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Pathology > Pharmacology Class 2020 Introduction,Pharmacodynamics and Drug Administration > Flashcards

Pharmacology Class 2020 Introduction,Pharmacodynamics and Drug Administration Flashcards

1
Q

Xenobiotics

A

synthesized outside the body

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2
Q

toxins

A

poisons that come from biologic orgin

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3
Q

poisons

A

produce harmful effects on the body.

The dose makes the poison

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4
Q

hormones

A

synthesized within the body

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5
Q

agonist

A

activates a process

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6
Q

anatagonist

A

inhibits effects

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7
Q

receptors

A

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

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8
Q

what are required of the drug to be specific?

A

size
shape
atomic composition
electrical charge

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9
Q

what is the MW of drug in order for it to bind?

A

100MW

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10
Q

do drugs over 1000MW diffuse readily through compartments of the body?

A

No, they must be administered directly to the site of their intended effect.

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11
Q

ligand

A

a molecule that binds to another molecule such as a drug, hormone or neurotransmitter

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12
Q

chirality

A

enatiomers which are mirror images of eachother.

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13
Q

racemic mixture

A

a drug that has a mix of both enatiomers or mirror images such as both the S and R enatiomer.

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14
Q

Why would we have only one enatiomer present in a drug?

A

because it may fit the target receptor better and create a superior effect than the other enatiomer.

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15
Q

Nonselective drugs

A

affects multiple receptors on different cells and tissues

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16
Q

selective drug

A

specific binding

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17
Q

What determines the quantitative relations between the dose and concentration of drug and pharmacologic effects?

A

Receptors

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18
Q

What is responsible for the selectivity of a drug?

A

Receptor

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19
Q

When a drug binds to a receptor, what is the general effect?

A

cascade of events

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20
Q

What does the bond between the drug and receptor determine?

A

The differences in the bind determines how well and how long a drug is going to bind.

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21
Q

what is the strongest bond between a drug and receptor?

A

Covalent Bond
They are strong and irreversible binding
Results when a pair of electrons is shared between two atoms.

Examples:
Aspirin
Sarin gas ( dangerous)
Penicillin

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22
Q

What is the weaker bond between a drug and receptor?

A

Electrostatic Bond

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23
Q

What type of bonds do you see in lipid drug receptors?

A

Hydrophobic

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24
Q

What is the most common use for aspirin today?

A

prevent platelet aggregation by binding covalently to Platelet COX-1 to prevent platelets from aggregating to other platelets and it takes 2 weeks for new platelets to be made.

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25
Q

How long does it take for aspirin to affect platelets in the body?

A

15 minutes

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26
Q

Which is more selective, covalent or electrostatic bonds?

A

Electrostatic

Because it is weaker, it requires the fit between the drug and receptor to be more precise so that it wont fall off unlike covalent which relies on its strength to hold on.

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27
Q

Why do we not want drugs to permanently bind to receptors?

A

it can produce toxic effects

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28
Q

What is the least common bond interaction?

A

Hydrophobic Bond

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29
Q

When a drug and receptor bind, what is formed?

A

D-R Complex

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30
Q

What binds to the same site as the Agonist?

A

Competitive Inhibitor/ Competitive Antagonist

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31
Q

Allosteric Activator

A

Binds to a different spot on the receptor to allow the receptor to have a confirmational change that makes it have more affinity for the drug

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32
Q

Agonist

A

Drugs that have an activating effect on a receptor

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33
Q

Full Agonist

A

Ligand or drug that bind only to the active form of the receptor to produce a Full Max effect. The plateau is the max on the graph.

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34
Q

Partial Agonist

A

Ligand binds to both the active and inactive forms of the receptor but with more affinity for the active form of the receptor. It does not reach the max effect

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35
Q

Antagonist

A

Blocks the agonist from binding to the receptor

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36
Q

How does partial agonist reduce the max effect of the Full Agonist?

A

Partial Agonist competes with the Full Agonist for the active receptors and prevents the Full Agonist from binding to all the receptor that it needs to in order to get their full effect.

It knocks off the Full Agonist from some of the receptors and you lose full effect of the Full Agonist.

Example:
Methadone drug is a Full Agonist

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37
Q

Inverse Agonist

A

Drugs that produce the opposite effects of the Agonist.

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38
Q

What is required for a drug to be an Inverse Agonist?

A

It must have constitutive Activity.

The key thing is that the receptor that it binds to must have constitutive activity which is the activity that occurs in the receptor when there is no ligand bound to it or baseline effect on its own.

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39
Q

What is the difference between an Inverse Agonist or Antagonist?

A

The antagonist blocks the agonist.

The Inverse Agonist brings down the activity of the receptor by producing the opposite effect.

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40
Q

Antagonist Types

A

Competitive
NonCompetitive
Allosteric Antagonist

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41
Q

Competitive Antagonist

A

Antagonist competes for the same binding spot as the ligand/ drug.

It is reversible because as you add more agonist the effects of the competitive antagonist can be overcome.

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42
Q

Spare Receptor

A

A receptor that does not bind to the drug when the drug concentration is sufficient to reach the max effect.

Example:

90% of receptors are bound produce max effect.
10% are spare receptors. ( Dont need to be bound to produce max effect)

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43
Q

Noncompetitive Antagonist

A

Bind to the receptor in irreversible manner.

Reduces the maximal response that an agonist can produce.

Cannot overcome effect of the noncompetitive antagonist by increasing concentration of agonist.

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44
Q

Phenochromocytoma

A

A tumor of the adrenal medulla. It produces excessive amounts of adrenaline and noradrenaline.

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45
Q

Mixed Agonist

A

Drugs have both agonistic and antagonistic properties.

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46
Q

Chemical Antagonism

A

A drug may antagonize the actions of a second drug by binding to and inactivating the second drug. It binds to the actual drug.

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47
Q

Physiologic Antagonism

A

Physiologic functions controlled by opposing regulatory pathways

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48
Q

Regulatory Proteins

A

Mediate actions of endogenous chemical signals such as neurotransmitter and hormones

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49
Q

Enzymes

A

Protein receptors that can be activated or inactivated by drugs. Drugs themselves can be enzymes.

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50
Q

Transport Proteins

A

Receptors that regulate movement of material

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51
Q

Structural Proteins

A

Structural Elements

Example: Tubulin

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52
Q

Colchicine

A

A drug that binds to a structural protein. It prevents microtubule assembly and thereby disrupts inflammasome activation.

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53
Q

What type of lipid soluble ligand affect gene expression?

A

steroids

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54
Q

What is the effect downregulation of receptors?

A

When ligand binding leads to internalization of the receptor. The synthesis of the receptors is less than the rate of receptor degredation.
Losing total number of cell surface receptors available to bind to the ligand which reduces the responsiveness of the receptor to the ligand.

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55
Q

What type of transmembrane signaling is available?

A

Enzyme

Nonenzyme

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56
Q

Tachyphylaxis

A

When responsiveness to a drug diminishes rapidly after administration of a drug which is acute tolerance.

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57
Q

Desensitization

A

cell’s responsiveness to ligand decreases

58
Q

Upregulation

A

An increase in the number of receptors on the surface of target cells.

59
Q

Resensitization

A

When you have been off a drug for a while and build up a tolerance that you want to get rid of and then when you start taking it again, the response is very high as your first time taking it.

60
Q

Graded Dose Response Curve

A

Graph of the change of dose vs the effect

61
Q

EC 50

A

the concentration that produces 50% of the maximal response

62
Q

EMax

A

The maximal response that can be produced by the drug

63
Q

Dose

A

The concentration of a drug.

64
Q

TD 50

A

The dose at which 50% of the subjects experienced a toxic effect

65
Q

LD 50

A

The dose at which 50% of the subjects died.

66
Q

Potency

A

The amount of the drug needed to produce a specified effect.

Potency is also the concentration needed for the drug to reach 50% effect

67
Q

Graded Response

A

There is a small response to a low dose of a drug and the response increases as the dose increases.
It is the affinity of the receptor for the drug and the number of receptors available.

68
Q

Relative Potency

A

The ratio of equi effective doses.

69
Q

Equipotent Dose

A

Increasing the dose of a less potent drug to get the same clinical response of a more potent drug.

Even if a drug is more potent, it does not mean that it is superior in therapeutic effect.

70
Q

What is a statin?

A

A cholesterol lowering drug

71
Q

Pharmacokinetics

A

Study of the time course of drug absorption, distribution, metabolism and elimination

72
Q

Pharmacodynamics

A

Effects of the drugs on the biological systems

73
Q

Mechanism of Action

MOA

A

The events that occur in the body that lead to a drug’s effect

74
Q

Drugs

A

Any substance that brings about a change in biologic function through its chemical actions

75
Q

Can drugs create physiologic responses?

A

No, the physiological process must be intrinsic to patient.

76
Q

What are the various forms of drugs?

A 
inorganic ions
nonpeptide organic molecules
nucleic acids
lipids
carbohydrates
small peptides
77
Q

EGF

A

Epidermal Growth Factor

78
Q

Quantal Dose Response

A

A dose response that is defined as either absent or present. All or none.
It is useful for finding the dose required to produce a specified response in each member of a population.

Example:
What dose is required to lower LDL by 50%?
What dose is required to lower SBP by 20mmHg?

79
Q

Therapeutic Range

A

Range between the minimum toxic dose and the minimum therapeutic dose.

80
Q

What is indicated by a higher TI index?

A

A greater margin for safety.

81
Q

What is indicated by a lower TI index?

A

A narrow therapeutic index with a high risk for toxic effects.

82
Q

Therapeutic Window

A

Range of concentration of drug in the plasma that provides therapeutic efficacy with minimal toxicity.

83
Q

Tubulin

A

A receptor for a drug that prevents gout formation.

84
Q

What is an example of a mixed agonist?

A

Buprenorphine

85
Q

What is the role of insulin?

A

To reduce plasma glucose levels.

86
Q

Which drug increases plasma glucose levels in the body?

A

Prednisone

87
Q

What is the chemical antagonist of Heparin?

A

Protamine because it binds to Heparin and neutralizes it.

Acts as a chemical antagonist

88
Q

The events that occur in the body to lead to a drug’s effect.

A

MOA

Mechanism of Action

89
Q

Drugs that affect the signaling of other drugs

A

Chemical Antagonist

90
Q

Drugs with the same chemical makeup but in different arrangements

A

Enatiomers

Example:
Ipratroprium for asthma
Atropine for bradycardia

91
Q

Maximal response that can be produced by a drug

A

E Max

92
Q

Concentration that produces 50% of the maximal response

A

EC 50

93
Q

Ligand only binds to the active form of the receptor

A

Full Agonist

94
Q

what factors affect the Oral Administration of a drug?

A 
pH
Tolerability
Patient Compliance
Liver metabolism
Circulation to the intestines
Hydrophobicity
Absorption capacity of patient in gut
95
Q

what are oral solids?

A

Tablets

Capsules

96
Q

Why do we use an enteric coated form of asprin?

A

To prevent stomach irritation due to be destroyed in low pH environment

97
Q

Why are oral liquid forms of the drug great?

A

easier to swallow for patients that have swallowing issues with muscle.
Pediatric patients
Elderly patients

98
Q

What is a disadvantage of oral liquid drugs?

A

Mistake in drug dosage

There is no controlled release like oral solid drug
there is a shorter shelf life because the medium of

Liquid makes it less stable than a solid would be.

99
Q

What is sublingual drug?

A

Administered under the tongue for systemic effect like

Examples: B12 or nitroglycerin

100
Q

What is a buccal drug?

A

A drug that is placed between the gum and cheek

Example: Nicotine gum

101
Q

What is a immediate release drug?

A

Releases drug as quickly as possible after administration and onset is minutes to hours.

The effectiveness is short

102
Q

What are the benefits of controlled release drugs?

A

Less frequency of administration of the drug

Decrease adverse effects by dampening the peak

Works overnight

Constant rate of release over dosing interval

103
Q

What is a modified release drug?

A

Used to describe products that alter the timing and or rate of the release of the drug substance in the formulation

104
Q

What is dose dumping?

A

A controlled release drug is taken with warm or hot water which could cause the drug to release all at once.

105
Q

What is the disadvantage of controlled drug release?

A

Difficult to modify the dose

Require patient education to tell patient not to take too many per hour due to controlled release

106
Q

What is the best time to use rectal route?

A

When the patient is incapacitated.

107
Q

What is the disadvantage of rectal route?

A

Could be inserted more distally which impair absorption.

108
Q

What is a delayed release drug?

A

The drug is released only at some point after the initial administration

Examples: Enteric Coated
Tablets
Colorectal Drugs

109
Q

Define Extended Release Drug

A

Slow uniform absorption of drug over 8 hours and longer therapeutic effect.

The advantage is that there is less frequent administration and better compliance

110
Q

Which is the more rapid form of administration of a drug that avoids absorption and metabolic issues?

A

Parental Administration which is an injection into an internal body compartment or cavity through IV and subcutaneous SC

111
Q

What us Sustained Release Drug?

A

Administered over a sustained period of time that is not at a constant rate in which plasma concentration may be variable

112
Q

What is the difference between Sustained and Controlled Release drug?

A

There is variability in plasma concentration of a sustained release and constant plasma concentration in controlled release drug.

113
Q

Why is inhalation drugs beneficial?

A

Useful for local delivery and reduces drug exposure and systemic side effects

114
Q

What are the advantages of parental administration of a drug?

A

More rapid

Extensive

Precise

More predictable than oral

115
Q

What are suspensions used for in parental administration?

A

Used for insoluble drugs that are suspended in aqueous or oil vehicle.

Suspensions increase stability for insoluble drugs or chemicals with decreased water solubility

It makes a slower release than water soluble which can produce a more sustained release.

116
Q

In what two ways are suspensions given?

A

SQ or IM

117
Q

What are emulsions used for?

A

Drugs that are irritating to the vein.

They increase stability of the drug

118
Q

What are dry powders?

A

Used to store unstable drugs

119
Q

What are the different depths of parental administration?

A

Intramuscular =IM
Into Vein= IV
Intradermal= between epidermis and dermis
Subcutaneous= SQ Just below dermis

120
Q

Tissue Plasmogen Activator ( TPA)

A

Breaks up blood clot

121
Q

What is F symbol ?

A

Amount of drug reaching systemic circulation + amount of drug given

122
Q

What is the risk of intramuscular or intravenous drug administration?

A

Introduction of bacteria.

We swab patient skin with alcohol first to prevent bacteria from getting into system.

123
Q

Which type of administration has the most disadvantages?

A

IV drug

124
Q

What are benefits of SQ administration?

A

Reduced risk to pathogens than IV

Slower absorption means longer effects

125
Q

What is wrong with vitamin K in SQ administration?

A

Absorption is erratic

126
Q

What are disadvantages of SQ?

A

Can only administer 1.5ml at a time

Unsuitable for irritating drugs

127
Q

What are the typical muscular sites of IM administration?

A

Deltoid
Ventrogluteal
Vastus Lateralis
Dorsogluteal

128
Q

What increases the absorption rate of an IM?

A

massage

heat

exercise

129
Q

What are the restrictions of IM?

A

Pain

Possible nerve damage of which the highest risk of nerve damage is in gluteal injections because Sciatic nerve damage.

Limited volume of drug can be given at 1.3ml

130
Q

What type of drugs are administered by intra articular?

A

Corticosteroids such as methylprednisone, triamcinolone, dexamethasone,hydrocortisone

Local Anesthetics such as lidocaine,bupivaccine

Common use: 
Arthritis
Gout
Bursitis
Tendonitis
131
Q

How would you administer a corticosteroid?

A

Intra articular

132
Q

What route of administration is used for local anesthetic?

A

intra articular

133
Q

What is the limit of dose for intra dermal administration?

A

0.1ml

134
Q

What is the use of intra dermal administration?

A

skin testing for TB

135
Q

What is intrathecal administration?

A

bypass blood brain barrier CSF

Used for spinal anesthesia ,CNS infections

136
Q

Where do we inject epidural?

A

Epidural space around spinal cord

137
Q

Where is intracavernous?

A

Injection into base of penis

138
Q

What is topical administration?

A

Good for localized arthritis.

Applied on top of the skin or mucous membranes

Examples: Creams , Ointment

139
Q

What is disadvantage of topical administration?

A

Reapplication 2-3 times per day

Slow absorption

140
Q

What are transdermal patches?

A

To release a certain amount of drug during a certain time period.

It is in place of oral drug administration

Used for systemic absorption with release into blood stream without being metabolized

Must be removed before MRI

Examples:

Nicotine
Hormonal

141
Q

What is the mechanism of the transdermal administration?

A

Pressure mechanisms in the patch forces the drug into the skin through pressure and can use heat too.

142
Q

What are opthalmic drugs?

A

pH sensitive

Require frequent dosing

Up to 80% of the drug can be systemically absorbed

Pathology (10 decks)

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