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Pharmacology Test #1 > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

Concentration of a drug at the site of action is dependent on

A

rate of absorption and blood flow to the site

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2
Q

how long a drug remains at the site in effective concentrations depends on

A

biotransformation (metabolism) and excretion

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3
Q

sites of drug action

A

extracellular
intracellular
on the cell surface

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4
Q

intracellular sites

A

drugs used to treat infections
drugs used for cancer chemotherapy
hormones such as estrogen

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5
Q

EC 50

A

way to measure the potency of a drug

drug concentration at which the drug is 50% effective

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6
Q

law of mass action

A

the effect of a drug is directly proportional to the amount of drug-receptor complex formed

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7
Q

rate of association

A

k1 [D][R]

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8
Q

rate of dissociation

A

k-1 [DR]

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9
Q

rate at equilibrium

A

rate of association is equal to the rate of dissociation

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10
Q

the lower the Kd?

A

the higher the affinity

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11
Q

Kd?

A

half of the receptors are bound by the drug

measure of affinity

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12
Q

assumptions made for the law of mass action

A
  1. the binding is totally reversible
  2. D and R only exist as free and bound
  3. all receptor sites are considered to have equivalent affinity for D and to be independent
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13
Q

Potency

A

the dose of a drug required to produce a particular effect of given intensity (comparison based on doses that produce the same effect)

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14
Q

Affinity

A

the ability of the drug to interact with the receptor

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15
Q

What does a strong agonist have?

A

high affinity and high efficacy

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16
Q

Maximal efficacy is often limited by?

A

toxicity

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17
Q

What is more important, efficacy or potency?

A

Efficacy

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18
Q

partial agonist

A

produces a reduced response even at full receptor occupancy

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19
Q

Receptor antagonist

A

a drug-receptor interaction that interferes with or prevents the development of a drug response by an agonist

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20
Q

three major types of receptor antagonists

A
  1. competitive
  2. mixed
  3. irreversible
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21
Q

How can you reverse a competitive antagonist?

A

increasing the dose of the agonist

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22
Q

describe the log dose-response curve for an agonist in the presence of a competitive antagonist

A

shifted to the right indicating a reduction in the effective potency of the agonist

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23
Q

shape of the log dose-response curve with a competitive antagonist

A

shape and maximal response are not altered

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24
Q

Noncompetitive antagonist

A

the antagonist produces its effect at a site of the receptor other than the site used by the agonist

25
Q

increasing noncompetitive antagonist concentrations do what to Kd and Emax?

A

increase Kd and decrease Emax of the agonist

26
Q

describe the log dose-response curve in the presence of a noncompetitive antagonist?

A

shifted to the right
the slope of the agonist curve and maximal response obtained are progressively decreased
at very high concentrations of antagonist, no amount of agonist can produce a response

27
Q

Describe the log dose-response curve in the presence of a noncompetitive antagonist.

A

shifted to the right
the slope of the agonist curve and maximal response obtained are progressively decreased
at very high concentrations of antagonist, no amount of agonist can produce a response

28
Q

Describe the log dose-response curve in the presence of an irreversible antagonist.

A

initially the dose-response curve is shifted to the right (resembles competitive)
as antagonist concentration is increased, maximal response obtained is progressively decreased (resembles noncompetitive inhibition)

29
Q

functional (physiological) antagonist

A

two drugs influence a physiological system but in opposite directions
each drug is unhindered in the ability to elicit its own characteristic response

30
Q

chemical antagonism

A

a chemical reaction occurs between an agonist and an antagonist to form an inactive product

31
Q

intracellular receptors

A

stimulate the transcription of genes in the nucleus by binding to specific DNA sequences near the gene whose expression is to be regulated

32
Q

therapeutic significance of intracellular receptors

A

drugs produce their effects after a characteristic lag period
effects can persist after the agonist concentration has been reduced to zero

33
Q

kinase

A

enzyme which adds a phosphate group to a substrate

34
Q

describe protein tyrosine kinases

A

receptor consists of an extracellular hormone-binding domain and a cytoplasmic enzyme domain with protein tyrosine kinase activity (spans the membrane once)

35
Q

protein tyrosine kinases usually act as

A

dimers

36
Q

How do ligand-gated channels work?

A

following ligand binding, the signal is transmitted across the plasma membrane by increasing transmembrane conductance of the relevant ion. Alters the electrical potential across the membrane.

37
Q

How do ligand-gated channels work?

A

Following ligand binding, the signal is transmitted across the plasma membrane by increasing transmembrane conductance of the relevant ion. Alters the electrical potential across the membrane.

38
Q

Types of receptors

A
  1. intracellular receptors
  2. protein tyrosine kinases
  3. ion channels
  4. GPCRs
39
Q

examples of second messengers

A
  1. cyclic AMP
  2. calcium ion
  3. phosphoinositides
40
Q

cAMP

A

effector enzyme is adenylyl cyclase and the enzyme converts ATP to cAMP
stimulates cAMP-dependent protein kinases

41
Q

calcium and phosphoinositides

A

effector enzyme is phospholipase C

results in the release of phosphoinositides and diacylglycerol

42
Q

cGMP

A

effector enzyme is guanyl cyclase

activates cGMP-dependent protein kinase

43
Q

Assumptions for quantal log-dose reponse relationships

A

At the dose given, the subject will respond to the maximum, or not at all

44
Q

threshold

A

the minimum effective dose of the drug which evokes an all-or-none pharmacological response

45
Q

normal frequency distribution

A

doses required to produce a specified quantal effect are log-normally distribulated

46
Q

median effective dose (ED50)

A

the dose required to produce the stated effect in 50% of the population

47
Q

median lethal dose (LD50) or

median toxic dose (TD50)

A

dose required to produce death in 50% of the population or a particular toxic effect in 50% of the population

48
Q

Therapeutic index or Ratio

A

the relative safety of a drug expressed as LD50/ED50

larger the ratio the greater the relative safety

49
Q

Graded log-dose response relationships

A

the responding system is capable of showing progressively increasing effects with increasing concentrations of the drug

50
Q

drug tolerance

A

condition of decreased responsiveness to a drug

51
Q

development of drug tolerance

A
  1. decrease in effective concentration of the agonist at the site of action
  2. decrease in the normal reactivity of the receptor
52
Q

Cross tolerance

A

tolerance develops to one drug that is also seen with drugs belonging to the same class

53
Q

tachyphylaxis

A

acute development of tolerance following rapid, repeated administration of a drug
(ex. ephedrine)

54
Q

drug allergy

A

an adverse response to a foreign chemical resulting from previous exposure to the substance

55
Q

Type I hypersensitivity

A

first exposure causes IgE to the produced
rapid onset
symptoms may be localized or systemic

56
Q

Type II hypersensitivity

A

antibody-dependent cytolytic reaction
IgG and IgM antibodies produced
antibodies activate the complement system
subsides within months after removal of drug

57
Q

Type III hypersensitivity

A

Immune complex formation
drug reacts in blood with soluble antibody (IgG)
resulting immune complex deposited in vascular endothelium
serum sickness, hemolysis and allergic nephritis
subsides 1-2 weeks after drug is removed

58
Q

Type IV hypersensitivity

A

delayed hypersensitivity hours or days after exposure
mediated by antigen contact with T lymphocyte
contact dermatitis with topic drugs

59
Q

Idiosyncratic reaction

A

a genetically determined abnormal reactivity to a drug

Pharmacology Test #1 (5 decks)

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