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Pharmacology Test 3 > Intro + Pain Control > Flashcards

Intro + Pain Control Flashcards

PK/PD, Opioids, NSAIDs, Neuropathic pain, RA, SLE, and OA

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

what does ADME stand for?

A

absorption distribution metabolism excretion

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4
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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5
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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6
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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7
Q

what are the 2 ways drugs are absorbed?

A

via enteral (GI tract) or parenteral route

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8
Q

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

A

oral,

sublingual,

rectal

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9
Q

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

A

inhalation, injection, topical, transdermal, implant

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10
Q

define bioavailability

A

% of drug that makes it into systemic circulation

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11
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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12
Q

what does a higher Vd mean?

A

there is more drug in tissue than the blood

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13
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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14
Q

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

A

5

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15
Q

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

A

4-5

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16
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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17
Q

Schedule I substance

A

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

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18
Q

Schedule II substance

A

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

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19
Q

Schedule III substance

A

lower abuse potential but still might lead to dependence

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20
Q

Schedule IV substance

A

still lower potential for abuse

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21
Q

Schedule V substance

A

lowest relative abuse potential

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22
Q

define specificity

A

drug binds to only one type of receptor

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23
Q

define selectivity

A

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

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24
Q

what is Emax?

A

maximal response receptors are saturated may cause toxicity

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25
Q

what is ED50?

A

effective dose to get 50% of expected response

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26
Q

how does ED50 relate to potency?

A

lower ED50 = more potent less drug required for effect

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27
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

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28
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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29
Q

what is TD50?

A

dose that is toxic for 50% of people

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30
Q

What is the Therapeutic Index?

A

a ratio of TD50 to ED50

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31
Q

What is the Naranjo Scale/

A

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

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32
Q

what are the 3 types of pain?

A

nociceptive neuropathic psychogenic

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33
Q

What neural structures are involved with ascending pain pathways?

A
  1. periphery sensory neurons
  2. dorsal horn of spinal cord
  3. brain stem
  4. thalamus
  5. somatosensory cortex
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34
Q

What does the descending pathway do?

A

modulate/suppression pain signals

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35
Q

where does the descending pathway originate?

A

periaqueductal gray matter of the mid-brain

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36
Q

Name some neurotransmitters in the nociceptive pathways

A

GABA, glutamate, serotonin, norepinephrine, adenosin

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37
Q

what is the MOA for opioids?

A

bind to opioid receptor in CNS to inhibit ascending pain pathways

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38
Q

What are the 3 main opioid receptors?

A

mu delta kappa

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39
Q

AE of opioids on CNS

A

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

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40
Q

AE peripheral effects of opioids

A

constipation urinary retention bronchospasm reduced GI motility Pruritus (itching)

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41
Q

what to notice for respiratory depression

A

labored breathing and decreased respiration rate

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42
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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43
Q

what is nociceptive pain?

A

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

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44
Q

when is nociceptive pain not localized?

A

when it originates from visera

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45
Q

what is neuropathic pain?

A

typically indicates nerve involvement burning, tingling sensation

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46
Q

what are the 2 primary nociceptive afferent neurons?

A

unmyelinated C fibers finely myelinated A delta fibers

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47
Q

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

A
  1. NMDA blocker
  2. substance P antagonists
  3. inhibition of NO synthesis
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48
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

49
Q

what are the three subtypes of DMARDs?

A
  1. Non-biologic
  2. Biologic (TNF/Non-TNF inhibitor)
50
Q

What is the basic MOA for DMARDs?

A

impacts mediators of inflammatory response

51
Q

What 3 drugs are Non-biologic DMARDs?

A
  1. Methotrexate
  2. Sulfasalazine
  3. Hydroxychloroquine
52
Q

DMARD (biologic TNF Inh) common AE

A
  1. headache
  2. infection
  3. antibody development
  4. IV infusion reactions (fever, hypotension, urticaria)
53
Q

DMARD (biologic TNF In) Boxed warnings

A

serious infections, secondary malignancies like lymphoma

54
Q

What is the MOA of Methrotrexate?

A

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

55
Q

methotrexate common AE

A

N/V/D, alopecia, malaise

56
Q

methotrexate less common AE

A
  1. increased liver function tests
  2. heptatoxicity
  3. nephrotoxicity
  4. thrombocytopenia
  5. bone marrow suppression
57
Q

Methotrexate PT concerns

A
  1. hydration
  2. photo-sensitivity
  3. caution: strengthening, stretching, deep tissue work, infection risk
58
Q

hydroxychloroquine AE

A
  1. dyspepsia
  2. nausea
  3. abdominal pain
  4. rashes
  5. nightmares and visual disturbances
59
Q

What DMARDs are indicated for lupus?

A
  1. methotrexate
  2. hydroxychloroquine (Plaquenil - also indicated for malaria)
60
Q

What drug is a Non-TNF inhibitor?

A

Rituximab

61
Q

rituximab AE

A
  1. injection/infusion reactions
  2. increased LFTs
  3. antibody development
62
Q

What 2 drugs are TNF Inhibitors?

A
  1. Adalimumab
  2. Etanercept
63
Q

AE TNF inhibitors

A

headache, antibody development, infection, IV reactions

64
Q

which DMARDs have boxed warnings?

A
  1. Adalimumab
  2. Etanercept
65
Q

Opioid drugs

A
  1. Codeine
  2. Hydrocodone
  3. Hydrocodone w/acetaminophen
  4. Morphine
  5. Oxycodone
  6. Oxycodone w/acetminophen
  7. Fentanyl
  8. Hydromorphone
  9. Meperidine
  10. Tramadol
  11. Methadone
66
Q

what opioid can be perscribed as an antitussive?

A

codeine

67
Q

Opioid common routes

A

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

68
Q

Opioid MOA

A

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

69
Q

Opioid AE CNS effects

A

sedation

nausea

respiratory depression

cough suppression

miosis

truncal rigidity

70
Q

Opioid Peripheral AE

A

constipation

urinary retention

bronchospasms

reduced GI motility

pruitis

71
Q

basic pathophysiology of cancer

A

uncontrolled cell growth

72
Q

what is Nadir?

A

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

73
Q

primary treatment (cure) for cancer

A
  1. surgery
  2. radiation
  3. chemotherapy
  4. biotherapy
74
Q

when is adjuvant therapy used?

A

after primary trx

75
Q

when is neoadjuvant therapy used?

A

before primary trx

76
Q

goals/stages of treatment

A
  1. cure
  2. control
  3. palliative
77
Q

what is palliative care?

A

decrease tumor burden, improve QOL, relieve pain

78
Q

Types of cancer trx

A
  1. radiation
  2. surgery
  3. pharmacotherapy,
79
Q

what is used to treat almost every solid tumor?

A

radiation

80
Q

Radiation trx AE

A
  1. significant damage to all tissues
  2. can result in fibrosis of lungs (location dependent)
  3. fatigue
81
Q

PT concerns for radiation

A

fatigue, location of tissue damage

82
Q

Cancer trx used to maximize tumor eradication

A

surgery

83
Q

PT considerations for surgery trx

A

wound complications, lymphedema, general post-op concerns

84
Q

what are the 3 types of pharmacotherapy?

A
  1. chemotherapy
  2. targeted therapy
  3. immunotherapy
85
Q

what is chemotherapy

A

drugs that inhibit growth and replication of cancer cells

86
Q

what is targeted therapy

A

blocks genes/proteins, specific genetic mutations

87
Q

what is immunotherapy

A

hormones and drugs that use the immune system to trx cancer

88
Q

majority of immunotherapy drugs utilize what?

A
  1. antibodies that end in -mab
  2. interferon
  3. interleukins (non-specific immunotherapy)
89
Q

what cancer AE should we be most concerned with?

A
  1. thrombocytopena
  2. neutropenia
  3. peripheral neuropathy
  4. pain
  5. infection
  6. mouth/throat
90
Q

special precautions for oral chemotherapy

A

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

91
Q

NSAID medications

A

Ibuprofen Naproxen Indomethacin Aspirin Celecoxib Meloxicam Diclofenac Trolamine salicylate

92
Q

NSAID indications

A

analgesia antipyretic anti-inflammatory

93
Q

Aspirin indications

A

analgesia antipyretic anti-inflammatory antithrombotic

94
Q

NSAID MOA

A

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

95
Q

how is Aspirin’s MOA different from other NSAIDS?

A

it irreversibly binds to COX enzymes, other NSAIDs reversibly bind

96
Q

general NSAID’s AE

A

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

97
Q

what NSAIDs are antithrombotic?

A

Aspirin

Celecoxib

Diclofenac

Trolamine Salicylate

Meloxicam

98
Q

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

A

Ibuprofen (motrin, Advil)

99
Q

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

A

Naproxen

100
Q

When should you avoid taking Celecoxib?

A

If you are at CV risk

101
Q

If you hae CV risk what NSAID should you avoid?

A

Celexocib

102
Q

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

A

TRUE

103
Q

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

A

TRUE

104
Q

Gabapentin indication

A

neuropathic pain

105
Q

Gabapentin drug class

A

GABA analog, anticonvulsant

106
Q

Gabapentin MOA

A

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

107
Q

Gabapentin AE

A

dizziness, drowsiness

108
Q

Azathioprine drug class

A

immunosuppresant

109
Q

Azathioprine indication

A
  1. SLE
  2. off label trx for MS
110
Q

Azathioprine MOA

A

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

111
Q

Azathioprine AE

A

N/V

112
Q

Hyaluronate indication

A

OA

113
Q

Hyaluronate MOA and AE

A
  1. MOA - viscoelastic solution to provide joint lubrication
  2. AE - injection site rxns, swelling, and rash
114
Q

anesthetic drugs

A
  1. lidocaine
  2. propofol
115
Q

anasthetic drugs indications

A

patient controlled analgesia

116
Q

general anasthetic common routes

A

IV, inhalation

117
Q

regional anasthetic common routes

A

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

118
Q

local anasthetic common routes

A

injection, topical

Pharmacology Test 3 (10 decks)

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