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[MT 6314] Pharmacology & Toxicology > Introduction to Pharmacology & Its General Principles > Flashcards

Introduction to Pharmacology & Its General Principles Flashcards

medyo oa

1
Q

What century where reliance on observation and experimentation began to replace theorizing in physiology and clinical medicine

A

End of 17th Century

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2
Q

Origin of ancient drugs

A

Plants

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3
Q

Science of drug preparation and the medical uses of drugs and identifies receptors

A

Materia Medica

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4
Q

The precursor to Pharmacology

A

Materia Medica

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5
Q

T/F: Any real understanding of the mechanisms of action of drugs was prevented by the absence of methods for purifying active agents from the crude materials that were available

A

True

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6
Q

Who developed the methods of experimental physiology and pharmacology; which has laid the foundation needed for understanding how drugs work at the organ and tissue levels.

A

Francois Magendie & Claude Bernard (Maganda & Cathryn Bernardo)

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7
Q

Real advances in basic pharmacology during this time were accompanied by an outburst of unscientific claims that marketed worthless patent medicines

A

Late 18th & Early 19th Century

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8
Q

Information accumulated about the drug action and biologic substrate of that action

A

Drug Receptor (1940s & 1950s)

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9
Q

Receptors for which no ligand has been discovered and whose function can only be guessed.

A

Orphan Receptors

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10
Q

Receptors and effectors do not function in isolation; they are strongly influenced by other receptors and by

A

Companion Regulatory Proteins

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11
Q

The relation of the individual’s genetic makeup to his or her response to specific drugs

A

Pharmacogenomics

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12
Q

Small segments of RNA can interfere with protein synthesis with extreme selectivity has led to investigation of __________ and __________ as therapeutic agents

A

small interfering RNAs (siRNAs), micro-RNAs (miRNAs)

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13
Q

Short nucleotide chains that are synthesized to be complementary to natural RNA or DNA, can interfere with the readout of genes and the transcription of RNA.

A

Antisense Oligonucleotides (ANOs)

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14
Q

T/F: All substances do not undergo certain circumstances to be toxic.

A

F; can undergo

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15
Q

T/F: Chemicals in botanicals (herbs and plant extracts, ”nutraceuticals”) are no different from chemicals in manufactured drugs except for the much greater proportion of impurities in botanicals.

A

T

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16
Q

T/F: All dietary supplements and all therapies promoted as health-enhancing, should meet the same standards of efficacy and safety as conventional drugs and medical therapies.

A

T

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17
Q

What are the 2 nature of drugs?

A

Pharmacodynamics & Pharmacokinetics

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18
Q

Pharmacodynamics or Pharmacokinetics?

Receptor, Receptor Sites

A

Pharmacodynamics

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19
Q

Pharmacodynamics or Pharmacokinetics?

Inert Binding Sites

A

Pharmacodynamics

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20
Q

Pharmacodynamics or Pharmacokinetics?

Movement of drugs in body

A

Pharmacokinetics?

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21
Q

Pharmacodynamics or Pharmacokinetics?

Absorption

A

Pharmacokinetics

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22
Q

Pharmacodynamics or Pharmacokinetics?

Distribution

A

Pharmacokinetics

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23
Q

Pharmacodynamics or Pharmacokinetics?

Metabolism

A

Pharmacokinetics

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24
Q

Pharmacodynamics or Pharmacokinetics?

Elimination

A

Pharmacokinetics

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25
Q

Drug Development & Regulation

A
  1. Safety & Efficacy
  2. Animal Testing
  3. Clinical Trials
  4. Patents & Generic Drugs
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26
Q

Body of knowledge concerned with action of chemicals on biologic systems, especially by binding to regulatory molecules (receptors) and activating or inhibiting normal body processes

A

Pharmacology

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27
Q

Activator

A

Agonist

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28
Q

Inhibitor

A

Antagonist

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29
Q

Target molecules or regulatory molecules in biological systems

A

Receptor

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30
Q

What do you call the new large molecule drugs that can be receptors themselves and bind endogenous molecules?

A

Biologicals

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31
Q

Drugs that may interact directly with other drugs

A

Chemical Antagonists

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32
Q

Drugs that interact almost exclusively with water molecules

A

Osmotic Agents

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33
Q

Who stated “The dose makes the poison”?

A

Paracelsus (1493 - 1541)

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34
Q

Area of pharmacology concerned with the use of chemicals in the prevention, diagnosis, and treatment of disease, especially in humans.

A

Medical Pharmacology

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35
Q

Area of pharmacology concerned with the undesirable effects of chemicals on biologic systems (e.g., poison)

A

Toxicology

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36
Q

T/F: It is the dose of the drugs that makes the drug lethal or poisonous.

A

T

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37
Q

Finds the exact mechanism of actions of drugs and identifies the receptors

A

Pharmacogenomics

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38
Q

Any substance that brings about change in biologic function through chemical actions (binds to receptors)

A

Drug

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39
Q

Specific molecule in the biologic system that plays a regulatory role

A

Receptor

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40
Q

T/F:

Receptor: No binding site = There is an effect in the body

A

F; no effect in the body

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41
Q

What kind of drugs that are usually easy to eliminate?

A

Water-soluble drugs

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42
Q

No receptor

A

Inert Substance

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43
Q

Chemical components of drugs similar to the human body

A
  1. Inorganic Ions
  2. Nonpeptide Organic Molecules
  3. Small peptides & proteins
  4. Nucleic Acids
  5. Lipids
  6. Carbohydrates
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44
Q

T/F: The body can process what it doesn’t t produce.

A

F; the body can’t process

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45
Q

Drugs may be synthesized within the body

A

Hormones

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46
Q

Chemicals that are not synthesized in the body

A

Xenobiotics

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47
Q

Drugs that have almost exclusively have harmful
effects.

A

Poisons

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48
Q

Poisons of biologic origin (i.e. synthesized by plants or animals) in contrast to inorganic poisons such as lead and arsenic.

A

Toxin

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49
Q

Physical Nature of Drugs

A
  1. Solid
  2. Liquid
  3. Gaseous
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50
Q

T/F: To interact chemically with its receptor, a drug molecule must have the appropriate size, electrical charge, shape, and atomic composition

A

T

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51
Q

Molecular weight of Lithium

A

7

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52
Q

Molecular weight of Thrombolytic Agents

A

50,000

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53
Q

What MW entails that receptors are small and for selective binding

A

100 MW

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54
Q

What MW is easily distributed but also easily be eliminated?

A

100 MW

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55
Q

MW: Upper limit wherein drugs can traverse within the different barriers of the body

A

1000 MW

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56
Q

MW that may not reach certain areas of the body

A

1000 MW

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57
Q

MW that cannot move within the body and cannot diffuse readily between the different
compartments of the body

A

> 1000 MW

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58
Q

MW that is given directly at the site of action and must be administered where they have their effect (usually proteins)

A

> 1000 MW

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59
Q

Why does >1000 MW have difficulty in traversing different sites of the body?

A

They have to fit in / They are prevented by the blood-brain barrier, blood-air barrier, etc.

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60
Q

Stereoisomerism / Can exist as enantiomeric pairs

A

Chirality

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61
Q

Affects the potency of the drugs

A

Chirality

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62
Q

A drug that interacts with adrenoceptors, has a single chiral center and thus two enantiomers.

A

Carvedilol

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63
Q

Potent beta receptor blocker

A

(S)(-) isomer

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64
Q

Weak beta receptor blocker

A

(R)(+) isomer

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65
Q

An intravenous anesthetic and racemic mixture.

A

Ketamine

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66
Q

Ketamine: (+/-) enantiomer is a more potent anesthetic and less toxic than the (+/–) enantiomer.

A

+ , -

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67
Q

T/F: Enzymes are usually stereoselective, one drug enantiomer is often more susceptible than the other to drug-metabolizing enzymes.

A

T

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68
Q

T/F: At present, only a small percentage of the chiral drugs are clinically marketed as the racemic mixtures the rest are available only as active isomers.

A

F; At present, only a small percentage of the chiral drugs are clinically marketed as the active isomer the rest are available only as racemic mixtures.

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69
Q

Mechanism for Drug Shapes

A

Lock and Key Mechanism

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70
Q

Binds to a specific site and activates the receptor which bring out the effect

A

Agonist Drugs

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71
Q

Binds to a receptor, competes with, and prevents binding by other molecules

A

Pharmacologic Antagonist

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72
Q

Binds at a different site other than the agonist binding site and increases agonist response

A

Allosteric Activators

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73
Q

Binds at a different site other than the agonist binding site and decreases agonist response

A

Allosteric Inhibitors

74
Q

Binds at the agonist binding site and decreases agonist response

A

Competitive Inhibitors

75
Q

Several other binding site in receptors and for other chemicals that bind to the receptors

A

Allosteric Site

76
Q

The presence of the antagonist at the receptor site will block access of agonists to the receptor and prevent the usual agonist effect.

A

Neutral Antagonism

77
Q

Produce increasing effects with increasing dose (Eventually saturate all receptors and response will plateau)

A

Agonist alone

78
Q

Agonist + Competitive Inhibitor

A

Require a higher dose to achieve the similar effect

79
Q

Agonist + Allosteric Activators

A

Enhances the response/effect produced by agonist with the same dose

80
Q

Agonist + Allosteric Inhibitors

A

Diminish the response/effect produced by agonist with the same dose

81
Q

Drug Receptor Bonds

Sharing of electrons
Strongest
Electrons are shared in order to stabilize these chemicals

A

Covalent Bonds

82
Q

Irreversible under biologic conditions / Cannot be easily dislodged

A

Covalent Bonds

83
Q

Drug Receptor Bonds

More common (+)(-) and weaker

A

Electrostatic Bonds

84
Q

Can we manipulate Electrostatic Bonds?

A

Yes

85
Q

Drug Receptor Bonds

Weakest and highly lipid-soluble drugs

A

Hydrophobic Bonds

86
Q

Interacts with lipids of cell membranes and in the interaction of drugs with the internal walls of receptors

A

Hydrophobic Bonds

87
Q

Action of the drug in the body

A

Pharmacodynamics

88
Q

Action of the body on the drug

A

Pharmacokinetics

89
Q

D + Receptor-Effector → _________ → Effect

A

Drug-Receptor-Effector

90
Q

D + R → _______ → Effector Molecule → Effect

A

Drug-Receptor Complex

91
Q

D + R → D-R Complex → ________ → Effector Molecule → Effect

A

Activation of Coupling Molecule

92
Q

Inhibition of metabolism of endogenous activator → _________ → Increased effect

A

Increased activator action on an effector molecule

93
Q

Occurs in the absence of the agonist. Some of the receptor pool must exist in Ra form and may produce same physiologic effect as agonist-induced activity

A

Constitutive / Basal Activity

94
Q

Activates receptor-effector system to the maximum extent (Ra-D pool) {activated form}

A

Full Agonist

95
Q

Binds to the same receptors and activate them in the same way but do not evoke as great a response

A

Partial Agonist

96
Q

Binds to a site on the receptor molecule separate from the agonist binding site

A

Allosteric Modulators

97
Q

Modifies receptor activity without blocking agonist activity

A

Allosteric Modulators

98
Q

May increase / decrease response to agonist and is also noncompetitive

A

Allosteric Modulators

99
Q

Drug has a stronger affinity for the Ri pool and reduces constitutive activity

A

Inverse Agonist

100
Q

Results in effects that are opposite of the effects produced by conventional agonists

A

Inverse Agonist

101
Q

Binds to a receptor, compete with and prevent binding by other molecules

A

Antagonist

102
Q

Inactive precursor and must be administered and converted to the active drug by biologic process inside the body

A

Prodrug

103
Q

Undergoes hepatic metabolism to be come a more active form that will enable them to reach target receptors

A

Prodrug

104
Q

Movement of molecules through the watery extracellular and intracellular spaces.

A

Permeation

105
Q

Movement of molecules through the watery extracellular and intracellular spaces.

A

Aqueous Diffusion

106
Q

Membranes of capillaries with small water-filled pores

Has passive processes

A

Aqueous Diffusion

107
Q

Governed by Fick’s Law

A

Aqueous Diffusion & Lipid Diffusion

108
Q

What diffusion?

Water-soluble drugs easily diffuse due to the presence of water intracellularly and extracellularly

A

Aqueous Diffusion

109
Q

Movement of molecules through membranes and other lipid structures

A

Lipid Diffusion

110
Q

Most important factor for drug permeation
Passive Process

A

Lipid Diffusion

111
Q

Drugs transported across barriers by mechanisms that carry similar endogenous substances

A

Transport by Special Carriers

112
Q

Its capacity is limited (limit rate of transport across membranes) and is not governed by Fick’s Law

A

Transport by Special Carriers

113
Q

Transport by Special Carriers

Needs energy
Against a concentration gradients

A

Activate Transport

114
Q

Transport by Special Carriers

No energy directly required
May utilize another concentration gradient of a substance / use an active receptor
Downhill

A

Facilitated Diffusion

115
Q

Binding to specialized components (receptors) on cell membranes

A

Endocytosis

116
Q

Internalization by infolding of the area of the membrane and contents of the vesicle are subsequently released into the cytoplasm

A

Endocytosis

117
Q

Permits very large or very lipid-insoluble (water soluble) chemicals to enter the cell

A

Endocytosis

  • B12 with intrinsic factor
  • Iron with transferrin
118
Q

Reverse process

Expulsion of membrane encapsulated material from the cell

A

Exocytosis

119
Q

Predicts the movement of molecules across a barrier

A

Fick’s Law of Diffusion

120
Q

Drug absorption is faster in organs with larger surface areas (e.g. small intestine) than from organs with smaller absorbing areas (e.g. stomach)

A

Fick’s Law of Diffusion

121
Q

Fick’s Formula

A

Rate = C1 - C2 x Permeability Coefficient / Thickness x Area

kaya nio n yn

122
Q

HHE: Higher Concentration

A

C1

123
Q

Lower Concentration

A

C2

124
Q

Intrinsic property of the drug; measure of the mobility of the drug in medium of the length of the diffusion path.

A

Permeability Coefficient

125
Q

Length of the diffusion path; Thicker means harder to permeate through.

A

Thickness

126
Q

Surface area of the membrane

A

Area

127
Q

Greater concentration difference = ______ ; ______ proportional to the rate

A

Faster equilibriation ; Directly

128
Q

↑ Permeability Coefficient = ___ Rate

A

↑

129
Q

Bigger Surface Area = _________ ; ________ proportional to rate

A

More areas to traverse ; Directly

130
Q

Is a function of the electrostatic charge (degree of ionization, polarity) of the molecule

A

Aqueous solubility of a drug

131
Q

Water molecules are attracted to (charged/uncharged) drug

A

Charged

132
Q

Lipid solubility of a molecule is _______ proportional to
its charge

A

Inversely

133
Q

Lipid Diffusion

Determines the fraction of molecules charged (ionized) versus uncharged (nonionized)

A

pH of the medium

134
Q

Fraction of molecules in the ionized state can be predicted by means of the H-H equation

A

Lipid Diffusion

135
Q

Clinically important when it is necessary to estimate or alter the partition of drugs between compartments of different pH

A

Henderson-Hasselbach Equation

136
Q

Formula for Henderson-Hasselbach

A

log (protonated) / (unprotonated) = pka - pH

137
Q

T/F: The HHE applies to both acid and basic drugs.

A

T

138
Q

T/F: In HHE, protonated means associated with a proton (a hydrogen ion / H+)

A

T

139
Q

Neutral molecule that can form a cation (+charged) by combining with a proton (hydrogen ion)

A

Weak Base

140
Q

Ionized, more polar, more water soluble when they are protonated

A

Weak Base

141
Q

Neutral molecule that can reversibly dissociate into an anion (-charged) a proton (hydrogen ion)

A

Weak Acid

142
Q

Not ionized, less polar, less water soluble when they are protonated

A

Weak Acid

143
Q

T/F: Large number of drugs are weak acids with amine containing molecules

A

F; weak bases

144
Q

T/F: Primary, secondary, and quarternary amines may undergo reversible protonation and vary their lipid solubility with pH, but tertiary amines are always in the poorly-lipid soluble charged form.

A

F

(1) Primary, secondar, tertiary
(2) but quarternary

145
Q

Amount absorbed into the systemic circulation amount of drug administered

A

Bioavailability

146
Q

Important parameter of Bioavailability

A

Blood Plasma - Looks into the amount of blood present in systemic circulation compared to amount of drug administered

147
Q
  • Maximum convenience
  • Absorption maybe slower, and less complete
A

Oral

148
Q

T/F: Some drugs have low bioavailability when given orally

A

T

149
Q
  • Instantaneous and complete absorption
  • Bioavailability by definition is 100%
  • Potentially more dangerous, high blood levels reached if administration is too rapid
A

Intravenous (IV) / Parenteral

150
Q
  • Absorption is often faster and more complete (higher bioavailability) than oral
  • Large volumes (>5 ml into each buttock) if the drug is not irritating
A

Intramuscular (IM)

151
Q

T/F: Heparin can be given by intramuscular route.

A

F; It will cause bleeding in the muscle

152
Q
  • Slower absorption than IM route
  • Heparin can be given by this route, does not cause hematoma
A

Subcutaneous

153
Q
  • Permits absorption direct into the systemic circulation, bypassing hepatic portal circuit and first-pass metabolism
  • Slow or fast depending on formulation of the product
A

Buccal and Sublingual

154
Q

In the pouch between gums and cheeks

A

Buccal Route

155
Q

Under the tongue

A

Sublingual Route

156
Q

T/F: Buccal and Sublingual routes offer different features when absorbed.

A

F; It offers the same features

157
Q

Tend to migrate upward in the rectum where absorption is partially into the portal circulation

A

Rectal (Suppository)

158
Q

T/F: Larger amounts of unpleasant drugs are better administered rectally

A

T

159
Q

For respiratory diseases

A

Inhalation

160
Q

Delivery closest to the target tissue

A

Inhalation

161
Q

Results into rapid absorption because of the rapid and thin alveolar surface area

A

Inhalation

162
Q

Drugs that are gases at room temperature (eg, nitrous oxide), or easily volatilized (anesthetics)

A

Inhalation

163
Q

Application to the skin or mucous membrane of the eye, nose, throat, airway, or vagina for local effect

A

Topical

164
Q

Rate of absorption varies with the area of application and drug’s formulation and absorption is slower compared to other routes

A

Topical

165
Q

Application to the skin for systemic effect and rate of absorption occurs very slowly

A

Transdermal

166
Q

Influences absorption from IM, subcutaneous, and in shock

A

Blood Flow

167
Q

T/F: High blood flow maintains a high drug depot-to-blood concentration gradient, which maximizes absorption

A

T

168
Q

Major determinant of the rate of absorption (Fick’s law)

A

Concentration

169
Q

Subject to first-pass effect

A
  1. Oral
170
Q

First-pass effect is avoided

A
  1. Intramuscular (IM)
  2. Subcutaneous
  3. Transdermal
171
Q

Partial avoidance of first-pass effect

A
  1. Rectal
172
Q

Significant amount of the agent is metabolized in the gut wall, portal circulation, and liver before it reaches the systemic circulation

A

First-pass effect

173
Q

Target of cocaine and some tricyclic antidepressants

A

NET

174
Q

Norepinephrine reuptake from synapse

A

NET

175
Q

Target of selective serotonin reuptake inhibitors and some tricyclic antidepressants

A

SERT

176
Q

Serotonin reuptake from synapse

A

SERT

176
Q

Target of reserpine and tetrabenazine

A

VMAT

176
Q

Transport of dopamine and norepinephrine into adrenergic vesicles in nerve endings

A

VMAT

177
Q

Transport of many xenobiotics out of cells

A

MDR1

178
Q

Leukotriene secretion

A

MRP1

[MT 6314] Pharmacology & Toxicology (20 decks)

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