Basic Principles I Flashcards

1
Q

pharmacology

A

-bio, biochem, phys, path, micro, psych, medicinal chem all go into pharmacology, which lead to pharmacodynamics, therapeutics and chemo, and tox (treatment of patients)

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2
Q

pharmacodynamics

A

-given meds, leading to a response

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3
Q

drug action

A
  • molecular action

- invisible

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4
Q

drug effect

A
  • pharmacologic effect

- visible response

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5
Q

selectivity

A
  • property of drug to cause a specific effect
  • few drugs produce a single effect
  • primary effect is desired and second may or may not be
  • can be one molecular action leading to multiple effects or two molecular action leading to combined effects
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6
Q

pharmacokinetic

A

-drug and elimination

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7
Q

pharmacodynamic

A

-how it works
-types of drug actions”
physiochemical and receptor interactions

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8
Q

physiochemical actions

A
  • simple chemical interactions
  • antacids
  • antiseptics
  • not very specific
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9
Q

receptor interactions

A
  • interaction of drug with physiologic receptors-macromolecules
  • most drugs
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10
Q

drug receptors

A
  • drug receptor interactions cause molecular events to occur in each cell
  • enough of these events cause a change in cell function
  • ultimately results in change in tissue function
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11
Q

receptors

A
  • macromolecules, particularly proteins
  • may be on or in a cell or free in the plasma or extracellular fluid
  • present as part of the normal biochemical and physiologic mechanisms and usually interact with endogenous compound
  • function both as ligand binder and as an effector
  • the natural ligand or a drug which resembles it can bind and modulate usual activity
  • each receptor occupied might be stimulated or inhibited
  • each cell in a tissue contains a large population of receptors that are easily accessible to drugs
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12
Q

receptors 2

A
  • each drug receptor interaction produces a small change in the biochemical or electrochemical homeostasis of the cell
  • cumulative effects of many drug receptor interactions will lead to a change in the function of the cell and then the tissue
  • when enough cells in a tissue are affected then the function of the tissue is altered and an observable pharmacologic response can be noted
  • maximal response is eventually reached which is related to the number of drug receptor interactions and the physiologic capacity of the tissue
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13
Q

types of receptors

A
  • membrane bound-neural synapse, ion channels
  • enzymes-intracellular or extra
  • structural macromolecules- MT
  • intracellular macro- steroid receptors, RNA
  • cell membrane itself- change electrical potential, fluidity
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14
Q

as subunit

A

-increases adenylyl cyclase and Ca currents

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15
Q

ai subunit

A

-decreases adenylyl cyclase and increases K currents

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16
Q

ao subinit

A

-decrease Ca currents

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17
Q

aq subunits

A

-increases phospholipase CB

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18
Q

a13 subunit

A

-increase Na/H exchange

19
Q

at subunit

A

-increases cCMP-phosphodiesterase (vision)

20
Q

aolf subunit

A

-increase adenylyl cyclase (olfaction)

21
Q

drug receptor bonds

A
  • reversible are ionic, van der waals, hydrogen

- irreversible is covalent

22
Q

receptor amp and transduction

A
  • aB together
  • GDP off, interaction with receptor and ligand, GTP binds
  • subunits split
  • action
  • GTPase on A gets rid of GTP
  • back together
23
Q

G proteins

A
  • regulate the activity of:
  • distinct effector proteins in the cell- enzymes, channels, transport proteins
  • can be multiple G proteins in a single cell
  • act as switches that are turned on by the receptor and turn themselves off in a few seconds
  • several drugs can stimulate different receptors but ultimately influence the same effector protein through the mediation of a G protein that is shared by different receptors
  • stimulus averaging or modulation can be achieved
24
Q

second messenger

A
  • also produce amplification of the drug receptor interaction
  • converts an even that happens outside the cell into a change that happens inside the cell
  • some second messengers can cause different effects in different tissues
  • changing the biochemical balance of substrates in metabolic pathways and activating or deactivating enzyme systems can have a profound effects on the function of the cells in a tissue
25
structure-activity relationships
- the structure of the drug determines how it will fit into the receptor - the better the fit, the better the stimulation - subtle changes in structure amongst a class of drugs can greatly influence effects
26
quantitative descriptions of drug action
-attempts to take experimental data, combine it with certain assumptions and make a model that works for most systems
27
interaction at eq
-drug + receptor equil with DR and leads to an effect
28
dose response relationships
- dose to % max response | - log dose to % makes it easier to make comparisons to other drugs and find effective doses
29
threshold
- beginning of the curve - dose of agonist at which a response begins - may relate to affinity of the agonist for the receptor
30
slope
- rate of rise of response on the steep portion of the curve | - log of EC50 also relates to affinity
31
maximal asymptote
-intensity of response is proportional to the fraction of receptors occupied -effect = Emax x D / Kd + D Kd is EC 50
32
intrinsic activity
- ability to stimulate the receptor once bound - relates to structure and influences efficacy and potency - greater intrinsic activity=greater efficacy
33
spare receptors
- not all receptors need to be occupied to achieve emax | - less efficacious agonists may need to occupy more receptors than highly efficacious agonists
34
secondary receptors
- outside of the target tissues | - may mediate other effects of the drug side effects
35
receptor regulation
- a cell can up or down regulate a population of receptors by changing the total number of receptors or their sensitivity - homeostasis - denervation hypersensitivity - desensitization
36
agonists
- bind to receptor and produce pharmacologic effect - bind to receptor and activate - can cause desensitization - better fit results in better results at lower doses - variations in intrinsic activity based on structure - better agonists need lower doses - can have same intrinsic activity- ability to achieve emax - can have different intrinsic activity and same affinity- bind the same but dont reach emax the same - can have different affinity and different intrinsic ability (different emax)
37
antagonists 1
-can cause hypersensitivity if stopped suddenly
38
efficacy
- stimulation after its bound - ability of a drug to activate the effector protein of the receptor once the drug is bound to the receptor - depends upon structure of drug
39
potency
- relate to the amount of drug needed for an effect - depends upon 1. biologic system- receptor density, efficiency of stimulus response mechanisms of the tissue 2. interaction of the drug with the receptor - affinity, efficacy
40
relative potency
- has horizontal relationship between two drugs | - increases EC 50 with different drug
41
relative efficacy
- vertical relationships | - reach higher emax
42
antagonists 2
- many things are learned about the structure and function of receptors from the use of antagonists - block binding of agonists and prevent the pharmacologic repsonse
43
competitive antagonists
- bind to same spot - can be overcome by enough agonists - just need more agonist - antagonist has weak bond and is easily reversed - two equilibriums-one to RL and one to RI - increases L shifts eq that way and same for increasing I
44
noncompetitive antagonists
- can't be overcome by increasing doses of agonist - receptors remain occupied by antagonist and not enough DR interactions occur to achieve emax - strong bond and not easily reversed - proton pumps - inhibitor can either change effector or binding site - if changes effector- ligand can bind but nothing happens- quad eq- bottom two inactive even after ligand binds (ligand plus inhibitor is inactive) - irreversible - can also change binding site- bind to it or attaching to a different portion and altering site - back to competitive eq- either ligand binds or inhibitor binds, but not both- reversible