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DPT Semester 1 > Pharmacology Test 1 > Flashcards

Pharmacology Test 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

absorptiondistributionmetabolismexcretion

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6
Q

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

A

identify new drug needFDA INDClinical trials

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7
Q

what are the 4 phases of clinical trials?

A
  1. safety2. efficacy3. larger and longer RCT4. 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 membrane2. passive diff thru aqueous channel3. 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-lifezero 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 channels2. G-protein-coupled receptors3. Kinase-linked receptors4. 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 receptorsvery quick (milliseconds)

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40
Q

receptor info for G-protein-coupled receptors?

A

Muscarinic ACh receptorsquick (seconds)

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41
Q

receptor info for Kinase-linked receptors?

A

Cytokine receptorslonger (hours)

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42
Q

receptor info for nuclear receptors?

A

estrogen receptors longer (hours)

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43
Q

what are 2 other drug targets?

A

enzymenon-human cells

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44
Q

define specificity

A

drug binds to only one type of receptor

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45
Q

define selectivity

A

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

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46
Q

what are the potential consequences of decreased specificity or selectivity?

A

less spec-selc = more AEless targeted approach

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47
Q

what is an agonist?

A

drugs that occupy receptors and activate them

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48
Q

what is an antagonist?

A

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

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49
Q

what is competitive antagonist?

A

agonist vs antagonisthigher concentration wins

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50
Q

what is noncompetitive antagonist?

A

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

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51
Q

what is a partial agonist?

A

similar to agonist but not a perfect fitlower dose leads to some agonist effecthigher dose blocks agonist, leads to diminished effect

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52
Q

what is a partial agonist?

A

similar to agonist but not a perfect fitlower dose leads to some agonist effecthigher dose blocks agonist, leads to diminished effect

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53
Q

what is Emax?

A

maximal responsereceptors are saturatedmay cause toxicity

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54
Q

what is ED50?

A

effective dose to get 50% of expected response

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55
Q

how does ED50 relate to potency?

A

lower ED50 = more potentless drug required for effect

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56
Q

Other forms of antagonism?

A

chemical, physiologic, pharmacokinetic receptor changes

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57
Q

What is a quantal-dose response curve?

A

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

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58
Q

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

A

the smallest effective dose among a population of people.

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59
Q

what is TD50?

A

dose that is toxic for 50% of people

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60
Q

What is the Therapeutic Index?

A

a ratio of TD50 to ED50

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61
Q

which is safer: Narrow or Wide therapeutic index?

A

wide therapeutic index

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62
Q

define adverse drug reaction (ADR)

A

response to a medicine which is noxious and unintended

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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

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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

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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

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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

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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

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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

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69
Q

what are boxed warnings?

A

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

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70
Q

What is the Naranjo Scale/

A

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

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71
Q

What could cause ADRs?

A

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

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72
Q

how to prevent ADRs

A

simplify med regimensassess adherenceevaluate changes in pt healthavoid polypharmacyuse ISMP recomendations

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73
Q

define synergistic interaction

A

produces a response > sum of responses to both drugs

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74
Q

define antagonists interaction

A

produce effect < response produced by each drug alone

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75
Q

What is pain?

A

an experience based on complex interactions of physical and psychological processes

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76
Q

what are the 3 types of pain?

A

nociceptiveneuropathicpsychogenic

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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

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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

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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

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80
Q

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

A

going from the thalamus to the somatosensory cortex of the brain

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81
Q

Where does interpretation of pain occur?

A

somatosensory cortex (cerebral cortex)

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82
Q

What does the descending pathway do?

A

modulate/suppression pain signals

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83
Q

where does the descending pathway originate?

A

periaqueductal gray matter of the mid-brain

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84
Q

Name some neurotransmitters in the nociceptive pathways

A

GABA, glutamate, serotonin, norepinephrine, adenosin

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85
Q

what is the MOA for opioids?

A

bind to opioid receptor in CNS to inhibit ascending pain pathways

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86
Q

What are the 3 main opioid receptors?

A

mudeltakappa

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87
Q

AE of opioids on CNS

A

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

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88
Q

AE peripheral effects of opioids

A

constipationurinary retentionbronchospasmreduced GI motilityPruritus (itching)

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89
Q

what to notice for respiratory depression

A

labored breathing and decreased respiration rate

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90
Q

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

A

TRUE

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91
Q

most opioid drugs bind to which receptor?

A

mu

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92
Q

effects associated with Mu opioid receptors

A

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

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93
Q

what is nociceptive pain?

A

produced by injurystabbing, aching, well-localized (exceptions)

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94
Q

when is nociceptive pain not localized?

A

when it originates from visera

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95
Q

what is neuropathic pain?

A

typically indicates nerve involvementburning, tingling sensation

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96
Q

what is psychogenic pain?

A

origin or relationship to pscyh d/o

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97
Q

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

A

FALSE

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98
Q

what are the 2 primary nociceptive afferent neurons?

A

unmyelinated C fibers finely myelinated A delta fibers

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99
Q

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

A

NMDA blockersubstance P antagonistsinhibition of NO synthesis

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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

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101
Q

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

A

diffuse pain sensation

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102
Q

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

A

localized, defined pain sensation

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103
Q

Ibuprofen trade name

A

Motrin Advil

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104
Q

Naproxen trade name

A

AleveNaprosyn

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105
Q

Indomethacin trade name

A

Indocin

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106
Q

Celecoxib trade name

A

Celebrex

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107
Q

Meloxicam trade name

A

Mobic

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108
Q

Diclofenac trade name

A

Voltaren

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109
Q

Trolamine salicylate trade name

A

Aspercreme

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110
Q

NSAID medications

A

IbuprofenNaproxenIndomethacinAspirinCelecoxibMeloxicamDiclofenacTrolamine salicylate

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111
Q

NSAID indications

A

analgesiaantipyreticanti-inflammatory

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112
Q

Aspirin indications

A

analgesiaantipyreticanti-inflammatoryantithrombotic

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113
Q

NSAID MOA

A

reversibly inhibits COX-1 and COX-2 enzymes to decrease prostaglandin formation

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114
Q

how is Aspirin’s MOA different from other NSAIDS?

A

it irreversibly binds to COX enzymes, other NSAIDs reversibly bind

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115
Q

general NSAID’s AE

A

GIN/VdyspepsiaulcersGI bleedingincreased BPnephrotoxicityCV risk

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116
Q

Rare Aspirin AE

A

skin rashphotosensitivitybronchospamsRaye Syndrome in Children

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117
Q

NSAIDs common routes

A

POtopical IMIV

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118
Q

Aspirin common routes

A

POrectal

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119
Q

Opioid drugs

A

CodeineHydrocodoneHydrocodone w/acetaminophenMorphineOxycodoneOxycodone w/acetminophenFentanylHydromorphoneMeperidineTramadol

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120
Q

Hydrocodone w/acetaminophen trade name

A

Vicodin

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121
Q

Morphine trade name

A

MS Contin

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122
Q

Oxycoden trade name

A

Oxycotin

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123
Q

Oxycodone w/acetaminophen trade name

A

Percocet

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124
Q

Fentanyl trade name

A

Duragesic

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125
Q

Hydromorphone trade name

A

Dilaudid

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126
Q

Meperidine trade name

A

Dermerol

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127
Q

what opioid can be perscribed as an antitussive?

A

codeine

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128
Q

Opioid Indication

A

analgesia

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129
Q

Opioid common routes

A

POrectalIVtopicalsubcutaneousintrathecalintranasaltransmucosaepidural

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130
Q

Opioid MOA

A

bind to opioid receptors in the CNS to inhibit ascending pain pathways

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131
Q

Opioid AE CNS effects

A

sedationnausearespiratory depressioncough suppressionmiosistruncal rigidity

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132
Q

Opioid Peripheral AE

A

constipationurinary retentionbronchospasmsreduced GI motilitypruitis

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133
Q

Acetaminophen trade name

A

Tylenol

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134
Q

Acetaminophen Indications

A

analgesiaantipyreticcombo with NSAID to reduce NSAID dose

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135
Q

Acetaminophen Common routes

A

POIVrectal

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136
Q

Acetaminophen MOA

A

inhibits prostaglandin synthesis in CNS

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137
Q

Acetaminophen AE

A

hepatotoxicity (esp w/alcohol)

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138
Q

Corticosteroids Drug List

A

Cortisone, Prednisone, Methylprednisolone, Prednisolone, Triamcinolone, Betamethasone

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139
Q

Corticosteroids Indication

A

RA, anti-inflammatory

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140
Q

Corticosteroids Common routes

A

PO, IV, intra-articular, topical

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141
Q

Corticosteroids MOA

A

decrease inflammation and suppress immune system

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142
Q

Short term corticosteroid AE

A

inc blood glucose, mood changes, fluid retention

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143
Q

Long term Corticosteroids AE

A

osteoporosis/ increased fracture risk, thin skin, muscle wasting, poor wound healing, adrenal suppression, Cushing’s disease, increased risk of infection from immunosuppression

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144
Q

brand name Gabapentin

A

Neurontin

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145
Q

Gabapentin indication

A

neuropathic pain

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146
Q

Gabapentin drug class

A

GABA analog, anticonvulsant

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147
Q

Gabapentin common route

A

PO

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148
Q

Gabapentin MOA

A

bind to alpha 2-delta subunit of a calcium channel to block its effects

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149
Q

Gabapentin AE

A

dizziness, drowsiness

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150
Q

Azathioprine drug class

A

immunosuppresant

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151
Q

Azathioprine indication

A

SLE

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152
Q

Azathioprine common routes

A

PO, injectible

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153
Q

Azathioprine MOA

A

decreases the immune response so the body doesn’t attack itself

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154
Q

Azathioprine AE

A

N/V

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155
Q

Hyaluronate trade name

A

Synvisc,Gel-One,Orthovisc

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156
Q

Hyaluronate indication

A

OA

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157
Q

Hyaluronate common route

A

injection

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158
Q

Hyaluronate MOA

A

viscoelastic solution to provide joint lubrication

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159
Q

Hyaluronate AE

A

injection site pain,swelling, rash

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160
Q

Lidocaine drug class

A

anesthetics

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161
Q

propofol drug class

A

anesthetics

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162
Q

anesthetic drugs

A

lidocaine, propofol

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163
Q

anasthetic drugs indications

A

patient controlled analgesia

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164
Q

general anasthetic common routes

A

IV, inhalation

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165
Q

regional anasthetic common routes

A

intrathecal, epidural, inflitration anesthesia, peripheral nerve block, IV, regional block

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166
Q

local anasthetic common routes

A

injection, topical

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167
Q

which antibiotic classes inhibit cell walls?

A

Penecillins, Cephalosporins Glycopeptides

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168
Q

which antibiotic classes inhibit protein synthesis?

A

Aminoglycides Tetracyclines Macrolides

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169
Q

which antibiotic classes inhibit DNA/RNA?

A

Fluoroquinolones, Nitroimidazole Antifolates

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170
Q

what pre/suffixes are associated with antibiotics that inhibit cell wall?

A

-cillin, ceph-, -vancin

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171
Q

what pre/suffixes are associated with antibiotics that inhibit protein synthesis?

A

-mycin -micin -cyclin

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172
Q

what pre/suffixes are associated with antibiotics that inhibit DNA/RNA?

A

-floxacin -idazole Sulfa-

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173
Q

Penecillins, Cephalosporins Glycopeptides

A

which antibiotic classes inhibit cell walls?

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174
Q

Aminoglycides Tetracyclines Macrolides

A

which antibiotic classes inhibit protein synthesis?

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175
Q

Fluoroguinolones, Nitroimidazole Antifolates

A

which antibiotic classes inhibit DNA/RNA?

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176
Q

-allinceph- -vancin

A

what pre/suffixes are associated with antibiotics that inhibit cell wall?

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177
Q

-mycin -micin -cyclin

A

what pre/suffixes are associated with antibiotics that inhibit protein synthesis?

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178
Q

-floxacin -idazole Sulfa-

A

what pre/suffixes are associated with antibiotics that inhibit DNA/RNA?

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179
Q

which antibiotic drug classes are gram +/-

A

Penecillins,

Tetracyclines

Macrolides

Antifolates

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180
Q

C-diff infection is treated using what antibiotic?

A

metronidazole

vancomycin

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181
Q

what antibiotic is used to treat respiratory infection?

A

macrolides

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182
Q

what antibiotic is used to treat community based pnemonia?

A

fluoroquinolones

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183
Q

what antibiotics are used to treat MRSA and Staph infections?

A

Linozolid

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184
Q

AE of antifolates

A

steven-johnson syndrome

allergies

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185
Q

AE of fluoroquinolones

A

Tendon rupure

hypoglycemia

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186
Q

AE of Penecillins

A

Allergies, GI distress

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187
Q

AE of cephalosporins

A

GI hypersentivity

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188
Q

AE of aminoglycides

A

ototoxicity

nephrotoxicity

photosensitivity

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189
Q

Macrolides AE

A

N/V/D

drug/drug interactions

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190
Q

AE Glycopeptides

A

hypotension (fall risk)

nephrotoxicity

redman syndrome

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191
Q

which antiobiotics can be administered as eye drops (opthalmic)?

A

Aminoglycocides

Fluoroquinolones

Macrolides

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192
Q

Nitroimidazole AE

A

GI

metallic taste

nausea

headache

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193
Q

which antiobiotics can rarely cause peripheral neuropathy?

A

Nitroimadzaole

194
Q

How would aminoglycocides increase fall risk?

A

affects vestibular function (ototoxicity

195
Q

potential AE of Linozolid

A

serotonin syndrome

thrombocytopenia

196
Q

PT specific pertaining to TB trx

A

CN VIII damage - increases fall risk

197
Q

tetracycline AE

A

GI distress, photosensitivity

198
Q

what broad AE should you be concerned about concerning antibiotics?

A

GI distress (specifically diarrhea)

199
Q

basic pathophysiology of cancer

A

uncontrolled cell growth

200
Q

causes of cancer

A

1). extrinsic: carcinogens 2). Intrinsic: genetic mutations/DNA sequences, viral agents, chronic irritation, genetic predisposition, oncogenes

201
Q

General stages of cell lifecycle

A

G0: cell at restG1: Pre-DNA S: DNA synthesisG2: pre-mitosisMitosis

202
Q

cell-cycle-specific (CCS) agents do what?

A

target specific phase of cell cycle

203
Q

what are CCS agents more effective on?

A

rapidly dividing tumors

204
Q

dose frequency of CCS agents

A

continuous infusion or frequent doses

205
Q

cell-cycle nonspecific (CCN) agents do what?

A

target the cell during it’s entire life cycle (including G0)

206
Q

What areas of the body are primarily adversely affected by chemotherapy?

A

bone marrow, GI, buccal mucosa, reproductive organs, hair follicles

207
Q

what are CCN agents more effective on?

A

slow large growing tumors

208
Q

dose frequency/timing of CCN agents

A

intermittently dose to reduce toxicities

209
Q

what is Nadir?

A

10-28 days when WBC is at it’s lowest, no trx given here

210
Q

what stage of the cell life cycle is chemotherapy not effective?

A

G0: cell at rest

211
Q

primary treatment (cure) for cancer

A

surgery, radiation, chemotherapy, biotherapy

212
Q

when is adjuvant therapy used?

A

after primary trx

213
Q

when is neoadjuvant therapy used?

A

before primary trx

214
Q

goals/stages of treatment

A

cure, controlpalliative

215
Q

what is palliative care?

A

decrease tumor burden, improve QOL, relieve pain

216
Q

Types of cancer trx

A

radiation, surgery, pharmacotherapy,

217
Q

what is used to treat almost every solid tumor?

A

radiation

218
Q

Radiation trx AE

A

1). significant damage to all tissues2). can result in fibrosis of lungs (location dependent)3). fatigue

219
Q

PT concerns for radiation

A

fatigue, location of tissue damage

220
Q

Cancer trx used to maximize tumor eradication

A

surgery

221
Q

PT considerations for surgery trx

A

wound complications, lymphedema, general post-op concerns

222
Q

what are the 3 types of pharmacotherapy?

A

1). chemotherapy2). targeted therapy 3). immunotherapy

223
Q

chemotherapy

A

drugs that inhibit growth and replication of cancer cells

224
Q

targeted therapy

A

blocks genes/proteins, specific genetic mutations

225
Q

immunotherapy

A

hormones and drugs that use the immune system to trx cancer

226
Q

majority of immunotherapy drugs utilize what?

A

antibodies that end in -mab, interferon, interleukins (non-specific immunotherapy)

227
Q

what cancer AE should we be most concerned with?

A

1). thrombocytopena2). neutropenia3). peripheral neuropathy4). pain5). infection6). mouth/throat

228
Q

special precautions for oral chemotherapy

A

wear gloves when touching laundry or bodily fluids (specific to the oral med)

229
Q

suffix associated with most antiviral drugs

A

-vir

230
Q

AE influenza A &amp; B

A

N/V/D, fever (the flu)

231
Q

which forms of Hepatitis do not have a vaccine?

A

C, D, E

232
Q

T/F: hepatitis D and E are common in the US

A

False

233
Q

how is hepatitis B treated?

A

1). Interferon (weekly injection)2). Nucleoside/Nucleotide analog (better, PO)

234
Q

AE of Interferon

A

flu-like symptoms

235
Q

common AE for DAAs

A

fatigue, weakness, headache, nausea

236
Q

PT concern with DAAs + corticosteroids

A

Bradycardia

237
Q

what does HIV target?

A

immune system -> CD4 T cells

238
Q

result of HIV progression?

A

decreased CD4 count leading to AIDS

239
Q

how is HIV treated?

A

HAART (Highly Active Antiretroviral Treatment)

240
Q

what is HAART?

A

combo therapy to increase efficacy and decrease resistance

241
Q

patient specific factor in successful management of HIV

A

ADHERENCE

242
Q

MOA of antivirals

A

target different points in lifecycle

243
Q

Rehab concerns specific to HIV

A

1). opportunistic infections2). Neuromuscular problems (myopathy, peripheral neuropathy)3). pt trx include pain management

244
Q

types of fungal infections

A

1). superficial2). systemic

245
Q

patients at risk for fungal infections

A

immunosuppression, antibacterial, diabetics, burn victims

246
Q

*antifungal drugs basic MOA

A

alter cell membrane permeability

247
Q

2 antifungal classes

A

1). polyenes, 2). azoles

248
Q

which antifungal drug class is broad spectrum

A

azoles

249
Q

PD implications of azoles

A

common CYP interactions

250
Q

which antifungals commonly have DDI?

A

Azoles

251
Q

Polyene drugs

A

Nystatin, Amphotericin B

252
Q

Nystatin AE

A

N/V/D, cramps (PO), rash, urticaria (topical)

253
Q

Azole drugs

A

Fluconazole, ketoconazole

254
Q

Azole drugs AE

A

N/V, photophobia, cardiac arrhythmia, menstrual irregularities,

255
Q

primary concern with antifungals

A

liver damage, elevated serum transaminasekidney damage

256
Q

What are the types of vaccines?

A

1). inactivated2). subunit/conjugated3). attenuated4). toxoid

257
Q

what is in an inactivated vaccine?

A

killed pathogen

258
Q

what is in a conjugated vaccine?

A

piece of the pathogen

259
Q

what is in a live attenuated vaccine?

A

weakened pathogen

260
Q

what is in a toxoid vaccine?

A

pathogen toxin instead of actual pathogen

261
Q

which vaccine is good for life?

A

life attenuated

262
Q

which vaccine should be avoided in immunocompromised populations?

A

life attenuated

263
Q

areas of virus lifecycle that a virus can impact

A

1). going into and out of cell (binding/budding)2). movement in cell (uncoating)3). replication (translation/transcription/assembly)

264
Q

what is used to treat Hepatitis C?

A

DAA

265
Q

What is a therapeutic concern when treating a patient with hepatitis C?

A

bradycardia

266
Q

for an acute infection of of Hepatitis A what is recommended?

A

rest, hyrdate, antipyretic drugs, AVOID acetaminophen, typically takes 2-6 months to recover

267
Q

name all the categories of antiviral drugs

A

antiherpes, anti-influenza, antihepatitis, miscellanis

268
Q

Opioid drugs

A

Codeine, Hydrocodone, Hydrocodone w/acetaminophen, Morphine, Oxycodone, Oxycodone w/acetminophen, Fentanyl, Hydromorphone, Meperidine, Tramadol, Methadone

269
Q

Hydrocodone w/acetaminophen trade name

A

Vicodin

270
Q

Morphine trade name

A

MS Contin

271
Q

Oxycoden trade name

A

Oxycotin

272
Q

Oxycodone w/acetaminophen trade name

A

Percocet

273
Q

Fentanyl trade name

A

Duragesic

274
Q

Hydromorphone trade name

A

Dilaudid

275
Q

Meperidine trade name

A

Dermerol

276
Q

what opioid can be perscribed as an antitussive?

A

codeine

277
Q

Opioid Indication

A

analgesia

278
Q

Opioid common routes

A

PO, rectal, IV, topical, subcutaneous, intrathecal, intranasal, transmucosa, epidural

279
Q

Opioid MOA

A

bind to opioid receptors in the CNS to inhibit ascending pain pathways

280
Q

Opioid AE CNS effects

A

sedation

nausea

respiratory depression

cough suppression

miosis

truncal rigidity

281
Q

Opioid Peripheral AE

A

constipation

urinary retention

bronchospasms

reduced GI motility

pruitis

282
Q

Which opioid drugs do not have trade names?

A

Codeine, Hydrocodone, Tamadol, Methadone

283
Q

DMARD drug list

A

Methotrexate, Sulfasalazine, Adalimumab, Etanercept, Rituximab Hydroxyhloroquine

284
Q

Non-biologic DMARDs

A

Methotrexate,SulfasalazineHydroxychloroquine

285
Q

DMARD (biologic TNF Inhibitor)

A

Adalimumab,Etanercept

286
Q

DMARD (biologic Non-TNF Inhibitor)

A

Rituximab

287
Q

Adalimumab trade name

A

Humira

288
Q

Etanercept trade

A

Enbrel

289
Q

Rituximab trade name

A

Rituxan

290
Q

DMARD indications

A

RA

291
Q

what else is methotrexate indicated for?

A

lupus

292
Q

Hydroxychloroquine Drug Class

A

DMARD (non-biologic)antimalarial

293
Q

Hydroxychloroquine trade name

A

Plaquenil

294
Q

Other indications for hydroxychloroquine?

A

lupus malaria

295
Q

What DMARDs are indicated for lupus?

A

methotrexatehydroxychloroquine

296
Q

DMARDs common routes

A

PO, IV, sub cutan

297
Q

which DMARDs have only the PO route?

A

methotrexate,sulfasalazinehydroxychloroquine

298
Q

which DMARDs are administered IV, or sub cut?

A

Adalimumab,etanerceptrituximab

299
Q

sulfasalazine and hydroxychloroquine MOA

A

impacts mediators of inflammatory response

300
Q

methotrexate MOA

A

possibly impacting IL-1, TNF-alpha, and leukotriene levels

301
Q

DMARD biologic TNF inhibitor MOA

A

bind TNF-alpha receptors to modulate downstream effects on inflammatory processes

302
Q

Rituximab MOA

A

basic MOA impacts inflammation process

303
Q

methotrexate common AE

A

N/V/D, alopecia, malaise

304
Q

methotrexate less common AE

A

increased liver function tests, heptatoxicity, nephrotoxicity, thrombocytopenia, bone marrow suppression

305
Q

sulfasalazine AE

A

Nausea, rash, hepatitis, pneumonitis, bone marrow suppression

306
Q

hydroxychloroquine AE

A

dyspepsia, nausea, abdominal pain, rashes, nightmares and visual disturbances

307
Q

rituximab AE

A

injection/infusion reactions, increased LFTs, antibody development

308
Q

DMARD (biologic TNF Inh) common AE

A

headache, infection, antibody development, IV infusion reactions (fever, hypotension, urticaria)

309
Q

DMARD (biologic TNF In) Boxed warnings

A

serious infections, secondary malignancies like lymphoma

310
Q

what are the three subtypes of DMARDs?

A

Non-biologic, Biologic (TNF/Non-TNF inhibitor)

311
Q

What 3 drugs are Non-biologic DMARDs?

A

Methotrexate, Sulfasalazine, Hydroxychloroquine

312
Q

What 2 drugs are TNF Inhibitors?

A

Adalimumab, Etanercept

313
Q

What drug is a Non-TNF inhibitor?

A

Tituximab

314
Q

How are biologic DMARDs usually administered?

A

IV, subcut.

315
Q

How are Non-biologic DMARDs usually administered?

A

PO

316
Q

What is the basic MOA for DMARDs?

A

impacts mediators of inflammatory response

317
Q

What is the MOA of Methrotrexate?

A

unknown, but possibly impacts IL-1, TNF-alpha, leukotreine levels

318
Q

AE of hydroxychloroquine

A

nightmares, visual disturbances, GI (N, dyspepsia), skin rash

319
Q

which DMARDs have boxed warnings?

A

Adalimumab, Etanercept

320
Q

AE TNF inhibitors

A

headache, antibody development, infection, IV reactions

321
Q

common AE Methotrexate

A

N/V/D, malaise, alopecia,

322
Q

AE Rituximab

A

increased LFTs, antibody development, injection infusion reaction

323
Q

rare AE Methotrexate

A

hepatotoxicity, nephrotoxicity, thrombocytopenia, bone marrow suppression

324
Q

MTX PT concerns

A

hydration, photo-sensitivity, caution: strengthening, stretching, deep tissue work, infection risk

325
Q

brand name Gabapentin

A

Neurontin

326
Q

Gabapentin indication

A

neuropathic pain

327
Q

Gabapentin drug class

A

GABA analog, anticonvulsant

328
Q

Gabapentin common route

A

PO

329
Q

Gabapentin MOA

A

bind to alpha 2-delta subunit of a calcium channel to block its effects

330
Q

Gabapentin AE

A

dizziness, drowsiness

331
Q

Azathioprine drug class

A

immunosuppresant

332
Q

Azathioprine indication

A

SLE

333
Q

Azathioprine common routes

A

PO, injectible

334
Q

Azathioprine MOA

A

decreases the immune response so the body doesn’t attack itself

335
Q

Azathioprine AE

A

N/V

336
Q

Hyaluronate trade name

A

Synvisc,Gel-One,Orthovisc

337
Q

Hyaluronate indication

A

OA

338
Q

Hyaluronate common route

A

injection

339
Q

Hyaluronate MOA

A

viscoelastic solution to provide joint lubrication

340
Q

Hyaluronate AE

A

injection site pain,swelling, rash

341
Q

Lidocaine drug class

A

anesthetics

342
Q

propofol drug class

A

anesthetics

343
Q

anesthetic drugs

A

lidocaine, propofol

344
Q

anasthetic drugs indications

A

patient controlled analgesia

345
Q

general anasthetic common routes

A

IV, inhalation

346
Q

regional anasthetic common routes

A

intrathecal, epidural, inflitration anesthesia, peripheral nerve block, IV, regional block

347
Q

local anasthetic common routes

A

injection, topical

348
Q

NSAID PT considerations

A

impacts muscle repair, injury recovery, and cartilage repair. caution against overuse and during Resistance training

349
Q

Opioid PT specific considerations

A

maximize PT scheduling to maximize pain relief, be aware of fall risk

350
Q

Fentanyl PT specific considerations

A

w/patches avoid using heat/hot pack

351
Q

Hydromorphone PT specific considerations

A

develop tolerance to all except constipation, miosis. Generally taken with a laxative

352
Q

Gabapentin PT specific considerations

A

higher chance of experiencing fall (due to dizziness)

353
Q

Corticosteroids PT specific considerations

A

diabetic pts can experience massive changes in blood sugar

354
Q

PT specific consideration for all DMARDs

A

keep pt hydrated

355
Q

methotrexate PT specific consideration

A

careful w/strengthening, stretching, deep tissue work. Lupus infection control (wash hands, etc.) Photo-sensitivity

356
Q

methotrexate PK/PD considerations

A

combo MTX w/another DMARD increase efficacy (but also toxicity). Give folic acid to reduce GI, hepatic and hematology toxicity

357
Q

Sulfasalazine PK/PD considerations

A

DMARDS + high-dose steroids = catabolic effect

358
Q

Azathioprine PT specific considerations

A

lupus infection control: wash hands, clean equipment, etx. Photosensitivity

359
Q

Hyaluronate PT specific considerations

A

mindful of swelling, rash following injections

360
Q

Anesthesia PT specific considerations

A

NM weakness, prolonged drowsiness, potential fall risk, impaired airway clearance

361
Q

what drug is usually safer than NSAIDs or elderly?

A

Acetaminophen

362
Q

what drug class would be prescribed for short-term RA treatment?

A

corticosteroids

363
Q

what is the gold standard treatment for RA?

A

methotrexate

364
Q

which drugs on our list have boxed warnings?

A

Azathioprine, Adalimumab, Etanercept, Methotrexate,

365
Q

NSAID medications

A

IbuprofenNaproxenIndomethacinAspirinCelecoxibMeloxicamDiclofenacTrolamine salicylate

366
Q

NSAID indications

A

analgesiaantipyreticanti-inflammatory

367
Q

Aspirin indications

A

analgesiaantipyreticanti-inflammatoryantithrombotic

368
Q

NSAID MOA

A

reversibly inhibits COX-1 and COX-2 enzymes to decrease prostaglandin formation

369
Q

how is Aspirin’s MOA different from other NSAIDS?

A

it irreversibly binds to COX enzymes, other NSAIDs reversibly bind

370
Q

general NSAID’s AE

A

N/V, dyspepsia, ulcers, GI bleeding, increased BP, nephrotoxicity, CV risk

371
Q

Rare Aspirin AE

A

skin rash, bleed and bruising,

photosensitivity,

bronchospams,

Raye Syndrome in Children

372
Q

NSAIDs common routes

A

PO

topical

IM

IV

373
Q

Aspirin common routes

A

POrectal

374
Q

what NSAIDs are antithrombotic?

A

Aspirin

Celecoxib

Diclofenac

Trolamine Salicylate

Meloxicam

375
Q

If you have GI risk which NSAID is the safest to take?

A

Ibuprofen (motrin, Advil)

376
Q

If you are at CV risk what is the safest NSAID to take?

A

Naproxen

377
Q

When should you avoid taking Celecoxib?

A

If you are at CV risk

378
Q

If you hae CV risk what NSAID should you avoid?

A

Celexocib

379
Q

If you have CV risk which NSAID is safest to take?

A

Naproxen

380
Q

If you have GI risk which NSAIDs are safe for you to take?

A

Celecoxib, Ibuprofen

381
Q

NSAIDs administered by what route give the lowest dose and for the shortest duration?

A

Topical

382
Q

T/F: someone with CHF shouldn’t take NSAIDs because it will increase their fluid retention

A

TRUE

383
Q

T/F: NSAIDs blunt the action of cardiovascular drugs?

A

TRUE

384
Q

If a patient is taking Ibuprofen, what should you watch out for?

A

Elderly, poor kidney function, history of GI bleed, any CV issues

385
Q

what else is methotrexate indicated for?

A

lupus

386
Q

Hydroxychloroquine trade name

A

Plaquenil

387
Q

Other indications for hydroxychloroquine?

A

lupus malaria

388
Q

What DMARDs are indicated for lupus?

A

methotrexatehydroxychloroquine

389
Q

DMARDs common routes

A

PO, IV, sub cutan

390
Q

which DMARDs have only the PO route?

A

methotrexate,sulfasalazinehydroxychloroquine

391
Q

which DMARDs are administered IV, or sub cut?

A

Adalimumab,etanerceptrituximab

392
Q

methotrexate common AE

A

N/V/D, alopecia, malaise

393
Q

methotrexate less common AE

A

increased liver function tests, heptatoxicity, nephrotoxicity, thrombocytopenia, bone marrow suppression

394
Q

sulfasalazine AE

A

Nausea, rash, hepatitis, pneumonitis, bone marrow suppression

395
Q

hydroxychloroquine AE

A

dyspepsia, nausea, abdominal pain, rashes, nightmares and visual disturbances

396
Q

rituximab AE

A

injection/infusion reactions, increased LFTs, antibody development

397
Q

DMARD (biologic TNF Inh) common AE

A

headache, infection, antibody development, IV infusion reactions (fever, hypotension, urticaria)

398
Q

DMARD (biologic TNF In) Boxed warnings

A

serious infections, secondary malignancies like lymphoma

399
Q

what are the three subtypes of DMARDs?

A

Non-biologic, Biologic (TNF/Non-TNF inhibitor)

400
Q

What 3 drugs are Non-biologic DMARDs?

A

Methotrexate, Sulfasalazine, Hydroxychloroquine

401
Q

What 2 drugs are TNF Inhibitors?

A

Adalimumab, Etanercept

402
Q

What drug is a Non-TNF inhibitor?

A

Rituximab

403
Q

How are biologic DMARDs usually administered?

A

IV, subcut.

404
Q

How are Non-biologic DMARDs usually administered?

A

PO

405
Q

What is the basic MOA for DMARDs?

A

impacts mediators of inflammatory response

406
Q

What is the MOA of Methrotrexate?

A

unknown, but possibly impacts IL-1, TNF-alpha, leukotreine levels

407
Q

AE of hydroxychloroquine

A

nightmares, visual disturbances, GI (N, dyspepsia), skin rash

408
Q

which DMARDs have boxed warnings?

A

Adalimumab, Etanercept

409
Q

AE TNF inhibitors

A

headache, antibody development, infection, IV reactions

410
Q

common AE Methotrexate

A

N/V/D, malaise, alopecia,

411
Q

AE Rituximab

A

increased LFTs, antibody development, injection infusion reaction

412
Q

rare AE Methotrexate

A

hepatotoxicity, nephrotoxicity, thrombocytopenia, bone marrow suppression

413
Q

MTX PT concerns

A

hydration, photo-sensitivity, caution: strengthening, stretching, deep tissue work, infection risk

414
Q

basic pathophysiology of cancer

A

uncontrolled cell growth

415
Q

causes of cancer

A

1). extrinsic: carcinogens 2). Intrinsic: genetic mutations/DNA sequences, viral agents, chronic irritation, genetic predisposition, oncogenes

416
Q

General stages of cell lifecycle

A

G0: cell at restG1: Pre-DNA S: DNA synthesisG2: pre-mitosisMitosis

417
Q

cell-cycle-specific (CCS) agents do what?

A

target specific phase of cell cycle

418
Q

what are CCS agents more effective on?

A

rapidly dividing tumors

419
Q

dose frequency of CCS agents

A

continuous infusion or frequent doses

420
Q

cell-cycle nonspecific (CCN) agents do what?

A

target the cell during it’s entire life cycle (including G0)

421
Q

What areas of the body are primarily adversely affected by chemotherapy?

A

bone marrow, GI, buccal mucosa, reproductive organs, hair follicles

422
Q

what are CCN agents more effective on?

A

slow large growing tumors

423
Q

dose frequency/timing of CCN agents

A

intermittently dose to reduce toxicities

424
Q

what is Nadir?

A

10-28 days when WBC is at it’s lowest, no trx given here

425
Q

what stage of the cell life cycle is chemotherapy not effective?

A

G0: cell at rest

426
Q

primary treatment (cure) for cancer

A

surgery, radiation, chemotherapy, biotherapy

427
Q

when is adjuvant therapy used?

A

after primary trx

428
Q

when is neoadjuvant therapy used?

A

before primary trx

429
Q

goals/stages of treatment

A

cure, controlpalliative

430
Q

what is palliative care?

A

decrease tumor burden, improve QOL, relieve pain

431
Q

Types of cancer trx

A

radiation, surgery, pharmacotherapy,

432
Q

what is used to treat almost every solid tumor?

A

radiation

433
Q

Radiation trx AE

A

1). significant damage to all tissues2). can result in fibrosis of lungs (location dependent)3). fatigue

434
Q

PT concerns for radiation

A

fatigue, location of tissue damage

435
Q

Cancer trx used to maximize tumor eradication

A

surgery

436
Q

PT considerations for surgery trx

A

wound complications, lymphedema, general post-op concerns

437
Q

what are the 3 types of pharmacotherapy?

A

1). chemotherapy2). targeted therapy 3). immunotherapy

438
Q

chemotherapy

A

drugs that inhibit growth and replication of cancer cells

439
Q

targeted therapy

A

blocks genes/proteins, specific genetic mutations

440
Q

immunotherapy

A

hormones and drugs that use the immune system to trx cancer

441
Q

majority of immunotherapy drugs utilize what?

A

antibodies that end in -mab, interferon, interleukins (non-specific immunotherapy)

442
Q

what cancer AE should we be most concerned with?

A

1). thrombocytopena2). neutropenia3). peripheral neuropathy4). pain5). infection6). mouth/throat

443
Q

special precautions for oral chemotherapy

A

wear gloves when touching laundry or bodily fluids (specific to the oral med)

444
Q

suffix associated with most antiviral drugs

A

-vir

445
Q

AE influenza A &amp; B

A

N/V/D, fever (the flu)

446
Q

which forms of Hepatitis do not have a vaccine?

A

C, D, E

447
Q

T/F: hepatitis D and E are common in the US

A

False

448
Q

how is hepatitis B treated?

A

1). Interferon (weekly injection)2). Nucleoside/Nucleotide analog (better, PO)

449
Q

AE of Interferon

A

flu-like symptoms

450
Q

common AE for DAAs

A

fatigue, weakness, headache, nausea

451
Q

PT concern with DAAs + corticosteroids

A

Bradycardia

452
Q

what does HIV target?

A

immune system -> CD4 T cells

453
Q

result of HIV progression?

A

decreased CD4 count leading to AIDS

454
Q

how is HIV treated?

A

HAART (Highly Active Antiretroviral Treatment)

455
Q

what is HAART?

A

combo therapy to increase efficacy and decrease resistance

456
Q

patient specific factor in successful management of HIV

A

ADHERENCE

457
Q

MOA of antivirals

A

target different points in lifecycle

458
Q

Rehab concerns specific to HIV

A

1). opportunistic infections2). Neuromuscular problems (myopathy, peripheral neuropathy)3). pt trx include pain management

459
Q

types of fungal infections

A

1). superficial2). systemic

460
Q

patients at risk for fungal infections

A

immunosuppression, antibacterial, diabetics, burn victims

461
Q

*antifungal drugs basic MOA

A

alter cell membrane permeability

462
Q

2 antifungal classes

A

1). polyenes, 2). azoles

463
Q

which antifungal drug class is broad spectrum

A

azoles

464
Q

PD implications of azoles

A

common CYP interactions

465
Q

which antifungals commonly have DDI?

A

Azoles

466
Q

Polyene drugs

A

Nystatin, Amphotericin B

467
Q

Nystatin AE

A

N/V/D, cramps (PO), rash, urticaria (topical)

468
Q

Azole drugs

A

Fluconazole, ketoconazole

469
Q

Azole drugs AE

A

N/V, photophobia, cardiac arrhythmia, menstrual irregularities,

470
Q

primary concern with antifungals

A

liver damage, elevated serum transaminasekidney damage

471
Q

What are the types of vaccines?

A

1). inactivated2). subunit/conjugated3). attenuated4). toxoid

472
Q

what is in an inactivated vaccine?

A

killed pathogen

473
Q

what is in a conjugated vaccine?

A

piece of the pathogen

474
Q

what is in a live attenuated vaccine?

A

weakened pathogen

475
Q

what is in a toxoid vaccine?

A

pathogen toxin instead of actual pathogen

476
Q

which vaccine is good for life?

A

life attenuated

477
Q

which vaccine should be avoided in immunocompromised populations?

A

life attenuated

478
Q

areas of virus lifecycle that a virus can impact

A

1). going into and out of cell (binding/budding)2). movement in cell (uncoating)3). replication (translation/transcription/assembly)

479
Q

what is used to treat Hepatitis C?

A

DAA

480
Q

What is a therapeutic concern when treating a patient with hepatitis C?

A

bradycardia

481
Q

for an acute infection of of Hepatitis A what is recommended?

A

rest, hyrdate, antipyretic drugs, AVOID acetaminophen, typically takes 2-6 months to recover

482
Q

name all the categories of antiviral drugs

A

antiherpes, anti-influenza, antihepatitis, miscellanis

DPT Semester 1 (12 decks)

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