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Pharmacology > Intro to Pharmacology (Exam 1) > Flashcards

Intro to Pharmacology (Exam 1) Flashcards

Understand the basic principles of Pharmacology and tie them to the dental practice

1
Q

Father of American Pharmacology

A

John Jacob Abel

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2
Q

1962 Kefauver-Harris Amendment

A

-Manufacturers must demonstrate the safety and efficacy of drugs -FDA regulates drug standards and testing and has the power to withdraw drugs already on the market

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3
Q

1983 Orphan Drug Act

A

Allows drug manufacturers to make drugs for the treatment of rare diseases

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4
Q

Pharmacodynamics: Definition

A

Mechanism of action of drugs

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5
Q

Pharmacokinetics: Definition

A

A: absorption D: distribution M: metabolism E: excretion

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6
Q

Pharmacogenomics: Definition

A

Study of genetic variations that causes differences in drug response among individuals or population

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7
Q

Therapeutics: Definition

A

Use of drugs for treatment of diseases

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8
Q

Toxicology: Definition

A

-Science of poisons and toxicity -Harmful effects of drugs and other chemicals and on the mechanisms by which toxic compounds produce pathologic changes, disease and death

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9
Q

Definition: Drug

A

A chemical other than food used in the prevention, diagnosis, alleviation, or cure of a disease

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10
Q

Definition: Poison

A

Any agent capable of producing a deleterious effect in a biological system, seriously injuring function or producing death -ANY chemical can act as a poison, the right DOSAGE differentiates a poison from a therapeutic remedy (Tylenol: 650mg vs 6000mg)

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11
Q

Definition: Prodrugs

A

Drugs that are inactive until acted on by enzymes in the body

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12
Q

Definition: Psychoactive drugs

A

Drugs that produce effects on the CNS, altering consciousness and perception (usually addictive)

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13
Q

Definition: Gateway Hypothesis

A

Types of drugs that, when used excessively, will lead to the use of more addictive drugs -Has many flaws and the Common Liability of Addiction (CLA) theory has more literature support -Ex: Tobacco, alcohol, marijuana

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14
Q

Definition: Common Liability of Addiction Theory

A

Suggests that individuals who abuse any drug are at a greater risk to develop any number of mental health disorders, including increased risk for abuse of other drugs

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15
Q

What are various usages for drugs?

A

-Diagnostic (radioactive iodine for thyroid, adenosine for heart arrythmias) -Prevention (Vaccines) -Treatment (cure or alleviation of symptoms)

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16
Q

True or False: Drugs cannot endow a tissue or cell with properties that they do not currently possess.

A

True

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17
Q

Effects of Drugs: Primary Effect

A

Desired therapeutic effect -Amphetamine (Dexedrine) for narcolepsy -Diphenhydramine (Benadryl) for allergic rhinitis/allergic reaction

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18
Q

Effects of Drugs: Side Effects

A

Predictable, dose-dependent on NON-TARGET organs -Amphetamine (Dexedrine) can cause increased heart rate -Diphenhydramine (Benadryl) can cause xerostomia

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19
Q

Effects of Drugs: Toxic Effects

A

Predictable, dose-related; they can act on TARGET and NON-TARGET organs -Ampetamine (Dexedrine) can lead to fatal arrhythmias/palpitations

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20
Q

Drug Nomenclature: Trade Name

A

Name the drug company used to register the drug -Capitalized and proprietary name registered with the US Patent Office

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21
Q

Drug Nomenclature: Generic Name

A

Non-Patented and non-proprietary name -Non-capitalized (acetaminophen is the generic name for Tylenol) -Official name of drug adopted by the US Adopted Name Council

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22
Q

Drug Nomenclature: Legend Drug

A

Requires a prescription

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23
Q

Drug Nomenclature: Non-legend Drug

A

OTC drug (non-prescription)

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24
Q

Drug Nomenclature: Orphan Drugs

A

Drugs developed to treat very rare disease such as Dornase alfa (Pulmozyme) for cystic fibrosis

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25
Q

Drug Nomenclature: Off-label Use

A

Use of an approved drug in another dosage form, for another indication, at higher doses, in a different patient population, or for use not mentioned in the approved labeling or package insert

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26
Q

1970 Controlled Substance Act

A

-Created drug schedules or classes for habit-forming drugs based on abuse potential -DEA places drugs on schedules and DEA number required to write prescriptions

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27
Q

Schedule 1 (C-1) Drug

A

-Highest abuse potential -Experimental or research-use only -Heroin, LSD, marijuana, hallucinogens

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28
Q

Schedule 2 (C-2) Drug

A

-High abuse potential -Written prescriptions ONLY -No Refills -Morphine, meperidine (Demerol), oxycodone (OxyContin), hydrocodone/acetaminophen (Vicodin)

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29
Q

Schedule 3 (C-3) Drug

A

-Moderate abuse potential -Prescriptions may be phoned in (NMT 5 refills or 6 month supply) -Codeine mixtures (Tylenol#3), ketamine, testosterone

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30
Q

Schedule 4 (C-4) Drug

A

-Low abuse potential -Written or phoned prescriptions allowed (NMT 5 refills or 6 month supply) -Benzodiazepines: diazepam (Valium), zolpidem (Ambien), or tramadol (Ultram)

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31
Q

Schedule 5 (C-5) Drug

A

-Lowest abuse potential -Can be purchased OTC in some states -Lyrica (Trade name) or some codeine-containing cough syrups

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32
Q

Drug Nomenclature: Bioavailability

A

Fraction of drug that reaches systemic circulation (F = 1) -F=1 (100%) for IV drugs

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33
Q

Drug Nomenclature: Bioequivalence

A

A generic drug generally produces a plasma level 80-120% of a brand name drug (CHEAPER) -BMN (brand medically necessary) if you don’t want the patient to get generic

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34
Q

Drug Regulation: FDA

A

Regulates the standard, quality, and manufacturing practice in drug manufacturing plants and approval of new drugs

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35
Q

Drug Regulation: FTC

A

Regulates trade practice, prohibits false advertising of food, non-prescription drugs and cosmetics

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36
Q

Drug Regulation: DEA

A

Regulates the manufacturing and distribution of drugs with high potential for abuse (narcotics, stimulants, and sedatives)

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37
Q

Drug Receptor Interactions Definition: Agonist

A

A drug capable of interacting with a receptor to produce a pharmacologic response -Has both AFFINITY and EFFICACY

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38
Q

Drug Receptor Interactions Definition: Affinity

A

The ability of the drug to bind to receptors

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39
Q

Drug Receptor Interactions Definition: Efficacy

A

The maximum intensity of effect or response that can be produced by a drug -Unique to Agonists (full agonist has intricate efficacy of 1)

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40
Q

Drug Receptor Interactions Definition: Antagonist

A

A drug that interacts with the receptors but no response is produced -AFFINITY (but no efficacy) -Can be reversed by adding more agonist

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41
Q

Drug Receptor Interactions Definition: Reserve (Spare) receptors

A

The fraction of receptors that are unoccupied even at 100% maximum response

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42
Q

Drug Receptor Interactions Definition: Partial agonist

A

A drug that is unable to produce maximal response, even at 100% receptor occupancy (No reserve receptors)

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43
Q

Drug Receptor Interactions Definition: Potency

A

The amount of drug needed to produce an effect -Compared to other drugs by measuring EC50 (effective concentration or concentration of drug to obtain 50% maximum response)

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44
Q

Sub-sensitivity and Pharmacodynamic Tolerance

A

The continuous or repeated exposure to agonists can decrease the number of post-synaptic receptors or decrease the affinity of the agonist for the receptors -Responsible for Pharmacodynamic Tolerance (increasing dosages are needed to produce the same pharmacologic effect) -Receptor down-regulation

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45
Q

Name the 5 types of Drug Receptors

A
  1. Ion Channel
  2. G-Protein Coupled Receptor
  3. Steroid
  4. Transmembrane Tyrosine Hydroxylase
  5. JAK-STAT Pathway
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46
Q

Supersensitivity

A

Continuous or repeated exposure to antagonists can increase the number of postsynaptic receptors

The response to the agonist will be intensified

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47
Q

3 Drug-Receptor Interaction Theories

A

Occupation Theory: Biological response of a drug is proportional to the number of receptors occupied

Rate Theory: the rate of the drug-receptor interaction is important

Drug-induced protein changes: agonists act by inducing a temporary structural change in the protein constituent of the receptor site

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48
Q

Threshold Dose

A

Minimum dose of a drug to observe an effect

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49
Q

Sub-threshold dose

A

Dose is too low to elicit an effect

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50
Q

Log Dose Response Curve

A
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51
Q

Graded Doses Response Curve

A
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52
Q

Quantal Dose Response Curve - Therapeutic Index

A
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53
Q

Therapeutic Index Definitions:

1) Narrow
2) Wide
3) ED50
4) LD50
5) Therapeutic index

A

1) Narrow - the two curves are close together
2) Wide - the two curves are far apart
3) ED50 - median effect dose - dose that will produce a specific response in 50% of the population
4) LD50 - median lethal dose - dose that will kill 50% of the population
5) Therapeutic index - LD50/ED50

*TI must be greater than 1.0 to have any clinical value and the greater the value, the safer the agent

54
Q

Non-Receptor Mechanisms of Drug Action

A

1) Antimetabolite
2) Chelating agents (Dimercaprol in mercury poisoning binds the heavy metals to form relatively stable, nontoxic soluble chelates excreted in urine)
3) Acid Base: Tums
4) Nonspecific action: Ethanol hand sanitizer disrupts the cell wall

55
Q

Placebo

A

Any therapy that lacks specific activity for the condition being treated

-Can have a powerful influence on outcome

56
Q

Drug Development Phases

A

Phase 1: 20-80 healthy volunteers - safety and dosage

Phase 2: 100-300 patient volunteers - efficacy and initial adverse effects

Phase 3: 1000-3000 patient volunteers - verify efficacy, monitor adverse effect

*FDA reviews data 2.5 years

Approved at 12 years

Phase 4: Post-marketing surveillance (not rigidly required by FDA)

57
Q

What does double-blinded mean?

A

Nobody knows (patient or provider) which treatment option they are receiving/giving

58
Q

Common Abbreviations

  1. ​​a
  2. ac
  3. pc
  4. qd
  5. qod
  6. qid
  7. bid
  8. tid
  9. h
  10. hs
  11. ud
  12. q
  13. prn
  14. po
  15. sq
A
59
Q

Pharmacokinetic Principles (ADME)

A

Absorption: Method of drug administration; dosage form of the drug; passage across biological membranes

Distribution: Plasma, specific tissue, non-specific tissue; protein bound; free drug pharmacologic effect

Metabolism: liver (major)

Excretion: kidney (major); sweat and milk (minor)

60
Q

Passage of Drug through Membranes: Passive Diffusion

A

-Most drugs enter this way (gases, hydrophobic, small polar); NOT large polar molecules or charged molecules

Non-ionized, lipid soluble drugs

Move down a concentration gradient and requires no energy

61
Q

Passage of Drug through Membranes: Pinocytosis (endocytosis)

A
  • Area of cell membrane invaginates around the target molecule and moves it into cell inside a vacuole
  • For molecules too large to traverse the membrane
62
Q

Passage of Drug through Membranes: Active transport

A
  • Protein pumps that require energy
  • Against a concentration gradient by a molecular pump
63
Q

Factors Affecting Passage of Drugs Across Membrane Barriers

A
64
Q

What is the Effect of pH on Drug Ionization and Membrane Passage

A

Cell membranes are more permeable to the non-ionized form of a drug than to the ionized form due to the greater lipophilicity of the non-ionized form

  • Low pH (acidic): majority non-ionized
  • High pH (basic) : majority ionized
65
Q

Absorption and factors that affect it

A

After a drug has permeated a membrane, it is absorbed (transfer of the drug into the bloodstream)

Factors:

  1. Dose
  2. Surface area available for absorption
  3. Route of drug administration
66
Q

Are nonionized molecules more lipid soluble or water soluble

A

Lipid soluble

67
Q

Where are weak acids better absorbed?

A

They are more nonionized in the stomach/stomach acid so it’s better absorbed there (aspirin)

68
Q

Where are weak bases better absorbed?

A

Weak bases are more nonionized in the small intestine so they are better absorbed there (codeine)

69
Q

Definition: Free drug

A

Active drug (not bound to protein); have pharmacological effect

70
Q

Where does metabolism mostly occur?

A

Liver

71
Q

Where does excretion predominately occur?

A

Kidney

72
Q

Where does elimination primarily occur?

A

Urine and feces

73
Q

What are the 2 major routes of administration?

A

Enteral and Parenteral

Enteral: oral (most common), sublingual or rectal

Parenteral: IV, IM, SQ (or SC)

74
Q

What are the advantages of the oral route of administration?

A

Convenient, allerfic reaction less likely to occur, and large absorbing area (Stomach, GI tract)

75
Q

What are the disadvantages of Oral administration?

A

Nausea, vomiting, slow onset (20-30 min), subjected to first pass effect (hepatic metabolism), presence of food in stomach may delay absorption, drugs destroyed by gastric acid wil become less available for absorption –> enteric coating of a drug protects it from gastric environment and may prevent/reduce gastric irritation

76
Q

What are the advantages of rectal drug administration?

A

NPO, nausea/vomiting, children, bypasses portal circulation, thus hepatic metabolism of drug is reduced

77
Q

What are the disadvantages of rectal administration?

A

Absorption is irregular and incomplete, inconvenient, potential irritation to rectal mucosa, poor adherence

78
Q

What are the advantages of Intravenous administration?

A

Immediate onset (most rapid 5-10 seconds), irritating solutions and large volumes can be given, use in emergency situations

79
Q

What are the disadvantages of intravenous administration?

A

Drug must be given in solution, sterility is essential

80
Q

What are the advantages of Intramuscular administration? Disadvantage?

A

Rapid absorption due to high blood flow through skeletal muscle, irritating substances can be administered, some depo (slow release) formulations are desired

Disadvantage: can hit a blood vessel by accident

81
Q

What are the advantages of subcutaneous administration? Disadvantages?

A

Advantages: slow but prolonged effect, implant pellets

Disadvantages: only non-irritating drugs can be used

82
Q

What are some of the other routes of administration?

A

Intrathecal/spine

Epidural

Intraosseous

Intradermal: Tb test and Local Anesthetics

Inhalation: gaseous and volatile drug aerosols, inhalation anesthetics (nitrous oxide)

Topical

Intranasal

Transdermal

83
Q

What is the first pass effect?

A

Oral drugs must pass through the liver before reaching systemic circulation

84
Q

Where are drugs filtered primarily? Metabolized?

A

Filtered: kidney

Metabolized: liver

85
Q

What does it mean to get enterohepatic circulation?

A

Some agents are eliminated into bile and are subjected to reabsorption, which may involve participation in enterohepatic circulation

This means that you may get longer duration of action

86
Q

What is volume of distribution? What does it measure?

A

Vd is the total amount of drug in the body (mg) and it is the measure of apparent space in the body available to contain the drug

87
Q

What type of drugs have a high Vd?

A

Lipid soluble drugs

88
Q

What is the Central compartment composed of? Peripheral?

A

Highly perfused organs

Less perfused

89
Q

What plasma proteins bind some drugs? Is this reversible? What are the repercussions of this binding?

A

Albumin and globulin

Binding process is reversible (equilibrium)

Once bound, the drug cannot cross the capillary wall (this serves as a storage depot for drug)

Bound drug does not cross the blood brain barrier

90
Q

What is biological effect proportional to?

A

Biological effect is proportional to FREE drug concentration in the plasma (plasma water)

91
Q

What happens when you prescribe both warfarin and diclofenac?

A

Because drugs with greater affinity for protein (diclofenac) will kick other med off and you get greater effect of the free med (warfarin)

92
Q

What are the different classifications of tissue distribution?

A

Specific: from plasma to target

Non-specific: tetracycline to bone enamel

Blood brain barrier: need small molecule to get into the brain due to tight junctions between endothelial cells of CNS

Placental barrier: leakiest barrier out there; few drugs are proven safe for pregnant women and should be avoided if possible

93
Q

What is tissue redistribution and why is it important to understand (Thiopental)?

A

The drug is transferred from one organ to another

Important because Thiopental for sedation dissipates quickly because it quickly is redistributed from the CNS to the skeletal tissue to the adipose tissue and the patient awakes in 5-6 minutes

94
Q

Define Metabolism (biotransformation)

A

Determines the intensity/duration of action of most drugs (usually terminates the action)

95
Q

What is the significance of metabolites?

A

Metabolites are usually less active, less lipid soluble, and more polar than the drug itself; are not reabsorbed by the kidney; excreted from the body

(oxidation is the body’s preferred pathway and the drug is ionized to become water-soluble for excretion)

96
Q

True or False: Drugs are usually metabolized from a lipid soluble drug to a lipid insoluble (hydrophilic) drug.

A

True

97
Q

Is the microsomal enzyme system specific or non-specific? What are examples of some of those enzymes and what is the preferred pathway?

A

Non-specific

Cytochrome P450, NADPH-Cytochrome P450 reductase

Oxidation

98
Q

What enzyme is responsible for most phase 1 inactivation reactions?

A

Cytochrome P450

99
Q

What happens when you have hepatic enzyme induction?

A

Pharmacologic effect is REDUCED

100
Q

What happens when you have hepatic enzyme inhibition? Why?

A

The pharmacologic effect of the drug is INCREASED

Because the metabolism of the drug is being slowed down so the duration of action is increased

101
Q

What is zero order kinetics?

A

A drug is metabolized at a constant rate

-I.e. alcohol is metabolized at a rate of 1 drink/hr

102
Q

What is First Order Kinetics?

A

A drug is eliminated at a constant fraction per unit time

-I.e. the more one takes, the more is eliminated; this occurs for most drugs

103
Q

What form are metabolized drugs excreted in: polar or non-polar?

A

More polar form

104
Q

What is half-life?

A

The time required for the body to eliminate 50% of the drug administered

105
Q

Drug Disappearance Curve (Picture)

A

The final net result of ADME of a drug can be described in the form of a drug disappearance curve, using blood or tissue concentration

106
Q

In general, how long does it take for the body to eliminate 94% of a drug?

A

4 half-lives

107
Q

Time Response Curve (Photo)

A

Latency - the time it takes before the drug starts to work = 0-1

Maximal effect (Efficacy) = 2

Duration of action = 1-5

108
Q

What is duration of action?

A

Time during which blood levels are above the minimum effective concentration

109
Q

When does maximum effect occur?

A

When absorption must be greater than elimination (measured by the time to peak action)

110
Q

Dosing Regimen: Maintenance dose

A

A drug administered in such a way as to achieve a steady state of drug in the body

-The amount of drug needed to maintain clinical effectiveness

[(Dosing rate)*(dosing interval)]/Oral Bioavailability

111
Q

Dosing Regimen: Loading Dose

A

The administration of an amount of drug that will raise the concentration of a drug in plasma to a target concentration of a drug in plasma to a target concentration for clinical effectiveness

-Dosed close to it’s half life (600mg loading dose; 300mg maintenance dose every 3-4hrs)

112
Q

Dosing Regimen: Steady State

A

A level of drug accumulation in the blood and tissue upon related dosing when the input of drug = the output of drug

113
Q

Creatinine clearance

A

An indicator of kidney function that affects renal elimination and dosing interval

Based on individual’s age, gender, weight, and lab serum creatinine (Scr)

114
Q

Synergism

A

The response obtained is greater than the algebraic sum of the independent effects of each drug

-Ex. Penicillin and streptomycin

115
Q

Potentiation

A

A drug does not have an effect on its own but increases the effect of a second drug

Ex. Clavulanic acid added to amoxicillin = Augmentin

116
Q

Addition/Summation

A

Response is equal to the algebraic sum of the independent effects (more common)

Ex. acetaminophen + codeine

117
Q

Antagonism

A

The clinical response of a drug is decreased by the administration of a second drug

Ex. Dubutamine (Beta1 agonist) and metoprolol (Beta1 antagonist)

118
Q

Mechanisms of Competitive Drug Antagonism

A

Log dose response graph

Green = increasing dose can restore pharmacologic response

119
Q

Physiological antagonism

A

The antagonist acts at a different site and by a different mechanism to produce an effect that is opposite and that counterbalances the effect of the agonist

Ex. Amphetamine and zoldipam (Ambien)

120
Q

Physical-chemical antagonism

A

The antagonist chemicaly or physcially interacts with and inactivates the agonist

-May not involve any receptor

Ex. minocycline (Minocin) and divalent cations (Ca++)

121
Q

Biochemical antagonism

A

The agonist may act as an enzyme inducer, thereby increasing the activity of the liver microsomal drug-metabolizing enzymes and rsults in the more rapid metabolism and inactivation of the agonist and other drugs taken concurrently

Ex. Hydrocarbons on tobacco smoke increase hepatic P450 enzymes leading to increased metabolism of warfarin = greater risk for clot development

122
Q

Tolerance

A

A decrease in pharmacologic effect of a drug after repeated administration

An increase in dosage of the same drug is needed to achieve the same response

This is related to receptor down-regulation (fewer receptors or less sensitive)

123
Q

Cross Tolerance

A

Tolerance of 1 drug leads to tolerance of another

-Opioid addict may require more local anesthetic to achieve profound anesthesia

124
Q
A
125
Q

What is the difference between physical dependence and psychological dependence?

A

Physical dependence=dependence

Psychological dependence=addiction

126
Q

What are the different types of adverse drug reactions?

A

Type A: predictable

Type B: unpredictable/idiosyncratic reactions; immunologic/allergic reactions; teratogenic effects; oncogenic effects

127
Q

What are side effects?

A

Most are predictable, dose-related, and extension of pharmacologic effects

Occur on non-target organs

128
Q

Toxic reactions

A

Predictable, dose-related but on target and non-target organs

129
Q

Allergic reactions

A

Unpredictable; not dose related

I: Immediate

II & III: Complement system activation; antibodies

IV: delayed hypersensitivity

130
Q
A

Pharmacology (7 decks)

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