Test I part I Flashcards

(50 cards)

1
Q

what is defined as the action of the body on the drug

A

pharmacokinetics

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2
Q

what is defined as the action of the drug on the body

A

pharmacodynamics

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3
Q

what is the concentration of drug in the blood plasma during the processes of absorption, distribution, metabolism, and elimination

A

pharmacokinetics

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4
Q

what is the physiological mechanism by which a drug produces its effects

A

pharmacodynamics

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5
Q

what is pharmacotoxicology

A

the study of the physiological mechanisms by which drugs produce their adverse effects/side effects in humans and environments

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6
Q

what are the 3 primary processes of pharmacokinetics

A

input
distribution
elimination

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7
Q

what is a drug?

A

any substance that brings about change in biologic function through its chemical actions

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8
Q

what are the fundamental things that drugs “DO”

A

-modify pre-existing conditions
- have multiple sites of action
- cause toxicity
- cause adverse effects
- contribute to cost of care

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9
Q

what is the difference between a drug and a poison

A

the dose

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10
Q

drugs that produce/enhance an effect similar to the natural effect of hormones, neurotransmitters, and other substances

A

agonist

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11
Q

Drugs that block/diminish the natural effects of hormones, neurotransmitters, or other drugs

A

antagonists

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12
Q

how do drug antagonists work?

A

-inhibit cell fx by occupying receptor sites
-bind to receptors but do NOT activate them
- fx to prevent agonists (natural or drug) from stimulating the receptor

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13
Q

GABA is an inhibitory NT. Thus if you give a GABA agonist, like propofol, what is the effect?

A

enhanced inhibition –> sleep

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14
Q

what are the different types of agonists?

A

full agonist
partial agonist
inverse agonist

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15
Q

what is a full agonist

A

shifts the majority of available receptors into the DR complex (enhancing effect of receptor)

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16
Q

what is a partial agonist

A

binds to the same receptors as full agonist; however, does not evoke as great of a response no matter how high the concentration

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17
Q

under what conditions can a partial agonist produce a dose-response curve similar to those seen with a full agonist?

A

when a full agonist is present with an irreversible antagonist

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18
Q

T/F: sufficiently high concentrations of agonists can exceed the effect of a given antagonists

A

true

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19
Q

what is an inverse agonist

A

a drug that when binds to receptor results in the opposite effect produced by conventional agonists at that receptor

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20
Q

T/F: all receptors are always active

A

false; they are either in an active or inactive state

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21
Q

what are the different types of antagonists

A

competitive
irreversible (noncompetitive)
chemical
physiologic

22
Q

competitive antagonist

A

progressively inhibits a response in the presence of a fixed concentration of agonist

23
Q

what is the effect if you have a high concentration of competitive antagonist?

A

can prevent the response completely

24
Q

presence of a competitive antagonist increases the _____________________ required for a given degree of response

A

agonist concentration

25
________________ fxs by forming a covalent bond with the receptor, therefore making it unavailable to bind with any agonist
irreversible (noncompetitive) antagonist
26
phenoxybenzamine is an alpha-1 blocker given for a pheochromocytoma surgery, this drug forms a covalent bond with the catecholamine receptors, preventing excretion of epi and norepi. phenoxybenzamine is an example of?
irreversible antagonist
27
a irreversible antagonist was given, but now due to unseen circumstances you need to give an agonist that fx's on those same receptors. What would be the effect?
number of unbound receptors may be too low for agonist to produce biological response even at high concentrations
28
what is a chemical antagonist
a drug that creates an ionic bond with another drug (neutralizing it), making it unavailable for a biological response and able to move across the membrane for elimination
29
giving protamine sulfate to reverse heparin is an example of what?
chemical antagonist
30
what are 2 examples of chemical antagonists?
protamine (+) for heparin (-) suggamadex (+) for Rocuronium (-)
31
what is a physiologic antagonist?
use of a drug to interrupt endogenous regulatory pathways mediated by different receptors
32
insulin and glucagon work on different receptor pathways and have opposing effects. thus, insulin and glucagon would be __________________
physiological antagonists
33
if you have a decrease in HR due to release of acetylcholine through the vagus nerve why would you choose atropine over isopro?
atropine fx on the acetylcholine receptors thus making it easier to control than isopro which also increases HR but does through B receptors
34
what is a poison?
a drugs that has almost exclusively harmful effects
35
what is a toxin?
poisons of biologic origin (plants or animals)
36
you can turn any drug into a ____________; however, _____________ are naturally occuring
poison; toxins
37
enantiomer
molecule that has a non-superimposable mirror image
38
enzymes and drug transporters are ________________, meaning they prefer one enantiomer over another
sterio-selective
39
the majority of drugs are ____________ mixtures of enantiomers, meaning 50% is less active, inactive or actively toxic
racemic
40
one chiral center yields ___________ stereoisomers
2
41
stereoisomers
isomers that differ in the 3-D orientation of atoms
42
Enantiomer
stereoisomers that are non-superimposable mirror images
43
racemic mixture
mixture of 2 equal quantities of 2 enantiomers
44
drug effects only last as long as ___________________
the drug occupies the receptor
45
___________________ is a strong chemical bond and in many cases NOT reversible under normal biologic conditions
covalent
46
what type of drug receptor bond is present with asprin and a platelet?
covalent; it blocks the synthesis of thromboxin A2 for the life of the plt (8-10) days
47
drugs that produce a covalent bond with their receptor, when would the effect of the drug stop?
until the DR complex is destroyed and a new receptor/enzyme is synthesized
48
due to the bond created with drug asprin to its receptor on a platelet, how long would you expect the effects of ASA to last? A. 4-8 days B. 8-10 days C. 6-12 days D. 8-12 days
B. 8-10 days forms a covalent bond so effects stay around until plt dies (life of 8-10 days)
49
_________________ drug-receptor bond is more common that covalent bonds, and strength ranges from relatively strong to weaker hydrogen bonds
electrostatic
50
most drug-receptor bonds fall into what area?
electrostatic