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01. Cardiopulm Renal > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

pharmacodynamics

A

effects of drugs on the body

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

pharmacokinetics

A

effects of the body on drugs

  • absorption
  • distribution
  • metabolism
  • elimination
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3
Q

receptor

A

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

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4
Q

inert binding site

A

a component of the biologic system to which a drug binds without changing any function

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5
Q

ligand

A

in pharmacology, a molecule like a hormone or a drug, which binds to a receptor

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6
Q

covalent bonds

A

irreversible; drug removal/receptor reactivation requires re-synthesis of the receptor or enzymatic removal of the drug

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7
Q

non-covalent bonds

A

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

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8
Q

relative strengths of noncovalent bonds

A

ionic bond > hydrogen bonds > hydrophobic interactions

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9
Q

affinity

A

how readily and tightly that drug binds to its receptor

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10
Q

high affinity

A

good drug-receptor interaction; less drug needed to produce a response

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11
Q

low affinity

A

poor drug-receptor interaction; more drug needed to produce a response

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12
Q

Kd

A

equilibrium dissociation constant; drug concentration at which 50% of the drug receptor binding sites are occupied by the drug

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13
Q

lower Kd

A

higher affinity of a drug for the receptor

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14
Q

higher Kd

A

lower affinity of a drug for a receptor

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15
Q

selectivity

A

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

  • measured by comparing affinities of a drug at different receptors
  • a more selective drug would affect fewer targets over a certain concentration range
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16
Q

intrinsic activity

A

the ability of a drug to change a receptor function and produce a physiological response upon binding to a receptor

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17
Q

agonists

A

bind to the receptor and stabilize it in a particular conformation (usually the active conformation) producing a physiological response ((intrinsic activity))

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18
Q

antagonists

A

bind to the receptor but do not change its function. They prevent the activation of the receptor in the presence of an agonist.

  • Do NOT have intrinsic activity
  • no pharmacological effect in the absence of an agonist
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19
Q

full agonists

A

fully activate receptors, produce a maximal pharmacological effect when all receptors are occupied, maximal intrinsic activity

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20
Q

partial agnoists

A

partially activate receptor upon binding, produce a sub-maximal pharmacological effect when all the receptors are occupied

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21
Q

inverse agnoists

A

produce an effect opposite to a full or partial agonist; decrease receptor signaling; decrease response at receptors
*intrinsic activity is present and related to the inhibition of receptor function

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22
Q

pharmacologic antagonism

A

action at the same receptor as endogenous ligands or agonist drugs

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23
Q

chemical antagonism

A

when chemical antagonist makes the other drug unavailable

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24
Q

physiologic antagonism

A

occurs between endogenous pathways regulated by different receptors

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25
Q

competitive antagonists

A

compete with endogenous chemicals or agonist drugs for binding of the receptor; can be displaced from the receptor by other drugs

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26
Q

noncompetitive antagonists

A

receptor inactivation is not surmountable

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27
Q

irreversible antagonists

A

irreversibly bind to and occlude the agonist site on the receptor by forming covalent

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28
Q

allosteric antagonists

A

bind to a site other than the agonist site to prevent or reduce agonist binding or activation of the receptor

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29
Q

competitive antagonism on dose-response curve

A

Agonist ED50 increases, Emax does not change (more linear graph)

30
Q

noncompetitive antagonism on dose response curve

A

agonist Emax decreases, EC50 does not change (more hyperbolic graph)

31
Q

dose response curve

A

the relationship between a drug and its effects is described quantitatively (drug dose on x-axis/effects on y-axis)

32
Q

what does a dose response curve look like if you plot it arithmetically?

A

hyperbolic curve

33
Q

what does a dose/response curve look like if you plot the logarithmic version?

A

sigmoidal curve

34
Q

what is Emax

A

the maximal effect that can be produced by the drug

35
Q

what is ED50

A

the effective dose 50. The dose of drug that produces 50% of its maximal effect

36
Q

graded response

A
  • the MAGNITUDE of the response

- typically a mean value within a population or person

37
Q

quantal response

A
  • binary
  • response or no response
  • requires a pre-defined response (falling asleep, etc.)
  • used to examine frequency of response
38
Q

quantal dose response curve

A

relate dose of a drug to the frequency of response within a population

39
Q

noncumulative quantal dose response curve

A

number or % of individuals responding at a dose of a drug and only at that dose

40
Q

cumulative quantal dose response curve

A

number or % of individuals responding at a dose of a drug AND at all doses lower than that dose

41
Q

TD50

A

median toxic dose

42
Q

LD50

A

median lethal dose

43
Q

therapeutic index formula

A

TI = TD50/ED50

*higher the TI, the safer the drug

44
Q

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

45
Q

wide therapeutic window

A

safer?

46
Q

narrow therapeutic window

A

more dangerous?

47
Q

potency

A

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

  • high affinity for receptor tends to be more potent
  • lower ED50 more potent
48
Q

efficacy

A

the maximal pharmacological effect that a drug can produce

  • equivalent to Emax
  • greater Emax, more efficacious the drug
49
Q

Five major classes of drug targets

A 
membrane receptors
nuclear receptors
ion channels
transport proteins
enzymes
50
Q

signal transduction

A

the process by which cells transmit, receive, and respond to information from their environment and from each other

51
Q

Components of signal transduction

A

1) ligand
2) receptor
3) intracellular signaling mechanisms within the target cell

52
Q

protein kinases

A

modify protein by covalently attaching phosphate group to an amino acid residue

i.e. tyrosine kinases, serine-threonine kinases

53
Q

phosphorylation

A

changes conformation of the protein, its activity, binding to other proteins, or localization within the cell

54
Q

transcription factors

A

proteins that bind to specific DNA sequences and thereby control the transcription of the genetic information from DNA to RNA

55
Q

specific action of transcription factors

A

activate or repress the recruitment of RNA polymerase to specific genes by binding to promoter regions of DNA (DNA sequence they bind is called the response element)

56
Q

what is the defining feature of transcription factors?

A

have DNA binding domain

57
Q

G protein coupled receptor structure

A

N terminal is extracellular
C terminal intracellular
7 transmembrane domain
Has alpha, beta, gamma subunits–> alpha dissociates with GTP when activated by ligand

58
Q

Gs protein family and target

A

Gs –> adenylyl cyclases–> AC activation

59
Q

Gi protein family and target

A

Gi –> adenylyl cyclases –> AC inhibition

60
Q

Gq protein family and target

A

Gq –> phospholipase C –> PLC activation

61
Q

G12/13 protein family and target

A

G12/13 –> Rho GTPases –> cytoskeletal rearrangements

62
Q

Desensitization of GPCR

A

A reduced cAMP response is observed in the continued presence of agonist. This desensitization occurs within a few minutes. Removal of agonist for a short amount of time can lead to resensitization

63
Q

Key signaling molecules in cAMP second messenger pathway

A

hormone receptor –>
stimulatory G protein –> adenylyl cyclase–>
phosphodiesterases that hydrolyze cAMP and cAMP dependent kinases with regulatory and catalytic subunits

64
Q

role of phosphodiesterase

A

regulates cAMP to 5’-AMP

65
Q

what is downstream of phospholipase C in G protein signaling?

A

IP3 and DAG

IP3 leads to release of calcium which binds to calmodulin

66
Q

What do receptor tyrosine kinases generally transmit signals for?

A

growth factors (IGF-1, insulin, VEGF, EGF, NGF, PDGF)

67
Q

general pathway of RTK activation

A

1) binding of growth factor
2) two receptors convert to active dimeric state by binding non-covalently
3) cytoplasmic domains of RTK are phosphorylated on Y subunit
4) phosphorylation of substrate proteins

68
Q

receptors coupled to janus kinases (JAKs)

A

hormones and cytokines

  • growth hormone (somatotropin)
  • erythropoietin
  • leptin
  • interferons
  • interleukins 2 to 10, 15
69
Q

JAK STAT pathway

A

1) form dimeric structure upon binding cytokine/ligand
2) JAK (protein tyrosine kinase) molecules are activated
3) phosphorylation of signal transducers
4) activation of STAT molecules
5) STAT molecules travel to the nucleus where they regulate transcription

70
Q

nuclear receptors

A

ligand activated transcription factors that modulate gene expression

  • produce effects after a lag period
  • effects can persist after the agonist concentration has been reduced to zero
71
Q

ligands of nuclear receptors

A

lipophilic molecules that are able to cross the cell membrane

  • steroid hormones
  • thyroid hormones
  • vitamin D, vitamin A
  • free fatty acids

01. Cardiopulm Renal (9 decks)

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