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pharmacology > principles of drug action > Flashcards

principles of drug action Flashcards

1
Q

what is the objective of drug therapy

A

provide max benefit with min harm

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2
Q

t/f: drug response determined by interaction within the body

A

true

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3
Q

what charge should most drugs have to be to go into a cell

A

neutral charge

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4
Q

ways that drugs can cross cell membrane (3)

A
  1. between spaces or channels
  2. transport system (p-glycoprotein)
  3. penetrate membrane directly (most drugs)
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5
Q

job of p-glycoprotein

A

protein that helps transport drug out of cell for elimination

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6
Q

p-glycoprotein and the liver?

A

transport drugs into bile for excretion

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7
Q

p-glycoprotein and the kidneys?

A

transports drugs into urine for elimination

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8
Q

p-glycoprotein and the placenta?

A

transports drugs back into maternal blood

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9
Q

p-glycoprotein and the brain?

A

transports drugs circulating blood to limit access to the brain

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10
Q

pharmacokinetics

A

study of drug movement throughout the body

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11
Q

absorption

A

movement of a drug from its site of administration into the blood

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12
Q

bioavailability

A

fraction of a drug that is absorbed into the circulation after administration
- can be different b/w generic + trade

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13
Q

explain how to determine bioavailability between IV and PO dose
at home –> PO levothyroxine 100mg
bioavailability IV = 1 and PO = 0.5
how much should the pt take IV at hosp?

A

pt had PO levothyroxine (Cynthroid) 100mg
–> routes always compared to IV
if IV ba = 1 and 100mg and PO = 0.5
then IV dose should be 50 mg

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14
Q

what are 6 factors that can affect absorption?

A
  1. solubility
  2. surface area
  3. ionization
  4. blood flow
  5. GI motility
  6. drug-drug/drug-food interactions
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15
Q

distribution

A

how drug molecule in bloodstream finds target receptor and into cells

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16
Q

what are 3 factors that can affect distribution?

A
  1. blood flow to tissues
  2. ability to leave blood
  3. ability to enter cells
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17
Q

what is tissue binding

A

some drugs = high affinity for specific tissues in body –> bind to tissue inappropriately –> attaches, no distribution

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18
Q

placental distribution vs BBB

A

opposite; drugs can easily pass through in the placenta, putting fetus at risk for whatever substances the mother is taking

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19
Q

protein binding

A

when drug is bound to protein = CAN’T pass through capillary walls (drug can’t do its job until unbound to protein)
- ex football player and cheerleader

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20
Q

high protein bound drug
- do you need higher or lower dose and why?

A

high affinity to protein, need HIGHER dose so that some drug molecules will able to distribute

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21
Q

low protein bound drug

A

low affinity to protein, do not necessarily need a higher dose since lower chance for the molecule to attach to protein

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22
Q

biotransformation/metabolism
- what chemical change occurs

A

how the body takes the drug molecule and transforms it into a different substance
lipophilic –> hydrophilic for excretions

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23
Q

does biotransformation always result in a smaller molecule?

A

naur

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24
Q

where are most drugs metabolized

A

liver

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25
Q

prodrug
- is first pass effect okay for prodrugs?

A

drug INACTIVE BEFORE metabolism by liver, then ACTIVATED
- first pass effect okay for prodrugs since the liver is needed to activate it

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26
Q

first pass effect

A

drug absorbed through GI tract –> splenic vein –> liver metabolize –> systemic circulation –> decreased amount of drug is available for the intended site
- only okay for prodrugs

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27
Q

t/f: drugs with high pass rates are given PO or G tube

A

FALSE
- given topical or IV to bypass liver metabolism

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28
Q

what are 7 factors affecting metabolism?

A
  1. age
  2. pregnancy
  3. drug metabolizing enzymes (P450)
  4. competition between drugs
  5. nutritional status
  6. disease
  7. genetics
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29
Q

excretion

A

how body gets rid of drug molecule

30
Q

what are 6 ways the body excretes drugs

A
  1. urine
  2. bile
  3. expired air
  4. breast milk
  5. sweat
  6. saliva
31
Q

what are 4 factors that affect excretion?

A
  1. renal function
  2. pH dependent ionization
  3. competition for active tubular transport
  4. age
32
Q

bile circulation (vicious cycle)
- what does this mean for the drug?

A

drug molecule gets absorbed in portal circulation and excreted into bile –> collecting in gall bladder –> returns to intestine through common bile duct and cycle continues
- drug has increased half life and prolonged duration of action

33
Q

p-450 system
- what is the most common isozyme

A

enzymes (CYPs) in liver that helps METABOLISM, each enzyme as specific drug or food to metabolize
- most common = CYP3a4

34
Q

what does the p-450 system determine

A

determines the SPEED at which drug is metabolized where we can start to see drug interaction
- some drugs induce or inhibit P450

35
Q

drug substrates

A

drugs metabolized by CYP enzyme

36
Q

drug enzyme inhibitors

A

drug inhibits action of CYP isoenzymes = contribute to toxic levels (bc no metabolizing drug)

37
Q

enzyme inducers

A

accelerate metabolism action of specific enzyme = drug level decrease fast

38
Q

_____ population’s P450 system has not been developed

A

infant

39
Q

_____ population’s P450 system has decreased and reduced action

A

elderly

40
Q

dangers of eating grapefruit while taking drugs

A

grapefruit can inhibit CYP3a4 = inhibit metabolism of drugs = risk of toxicity

41
Q

what are 4 variables that influence dose of drug

A
  1. maintenance and loading dose
  2. blood concentration
  3. potency
  4. efficacy
42
Q

maintenance vs loading dose

A

maintenance: daily dose
loading dose: larger than usual dose to reach therapeutic effect faster

43
Q

why does blood concentration determine drug dose

A

helps determine if dose is in therapeutic range, toxic, or subtherapeutic

44
Q

potency

A

amount of drug that must be given to produce particular response (DOSE NEEDED TO PROD EFFECTS)

45
Q

efficacy

A

how well a drug produces its desired effect

46
Q

adverse response vs side effect

A

adverse response: unexpected or unintended response
side effect: unavoidable secondary drug effect produced at therapeutic doses, usually predictable

47
Q

cumulative effects
- example

A

rate of admin exceeds rate of biotransformation and elimination
ex. chemotherapy can accumulate in body

48
Q

idiosyncratic response
- ex?

A

what happened to patient is OPPOSITE than what is expected to happen
- benadryl supposed to make you drowsy –> makes some ppl wide awake

49
Q

anaphylactic reaction

A

more severe allergic reaction that impairs breathing and circulation

50
Q

iatrogenic response

A

due to physician or treatment –> given too much drug –> toxicity

51
Q

pharmacodynamics

A

what the DRUG is doing to the BODY, how the drug effects the body

52
Q

how do drugs create an effect

A

attach to a receptor

53
Q

agonist

A

stimulates a cell (turn ON)

54
Q

antagonist

A

blocks a cell (turn OFF), prevents another chemical from attaching and causing an effect

55
Q

competitive antagonist
- ex?

A

can be overcome if increasing the dose of the agonist; can fall off and another chemical can attach and turn back ON
- ex. naloxone and opioids

56
Q

non competitive antagonist
- ex?

A

irreversibly binds until cell dies
- ex. aspirin prevents platelets from being sticky

57
Q

chemical antagonist
- ex?

A

receptorless drug; doesn’t sit on receptor but instead attaches to target cell to change its shape to prevent it from attaching to a receptor
- ex. protamine sulfate: sits on heparin and reverses its action

58
Q

selectivity/selective toxicity (and what does this have to do with receptors?

A

ability of a drug to injure a target cell/organism without injuring other cells
(more receptors drug can sit on = more side effects = less selectivity)

59
Q

t/f: when a drug has narrow therapeutic range, there is a higher risk for toxicity OR for drug to not work

A

true

60
Q

half life
- what does this determine

A

how long before half of a drug is removed from the body = DETERMINES DOSING INTERVAL

61
Q

what determines the dosing interval for a drug

A

half life

62
Q

what route to admin short half life meds?

A

continuous or IV (EPI)

63
Q

steady state/plateau

A

point where amount of drug being admin and amount of drug being eliminated balance off and are equal in which increasing dose has no effect

64
Q

what is measured once steady state is achieved

A

full pharmacotherapeutic response of drug dose

65
Q

it takes ____ half lives to reach steady state and ____ half lives after quitting cold turnkey to be fully eliminated

A

4-5

66
Q

drug interactions

A

change in magnitude or duration of a response to one drug in presence of another a drug (increase or decreased response)

67
Q

additive effects
- ex?

A

drug a (1) + drug b (1) = 2; drugs that if put together, give better effect
- tylenol + codeine

68
Q

synergist effects
- ex?

A

drug a (1) + drug b (1) = 3; drugs that if put together, give more enhanced effect
- analopril (ace inhibitor) + HCTZ (diuretic) - lower BP

69
Q

potentiation

A

drug a (1/2) + drug b (1) = 2; give one drug to help another drug work

70
Q

antagonism
- ex?

A

drug a (1) + drug b(1) = 0; admin drugs together will cancel any effect, one drug blocks another
- ex: Narcan blocks morphine

pharmacology (15 decks)

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