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

(73 cards)

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
drugs that binds to and activate receptor
agonist
26
how tightly a drug binds to receptor
affinity
27
amount of drug necessary to elicit a response
potency
28
drugs ability to produce the maximal desired response
efficacy
29
what happens to the dose if there is higher potency
smaller effective dose
30
when determining a drugs usefulness, is potency or efficacy more important?
efficacy
31
equi-potency
relative doses of two drugs to get the same efficacy
32
full vs partial agonist
produces a full (100%) response vs partially activating receptor regardless the conc.
33
antagonist
bind to receptor but block activation
34
*competitive antagonist
compete with other drugs--- binds to receptor and prevent binding by OTHER molecultes
35
allosteric antagonism
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
chemical antagonism
binds directly to agonist
37
functional antagonism
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
reversible antagonists
readily dissociate from their target | --when drug is gone it goes back to normal fx
39
irreversible antagonists
form a permanent, irreversible chemical bond with their receptor --until body can produce new targets
40
what is the difference b/w competitive and noncomp antagonist
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
some effects of opiods
analgesia, euphoria, resp depression, CNS depression, miosis
42
differ b/t high and low specificity
high- ONE type of receptor, limited toxicity ex (antibiotics) low- MULT receptor activities and more adverse effects (chemotherapy)
43
explain racemic mixture
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
what happens to the efficacy of the drug during down regulation
goes down | -- less effect due to decreasing receptors
45
in order to retain effectiveness during down regulation...
have to increase dose
46
antagonist cause ____ and agonist cause _____
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
bioavailability
amt of drug that is ABSORBED through a given route | -IV is faster than oral
48
first pass effect
when drug is absorbed through GI, *liver metabolizes a portion prior to entering systemic cyrculation
49
prodrug
drug that must be activated before being physiologically active (liver)
50
volume of distribution
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
name routes of administration
- IV - IM - subcutaneous - sublingual - oral - rectal - inhalation - transdermal
52
which ROA has the most rapid onset AND highest bioavailability
IV
53
which ROA has a large volume
Intramuscular (IM)
54
which ROA have 1st pass effect and which is most significant
oral*** - rectal - transdermal
55
what's meant by tritatable
continuous dosing
56
extravasation
drugs injected to tissue instead of vein
57
intraosseous
needle into bone marrow | -useful in emergent situations
58
what is a disadvantage of subQ
may cause pain or necrosis (anticoag)
59
what is an intrathecal ROA
injected in spinal cord- CSF, chemo - has slow absorption - placement is key - headaches
60
enteric coating
resist stomach acids to later be absorbed and have a high bioavail.
61
who oversees all the drugs administered?
FDA | -food and drug admin.
62
phase 1 in clinical testing of medication
HEALTHY pts determining dose, safety, and kinetics (how its absorbed)
63
phase 2- testing medication
testing on pt with dz- determine efficacy
64
phase 3- medication
more ppl to further establish safety and efficacy
65
why can meds be so expensive
paying for the others that failed
66
how many years does it take till patent expires
20 years
67
bioequivalence
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
contact dependent (signaling)
cells must be direct contact
69
paracrine signaling
signals are released into space but rapidly taken by other cells or destroyed by enzymes
70
synaptic signaling
very specific and very rapid delivery - neurotransmitters
71
endocrine signaling
slow and nonspecific | -via bloodstream by hormones
72
digoxin
used for arrhythmia and congestive heart failure
73
three cell surface binding vs one intracellular
-ion channels -g-coupled -enzyme linked and intracellular: (thyroid/steroid)