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(OMS2) SBL Exam 1 Pharm Week > Pharmacodynamics (Konorev) > Flashcards

Pharmacodynamics (Konorev) Flashcards

1
Q

Define pharmacodynamics

A

effects of drugs on the body including:

  • drug receptors
  • dose-response curves
  • mechanisms of drug actions
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2
Q

Define receptor vs. ligand in regards to pharmacology

A

receptor: a specific molecule in a biological system that plays a regulatory role. Receptor interacts with a drug and initiates the biochemical events leading to drug effects

ligand: it is a molecule like a hormone or drug which binds to a receptor

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3
Q

What is a dose-response curve

A

the relationship between a drug and its effects is described quantitatively using a dose-response curve

when you plot drug dose arithmetically on the x-axis vs. drug effect on the y-axis you typically get what is called a hyperbolic curve

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4
Q

How is a concentration-effect curve commonly presented?

A

by graphing the logarithm of the drug dose vs. the response in which case you get a sigmoidal curve

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5
Q

Define Emax

Define ED50

A

Emax is teh maxmial effect that can be produced by the drug

ED50 is the effective dose 50 or the dose of the drug that produces 50% of its maximal effect

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6
Q

What is a graded response (curve)?

A

Answers: How Much?

  • Magnitude of a response varies continuously
  • typically represents the mean value within a population or a single subject
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7
Q

What is the quantal dose-response (curve)?

A

All or none, yes/no binary responses

answers the question: Does the response? occur, or how many?

  • requires a pre-defined response
  • used to examine the frequency of a response within a large population
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8
Q

What is a non-cumulative quantal dose response curve?

A

Number of % of individuals responding at a dose of a drug and only at that dose

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9
Q

What is a cumulative quantal dose response curve?

A

Number of % of individuals responding at a dose of a drug and at all doses lower than that dose

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10
Q

Define:

ED50

TD50

LD50

A

ED50: median effective dose

TD50: median toxic dose

LD50: median lethal dose

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11
Q

Drug safety index can be described by the therapeutic index

A

TI=TD50/ED50 (the higher the TI, the safer the drug)

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12
Q

What is the therapeutic window?

A

the range of doses of a drug or of its concentration in a bodily system that provides for the safe and effective therapy

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13
Q

Define drug potency

A

describes the amount of drug required to produce a specific pharmacological effect

  • Describes the amount of a drug required to produce a specific effect
  • represented by the ED50
  • the lower the ED50, the more potent the drug
  • determines the drug dose to be used clinically
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14
Q

Define drug efficacy

A

describes the maximal pharmacological effect that a drug can produce

  • represented by the Emax
  • the greater the Emax, the more efficacious the drug
  • efficacy is related to the total number of receptors available to bind a drug
  • determines the magnitude of clinical effect
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15
Q

What are the four ways a drug can interact with its receptor?

A

binding

affinity

selectivity

intrinsic activity

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16
Q

Describe covalent drug-receptor binding

A

irreversible, requires resynthesis of the receptor or enzymatic removal of the drug

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17
Q

Describe non-covalent drug-receptor binding

A

reversible, most drugs bind to receptors via non-covalent bonds

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18
Q

Describe affinity of a drug for a receptor

A

The affinity of a drug for its receptor describes how readily and tightly that drug binds to its receptor

  • high affinity: strong drug-receptor interaction, less drug needed to produce a response
  • low affinity: poor drug receptor interaction; more drug needed to produce a response
19
Q

What is Kd?

A

describes affinity

drug concentration at which 50% of the drug receptor binding sites are occupied by the drug

unit is in molar concentrations

lower Kd indicates higher affinity for receptor

higher Kd indicates lower affinity of a drug for a receptor

20
Q

Describe drug selectivity

A

Selectivity is a property of a drug determined by its affinities at various binding sites

measured by comparing affinities of a drug to different receptors

a more selective drug would have higher Kd ratio and affect fewer targets over a specific concentration range

21
Q

How does selectivity relate to adverse effects

A

more selective drugs have fewer adverse effects

less selective drugs have more adverse effects

22
Q

What is Intrinsic activity?

A

intrinsic activity describes the ability of a drug to change a receptor function and produce a physiological response upon its binding to a receptor

23
Q

What is an agonist?

Does it have intrinsic activity?

A

an agonist binds to the receptor and stabilize it in a particular conformation, producing a physiological response

Has intrinsic activity

24
Q

What is an antagonist?

Does it have intrinsic activity?

A

A receptor antagonist binds to the receptor but do no change its function. They prevent activation of the receptor in the presence of an agonist

Does not have intrinsic activity

25
Q

What is a full agonist?

A

Fully activate receptors

produce a maximal pharmacological effect when all receptors are occupied

maximal intrinsic activity

26
Q

What is a partial agonist?

A

partially activate the receptor upon binding

produce a sub-maximal pharmacological effect when all receptors are occupied

intrinsic efficacy caries depending on drug, but is always submaximal

27
Q

What is an inverse agonist?

A

produces an effect opposite to a full or partial agonist

  • decreases receptor signaling
  • decreases response at receptors with a significant level of constitutive receptor activity
  • intrinsic activity is present and related to the inhibition of receptor function
28
Q

What is pharmacologic (receptor) antagonism?

A

action at the same receptor as endogenous ligands or agonist drugs

29
Q

What is chemical antagonism?

A

When chemical antagonist makes the other drug unavailable

30
Q

What is physiologic antagonism?

A

occurs between endogenous pathways regulated by different receptors

31
Q

What are competitive antagonists?

A
  • compete with endogenous chemicals or agonist drugs for binding the receptor
  • can be displaced from the receptor by other drugs (effects are surmountable)
32
Q

What are non-competitive antagonists?

A
  • receptor inactivation is not surmountable
  • irreversible antagonists: irreversibly bind to and occlude the agonist site on the receptor by forming covalent bonds
  • allosteric antagonists: bind to a site other than the agonist site to prevent or reduce agonist binding or activation of the receptor
33
Q

How does EC50 and Emax change in competitive antagonism?

A

Agonist EC50 increases

Emax does not change

34
Q

How does Emax and EC50 change in noncompetitive antagonism?

A

EC50 does not change

Agonist Emax decreases

35
Q

How do full agonists work?

A

mimic actions of endogenous chemicals at receptors

example: activation of mu opioid receptors by opioid analgesics such as morphine and codeine

36
Q

How to antagonists, partial and inverse agonists, work?

A

block the actions of endogenous lignads at receptors

example: blockade of the a1 adrenoceptors receptors by the antihypertensive drug, prazosin

37
Q

What are the major classes of drug targets?

A

membrane receptors

nuclear receptors

ion channels

transport proteins

enzymes

drugs are designed to target important regulatory proteins in the existing cell signaling pathways

38
Q

G protein families:

A

Gs-AC activation

Gi-AC inhibition

Gq-PLC activation

G12/13-Rho GTPases, cytoskeletal rearrangements

39
Q

GPCR signaling cascades are either

A

cyclic AMP second messenger pathway lead or DAg/IP3 lead

40
Q

JAKs transmit the effect of a number of hormones and cytokines to activate the JAK-STAT pathway including

A

growth hormone (somatotropin)

erythropoietin

letpin

itnerferons

interleukins 1-10, 15

41
Q

RTKs transmit the action of growth factors such as

A

IGF-1

insulin

VEGF

EGF

NGF

PDGF

42
Q

RTK signaling pathways as drug targets for oncogenes in growth factor pathways including

A

overexpression or amplifications of GF

point mutations or amplifications of GF receptors

point mutations in RAS

point mutations in Raf

targeted anticancer drugs inhibit upregulated growth factor signalging

43
Q

nuclear receptors are ligand-activated transcription factors that modulate gene expression

A

ligands are lipophilic molecules that are able to cross cell membranes including

steroids and thyroid hormones

vitamines A and D

lipid mediators

44
Q

Ion channels as drug targets used for

A

maintaining resting membrane potential

shape action potentials

change the concentration of ions in cytosol

(used for arrythmias, angina pectoris, hypertension, constipation)

(OMS2) SBL Exam 1 Pharm Week (6 decks)

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