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316 Pharmacology > Exam 1: Pharmacologic management, Pain and Inflammation > Flashcards

Exam 1: Pharmacologic management, Pain and Inflammation Flashcards

1
Q

Duge classification: Prednisone

A

Corticosteroid; anti-inflammatory

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2
Q

Indication: Prednisone

A
  • Allergy state (asthma, anaphylaxis)
  • autoimmune disorders
  • Inflammatory bowel disease
  • Endocrine disorders (replacement therapy)
  • Neoplastic disease (In conjunction w/ anticancer agents)
  • Prevention of transplant rejection
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3
Q

MoA: Prednisone

A
  • Inhibits synthesis of inflammatory chemical mediators
  • – Decrease in swelling, warmth, redness, and pain
  • Interrupts inflammatory processes
  • Suppresses the infiltration of inflammatory cells (Leukocytes)
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4
Q

Side effects: Prednisone

A
  • Adrenal suppression: Suppressions of hypothalamic-pituitary-adrenal (HPA) axis; HPA suppression may lead to adrenal crisis;
  • Immunosuppression: Prolonged use of corticosteroids may mask acute infections & Increase the incidence of secondary infection due to suppression of host defenses
  • Increased glucose levels/hyperglycemia (caution in diabetics)
  • Peptic ulcer disease (Increases perforation risk)
  • Latrogenic Cushing’s syndrome
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5
Q

three broad categories of medications when treating a patient with acute pain

A
  • Non-opioid analgesics
  • Opioid analgesics
  • Analgesic adjuvants
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6
Q

Analgesia

A

the relief of pain without loss of consciousness

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7
Q

Non- opioid

A

Medications that reduce inflammation &/or pain arising from injured tissue; exert analgesic, anti-inflammatory, & Antipyretic effects

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8
Q

Discontinuation of corticosteroids should be

A

Done slowly! (usually over 7 days)

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9
Q

Opioids

A

A morphine-like medication that produces pain relief, natural, semi-synthetic, & synthetic medications that relieve pain by binding to opioid receptors in the nervous system

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10
Q

Analgesic adjuvant

A

A medication that is not the primary analgesic but rather a medication research has shown to have independent or additive analgesic properties (anti-convulsants; antidepressants)

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11
Q

Non-opioid analgesics have a role in a wide spectrum of acute and chronic pain such as

A
  • Post-operative pain
  • cancer pain
  • arthritis
  • headache
  • menstrual cramps
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12
Q

What drug classification should be considered initially for pain management

A

Non-opioid analgesics

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13
Q

All medication of non opioid are _____ except for ____

A

NSAIDS! except for acetaminophen

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14
Q

Non- opioid analgesics have significant

A

Opioid dose-sparing properties, thereby reduction opioid-related side effects
(giving non-opioids in conjunction with opioids so we dont give too much opioids)

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15
Q

Examples of non-opioid analgesics

A

Acetaminophen
aspirin
ibuprofen
ketoralac

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16
Q

Non-opioids analgesics differ from opioids….

A
  • Ceiling effect to analgesics (non-opioids stop working after a certain point_
  • they do not produce tolerance or physical/psychological dependency
  • antipyretic
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17
Q

Primary MoA (NSAIDS):

A

-inhabitation of cyclooxygenase (COX), thereby preventing the formation of prostaglandins, which will decrease pain sensitivity

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18
Q

Prostaglandins

A

Group of chemicals found in almost all tissues

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19
Q

How/where do prostaglandins act

A

act locally (paracrine) on the tissues were they are synthesized as a result of normal and pathophysiologic processes

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20
Q

Physiological stimulus triggers what

A

COX 1

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21
Q

COX 1 effects

A 
TXA 2 (platlete aggreg. vasoconstriction)
PGI 2 (vasodilation, GI-mucosal protection)
PGE1/PGE2 (Kidney, GI-Tract, CNS)
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22
Q

Inflammatory stimulus effects

A

COX2

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23
Q

COX 2 effects

A

Inflammatory site

—-Causes pain sensitization, vasodilation

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24
Q

Many Nsaids are

A

Non-selective, so they inhibit both COX 1 & 2

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25
Q

Why are NSAIDS hard on the stomach

A

Because it’s non-selective, it blocks COX 1 protection

—– Blocking Cox 1 can cause ulcers, blood thinning, urinary tract issues

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26
Q

Cox 1 is

A

Constitutive

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27
Q

Cox 2 is

A

Inducible

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28
Q

Aspirin drug classification

A
  • Salicylate
  • NSAID
  • Antiplatelet agent
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29
Q

Non-selective inhibitor of COX causes

A

Anti-inflammatory
Analgesic
Antipyretic
Anti-platelet

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30
Q

Salicylates

A

type of drugs found in many OTC

Aspirin is the most common

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31
Q

Indication: Aspirin

A

mild to moderate pain, fever, myalgia

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32
Q

MoA: Aspirin

A

-Inhibits cyclooxygenase (COX) in periphery, decrease pain and inflammation
-blocks effects of PG synthesis at hypothalamus, which decrease fever
-

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33
Q

Adverse effects for aspirer are rare when

A

taken short term at normal doses

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34
Q

Side effects of aspirin

A
  • -8th cranial nerve stimualtion, ear ringing
  • GI irritation, gastric ulceration/perforation/bleeding
  • Increase ulceration risk when taken concurrently with corticosteroids or if combined with alcohol
  • prolonged bleeding, intensify anticoagulant effects of anticoagulants
  • renal impairment (especially in elderly and those with renal dysfunction
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35
Q

Cautions with aspirin

A
  • bleeding abnormalities
  • use of anticoagulants
  • peptic ulcer disease
  • child and adolescents under 19 with possible viral infections because of risk of Reye’s syndrome
  • pregnancy and lactation
  • Drug interactions: Warfarin, steroids, alcohol, other NSAIDS
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35
Q

Cautions with aspirin

A
  • bleeding abnormalities
  • use of anticoagulants
  • peptic ulcer disease
  • child and adolescents under 19 with possible viral infections because of risk of Reye’s syndrome
  • pregnancy and lactation
  • Drug interactions: Warfarin, steroids, alcohol, other NSAIDS
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36
Q

take Aspirin with a

A

Full glass of water, enteric coated can also help decrease stomach irritation

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37
Q

Salicylism

A

toxic effects of OD with salicylic acid or its salts

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38
Q

side effects of salicylates

A
  • Dizziness
  • tinnitus
  • nausea/vomiting
  • fluid and electrolyte deficiencies
  • metal confusion, lethargy
  • fever
  • Hyperventilation
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39
Q

Non-salicylate NSAIDS

A

-analgesic
-Anti-inflammatory
-antipyretic
Gastric ulceration & Renal impairment!!!!

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40
Q

Opposed to salicylate NSAIDS, Non-salicylate NSAIDs inhibit

A

platelet aggregation by REVERSIBLY inhabiting prostaglandin synthesis

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41
Q

Inhibition of platelet aggregation last only as long

A

as there is an effective serum drug concentration

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42
Q

Non salicylate NSAIDS do NOT

A

protect against MI, TIA, Stroke

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43
Q

NSAIDS may increase risk of

A

Thrombotic events

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44
Q

Salicylate NSAIDS MOA (one difference from Non-salicylate)

A

irreversibly inhibits platelet aggregation by blocking formation of thromboxane A2

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45
Q

Drug Classification: Ibuprofen

A

Non-salicylate, NSAID, Propionic acid derivative

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46
Q

Indictions: Ibuprofen

A

Milt to moderate pain , fever, and inflammation, dysmenorrhea, musculoskeletal pain; chronic treatment or rheumatoid & osteoarthritis

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47
Q

MoA of Ibuprofen

A

Inhibits prostaglandin synthesis by blocked COX (inhibits both cox 1 & 2)

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48
Q

Ibuprofen causes less

A

gastric bleeding and less platelet aggregation inhibition than aspirin

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49
Q

Ibuprofen black box warning

A
  • associated with increased risk of adverse CV thrombotic events, including fatal MI and Stroke
  • increase risk of GI irritation, inflammation, ulceration, bleeding, and perforation
  • contradicts treatment of preoperative pain in the setting or coronary artery bypass graft surgery
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50
Q

Drug classification of Ketorolac

A

Non-salicylate, NSAID, acetic acid derivative

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51
Q

Ketorolac is used for ______ relief of moderate to sever pain

A

Short term

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52
Q

indication for ketorolac

A
  • Powerful analgesic
  • Post-operative pain, as effective as morphine
  • minimal anti-inflammatory actions
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53
Q

Route for ketorolac

A

IM, IV, PO, Ophthalmic, intranasal

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54
Q

Side effects: Ketorolac

A
  • very high potential for GI bleeding (increase Cox 1 selectivity)
  • do not combine with other NSAIDS
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55
Q

How long should onetime ketorolac

A

No more than 5 days

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56
Q

ketorolac is contraindicated in patients with

A

renal impairment and peptic ulcer disease

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57
Q

ketorolac black box warning

A
  • inhibit platelet function
  • increased risk of CV thrombotic events, MI, stroke
  • increase risk for gastrointestinal irritation, inflammation, ulceration, bleeding, and perforation
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58
Q

Maximum daily use of ketorolac

A

40 mg

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59
Q

Drug classification of celecoxib

A

Non-salicylate, NSAID, Selective COX-2 inhibitor

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60
Q

MoA & therapeutic effect: Celecoxib

A

selective inhibition of COX 2 which decreases pain and inflammation

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61
Q

Does celecoxib inhibit platelet aggregation?

A

NO! because it does not target COX 1

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62
Q

Use celecoxib cautiously with patents who have

A

Cardiovascular risk factors

  • hypetension
  • DM
  • Dyslipidemia
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63
Q

Drug class: Acetaminophen

A

Non-NSAID, Antipyretic, non-opioid analgesic

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64
Q

Route of acetaminophen

A

PO, PR, IV for post op

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65
Q

Indication from acetaminophen

A
  • mild to moderate pain associated with variety of conditions
  • antipyretic: Drug choice for fever in children
  • Releif of musculoskeletal pain associated with arthritis
  • prophylaxis for children receiving Diphtheria-Pertussis-tetanus(DPT)
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66
Q

Is acetaminophen an NSAID?

A

NO

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67
Q

How does acetaminophen differ from NSAIDS?

A

They are more central analgesic effect (Blockage of central PGs)

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68
Q

Acetaminophen has fewer side effects compared to NSAIDS like

A
  • no anti-inflammatory effects
  • no anti-platelet effects
  • rarely causes GI problems
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69
Q

Acetaminophen may cause

A

HEPATOTOXICITY, hepatic necrosis, liver failure

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70
Q

Antidotes for acetaminophen OD

A
  • acetylcysteine

- give within 8 hours of ingestion

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71
Q

Acetaminophen should no exceed

A

4 g/day, 3000mg/day for extra strength, and 3250mg for regular strength

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72
Q

What kind of injury and hypersensitivity reaction occur with acetaminophen

A

liver injury and hypersensitivity reactions like anaphylaxis

73
Q

Opioids are divided into 2 groups

A
  1. agonists (pure agonists, mu receptor)

1. agonist-antagonist (Mu and KAPPA receptor)

74
Q

opioids are used for

A

Moderate to severe pain; preoperative sedation and reduction of anxiety

75
Q

Opioids bind to

A

opioid receptors producing effects that mimic the action of endogenous opioids

76
Q

example of opioids that are available with aspirin or Tylenol

A

Vicodin, Percocet

77
Q

examples of opioids

A 
morphine 
codeine
fentanyl 
hydrocodone
hydromorphone
oxycodone
78
Q

opioid agonists mimic

A

effects of naturally occurring opioids (endorphins, enkephalins)

79
Q

three main opioid receptors

A

Mu
Kappa
Delta

80
Q

Most important receptors in pharmacology

A

Mu

Kappa

81
Q

opioid receptors in the body

A 
brain 
brainstem 
spinal cord 
peripheral neurons 
intestine
82
Q

3 therapeutic effects of opioids

A
  • analgesia
  • sedation
  • euphoria
83
Q

3 non therapeutic effects of opioids

A
  • respiratory depression
  • constipation
  • dependency/addiction
84
Q

other effects of opioids

A 
orthostatic hypotension 
decrease cough reflex 
miosis 
emesis 
urinary retention 
urticaria 
increase intracranial pressure
85
Q

Drug to drug consideration for opioids

A
  • Increase CNS depression when given with CNS depressants (benzodiazepine, alcohol)
  • antihypertensive medications: can lead to increase hypotensive effect
  • Increase anticholinergic effects (constipation, urinary retention) when given with anticholinergic agents
86
Q

morphine sulfate is a

A

prototype opioid analgesic

87
Q

routes of morphine sulfate

A

PO, IM, IV, SQ, epidural, intrathecal

88
Q

MoA morphine sulfate

A

Primarily binds to MU receptors, mimicking the action of endogenous opiods, producing multiple pharmacological effects

89
Q

morphine sulfate main therapeutic effect

A

analgesia

90
Q

Morphine sulfate have a significant ________

A

first pass metabolism (rarely given PO)

91
Q

Repeated use of morphine sulfate use can produce a tolerance to

A

respiratory depressant
analgesic
euphoric
sedative effects

92
Q

If someone is given opioids but has a respiratory rate of less than 8-10, what do you do?

A

Hold the mediation and CONTACT PROVIDER!

Cannot give something different without provider approval

93
Q

is morphine sulfate a high alert medication

A

yes, it has a heightened risk of causing significant patient harm

94
Q

drug class: fentanyl

A

Opioid agonist

95
Q

route of fentanyl

A

Parenteral
Transdermal
Transmucosal
epidural , intrathecal

96
Q

Potency of fentanyl

A

High potency: 100 times that of morphine

97
Q

is fentanyl a high alert medication

A

yes

98
Q

indiction of parenteral fentanyl

A

used in combination with other agents for induction & maintenance of surgical anesthesia

99
Q

indication of transdermal fentanyl

A

life-threatening respiratory depression is a special concern with transdermal patch because of delayed onset of effects

100
Q

fentanyl should only be used with patents who are

A

opioid tolerant and should not be used to in patients who are not opioid tolerant

101
Q

drug class of pentazocine

A

Opioid agonist-antagonist; analgesic

102
Q

pentazocine is ____ of kappa receptor and ____ of mu receptor

A

agonist of kappa receptors; weak antagonist of MU receptor

103
Q

Indication for pentazocine

A

moderate pain

104
Q

Route for pentazocine

A

PO only

105
Q

what can pentazocine do to a patient who is physically dependent on a pure opioid agonist?

A

can precipitate withdraw symptoms

106
Q

lidocaine is a

A

Topical analgesic, local anesthetic

107
Q

Route for lidocaine

A

aerosol spray, cream, gel, lotion, ointment, patch, solution

108
Q

MoA: lidocaine

A

Blocks both the initiation & conduction of nerve impulses by decreasing the neuronal membrane’s permeability to Na+ ions

Inhibition of depolarization—-> blockage of pain conduction

109
Q

Only NSAID given via IV

A

Ketorolac

110
Q

Opioid antagonists

A

Brind strongly to opioid receptors without receptor activation

  • – Block effects of narcotics
  • –useful in reversing narcotic respiratory depression or hypotension
111
Q

Acute narcotic abstinence syndrome

A 
Nausea/vomiting 
Sweating 
Tachycardia 
Hypertension 
Tremors 
Anxiety
112
Q

Opioid antagonists indications

A

Reverses the effects of narcotics, manages known or suspected narcotic overdose

113
Q

Naltrexone

A

used orally in the management of alcohol or narcotic dependence

114
Q

Naloxone route

A

Iv, Im, SQ, via ETT

115
Q

Naloxone acts as

A

a competitive antagonist at opioid receptors —> blocking opioid actions

116
Q

Naloxone reverses adverse side effects of opioids like

A

Respiratory depression, sedation, euphoria, coma, analgesia

117
Q

Naloxone has a _____ metabolism

A

High first pass metabolism (give IV)

118
Q

Naoloxone must be given in ___ doses

A

Small doses until adequate response is recieved

119
Q

Half life of naloxone

A

short, will require repeat dosing

120
Q

Sedation scale 1

A

Awake and alert

121
Q

Sedation scale 2

A

Slightly drowsy, easily aroused

122
Q

Sedation scale 3

A

frequently drowsy, arousable, drifts off to sleep during conversation

123
Q

Sedation scale 4

A

somnolent, minimal or no response to physical stimulation

124
Q

Tolerance

A

a decerase in sensitivity to opioids resulting in less effect from the same dose, or the need for progressively larger doses to maintain the same effect

125
Q

Physical dependence

A

A physiological adaptation to a drug characterized by the emergence of a withdrawal syndrome if the drug is abruptly stopped, reduced in dose, or antagonized

126
Q

Addiction

A

A pattern of compulsive drug use characterized by a continued craving for the drug & the need to experience its psychic effects & not pain relief; characterized by

  1. loss of control over the drug use
  2. compulsive use
  3. continued use despite harm
127
Q

Pseudoaddiction

A

drug seeking behavior caused by need for better pain relief

128
Q

Is acetaminophen anti-inflammatory?

A

No!

129
Q

What to avoid when giving acetaminophen

A

Individuals who drink and have a toxic liver

130
Q

Acetaminophen is “good for” individuals who

A
  • Have peptic ulcer
  • Hemophilia
  • Children with viral infection

-Good alternative for NSAIDS to decrease risk of bleeding

131
Q

does acetaminophen cause GI problems

A

Rarely, but can still happen!

132
Q

NSAIDs are not good for individuals with

A
  • Renal failure
  • Peptic ulcers
  • Asthma
  • Hypertension
  • taking anticoagulants
133
Q

In general, NSAIDS moA

A

Inhibit cyclooxyenase (COX)

134
Q

Inhibiting COX 1 can cause

A

Vasoconstriction
Bronchoconstriction
Decrease in renal and GI protection
Deceased platelet aggregation

135
Q

Non-selective non-salicylates

A

Ibuprofen
Meloxicam
Ketorolac

136
Q

Although ketorlac is a non-selective non salicylate, which COX are they more “drawn to”

A

Cox 1

137
Q

Cox 2 decreases or prevents

A

Inflammation and fever

138
Q

Does cox 2 cause decrease platelet aggregation?

A

No, COX 2 normally inhibits platelet aggr. but since celecoxib inhibits COX 2, it may promote it rather than inhibit

139
Q

Inhibiting Cox 2 causes an increase risk of

A

Myocardial infarction/stroke

140
Q

Inhibiting COX 2 causes

A
  • Decrease inflammation and fever
  • Decrease pain sensitivity
  • Inhibits the decreasing of platelet aggregation
141
Q

Opioid antagonists reverse

A

Hypotension and respiratory depression

142
Q

Side effects of opioid antagonist

A

Hypertension
tachycardia
sweating
anxiety

143
Q

Opioids =

A

low and slow vitals

Decreased HR, BP, RR, Brain

144
Q

Opioids should be avoided for

A

Old individuals
pregnant
hypotension
hepatic or renal failure

145
Q

high risk for death and how to prioritize

A
  • advanced age 70<
  • pulmonary disease
  • Post surgery

Choose patient that is oldest and then the most recent surgery

146
Q

Do opioids have any fever/inflammation reduction effects?

A

NO

147
Q

Common side effects of opioid agonists that does not cause alert

A
  • burning when injecting
  • Itching
  • Nausea/vomitting
148
Q

What side effects call for opioid antagonist

A

Respiratory rate <12
Unarousable
Falling asleep while talking

149
Q

What should you do before giving a new fentanyl patch?

A

Remove the first before adding the second

150
Q

Pain is classifies in terms of

A
  • Onset and duration
  • source
  • disease or other conditions that cause it
151
Q

nociception

A

sensation of perception of pain; processing of pain signals

152
Q

Nocireceptors

A
  • subclass of sensory nerves ( A&C) that transmit pain signals to cranial nervous system from other body parts; have free nerve endings that are found in most tissues in the body
153
Q

Nociceptors respond to

A

Noxious stimuli

154
Q

Examples of noxious stimuli

A

thermal, chemical, mechanical

155
Q

How do nociceptors perform a protective function

A

identifying changes that may endanger the body

156
Q

A-delta and A-beta fibers are

A

Afferent nerve fibers

157
Q

A delta fibers are

A

most myelinated, large diameter

FAST

158
Q

A delta fibers are responsible for

A

Acute, sharp pain

159
Q

A-beta fiber is the second most

A

myelinated, 2nd fastest, and second in diameter

160
Q

A beta fiber are

A

Sensitive

161
Q

Stimulation of A-beta fibers can

A

prevent nociceptive fibers from reaching high center in the brain, which reduce pain

162
Q

are C-fibers myelinated?

A

No they are unmyelinated with a small diameter and slow

163
Q

C-fiber is responsible for

A

Fibromyalgia, aching, and chronic pain

164
Q

Most numerous type of nociceptor

A

C-fiber

165
Q

How can A-delta or C-fiber be overridden?

A

Stimulation of A-beta can override stimulus

166
Q

Gating mechanism is located in the

A

Dorsal horn of the spinal cord

167
Q

Opening/closing of the spinothalamic response to C fiber activity can be induced by

A
  • Stimulating mechanoreceptive afferent

- Efferent stimulation from the brain, which inhibit transmission

168
Q

When nerves receive non-painful signals such as vibration or cold,

A

the brain closes the gate on the pain signals

169
Q

If gate is open, then

A

Pain impulses reach the brain

170
Q

gate is closed by incoming impulses from large fibers or from the brain, how is gate opened?

A

impulses from smaller fibers

171
Q

Nociception involves 4 basic processes

A

Transduction
Transmission
Perception
Modulation

172
Q

Acute inflammation characterized by

A

Localized signs: redness, swelling, pain and loss of function

173
Q

Systemic signs of acute inflammation

A

Pyrexia and leukocytosis (Increase WBC)

174
Q

Intracellular cation, Potassium, causes

A

increase sensitivity to pain

175
Q

Serotonin (5HT) causes

A

Capillary vasodilation and increase permeability

- warmth and localized swelling

176
Q

Bradykinin (BK) results in q

A

Increase sensitivity to pain

177
Q

Histamine (H)

A

Capillary vasodilation and increase permeability

- warmth and localized swelling

178
Q

Prostaglandins (PG) results in

A

Increase sensitivity to pain and vasodilation

179
Q

Substance P )SP results in

A

Transmit pain to higher brain centers

316 Pharmacology (19 decks)

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