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CPR Exam 1 > DSA 1 > Flashcards

DSA 1 Flashcards

1
Q

What is pharmacodynamics?

A

How the drug affects the body MOA, type of receptor it binds to, and dose-response curves

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2
Q

What is pharmacokinetics

A

How the body affects the drug; ADME (absorption, distribution, metabolism and elimination)

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3
Q

Receptor + drug => activates receptor => initiates biochemical effects => cause drug effects Receptors have a _______ role.

A

regulatory

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4
Q

Inert binding site is?

A

where a drug binds, however it does not change fx.

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5
Q

Ligand is a?

A

hormone or a drug that binds to a receptor.

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6
Q

If a drug-receptor bind covalently, the interaction is ______.

A

Irreversible

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7
Q

If a drug-receptor binds non-covalently, the interaction is ________.

A

Reversible

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8
Q

If a drug-receptor bind covalently, removal of the drug or re-activation of the receptor requires what?

A

REmake a receptor or remove the drug using an enzyme

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9
Q

Most drugs bind to receptors ______

A

NON-covalently

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10
Q

List non-covalent interactions from strongest => weakest.

A
  • Ionic: [position ion] + [negative ion] - Hydrogen bonds: - Hydrophobic interactions: hydrophobic regions of drug + receptor interact.
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11
Q

What 3 factors describe how well a drug and receptor interact?

A
  1. Affinity 2. Selectivity 3. Intrinsic activity
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12
Q

What is affinity?

A

how well a drug binds to a receptor

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13
Q

High affinity: _____ interaction and ____ drug is needed to create a response.

A

good LESS

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14
Q

Low affinity: ____ interaction and ___ drug is needed to make a response.

A

BAD MORE

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15
Q

What is KD?

A

KD (Equilibrium dissociation constant) is the concentration of the drug where 50% of the receptors are occupied.

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16
Q

What is the relationship between affinity and KD?

A

High affinity = lower KD Lower affinity= higher KD because we need more the drug to occupy 50% of the receptors

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17
Q

Selectivity of a drug is? What determines a drugs selectivity

A

Selectivity is the degree to which a drug acts on a given site relative to other site (within a range) It is determined by the drugs affinity at different binding sites.

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18
Q

What is a intrinsic activity?

A

The ability for the drug to produce a physiological response when it binds to a receptor

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19
Q

Which have intrinsic activity; agonist or ANT?

A

Agonists: not ANT

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20
Q

What happens when a AGO binds to receptor

A

=> stabilizes it in active confirmation => cause a physiological response

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21
Q

ANT do not have physiological response. What do they do then?

A

They do not change the function but they bind => if ago is present, prevent the activation.

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22
Q

what do ANT do when an AGO is NOT present?

A

no effect

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23
Q

Full AGO: _____ activate receptors, produce a ______ effect when bound to all receptors and have _____ intrinsic activity.

A

Fully; max; max

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24
Q

Partial AGO ______ activate receptors, produce a ______ effect when bound to all receptors and intrinsic efficacy _________.

A

partially sub-max IA will depend on the drug but it is always sub-max

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25
Q

A partial AGO will have _____ affinity for both Ri and Ra forms

A

intermediate

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26
Q

What do inverse AGO do?

A

Has the opposite effect of a full/partial AGO; decrease receptor signaling, decrease response, its IA will inhibit the function of the receptor

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27
Q

ANT has _____ affinity for both Ri (inactive receptor that produces no effect) and Ra (active receptor that can activate downstream mechanisms that produces a small observable effect, even in the absence of ligands) and have ____ level of constitutive activity.

A

equal; same

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28
Q

___________ is have action at the same reeptor as endogenous ligands or AGO drugs ______ occurs when a chemical ANT prevents drug from binding

A

Pharmacologic ANT Chemical ANT

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29
Q

Inverse AGO have a higher affinity for the ____ form

A

Ri

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30
Q

What are the types of pharmacologic ANT?

A
  1. Competitive ANT 2. Non-competitive ANT; includes both irreversible ANT and allosteric ANT.
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31
Q

_________ irreversibly (covalently) and block where AGO bind.

A

Irreversible ANT

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32
Q

________ bind to ANOTHER site than the AGO site to prevent or reduce the AGO from binding or activation of the receptor.

A

Allosteric ANT

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33
Q

Competitive ANT: higher concentrations of the AGO are required to displace the ANT and cause an effect (shifts to the ____)

A

right

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34
Q

EC50 is what?

A

concentration of a drug that gives HALF of the max response.

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35
Q

What is Vmax

A

max rate of reaction when all receptors are bound

36
Q

Competitive ANT: EC50 ____; Vmax ____

A

EC50 increases Vmax: does not change

37
Q

Noncompetitive ANT: EC50 _____; Vmax ____

A

EC50 does not change Vmax: decreases

38
Q

The dose-response curve makes a _______ when plotted arithmetically.

A

hyperbolic curve

39
Q
  1. The dose-response curve makes a ________ curve when it is plotted using a logarithm: most common!!!!
A

Sigmoidal

40
Q
  1. Describe the dose-response curve parameters, such as ED50 and Emax.
A

Emax: max effect that a drug can make

ED50 (effective dose): dose of the drug that makes 50% of the max effect

41
Q

Distinguish between quantal and graded responses and recognize when a response is graded vs. quantal.

A
  • Graded response (how much) of a drug will produce a certain response; it is usually a mean in a population and the magnitude will vary.
  • Quantal response (all or none/binary) asks if a response will occur and requires a pre-defined response and is used to describ e a frequency of a response in a large population
42
Q

A ____ response is seen an a individual/mean value in a population and increases with dose.

A

Graded response

43
Q

_______ response is seen in a population and is either [present/absent] in a single person.

A

Quantal response

44
Q

What 2 questions do quantal responses answer?

A
  • 1. In how many (in how many people will death occur)
  • 2. Does the response occur or not (yes or no)
45
Q

What questions do graded responses answer?

A

How much

Usually a mean value in a population or a single person

46
Q

Non-cumulative quantal dose-response curve: shows us what?

A

the # of ppl that response AT a dose and ONLY at that dose

  1. 20% of people in the population who take 10 mg of a drug will die
47
Q

Cumulative quantal dose-response curve shows us what?

A

of people that response at a dose and at ALL doses lower than those dose.

  1. 20% of people in population who take up 10 mg of a drug will die.
48
Q

Median effective dose (ED50) is?

A

the dose where 50% of the population react to the drug

49
Q

TD50

A

median toxic dose

50
Q

LD50

A

median lethal dose

51
Q

TI

A

Therapetuic index (TI) calculates the safety of a drug

Higher TI=safer

TI= TD50/ED50

52
Q

therapeutic window

A

Range of doses of a drug or its concentration in the body that are safe and effective

53
Q

Potency

A

the dose of drug needed to create a specific pharmacological effect

54
Q

More potent drugs have _____ ED50

A

lower

55
Q

More potent drugs will have a _____ affinity and a _____ KD

A

higher

lower

56
Q

On a sigmoidal DR curve, potency increases as EC50 ____

Potency increases going from _____

A

decreases

R => L

57
Q

Efficacy is?

A

can be measured by Emax;

it is the max effect a drug can produce.

58
Q

Efficacy is related to?

What is it used to determine?

A

Total number of receptors that are available for drug to bind to.

Determine the magnitude of clinical effect

59
Q

High ____ => more effective

A

High Emax

60
Q

On a DR, efficacy increases as a curve _____

A

goes up

61
Q

What do drugs target? (6)

A

1. Membrane receptors

2. Cytoplasmic receptors

3. Nuclear receptors

4. Ion channels,

5. Transport proteins

6. enzymes

62
Q

Kinases do what?

A

covalently phosphorylate a protein using a phosphate lost from ATP => ADP

63
Q

Transcription factors (TFs) bind to DNA using its _________ (defining feature) at the ______________, located near coding sequence of gene, and control transcription from DNA => RNA

A
  • DNA-binding domain
  • Response element (enhancer or promotor region)
64
Q

TF MOA?

A

Promote the recruiment of RNA polymerase to genes via activators

Inhibit the recruitment of RNA polyermase to genes via inhibitors

65
Q

1/3 of drugs act on GCPR, which are heterotrimeric (alpha, beta and y subunits)

What is the G-protein cycle?

A
  1. AGO binds and activates the GCPR
  2. Promotes release of GDP from alpha protein
  3. GTP then binds to nucleotide binding site
  4. Alpha-protein + GTP => causes G-protein to bind to the effector enzyme or ion channel.
  5. Hydrolysis of GTP -> GDP => signal terminated.
66
Q

which G-protein:

+ AC and Src tyrosine kinases

A

Gs

67
Q

What does Gi Gprotein do?

A
  • Inhibit AC 13, 5 and 6
  • Activate tyrosine kinase Src
68
Q

What does Gq do?

A

+ PLC CB

69
Q

G 12/13 does what?

A

+ Rho GTPases => Cytoskeletal rearrangements

70
Q

Describe the process of densitization.

A
  • AGO binds to cell => cAMP
  • Continued prescence will reduce cAMP ersponse after a few minutes.
  • If AGO is removed after a short time, cells revoer FULL responsiveness to an additional AGO “resensitization”.
    • Resensization does NOT occur if the cells are exposed to AGO repeatedly or for a long time
71
Q

What is the process of resensitization?

A
    1. AGO binds to a receptor => initiates signaling by promoting the receptor interaction with G protein
    1. GRK (G-protein-coupled receptor kinase) phosphorylates [AGO + receptor], preventing the Gs protein from binding to the receptor and promoting B-arrestin to bind.
    1. Receptor-arrestin complex bind to coated pits, which internalizes the receptor.
    1. AGO dissociated from internalized receptor => reduces B-Arr binding affinity, allowing phosphotase to dephosphorylate the receptor
    1. Receptor returns to plasma membrane
72
Q

What promotes the DOWN-regulation of a receptor, instead of densitization?

A

Following the processes that occured before, if the AGO does not dissociate from the internalized receptor => B-arrestin will stay bound => receptor is broken down by lysosomes.

73
Q

27. Describe signaling involving cyclic AMP system and the role phosphodiesterase in regulating the intracellular concentration of this signaling intermediate.

A
  1. AGO binds to GCPR
  2. +Gs
  3. +AC (converts ATP => cAMP
  4. cAMP activates PKA

PDE hydrolyzes cAMP to 5’AMP

74
Q

Gq: Gq => PLC => PIP2 will split into IP3 and DAG

IP3 causes Ca2+ to be released from ____

What does DAG do?

A

SR

+ PKC

75
Q

What receptors trasmit the action of growth factors?

A

RTKs (receptor tyrosine kinases)

76
Q

Describe receptor tyrosine kinase signaling,

A
  1. RTK is a transmembrane receptor: GFs bind (IGF, insulin, VEGF, EFG, NGF and PDGF),
  2. Receptor converts from inactive monomeric state => active dimeric state, where 2 receptor polypeptides bind non-covalently.

3. Cytoplasmic domain is phosphorylated on tyrosine resides

4. Activate and phosphorylates substrates (ATP-ADP)

77
Q

Receptors coupled to JAK kinases are coupled to JAKs, ______ tyrosine kinases.

A

cytosolic tryrosine kinases

78
Q

receptors coupled to JAKs trasmit the effects of what?

A

1. Growth hormones (somatotropin)

2. Erythropoeitin

3. Leptin

4. Interferons

5. IL 2-10 and 15

79
Q

ONce JAK kinases are activated, what do they do?

A
  • Phosphorylate signal transducers and activate transcription (STAT) molecules
  • STAT dimers => go to nucleus => regulate transcription
80
Q

Nuclear receptors are ______ TF that do what?

What binds to them?

A

Ligand-activated

modulate gene expression

-lipophillic molecules (steroids, thyroid, vitD/A, lipid mediateors)

81
Q

Name nuclear receptors

A

1. androgen receptor

2. estrogen receptor

3. progesterone receptor

4. Glucocorticoid receptors

5. Mineralcorticoid receptors

82
Q

When do hormones that bind to nuclear receptors cause effects?

How long do they last?

A

Produce effects after a LAG period of several hours or days

Effects can persist even afer concentration of AGO is 0

83
Q

Drug A is a partial AGO. Drug B is a full AGO. Thus, drug A has a _____ Emax than drug B.

A

lower

84
Q

In the absence of other drugs, pindolol causes increase in HR by activating B-AR. When highly effective B-AR stimulants are present, pindolol causes a decrease in HR. Thus, it should be classified as a _______

A

Partial AGO

85
Q

Competitive ANT: Agonist EC50 ____; Emax _____

Noncompetitive ANT: EC50 ______ but AGO Emax ______.

A

Competitive ANT: Agonist EC50 increases; Emax does not change

Noncompetitive ANT: EC50 does not change but AGO Emax decreases.

86
Q
A

CPR Exam 1 (19 decks)

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