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Pharmacodynamics > Unit 1- Intro, Routes Of Admin and Receptor Theory > Flashcards

Unit 1- Intro, Routes Of Admin and Receptor Theory Flashcards

1
Q

two types of drug names

A

trade vs generic

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2
Q

generic name

A

nonproprietary- chemical name of a compound approved by the FDA i.e. ibuprofen
-PANCE

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3
Q

trade name

A

proprietary name (trademark)

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4
Q

pharmacology define

A

study of drugs in the body, including interactions between drugs
-dynamics + kinetics

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5
Q

pharmacodynamics

A

mechanism of action (MAO) of the DRUG in the body
“what does the drug physically do to the body”
i.e. ethanol- loss of inhibition, slurring of speech

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6
Q

pharmacokinetics

A

what the BODY does TO drug

-absorbs, distributes, metabolizes or excretes

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7
Q

T/F effects of drug vary by pt

A

true

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8
Q

the relationship between drug conc. and effect on body

A

pharmacodynamics

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9
Q

effects of a drug can either be ____ or toxic

A

therapeutic/efficacy

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10
Q

pharmacogenomics

A
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11
Q

define drug

A

any substance that brings about a change in biologic fx through its chemical ax (key)

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12
Q

receptor

A

component of a cell or organism that interacts with a drug

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13
Q

what is known as a lock and key

A

receptor vs effect of drug

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14
Q

where can a receptor be located?

A

intracellularly or on the surface

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15
Q

what initiates the chain of biochemical events and what does it lead to?

A

receptor; to the drugs effect

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16
Q

most receptors are mainly ____

A

proteins

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17
Q

upregulation

A

a lot of slots on receptor to bind

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18
Q

downregulation/resistant

A

no slots on receptor for drugs to bind

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19
Q

apoptosis

A

cell death

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20
Q

ligand

A

molecule that bind to receptor involved in chemical signaling

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21
Q

what are some examples of ligands

A

neurotransmitter, hormone, drug, messenger molecultes

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22
Q

hormone

A

natural substance that is produced IN the body and that influences the way the body grows or develops

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23
Q

xenobiotic

A

chemical compound that is FOREIGN to a living organism

i.e. acetometophin is not made by the body so its foreign

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24
Q

toxin vs toxicant

A

biologic (snake venom, botox(bacteria)) vs nonbiologic (led, pharma)

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25
Q

drugs that binds to and activate receptor

A

agonist

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26
Q

how tightly a drug binds to receptor

A

affinity

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27
Q

amount of drug necessary to elicit a response

A

potency

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28
Q

drugs ability to produce the maximal desired response

A

efficacy

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29
Q

what happens to the dose if there is higher potency

A

smaller effective dose

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30
Q

when determining a drugs usefulness, is potency or efficacy more important?

A

efficacy

31
Q

equi-potency

A

relative doses of two drugs to get the same efficacy

32
Q

full vs partial agonist

A

produces a full (100%) response vs partially activating receptor regardless the conc.

33
Q

antagonist

A

bind to receptor but block activation

34
Q

*competitive antagonist

A

compete with other drugs— binds to receptor and prevent binding by OTHER molecultes

35
Q

allosteric antagonism

A

binds to allosteric site on receptor to prevent agonist action
AKA– binds to different site on receptor changing structure thus preventing other things from binding

36
Q

chemical antagonism

A

binds directly to agonist

37
Q

functional antagonism

A

indirectly inhibits physiologic actions of the agonist
ex: treating somebody with asthma and DM give steroids and insulin which have opposing effects on glucose
… interactions that fight with effect

38
Q

reversible antagonists

A

readily dissociate from their target

–when drug is gone it goes back to normal fx

39
Q

irreversible antagonists

A

form a permanent, irreversible chemical bond with their receptor
–until body can produce new targets

40
Q

what is the difference b/w competitive and noncomp antagonist

A

comp- agonist/antagonist CONC. determines effect.. a higher amt of agonist can reverse antagonist vice versa
noncomp-binds to receptor with STRONG affinity that receptor is no longer available to bind to agonist regardless of the conc.

41
Q

some effects of opiods

A

analgesia, euphoria, resp depression, CNS depression, miosis

42
Q

differ b/t high and low specificity

A

high- ONE type of receptor, limited toxicity ex (antibiotics)
low- MULT receptor activities and more adverse effects (chemotherapy)

43
Q

explain racemic mixture

A

there’s a r./l. hand of drug (50/50 mixture)
-one enantiomer may either cause a therapeutic effect or a toxic effect..
pharm try to separate it to reduce side effects… essentially sell it for more $$$$ esp when finding omething new

44
Q

what happens to the efficacy of the drug during down regulation

A

goes down

– less effect due to decreasing receptors

45
Q

in order to retain effectiveness during down regulation…

A

have to increase dose

46
Q

antagonist cause ____ and agonist cause _____

A

upregulation- too much blockage so body says to bring new cells for more open slots
downregulation- not enough spots due to too much activity

47
Q

bioavailability

A

amt of drug that is ABSORBED through a given route

-IV is faster than oral

48
Q

first pass effect

A

when drug is absorbed through GI, *liver metabolizes a portion prior to entering systemic cyrculation

49
Q

prodrug

A

drug that must be activated before being physiologically active (liver)

50
Q

volume of distribution

A

measure of apparent space in the body available to contain the drug

  • how far drugs distribute into tissue vs stay in central blood supply
    i. e. THC, high VD bc it stays in the fat
51
Q

name routes of administration

A
  • IV
  • IM
  • subcutaneous
  • sublingual
  • oral
  • rectal
  • inhalation
  • transdermal
52
Q

which ROA has the most rapid onset AND highest bioavailability

A

IV

53
Q

which ROA has a large volume

A

Intramuscular (IM)

54
Q

which ROA have 1st pass effect and which is most significant

A

oral***

  • rectal
  • transdermal
55
Q

what’s meant by tritatable

A

continuous dosing

56
Q

extravasation

A

drugs injected to tissue instead of vein

57
Q

intraosseous

A

needle into bone marrow

-useful in emergent situations

58
Q

what is a disadvantage of subQ

A

may cause pain or necrosis (anticoag)

59
Q

what is an intrathecal ROA

A

injected in spinal cord- CSF, chemo

  • has slow absorption
  • placement is key
  • headaches
60
Q

enteric coating

A

resist stomach acids to later be absorbed and have a high bioavail.

61
Q

who oversees all the drugs administered?

A

FDA

-food and drug admin.

62
Q

phase 1 in clinical testing of medication

A

HEALTHY pts determining dose, safety, and kinetics (how its absorbed)

63
Q

phase 2- testing medication

A

testing on pt with dz- determine efficacy

64
Q

phase 3- medication

A

more ppl to further establish safety and efficacy

65
Q

why can meds be so expensive

A

paying for the others that failed

66
Q

how many years does it take till patent expires

A

20 years

67
Q

bioequivalence

A

when 2 different drugs contain same active ingredients and are identical in strength/conc., dosage form, and ROA
ex: same drug diff manufacturers, generic

68
Q

contact dependent (signaling)

A

cells must be direct contact

69
Q

paracrine signaling

A

signals are released into space but rapidly taken by other cells or destroyed by enzymes

70
Q

synaptic signaling

A

very specific and very rapid delivery - neurotransmitters

71
Q

endocrine signaling

A

slow and nonspecific

-via bloodstream by hormones

72
Q

digoxin

A

used for arrhythmia and congestive heart failure

73
Q

three cell surface binding vs one intracellular

A

-ion channels
-g-coupled
-enzyme linked
and intracellular: (thyroid/steroid)

Pharmacodynamics (6 decks)

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