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Pharmacology I > Test I part I > Flashcards

Test I part I Flashcards

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
Q

________________ fxs by forming a covalent bond with the receptor, therefore making it unavailable to bind with any agonist

A

irreversible (noncompetitive) antagonist

26
Q

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?

A

irreversible antagonist

27
Q

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?

A

number of unbound receptors may be too low for agonist to produce biological response even at high concentrations

28
Q

what is a chemical antagonist

A

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
Q

giving protamine sulfate to reverse heparin is an example of what?

A

chemical antagonist

30
Q

what are 2 examples of chemical antagonists?

A

protamine (+) for heparin (-)
suggamadex (+) for Rocuronium (-)

31
Q

what is a physiologic antagonist?

A

use of a drug to interrupt endogenous regulatory pathways mediated by different receptors

32
Q

insulin and glucagon work on different receptor pathways and have opposing effects. thus, insulin and glucagon would be __________________

A

physiological antagonists

33
Q

if you have a decrease in HR due to release of acetylcholine through the vagus nerve why would you choose atropine over isopro?

A

atropine fx on the acetylcholine receptors thus making it easier to control than isopro which also increases HR but does through B receptors

34
Q

what is a poison?

A

a drugs that has almost exclusively harmful effects

35
Q

what is a toxin?

A

poisons of biologic origin (plants or animals)

36
Q

you can turn any drug into a ____________; however, _____________ are naturally occuring

A

poison; toxins

37
Q

enantiomer

A

molecule that has a non-superimposable mirror image

38
Q

enzymes and drug transporters are ________________, meaning they prefer one enantiomer over another

A

sterio-selective

39
Q

the majority of drugs are ____________ mixtures of enantiomers, meaning 50% is less active, inactive or actively toxic

A

racemic

40
Q

one chiral center yields ___________ stereoisomers

A

2

41
Q

stereoisomers

A

isomers that differ in the 3-D orientation of atoms

42
Q

Enantiomer

A

stereoisomers that are non-superimposable mirror images

43
Q

racemic mixture

A

mixture of 2 equal quantities of 2 enantiomers

44
Q

drug effects only last as long as ___________________

A

the drug occupies the receptor

45
Q

___________________ is a strong chemical bond and in many cases NOT reversible under normal biologic conditions

A

covalent

46
Q

what type of drug receptor bond is present with asprin and a platelet?

A

covalent; it blocks the synthesis of thromboxin A2 for the life of the plt (8-10) days

47
Q

drugs that produce a covalent bond with their receptor, when would the effect of the drug stop?

A

until the DR complex is destroyed and a new receptor/enzyme is synthesized

48
Q

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

A

B. 8-10 days

forms a covalent bond so effects stay around until plt dies (life of 8-10 days)

49
Q

_________________ drug-receptor bond is more common that covalent bonds, and strength ranges from relatively strong to weaker hydrogen bonds

A

electrostatic

50
Q

most drug-receptor bonds fall into what area?

A

electrostatic

Pharmacology I (16 decks)

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