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Pharmacology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Pharmacokinetics definition

A

what the body does to a drug involves ADME

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2
Q

Pharmacodynamics definition

A

how a drug affects a body

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3
Q

T/F: pharmacy and pharmacology mean the same thing?

A

False

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4
Q

Pharmacotherapeutics definition

A

study of the therapeutic use and effects of drugs in the treatment or prevention of disease

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5
Q

what does ADME stand for?

A

absorption distribution metabolism excretion

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6
Q

what are the 3 steps in the FDA drug approval process?

A

identify new drug need FDA IND Clinical trials

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7
Q

what are the 4 phases of clinical trials?

A
  1. safety 2. efficacy 3. larger and longer RCT 4. post marketing surveillance
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8
Q

Off-label and Off-patent difference?

A

off-patent = not paying original develop, anyone can make it;

off-label = not original/FDA approved use for drug

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9
Q

is off-label use illegal?

A

no (unless unethical) illegal to market off-label use though

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10
Q

3 ways drugs are named

A

chemical, generic, brand/trade names

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11
Q

define brand/trade name for drugs

A

drug marketed under a proprietary, trademark-protected name

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12
Q

how are controlled substances classified?

A

into 5 schedules, schedule 1 has the highest abuse and dependence level and no medical purpose

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13
Q

what are the 2 ways drugs are absorbed?

A

via enteral (GI tract) or parenteral route

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14
Q

what are 3 drug types that are absorbed via enteral route?

A

oral,

sublingual,

rectal

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15
Q

what are 5 drug types that are absorbed via parenteral route?

A

inhalation, injection, topical, transdermal, implant

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16
Q

what are the 3 main pathways a drug gets to a target?

A
  1. passive diff thru lipid membrane 2. passive diff thru aqueous channel 3. carrier-mediated
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17
Q

define bioavailability

A

% of drug that makes it into systemic circulation

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18
Q

what is the first-pass effect/metabolim/elimination?

A

Oral medications that are taken will exit the stomach and can be absorbed up to the liver via the portal vein which can result in a large percentage of the drug being broken down and thus resulting in a decreased bioavailability of that drug.

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19
Q

What does volume of distribution tell us?

A

how extensively a drug is distributed to the rest of the body compared to the plasma

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20
Q

what does a higher Vd mean?

A

there is more drug in tissue than the blood

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21
Q

what are CYP enzymes?

A

enzymes that catalyze reactions to break down drugs, mainly in the liver

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22
Q

how are CYPs affected by drug-drug interactions?

A

some drugs induce or inhibit CYP which affects the bioavailability of other drugs

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23
Q

what is the difference between first-order and zero order elimination?

A

first-order has a constant half-life zero order has a constant elimination rate

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24
Q

how many half-lives before a drug is considered “cleared”?

A

5

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25
Q

how many half-lives does it take to reach “steady state”?

A

4-5

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26
Q

define steady state as it pertains to dosing

A

amount of drug excreted in specific time frame = amount of drug administered often equal to time to reach therapeutic effect

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27
Q

define volume of distribution (Vd)

A

the ratio of the amount of drug in the total body to the concentration of drug in the plasma

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28
Q

define drug

A

articles intended for use in the diagnosis, cure, mitigation, treatment, or prevention of disease in man or other animals

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29
Q

what is toxicology?

A

the study of the harmful effects of chemicals, side effects or adverse effects

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30
Q

Schedule I substance

A

regarded as having the highest potential for abuse and addiction (THC, LSD, heroin, ecstasy)

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31
Q

Schedule II substance

A

approved for specific uses but still have a high potential for addiction (opioids/narcotics)

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32
Q

Schedule III substance

A

lower abuse potential but still might lead to dependence

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33
Q

Schedule IV substance

A

still lower potential for abuse

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34
Q

Schedule V substance

A

lowest relative abuse potential

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35
Q

define dose

A

the amount of drug given at any one time

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36
Q

define dosage

A

the frequency with which a drug dose is to be given

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37
Q

What are the 4 drug receptor types?

A
  1. ligand-gated ion channels 2. G-protein-coupled receptors 3. Kinase-linked receptors 4. Nuclear receptors (DNA coupled)
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38
Q

what is pharmacodynamics?

A

the study of the biochemical and physiological effects of drugs on the body and underlying pathologies

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39
Q

receptor info for ligand-gated ion channels?

A

nicotinic ACh receptors very quick (milliseconds)

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40
Q

receptor info for G-protein-coupled receptors?

A

Muscarinic ACh receptors quick (seconds)

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41
Q

receptor info for Kinase-linked receptors?

A

Cytokine receptors longer (hours)

42
Q

receptor info for nuclear receptors?

A

estrogen receptors longer (hours)

43
Q

what are 2 other drug targets?

A

enzyme non-human cells

44
Q

define specificity

A

drug binds to only one type of receptor

45
Q

define selectivity

A

can bind to a multiple subtypes of a receptor but it prefers one

46
Q

what are the potential consequences of decreased specificity or selectivity?

A

less spec-selc = more AE less targeted approach

47
Q

what is an agonist?

A

drugs that occupy receptors and activate them

48
Q

what is an antagonist?

A

drugs that occupy receptors but don’t activate them block activation by agonist

49
Q

what is competitive antagonist?

A

agonist vs antagonist higher concentration wins

50
Q

what is noncompetitive antagonist?

A

antagonist binds to secondary receptor, cannot leave, shuts down/blocks agonist effects

51
Q

what is a partial agonist?

A

similar to agonist but not a perfect fit lower dose leads to some agonist effect higher dose blocks agonist, leads to diminished effect

52
Q

what is a partial agonist?

A

similar to agonist but not a perfect fit lower dose leads to some agonist effect higher dose blocks agonist, leads to diminished effect

53
Q

what is Emax?

A

maximal response receptors are saturated may cause toxicity

54
Q

what is ED50?

A

effective dose to get 50% of expected response

55
Q

how does ED50 relate to potency?

A

lower ED50 = more potent less drug required for effect

56
Q

Other forms of antagonism?

A

chemical, physiologic, pharmacokinetic receptor changes

57
Q

What is a quantal-dose response curve?

A

used to compare safety of a drug tracks % or # of population who has a particular reponse at a given dose

58
Q

what can a quantal-dose response curve help us find?

A

the smallest effective dose among a population of people.

59
Q

what is TD50?

A

dose that is toxic for 50% of people

60
Q

What is the Therapeutic Index?

A

a ratio of TD50 to ED50

61
Q

which is safer: Narrow or Wide therapeutic index?

A

wide therapeutic index

62
Q

define adverse drug reaction (ADR)

A

response to a medicine which is noxious and unintended

63
Q

side effect

A

any unintended effect of a pharmaceutical product occurring at doses normally used by a patient which is related to the pharmacological properties of the drug

64
Q

medication error

A

any preventable event that may cause or lead to inappropriate medication use or patient harm while the medication is in the control of the health care pro, pt, or consumer

65
Q

define side effect

A

any unintended effect of a pharmaceutical product occurring at doses normally used by a patient which is related to the pharmacological properties of the drug

66
Q

define medication error

A

any preventable event that may cause or lead to inappropriate medication use or patient harm while the medication is in the control of the health care pro, pt, or consumer

67
Q

define adverse event/experience

A

any untoward medical occurrence that may present during treatment with a medicine but which does not necessarily have a causal relationship with this treatment

68
Q

serious adverse event is any event that is:

A

1) . fatal/life threatening
2) .permanently/sig disabling
3) . requires/prolongs hospitalization
4) . causes congenital anomaly
5) . requires intervention

69
Q

what are boxed warnings?

A

FDA designation added to labels, calls attention to serious/life threatening risk

70
Q

What is the Naranjo Scale/

A

a questionnaire that helps to determine if a pt is suffering from AE

71
Q

What could cause ADRs?

A

1) . patient specific factors
2) . drug-drug interactions
3) . HCP error
4) . Nonadherence

72
Q

how to prevent ADRs

A

simplify med regimens assess adherence evaluate changes in pt health avoid polypharmacy use ISMP recomendations

73
Q

define synergistic interaction

A

produces a response > sum of responses to both drugs

74
Q

define antagonists interaction

A

produce effect < response produced by each drug alone

75
Q

What is pain?

A

an experience based on complex interactions of physical and psychological processes

76
Q

what are the 3 types of pain?

A

nociceptive neuropathic psychogenic

77
Q

What neural structures are involved with ascending pain pathways?

A

periphery sensory neurons, dorsal horn of spinal cord, brain stem, thalamus, somatosensory cortex

78
Q

where would you find 1st order neurons in ascending pathways?

A

going from the injury site to the dorsal horn of the spinal cord

79
Q

where would you find 2nd order neurons in ascending pathways?

A

going from the dorsal horn of the spinal cord, crossing over then ascending up to the thalamus

80
Q

where would you find 3rd order neurons in ascending pathways?

A

going from the thalamus to the somatosensory cortex of the brain

81
Q

Where does interpretation of pain occur?

A

somatosensory cortex (cerebral cortex)

82
Q

What does the descending pathway do?

A

modulate/suppression pain signals

83
Q

where does the descending pathway originate?

A

periaqueductal gray matter of the mid-brain

84
Q

Name some neurotransmitters in the nociceptive pathways

A

GABA, glutamate, serotonin, norepinephrine, adenosin

85
Q

what is the MOA for opioids?

A

bind to opioid receptor in CNS to inhibit ascending pain pathways

86
Q

What are the 3 main opioid receptors?

A

mu delta kappa

87
Q

AE of opioids on CNS

A

sedation, nausea, respiratory depression, cough suppression, miosis (pinpoint pupil), truncal rigidity

88
Q

AE peripheral effects of opioids

A

constipation urinary retention bronchospasm reduced GI motility Pruritus (itching)

89
Q

what to notice for respiratory depression

A

labored breathing and decreased respiration rate

90
Q

T/F: respiratory depression from opioid can occur even at usual doses

A

TRUE

91
Q

most opioid drugs bind to which receptor?

A

mu

92
Q

effects associated with Mu opioid receptors

A

analgesia, euphoria, respiratory depression, bradycardia, emesis, slowed GI motility, pruritis, high abuse/dependence potential

93
Q

what is nociceptive pain?

A

produced by injury stabbing, aching, well-localized (exceptions)

94
Q

when is nociceptive pain not localized?

A

when it originates from visera

95
Q

what is neuropathic pain?

A

typically indicates nerve involvement burning, tingling sensation

96
Q

what is psychogenic pain?

A

origin or relationship to pscyh d/o

97
Q

T/F: the 3 types of pain are mutually exclusive and cannot have overlap?

A

FALSE

98
Q

what are the 2 primary nociceptive afferent neurons?

A

unmyelinated C fibers finely myelinated A delta fibers

99
Q

in the dorsal horn, what neurotransmitters inhibit pain signal propagation?

A

NMDA blocker substance P antagonists inhibition of NO synthesis

100
Q

what is the substantia gelatinosa?

A

a collection of gray cells (in dorsal horn) act like gate keeper to regulate pain signals from nociceptive fibers

101
Q

what type of pain is usually created by unmyelinated C fibers?

A

diffuse pain sensation

102
Q

what type of pain is usually created by finely myelinated A delta fibers?

A

localized, defined pain sensation

Pharmacology (10 decks)

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