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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
Q

ideal chemical is

A

water and lipid soluble

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26
Q

1st peak

A

blood

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27
Q

2nd

A

vascular/vessel rich group

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28
Q

3rd peak

A

muscle, highly vascularized

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29
Q

4th peak

A

fat, could serve as a slow release reservoir

could be pumping the drug back into the bloodstream for longer

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30
Q

compartmental distribution

A

gradual decrease of drug in blood
being eliminated and broken down by liver
has traveled into other compartments

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31
Q

volume of distribution eqn

A

dose/[drug in plasma]

low for drugs contained in plasma, high for drugs distributed to muscle or adipose

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32
Q

high volume of dist.

A

drug could spread to a lot of places and do things beyond the intended purpose

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33
Q

42L

A

middle Vd value,
less than this: remain in plasma (aspirin)
greater: moves out more readily (morphine)

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34
Q

sites of metabolism

A 
liver: primary
kidneys
lungs
skin
GI
35
Q

biotransformation

A

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
Q

metabolite

A

breakdown product of metabolism

37
Q

phase 1 reaction metabolic pathway

A

modification thru oxidation, reduction or hydrolysis

most common oxidative pathway: CYP3A4

38
Q

phase 2 reactions

A

conjugate a drug to form a large polar molecule

enhance the solubility and excretion in urine or bile

39
Q

liver enzyme inducers

A

causes other meds to be metabolized faster

turns up rate of enzymitic pathways

40
Q

liver enzyme inhibitors

A

turns down the rate of pathways

causes other meds to be metabolized more slowly

41
Q

individual variables in metabolism

A 
pharmacogenomics
age and gender
diet and enviroment
metabolic drug interactions
diseases
42
Q

excretion

A

renal is primary route
renal ex. relies of water solubility
also excreted in small amounts via bile, feces, lungs, and skin

43
Q

half life

A

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
Q

things that decrease 1/2 life

A

aging (bc you lose muscle mass, also more likely to inc), enzyme induction

45
Q

things that increase 1/2 life

A

obesity, enzyme inhibition, organ failure

46
Q

the more frequent small doses

A

the more desired effects you get

47
Q

infrequent large doses

A

more likely to fluxuate in and out of the therapeutic range

48
Q

how long to reach a setady state/effectively elimate a drug

A

4-5 half lives

49
Q

macromolecules

A

bind with receptor proteins

50
Q

liklihood of binding is equal to

A

the affinty for the receptor

51
Q

high affinity molecules

A

could have a low concentration and get a high response

52
Q

low affinity

A

could have a high concentration and have a lower response

53
Q

ion channel receptors

A

ligand gated

ion flow through ligands

54
Q

G-protein coupled

A

most common in humans

transmambrane domains, loops form binding sites

55
Q

guanine diphosphate

A

not used as a source of energy but more as an on/off switch

56
Q

enzyme coupled

A

ligand linked to an enzyme, activity inside cell

57
Q

intracellular

A 
within nucleus
influence gene transcription
highly lipid soluble
substances that can diffuse into cells
ie)steroids
58
Q

1st messenger

A

drug molecule

59
Q

2nd messenger

A

G protein complex

receptors could be stimulating or inhibitory

60
Q

prolonged increase in stimulation

A

decrease in receptor function

61
Q

desensitization

A

doesnt last long

increase in stim

62
Q

supersensitivity

A

decreased stim

minutes to hours

63
Q

inactivation

A

doesnt allow ligand to bind in response to excess stim

64
Q

down regulation

A

increased stim

65
Q

upregulation

A

decreased stim

66
Q

increased stim

A

decrease in receptor function, tolerance

67
Q

dec. stim

A

inc in receptor function

68
Q

rebound

A

can occur with abrupt withdrawl, all receptors available, BP inc a lot, infarctions

69
Q

agonist

A

some affinty for a receptor, binds, causes some response

70
Q

antagonist

A

“blockers”

binds and no response, nothing happens, makes it so agonists cant bind

71
Q

non-receptor antagonists

A

either limit ability of agonists or give an opposite effct

chemical: renders agonists inactive
physiological: opposite effects of another drug

72
Q

receptor antagonists

A

competitive or non

reversible or non

73
Q

competitive antagonists

A

either they win or the agonist does depending on [], competes with agonist for same spot

74
Q

noncompetitive antagonists

A

when when agonist binds, the channel wont open

75
Q

partial agonist

A

activates receptor but produces only a partial response, even when all site bound

76
Q

threshold dose

A

dose needed to see a response

77
Q

ceiling effect

A

no furthin inc in response, saturation and all receptors bound

78
Q

efficacy

A

magnitude of the response that can be acheived by the med

79
Q

potency

A

lower dose to produce the same effect

80
Q

ED50

A

dose at which 50% of pop acheives therapeutic effect

81
Q

TD50

A

dose at which 50 of pop experiences a toxic effect

82
Q

LD50

A

lethal effect

83
Q

therapeutic index eqn

A

bigger number is safer/better

TD50/ED50

Bioscience Emily Clipston (9 decks)

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