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Bioscience Emily Clipston > quiz 4 > Flashcards

quiz 4 Flashcards

1
Q

best place to find up to date information on drugs?

A

online

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2
Q

pharmacology

A

the study of drugs

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3
Q

drug

A

any chemical agent that affects the processes of living organisms

any substance that alters the physiology of an organism whether that alteration is beneficial or harmful

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4
Q

pharmacotherapeutics

A

use of drugs in the prevention, treatment, or dx of the disease

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5
Q

pharmacokinetics

A

time-dependent changes of both plasma drug concentration and the total amount of drugs in the body

WHAT THE BODY DOES TO THE DRUG

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6
Q

pharmacodynamics

A

the quantitative effects of a drug on the body

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7
Q

ADME

A

absorption
distribution
metabolism
elimination

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8
Q

enteral

A

GI tract used to get the drug into the body (pill, oral administration)
includes oral, sublingual, and rectal meds

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9
Q

parenteral

A

injection
no GI tract
includes intravenous, intramuscular, subcutaneous

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10
Q

route of administration is dependent on

A
  1. lipid or water soluble?
  2. ionized?
  3. speed of action desired?
  4. systemic or local
  5. enteral vs parenteral
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11
Q

bioavailability equation

A

plasma concentration/dose

injected meds have close to 100% bioavailability

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12
Q

enteral advantages

A 
safe, easy, convenient
inexpensive, no pain, no infection
no rapid spikes in plasma level
large vascular network available
gradual entry
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13
Q

enteral disadvantages

A 
pathway is variable and complex
slow delivery
requires functioning Gi tract
first pass effect
harsh GI environments
GI irritation
need lipid soluble and neutral drugs
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14
Q

first pass effect

A

liver metabolizes the drug before systemic circulation, decreased bioavailability

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15
Q

parenteral advantages

A 
rapid delivery
high availability
avoids first pass metabolism
avoids GI
good control of delivered dose
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16
Q

parenteral disadvantages

A 
irreversible
infection risk
pain, fear
need for skilled delivery
limited delivery with spinal cord and intramuscular
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17
Q

inhalation

A

next fastest after injection
large SA, rapid delivery
localized effects
complicated for self delivery

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18
Q

intranasal

A

up the nose, localized

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19
Q

inthrathecal

A

anatomical sheath into subarachnoid space, baclafin

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20
Q

topical

A

lotion

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21
Q

transdermal

A

across or through the skin

ie. patch

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22
Q

phonophoresis

A

using ultrasound to drive drugs into the skin

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23
Q

ionophoresis

A

electrical current to drive drugs through the skin

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24
Q

distribution

A

uptake depends on blood flow
the more vascularized, the more uptake

via circulation
variation in organs and tissues ability to take up the drug
non vascular tissue and plasma proteins can take up or bind drugs

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25
ideal chemical is
water and lipid soluble
26
1st peak
blood
27
2nd
vascular/vessel rich group
28
3rd peak
muscle, highly vascularized
29
4th peak
fat, could serve as a slow release reservoir | could be pumping the drug back into the bloodstream for longer
30
compartmental distribution
gradual decrease of drug in blood being eliminated and broken down by liver has traveled into other compartments
31
volume of distribution eqn
dose/[drug in plasma] | low for drugs contained in plasma, high for drugs distributed to muscle or adipose
32
high volume of dist.
drug could spread to a lot of places and do things beyond the intended purpose
33
42L
middle Vd value, less than this: remain in plasma (aspirin) greater: moves out more readily (morphine)
34
sites of metabolism
``` liver: primary kidneys lungs skin GI ```
35
biotransformation
alters drug in 4 ways: 1. conversion of active to inactive 2. conversion of active to toxic or active metabolite 3. conversion of active prodrug (becomes activated) to active drug 4. conversion of unexcretable drug to excretable metabolite
36
metabolite
breakdown product of metabolism
37
phase 1 reaction metabolic pathway
modification thru oxidation, reduction or hydrolysis | most common oxidative pathway: CYP3A4
38
phase 2 reactions
conjugate a drug to form a large polar molecule | enhance the solubility and excretion in urine or bile
39
liver enzyme inducers
causes other meds to be metabolized faster | turns up rate of enzymitic pathways
40
liver enzyme inhibitors
turns down the rate of pathways | causes other meds to be metabolized more slowly
41
individual variables in metabolism
``` pharmacogenomics age and gender diet and enviroment metabolic drug interactions diseases ```
42
excretion
renal is primary route renal ex. relies of water solubility also excreted in small amounts via bile, feces, lungs, and skin
43
half life
time over which the drug concentraction in the plasma decreases to 1/2 ranges from days to minutes drugs with higher half lives are likely to be more concerning
44
things that decrease 1/2 life
aging (bc you lose muscle mass, also more likely to inc), enzyme induction
45
things that increase 1/2 life
obesity, enzyme inhibition, organ failure
46
the more frequent small doses
the more desired effects you get
47
infrequent large doses
more likely to fluxuate in and out of the therapeutic range
48
how long to reach a setady state/effectively elimate a drug
4-5 half lives
49
macromolecules
bind with receptor proteins
50
liklihood of binding is equal to
the affinty for the receptor
51
high affinity molecules
could have a low concentration and get a high response
52
low affinity
could have a high concentration and have a lower response
53
ion channel receptors
ligand gated | ion flow through ligands
54
G-protein coupled
most common in humans | transmambrane domains, loops form binding sites
55
guanine diphosphate
not used as a source of energy but more as an on/off switch
56
enzyme coupled
ligand linked to an enzyme, activity inside cell
57
intracellular
``` within nucleus influence gene transcription highly lipid soluble substances that can diffuse into cells ie)steroids ```
58
1st messenger
drug molecule
59
2nd messenger
G protein complex | receptors could be stimulating or inhibitory
60
prolonged increase in stimulation
decrease in receptor function
61
desensitization
doesnt last long | increase in stim
62
supersensitivity
decreased stim | minutes to hours
63
inactivation
doesnt allow ligand to bind in response to excess stim
64
down regulation
increased stim
65
upregulation
decreased stim
66
increased stim
decrease in receptor function, tolerance
67
dec. stim
inc in receptor function
68
rebound
can occur with abrupt withdrawl, all receptors available, BP inc a lot, infarctions
69
agonist
some affinty for a receptor, binds, causes some response
70
antagonist
"blockers" | binds and no response, nothing happens, makes it so agonists cant bind
71
non-receptor antagonists
either limit ability of agonists or give an opposite effct chemical: renders agonists inactive physiological: opposite effects of another drug
72
receptor antagonists
competitive or non | reversible or non
73
competitive antagonists
either they win or the agonist does depending on [], competes with agonist for same spot
74
noncompetitive antagonists
when when agonist binds, the channel wont open
75
partial agonist
activates receptor but produces only a partial response, even when all site bound
76
threshold dose
dose needed to see a response
77
ceiling effect
no furthin inc in response, saturation and all receptors bound
78
efficacy
magnitude of the response that can be acheived by the med
79
potency
lower dose to produce the same effect
80
ED50
dose at which 50% of pop acheives therapeutic effect
81
TD50
dose at which 50 of pop experiences a toxic effect
82
LD50
lethal effect
83
therapeutic index eqn
bigger number is safer/better | TD50/ED50

Bioscience Emily Clipston (9 decks)

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