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Pharmacology > EXAM #1: PHARMACODYNAMICS > Flashcards

EXAM #1: PHARMACODYNAMICS Flashcards

1
Q

Generally, what is the pharmacodynamics?

A

“What the drug does to the body.”

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2
Q

What are the five categories of receptors?

A

1) Intracellular receptors
2) Receptors with intrinsic enzyme activity
3) Receptors that directly associated with intracellular enzymes
4) Ligand-gated ion channels
5) 7-membrane spanning receptors (GPRC)

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3
Q

What type of ligands bind intracellular receptors?

A

LIPOPHILLIC ligands e.g.

  • Steroids
  • Thyroid hormone
  • Fat-soluble vitamins
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4
Q

What is the general consequence of ligand binding with an intracellular receptor?

A

Change in gene transcription

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5
Q

Describe the structure of a receptor with intrinsic enzymatic activity.

A
  • Single membrane spanning domain
  • Extracellular domain binds ligand
  • Intracellular domain contains enzymatic activity
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6
Q

What is the difference between a receptor with intrinsic enzymatic activity and a receptor that directly associates with intracellular enzymes?

A

Transmembrane domain associated with an enzyme instead of containing intrinsic activity itself

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7
Q

Describe the general structure of a ligand-gated receptor. What types of substances typically interact with ligand-gated channels?

A
  • Multimeric complex of several transmembrane domains that form a barrel in the membrane
  • Hormones and neurotransmitters
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8
Q

What is a 7MSR? What types of signals are propagated through a 7MSR?

A

“7 Membrane Spanning Receptors” that mediated:

  • G-protein coupled signals
  • G-protein independent signals
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9
Q

What are estrogen receptors and Vitamin A receptors examples of?

A

Intracellular receptors

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10
Q

What are epidermal growth factor receptor (EGFR), insulin receptor (IR), and transforming growth factor receptor (TGF-BR) examples of?

A

Receptor with intrinsic enzymatic activity

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11
Q

What receptor type associates with kinases and proteases including IL-3R, erythropoetin receptor, and the leptin receptor?

A

Receptors that directly associated with intracellular receptors

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12
Q

What type of receptor is the nicotinic acetylcholine receptor (NAChR)?

A

Ligand-gated

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13
Q

What type of receptor are the B-adrenergic, odorant, rhodopsin, frizzled, and smoothened receptors?

A

7MSR or G-protein coupled

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14
Q

What is a typical stimulus for receptor downregulation?

A

Continued simulation of the receptor

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15
Q

What is a typical stimulus for receptor upregulation?

A

Continued exposure to an inhibitor

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16
Q

What is Kd?

A
  • Dissociation constant

- Ligand concentration at a point at which 50% of receptors are bound

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17
Q

Write the two different equations for Kd.

A

N/A

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18
Q

Draw and label a graph of drug concentration (C) vs Receptor-bound drug (B). Be sure to include Kd and Bmax.

A

N/A

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19
Q

What does Kd represent?

A

Affinity of a ligand for a receptor

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20
Q

What does a small Kd indicate? What does a large Kd indicate?

A

Small Kd= high affinity

Large Kd= low affinity

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21
Q

Example from powerpoint.

A

IP

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22
Q

Draw the dose-response curve on a drug concentration (C) vs. drug effect (E) graph. Be sure to include EC50 and Emax.

A

N/A

23
Q

What is the EC50?

A

Concentration of drug that produces half-maximal effect.

24
Q

What is potency a comparison of? What is potency conceptually?

A
  • EC50
  • Potency is a measurement of relative affinity and effectiveness of two or more drugs.

*****A drug with a LOWER EC50 is MORE potent.

25
Q

What is efficacy a comparison of? What is efficacy conceptually?

A
  • Emax
  • Efficacy is the maximal effect a drug can induce.

*****A drug with a higher maximal effect is more efficacious.

26
Q

If drug A has a lower EC50 than drug B, what does this indicate about drug B?

A

Drug A is MORE potent

27
Q

Are potency and efficacy independent or dependent on each other?

A

INDEPENDENT

28
Q

What is an agonist?

A

A ligand that binds to a receptor AND produces a response

*****Response can be molecular, cellular, or physiological

29
Q

What is an antagnoist?

A

A ligand that binds to a receptor and INHIBITS the response produced by the agonist

30
Q

What is the difference between a competitive and noncompetitive antagonist?

A

Competitive= agonist and antagonist compete for the same binding site

Noncompetitive= agonist and antagonist bind at DIFFERENT sites

31
Q

How does a competitive antagonist alter the dose-response curve?

A
  • Shift in the EC50 to the RIGHT

- Emax is stall achievable

32
Q

How does a noncompetitive antagonist alter the dose-response curve?

A

Decrease in Emax

**Note that the agnoist’s affinity (EC50) for the receptor may not be changed by the noncompetitive antagonist

33
Q

How can you overcome the effects of a competitive antagonist?

A

Administer more agonist

34
Q

What is a partial agonist?

A
  • Drug that produces a lower than maximal response compared to the agonist i.e. lower Emax/ efficacy
  • Binding of the partial agonist also DECREASES binding of the agonist

*****Note that the partial agonist evokes a partial response, whereas a noncompetitive antagonist inhibits a response. BOTH decrease Emax.

35
Q

How can a partial agonist be used clinically?

A
  • Administration of a partial agonist decreases binding of the full agonist
  • A partial agonist can be given to decrease the effect of an endogenous substance (full agonist)

E.g. epinephrine as the endogenous substance, drug as a partial agonist–blunts the normal physiologic response

36
Q

See ppt. example question on “dose response curve.”

A

B is most potent (lower ED50)

A, C, and D are equally efficacious (but differ in potency)

37
Q

See ppt. example question on “dose response curve 2.0”

A

B and C are competitive inhibitors

D and E are non-competitive inhibitors

38
Q

What is a quantal dose response curve?

A

Graph of dose (x) vs. % individuals responding (y)

39
Q

What is the quantal dose response curve used for?

A

Describing the:

  • Effective dose
  • Toxic dose
  • Lethal dose
40
Q

What is the ED50?

A

“Median Effective Dose”

  • Dose at which 50% of individuals exhibit a specific quantal response
41
Q

What is the TD50?

A

“Median Toxic Dose”

  • Dose at which a specific toxic effect occurs within 50% of the individuals tested

*****Note that this is typically further to the right on the quantal dose-effect curve than the ED50

42
Q

What is the LD50?

A

“Median Lethal Dose”

  • Dose that is lethal for 50% of individuals tested
43
Q

What is the TI? What is the TI an indication of?

A

TI= Therapeutic Index

The TI is a measure of SAFETY

44
Q

What is the equation for the TI?

A

TD50/ED50

45
Q

Is a drug with a large TI, more safe or less safe than a drug with a small TI?

A

Greater TI= MORE SAFE

46
Q

Answer the case presentation example on TI?

A

A= 4,000/100= 40
*Safer

B= 1,000/200= 5

47
Q

Draw a quantal dose-effect curve representing the TI examples from the ppt.

A

N/A

48
Q

What is tolerance?

A

Decreased drug response following repeated administration

49
Q

What is sensitization?

A

“Reverse tolerance”

  • Increase in drug response following repeated administration
50
Q

What does tolerance look like on a dose-response curve? Sensitization?

A

Tolerance= shift to the right

Sensitization= shift to the left

51
Q

What are the causes of tolerance?

A

1) Phamacokinetic changes i.e. a change in metabolism
2) Change in pharmacodynamic parameters i.e. downregulation/ decrease in receptor number
3) Behavioral changes i.e. patient predicts response to drug and mentally compensates for it

52
Q

What is the additive effect of multi-drug therapy?

A

Two drugs given together produce an effect consistent with the combined potency of the drugs

53
Q

What is the synergistic effect of multi-drug therapy?

A

Two drugs produce a response that is GREATER than the sum of the agent’s potency

Pharmacology (64 decks)

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