics

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11
Q

together with the internist, Bernhard Naunyn, founded the first journal of pharmacology, which has since been published without interruption

A

Oswald Schmiedeberg

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12
Q

founded the first institute of pharmacology at the University of Dorpat (Estonia) in 1847, ushering in pharmacology as an independent scientific discipline

A

Rudolf Buccheim

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13
Q

FAther of Anesthesiology

A

Philippus Theophrastus Aureolus Bombastus von Hohenheim

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14
Q

Father of American Pharmacology

A

John J. Abel

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15
Q

first formalized receptor theory in the early 1920s by applying the Law of Mass Action to drug-receptor interactions

A

Alexander J. Clark

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16
Q

selective toxicity

A

P. Ehrlich

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17
Q

Father of modern pharmacology

A

Oswald Schmiedeberg

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18
Q

“The empiricists say that all is found by experience. We, however, maintain that it is found in part by experience, in part by theory. Neither experience nor theory alone is apt to discover all.”

A

Claudius Galen

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19
Q

“The science of medicines is a theoretical, i.e., explanatory, one. It is to provide us with knowledge by which our judgment about the utility of medicines can be validated at the bedside.”

A

Rudolf Buccheim

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20
Q

“I pondered at length. Finally I resolved to clarify the matter by experiments.”

A

Johann Jakob Wepfer

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21
Q

“If you want to explain any poison properly, what then isn‘t a poison? All things
are poison, nothing is without poison; the dose alone causes a thing not to be poison.”

A

Philippus Theophrastus Aureolus Bombastus von Hohenheim

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22
Q

he strove to explain the chemical properties of drugs

A

Rudolf Buccheim

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23
Q

Effects of drug are brought about by what?

A

Drug-receptor interaction

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24
Q

ability to bind to a receptor

A

Affinity

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25
Q

ability to generate a series of biochemical events leading to an effect

A

Intrinsic Activity

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26
Q

combining of a drug molecule with the receptor for which it has affinity,

A

Drug-receptor interaction

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27
Q

drugs initiation of a pharmacologic response by its___

A

intrinsic activity

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28
Q

Serves as the ligand

A

drug

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29
Q

serves as the substrate

A

receptor

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30
Q

pharmacological action is not directly dependent on chemical

structure

A

Structural Nonspecific Drugs

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31
Q

pharmacological action results primarily from their chemical

structure

A

Structural Specific Drugs

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32
Q

Examples of SND

A

NO and Halothane

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33
Q

Examples of SSD

A

Antibiotics, sulfonamides

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34
Q

component of a cell or organism that interacts with a drug and initiates the chain of events leading to the drug’s observed effects

A

receptor

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35
Q

4 theories of Drugreceptor

A
  1. Hypothesis of Clark
  2. Hypothesis of Ariëns and Stephenson
  3. Hypothesis of Paton
  4. Lock and Key Hypothesis
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36
Q

T/F Receptors are usually protein or proteinaceous materials

A

True

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37
Q

aka Rate Theory

A

Hypothesis of Paton

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38
Q

effectiveness lasts as long as the receptor is occupied

A

Hypothesis of Ariens and Stephenson/ occupation Theory

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39
Q

Only dependent on the afifnity

A

Hypothesis of Clark

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40
Q

Hypothesis of Ariens and Stephenson is aka

A

Occupation Theory

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41
Q

drug molecule must fit into a receptor like a key fits into a lock

A

Lock and Key Hypothesis

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42
Q

effectiveness does not depend upon actual occupation of the receptor, but upon obtaining the proper stimulus only

A

Rate Theory/ Hypothesis of PAthon

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43
Q

depends on the affinity and intrinsic activity of the drug

A

Occupation Theory/H of Ariens and Stephenson

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44
Q

Types of receptors

A

TIGOK

  1. Transmembrane ion channels
  2. Intracellular hormone receptors
  3. G protein-linked transmembrane receptors
  4. Other mechanisms
  5. Kinase-linked transmembrane receptors
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45
Q

open & close to allow the selective transport of ions across membranes

A

Transmembrane ion channels

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46
Q

two types of Transmembrane ion channels

A

Ligand and Voltage gated

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47
Q

GABA receptor is what kind of TIC

A

Ligand Gated

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48
Q

signal transducer that conveys information from the receptor to the second messenger systems

A

G-protein system

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49
Q

structures related to g protein-linked receptors

A
  1. amino terminal
  2. heptahelical polypeptide
    chain
  3. carboxyl terminal
  4. G-protein
  5. second messenger systems
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50
Q

T/F g-protein system consists of 4 different subunits namely alpha beta gamma and sigma

A

F. first three lang ang true

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51
Q

activates phospholipase C

A

Gq

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52
Q

activates adenylyl cyclase

A

Gs

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53
Q

Inhibits adenylyl cyclase

A

Gi

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54
Q

synthesized from guanosine triphosphate (GTP) by guanylyl cyclase

A

cGMP

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55
Q

types of second messenger systems

A

Cyclic nucleotide system and Phosphatidylinositol system

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56
Q

T/F cAMP is synthesized from adenosine triphosphate (ATP) by guanylyl cyclase

A

False. Adenylyl cyclase dapat

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57
Q

T/F only DAG is synthesized from phosphatidylinositol 4,5- bisphosphate (PIP2) by phospholipase C

A

F. Both IP3 and DAG

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58
Q

meaning of IP3

A

inositol 1,4,5-trisphosphate

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59
Q

inositol 1,4,5-trisphosphate and diacylglycerol are both synthesized from ________ by __________

A

phosphatidylinositol 4,5-biphosphate (IP2); phospholipase C

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60
Q

kinase linked receptors are polypeptides consisting of

A

extracellular hormone-

binding domain and cytoplasmic enzyme domain

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61
Q

give examples of kinase-linked receptors

A
  • insulin
  • epidermal growth factor (EGF)
  • platelet-derived growth factor (PDGF)
  • atrial natriuretic peptide (ANP)
  • transforming growth factor-beta (TGF-β)
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62
Q

types of cytoplasmic enzyme domain

A
  • tyrosine kinase
  • serine kinase
  • guanylyl cyclase
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63
Q

where lipid-soluble ligands bind

A

Intracellular hormone receptors

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64
Q

T/F Hormones and nitric oxide are G protein-linked receptors

A

F. Intracellular sila

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65
Q

Classifications of Drug Action

A
  1. Agonist
  2. Antagonist
  3. Partial agonist
  4. Inverse agonist
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66
Q

binds to a receptor but does not activate it

A

Receptor Antagonist

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67
Q

mimics the effects of endogenous ligands

A

Agonist

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68
Q

types of antagonist

A
  1. Receptor
  2. Physiologic
  3. Chemical
69
Q

drug showing both agonist and antagonist activities

A

Partial agonist

70
Q

T/F Antagonist has both affinity and intrinsic activities

A

F. Agonist yun

71
Q

shifts the equilibrium towards the inactive form of the receptor

A

Inverse Agonist

72
Q

does not use a receptor; binds to and inactivates a drug

A

Chemical Antagonist

73
Q

produces effects opposite that of the agonist by binding to a different receptor

A

Physiologic Antagonist

74
Q

T/F Non-competitive Receptor Antagonist is a reversible type of antagonist

A

F. Irreversible yun.

75
Q

T/F Receptor Antagonist has intrinsic activity but lacks affinity

A

F. Baliktad

76
Q

competes with the endogenous ligand for the same receptor

A

Competitive RA

77
Q

T/F Partial Agonist acts as an agonist at high natural ligand concentration

A

Antagonist yun

78
Q

Examples of this are heparin & protamine sulfate; BAL & heavy metals

A

Chemical Antagonist

79
Q

binds to other sites present in the receptor (called allosteric sites); causes a conformation change at active site

A

Noncompetitive RA

80
Q

Give examples of Physiologic Antagonist

A

isoproterenol & acetylcholine; glucocorticoid & insulin

81
Q

T/F Inverse agonist increases intrinsic activity

A

F. Decreases

82
Q

indicate the potential variability of responsiveness among individuals

A

Quantal dose-response curves

83
Q

Properties in which graded dose-response curves are based

A

Potency and Efficacy

84
Q

minimum dose that produces efficacy

A

Ceiling dose

85
Q

concentration (EC50) or dose (ED50) of a drug required to produce 50% of the drug’s maximal effect

A

Potency

86
Q

maximum achievable response

A

Efficacy

87
Q

T/F Slope of the curve of a graded dose-response curves is the degree of change in response with change in dose

A

T

88
Q

generate information regarding the margin of safety to be expected from a particular drug used to produce a specified effect

A

Quantal dose-response curves

89
Q

A ratio that compares the blood concentration at which a drug becomes toxic and the concentration at which the drug is effective.

A

Therapeutic Index

90
Q

T/F The smaller the TI, the safer the drug

A

F

91
Q

dose producing toxic effects in 50% of test population

A

Median toxic dose (TD50)

92
Q

dose producing beneficial effects in 50% of test population

A

Median effective dose (ED50)

93
Q

dose producing death in 50% of test population

A

Median lethal dose (LD50)

94
Q

an indicator of the possible margin of safety of a drug

A

TI

95
Q

a drug with no inherent activity will enhance the effect of another drug

A

Potentiation

96
Q

response is equal to the combined effects of individual drugs

A

Addition

97
Q

response is greater than the combined effects of the individual drugs

A

Synergism

98
Q

Flecainide and Verapamil are examples of what enhancement of drug effects

A

Addition (inc neg inotropic and chronotropic effects)

99
Q

T/F Amoxicillin + Clavulanic acid are syngeristic

A

F. Potentiation

100
Q

Example of synergistic

A

Sulfamethoxazole + Trimethoprim (bactericidal effect)

101
Q

Answers what the body does to the drug

A

Pharmacokinetics

102
Q

ADME of drugs

A

Pharmacokinetics

103
Q

answers what the drug does to the body

A

Pharmacodynamics

104
Q

rate of reaction is dependent of the drug concentration remaining

A

First order

105
Q

unit of k in zero order kinetics

A

C/t

106
Q

rate of reaction is independent of the concentration of the drug remaining

A

zero-order kinetics

107
Q

equation for zeroorder

A

C = -k0t + C0

108
Q

unit for k in first order

A

1/t

109
Q

logarithm equation for first order

A

ln C = -kt + ln C0

110
Q

time it takes for the drug concentration to decrease by 50%

A

Half-life

111
Q

T/F first order halflife depends on the initial concentration

A

F. t1/2=0.693/k

112
Q

equation for zero-order half life

A

t1/2=0.5Co/ko

113
Q

drug is bound to the surface of the skin or mucosa

A

Adsorption

114
Q

T/F ionized form of the drug is absorbed

A

F. unionized

115
Q

T/F drugs going in extravascular routes are not 100% absorbed

A

T

116
Q

process of uptake of the drug from the site of administration into the systemic circulation

A

Absorption

117
Q

drug reaches the deeper layers of the skin but not the capillaries

A

Penetration

118
Q

prerequisite form of drug

A

in aqueous solution

119
Q

Mechanism of drug absorption in which organic anion complex with cation of the membrane

A

Ion-pair Transport

120
Q

against concentration gradient and requires ATP

A

Active Transport

121
Q

along concentration gradient (higher to lower concentration)

A

Passive Diffusion

122
Q

what law guides passive diffusion

A

Fick’s Law of Diffusion

123
Q

T/F Active transport is mediated by carriers

A

T

124
Q

involves vesicular transport, phagocytosis and pinocytosis

A

Endocytosis

125
Q

T/F only active transport is mediated by carriers and is subject to competitive inhibition and saturation

A

F. even facilitated transport

126
Q

movement along with the solvent through membrane pores with diameter of 7-10Å

A

Convective Transport

127
Q

does not require ATP, along concentration gradient. example is Vit B12

A

Facilitated Transport

128
Q

T/F Vit A, B, D, E and K are examples of substances transported via endocytosis

A

F. walang B

129
Q

hypothetical volume that contains a certain drug concentration

A

Compartment

130
Q

central component of the body

A

Circulatory System

131
Q

measure of drug absorbed in the body

A

AUC

132
Q

AUC follows what rule

A

Trapezoidal Rule

133
Q

is established when two drug products have similar BA

A

Bioequivalence

134
Q

the relative amount of drug from an administered dosage form which enters the systemic circulation and the rate at which the drug appears in the blood stream

A

Bioavailability

135
Q

formula for volume of distribution

A

Vd=Dose/Cp

136
Q

Process in which drug leaves the systemic circulation and enters the cells

A

Distribution

137
Q

a hypothetical volume of body fluid* that would be required to dissolve the total amount of drug at the same concentration as that found in the blood

A

volume of distribution

138
Q

T/F Protein binding is a weak reversible force that delays urinary excretion and decreases elimination halflife

A

F. inc elimination halflife

139
Q

protein that binds basic drugs

A

AAG (alpha-acid glycoprotein)

140
Q

protein that binds acid drugs

A

albumin

141
Q

converts drugs into water-soluble, less toxic and inactive metabolites

A

Metabolism

142
Q

other name for metabolism

A

biotransformation

143
Q

major organ for metabolism

A

liver

144
Q

phase of metabolism in which hepatic enzymes are stimulated resulting to a faster metabolism

A

Enzyme induction

145
Q

drugs that undergo enzyme induction

A

PRC (phenobarbital, phenytoin, rifampicin and carbamazepine)

146
Q

functionalization phase of metabolism

A

Phase 1

147
Q

T/F phase 1 involves synthetic rxns

A

F. 2 yun.

148
Q

phase in which hepatic enzymes are inhibited and there is an increase in pharmacological effect or possible toxicity

A

Enzyme inhibition

149
Q

phase 2 is the

A

conjugation phase

150
Q

T/F Phase 2 involves oxidation , reduction and hydrolysis

A

F. 1 yun

151
Q

drugs that undergo enzyme inhibition

A 
MEDVICK
M–metronidazole
E–erythromycin
D–disulfiram
V–valproicacid
I–isoniazid
C–cimetidine,chloramphenicol
K–ketoconazole
152
Q

the phenomenon in which drugs emptied via bile into the small intestine can be reabsorbed from the intestinal lumen into systemic circulation

A

Biliary Recycling

153
Q

other name for biliary recycling

A

Enterohepatic recirculation

154
Q

actual unit where elimination takes place

A

nephron

155
Q

major organ in excretion

A

kidney

156
Q

final elimination from the body’s systemic circulation via:

A
  • the kidney into urine
  • bile* and saliva into intestines and into feces
  • sweat
  • skin
  • milk
157
Q

biochemical product of muscle metabolism

A

creatinine

158
Q

what equation is used in calculation creatinine clearance

A

Cockcroft and Gault Equation

159
Q

T/F Glomerular filtration filters high MW molecules

A

F

160
Q

Cockcroft and Gault Equation

A

CC=([{140-Age in yrs}xBW]/serumcreatinine(mg/dL)x72) xF

161
Q

Factor for female (CandG eq)

A

0.85

162
Q

occurs in the distal convoluted tubule

A

Tubular Reabsorption

163
Q

occurs in the proximal convoluted tubule

A

Tubular Secretion

164
Q

T/F unionized form of the drug is secreted

A

F. ionized

165
Q

equation that guides tubular reabsorption

A

Henderson-Hasselbalch Eq

166
Q

urinary acidifier

A

Ascorbic acid

167
Q

urinary alkalinizer

A

NaHCO3

168
Q

measure of drug elimination from the body or the volume of fluid cleared of drug from the body per unit
time

A

Drug clearance

PCOL (3 decks)

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