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Farm > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

What’s the difference between pharmacokinetics and pharmacodynamics?

A

Pharmacokinetics: Body’s effect on the drug: ADME = absorption, distribution, metabolism, excretion
PharmacoDynamics: Drug’s effect on the body: dose-response and drug-receptor relationships

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2
Q

__ is the cornerstone of pharmacology.

A

The receptor

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3
Q

The __ is the drug whose interaction with the receptor __ a biological response.

A

agonist; stimulates

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4
Q

Main effect

A

characteristic intended effect

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5
Q

Side effect

A

unwanted or bothersome effect USUALLY RELATED to the main effect

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6
Q

Toxic effect

A

harmful or adverse effect of the drug; generally NOT DIRECTLY RELATED to main effect
often related to excessively high drug concentrations

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7
Q

“How quickly will the drug act?” is a question of … (pharmaco-dynamics or -kinetics)

A

Pharmacokinetics

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8
Q

What are the the three general sites of drug action?

A

1) Intracellular
2) Extracellular
3) Cell surface

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9
Q

Neutralization of excessive gastric acid by antacids is an example of which site of action?

A

Extracellular (also, heparin in preventing blood coagulation)

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10
Q

Hormone treatment is an example of which site of action?

A

Intracellular (also, cancer chemotherapy and infection tx)

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11
Q

Agonist

A

Drug that binds to receptor and stimulates a biological response

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12
Q

Antagonist

A

Drug that binds to a receptor without altering receptor function (doesn’t stimulate a response)

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13
Q

EC(50)

A

The concentration of a drug at which the drug effect is either at 50% of its maximum or compared to another known drug with the same effects

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14
Q

Law of mass action

A

[D] + [R] –> [DR] –> Effect

Words: Effect of a drug is directly proportional to the amount of drug-receptor complexes formed

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15
Q

Rate of association =

A

= k(1) [D][R]

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16
Q

Rate of dissociation =

A

= k (-1) [DR]

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17
Q

Equilibrium Dissociation Constant

A

rate of assoc. = rate of dissoc. at equilibrium; therefore, [D][R}/[DR] = K(D)

The lower the K(D) the higher the affinity

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18
Q

How can you determine the number of occupied receptors from the drug concentration, max % of bound receptors (B) and K(D)?

A

C x B / C + K(D)

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19
Q

What are the three assumptions being made in the law of mass action?

A

1) 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 (vs. cooperativity)

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20
Q

Potency

A

The dose of a drug required to produce a particular effect of given intensity (usually measured as ED50). A response measurement.

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21
Q

Affinity

A

The ability of the drug to interact with the receptor (measured as K(D)). Usually in vitro.

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22
Q

Efficacy

A

Biological response resulting from drug-receptor interaction. (Typically plotted along y-axis)

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23
Q

Maximal efficacy is often limited by ___.

A

Toxicity

24
Q

Partial agonist

A

Work by shifting equilibrium of a receptor to be stimulated more frequently but not as much so as the full agonist.

25
Q

Look at the “example of concepts” slide to differentiate potency, efficacy, agonists, and partial agonists.

A

Just do it…

26
Q

Log dose-response curve when adding competitive antagonist

A

Magnitude of shift to the right is proportional to the concentration of antagonist added; the shape and maximal response are not altered

27
Q

Spare receptors

A

when a maximal response can be elicited by an agonist at a concentration that does not result in 100% occupancy of available receptors
Important in the action of irreversible antagonists

28
Q

What makes a competitive antagonist irreversible?

A

The covalent binding (usually to the same site as the agonist)

29
Q

Noncompetitive antagonist

A

Different binding site; the antagonism cannot be completely reversed by increasing the concentration of agonist –> decrease Emax by occupying receptors
** Is reversible with drug withdrawal **

30
Q

As dose of noncompetitive antagonist is increased the ___ is progressively decreased.

A

Maximal response

31
Q

Functional (physiological) antagonism

A

two drugs influence the same physiological system but in opposite directions

Exp. Ach decreased blood pressure, but can be offset by epinephrine

32
Q

Chemical antagonism

A

Direct i/a of agonist and antagonist where they react and form an inactive product

Exp. calcium-containing antacids and tetracycline antibiotics

33
Q

Threshold of quantal log dose-response curves

A

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

34
Q

How does one make a quantal dose-response curve?

A

Doses required to produce a specified (yes or no) effect are log-normally distributed.
Responses are then summated for each given dose and the resulting cumulative frequency distribution constitutes the curve

35
Q

ED(50)

A

= Median effective dose

= Dose required to produce the stated effect in 50% of the population

36
Q

LD(50) or TD(50)

A

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

37
Q

Therapeutic Index

A

The relative safety of a drug expressed as the ratio of LD(50):ED(50)
-Larger ratio–> greater relative safety

38
Q

This type of drug produces its effects after a characteristic lag period (can not alter a pathologic state within minutes).

A

Intracellular/hormonal drugs

Effect can persist long after the agonist concentration is reduced to zero.

39
Q

What is an important structural characteristic of protein tyrosine kinases?

A

The span the lipid bilayer ONE time. –> Usually act as dimers.

Exps. Insulin, EGF, and platelet derived growth factor receptors

40
Q

How is protein tyrosine kinase activity turned off?

A

Receptor down regulation by stimulating endocytosis once the receptor is stimulated.

41
Q

Ach, GABA, and many excitatory a.a. like glycine, aspartate, and glutamate are examples of _

A

Drugs that acts as ligands for gated ion channels

42
Q

How does the lag of action in ligand-gated channels/drugs compare to intracellular drugs?

A

Time elapsed after ligand/agonist binding to cellular response is often milliseconds- much shorter than that of intracellular drugs that must induce genetic change to have an effect.

43
Q

Adrenergic amines, serotonin, acetylcholine (for muscarinic effects) are examples of __.

A

Ligands for g-protein coupled receptors

44
Q

Effector enzyme and target enzymes of cAMP

A

Effector enzyme- adenylyl cyclase

Stimulates cAMP-dependent protein kinases (also EPAC)

45
Q

Effector enzyme and effects of phosphoinositides and diacylglycerol

A

Effector enzyme- phospholipase C (PLC)–> releases IP3 and DAG

IP3-release of calcium
DAG- can activate protein kinase C

46
Q

Effector enzyme and effects of cGMP

A

Effector enzyme- guanyl cyclase
Activates cGMP-dependent protein kinases
Much more specific than other messenger systems

47
Q

“Drug disposition tolerance”

A

a decrease in effective concentration of the agonist at the site of action–> decreased effect of drug

Exp. Phenobarbital increases rate of biotransformation of a number of drugs which are metabolized by liver enzymes

48
Q

“Cellular or pharmacologic tolerance”

A

a decrease in the normal reactivity of the receptors i.e. down regulation or change in receptor affinity

Most often seen with CNS drugs (narcotics, depressants, stimulants)

49
Q

Tachyphylaxis

A

ACUTE development of tolerance following rapid, repeated administration of a drug. Often happens when drugs have an indirect effect on target response.

Can NOT overcome this type of tolerance with increasing dose

50
Q

What is an example of a drug that causes tachyphylaxis?

A

Ephedrine

51
Q

Idiosyncratic reaction

A

a genetically-determined abnormal reactivity to a drug ; often due to differences in drug metabolizing enzymes

52
Q

Type I Hypersensitivity (briefly)

A
  • Immediate hypersensitivity or anaphylaxis
  • IgE production
  • IgE becomes fixed to mast cells
  • Subsequent exposure causes drug to bind to IgE and histamine, PGs etc to be released
53
Q

Type II Hypersensitivity (briefly)

A
  • Antibody and complement mediated cytolytic reaction
  • Drug binds to cell surface –> makes cell look foreign
  • IgG and IgM activate classic complement system
  • Blood cells are primary target tissues
  • Subsides within months after removal of drug
54
Q

Type III Hypersensitivity (briefly)

A
  • Immune complexes
  • Drug reacts in the blood with soluble IgG
  • Immune complex is deposited in vascular endothelium
  • Cell mediated immune response–> local inflammation and complement activation
  • SERUM SICKNESS, hemolysis and allergic nephritis
  • Subsides 1-2 weeks after drug is removed
55
Q

Type IV Hypersensitivity (EXTENDED VERSION)… jk (briefly)

A
  • Delayed hypersensitivty (lymphocyte mediated)
  • Hours or days after exposure
  • Mediated by antigen contact with sensitized T cells and macrophages
  • Release of lymphokines/cytokines
  • Influx of neutrophils and macrophages
  • CONTACT DERMATITIS/TOPICAL DRUGS

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