Exam 1: Pharmacologic management, Pain and Inflammation Flashcards
1
Q
Duge classification: Prednisone
A
Corticosteroid; anti-inflammatory
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
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)
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
5
Q
three broad categories of medications when treating a patient with acute pain
A
- Non-opioid analgesics
- Opioid analgesics
- Analgesic adjuvants
6
Q
Analgesia
A
the relief of pain without loss of consciousness
7
Q
Non- opioid
A
Medications that reduce inflammation &/or pain arising from injured tissue; exert analgesic, anti-inflammatory, & Antipyretic effects
8
Q
Discontinuation of corticosteroids should be
A
Done slowly! (usually over 7 days)
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
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)
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
12
Q
What drug classification should be considered initially for pain management
A
Non-opioid analgesics
13
Q
All medication of non opioid are _____ except for ____
A
NSAIDS! except for acetaminophen
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)
15
Q
Examples of non-opioid analgesics
A
Acetaminophen
aspirin
ibuprofen
ketoralac
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
17
Q
Primary MoA (NSAIDS):
A
-inhabitation of cyclooxygenase (COX), thereby preventing the formation of prostaglandins, which will decrease pain sensitivity
18
Q
Prostaglandins
A
Group of chemicals found in almost all tissues
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
20
Q
Physiological stimulus triggers what
A
COX 1
21
Q
COX 1 effects
A
TXA 2 (platlete aggreg. vasoconstriction) PGI 2 (vasodilation, GI-mucosal protection) PGE1/PGE2 (Kidney, GI-Tract, CNS)
22
Q
Inflammatory stimulus effects
A
COX2
23
Q
COX 2 effects
A
Inflammatory site
—-Causes pain sensitization, vasodilation
24
Q
Many Nsaids are
A
Non-selective, so they inhibit both COX 1 & 2
25
Why are NSAIDS hard on the stomach
Because it's non-selective, it blocks COX 1 protection
| ----- Blocking Cox 1 can cause ulcers, blood thinning, urinary tract issues
26
Cox 1 is
Constitutive
27
Cox 2 is
Inducible
28
Aspirin drug classification
- Salicylate
- NSAID
- Antiplatelet agent
29
Non-selective inhibitor of COX causes
Anti-inflammatory
Analgesic
Antipyretic
Anti-platelet
30
Salicylates
type of drugs found in many OTC
| Aspirin is the most common
31
Indication: Aspirin
mild to moderate pain, fever, myalgia
32
MoA: Aspirin
-Inhibits cyclooxygenase (COX) in periphery, decrease pain and inflammation
-blocks effects of PG synthesis at hypothalamus, which decrease fever
-
33
Adverse effects for aspirer are rare when
taken short term at normal doses
34
Side effects of aspirin
- -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
35
Cautions with aspirin
- 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
35
Cautions with aspirin
- 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
36
take Aspirin with a
Full glass of water, enteric coated can also help decrease stomach irritation
37
Salicylism
toxic effects of OD with salicylic acid or its salts
38
side effects of salicylates
- Dizziness
- tinnitus
- nausea/vomiting
- fluid and electrolyte deficiencies
- metal confusion, lethargy
- fever
- Hyperventilation
39
Non-salicylate NSAIDS
-analgesic
-Anti-inflammatory
-antipyretic
Gastric ulceration & Renal impairment!!!!
40
Opposed to salicylate NSAIDS, Non-salicylate NSAIDs inhibit
platelet aggregation by REVERSIBLY inhabiting prostaglandin synthesis
41
Inhibition of platelet aggregation last only as long
as there is an effective serum drug concentration
42
Non salicylate NSAIDS do NOT
protect against MI, TIA, Stroke
43
NSAIDS may increase risk of
Thrombotic events
44
Salicylate NSAIDS MOA (one difference from Non-salicylate)
irreversibly inhibits platelet aggregation by blocking formation of thromboxane A2
45
Drug Classification: Ibuprofen
Non-salicylate, NSAID, Propionic acid derivative
46
Indictions: Ibuprofen
Milt to moderate pain , fever, and inflammation, dysmenorrhea, musculoskeletal pain; chronic treatment or rheumatoid & osteoarthritis
47
MoA of Ibuprofen
Inhibits prostaglandin synthesis by blocked COX (inhibits both cox 1 & 2)
48
Ibuprofen causes less
gastric bleeding and less platelet aggregation inhibition than aspirin
49
Ibuprofen black box warning
- 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
50
Drug classification of Ketorolac
Non-salicylate, NSAID, acetic acid derivative
51
Ketorolac is used for ______ relief of moderate to sever pain
Short term
52
indication for ketorolac
- Powerful analgesic
- Post-operative pain, as effective as morphine
- minimal anti-inflammatory actions
53
Route for ketorolac
IM, IV, PO, Ophthalmic, intranasal
54
Side effects: Ketorolac
- very high potential for GI bleeding (increase Cox 1 selectivity)
- do not combine with other NSAIDS
55
How long should onetime ketorolac
No more than 5 days
56
ketorolac is contraindicated in patients with
renal impairment and peptic ulcer disease
57
ketorolac black box warning
- inhibit platelet function
- increased risk of CV thrombotic events, MI, stroke
- increase risk for gastrointestinal irritation, inflammation, ulceration, bleeding, and perforation
58
Maximum daily use of ketorolac
40 mg
59
Drug classification of celecoxib
Non-salicylate, NSAID, Selective COX-2 inhibitor
60
MoA & therapeutic effect: Celecoxib
selective inhibition of COX 2 which decreases pain and inflammation
61
Does celecoxib inhibit platelet aggregation?
NO! because it does not target COX 1
62
Use celecoxib cautiously with patents who have
Cardiovascular risk factors
- hypetension
- DM
- Dyslipidemia
63
Drug class: Acetaminophen
Non-NSAID, Antipyretic, non-opioid analgesic
64
Route of acetaminophen
PO, PR, IV for post op
65
Indication from acetaminophen
- 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)
66
Is acetaminophen an NSAID?
NO
67
How does acetaminophen differ from NSAIDS?
They are more central analgesic effect (Blockage of central PGs)
68
Acetaminophen has fewer side effects compared to NSAIDS like
- no anti-inflammatory effects
- no anti-platelet effects
- rarely causes GI problems
69
Acetaminophen may cause
HEPATOTOXICITY, hepatic necrosis, liver failure
70
Antidotes for acetaminophen OD
- acetylcysteine
| - give within 8 hours of ingestion
71
Acetaminophen should no exceed
4 g/day, 3000mg/day for extra strength, and 3250mg for regular strength
72
What kind of injury and hypersensitivity reaction occur with acetaminophen
liver injury and hypersensitivity reactions like anaphylaxis
73
Opioids are divided into 2 groups
1. agonists (pure agonists, mu receptor)
| 1. agonist-antagonist (Mu and KAPPA receptor)
74
opioids are used for
Moderate to severe pain; preoperative sedation and reduction of anxiety
75
Opioids bind to
opioid receptors producing effects that mimic the action of endogenous opioids
76
example of opioids that are available with aspirin or Tylenol
Vicodin, Percocet
77
examples of opioids
```
morphine
codeine
fentanyl
hydrocodone
hydromorphone
oxycodone
```
78
opioid agonists mimic
effects of naturally occurring opioids (endorphins, enkephalins)
79
three main opioid receptors
Mu
Kappa
Delta
80
Most important receptors in pharmacology
Mu
| Kappa
81
opioid receptors in the body
```
brain
brainstem
spinal cord
peripheral neurons
intestine
```
82
3 therapeutic effects of opioids
- analgesia
- sedation
- euphoria
83
3 non therapeutic effects of opioids
- respiratory depression
- constipation
- dependency/addiction
84
other effects of opioids
```
orthostatic hypotension
decrease cough reflex
miosis
emesis
urinary retention
urticaria
increase intracranial pressure
```
85
Drug to drug consideration for opioids
- 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
morphine sulfate is a
prototype opioid analgesic
87
routes of morphine sulfate
PO, IM, IV, SQ, epidural, intrathecal
88
MoA morphine sulfate
Primarily binds to MU receptors, mimicking the action of endogenous opiods, producing multiple pharmacological effects
89
morphine sulfate main therapeutic effect
analgesia
90
Morphine sulfate have a significant ________
first pass metabolism (rarely given PO)
91
Repeated use of morphine sulfate use can produce a tolerance to
respiratory depressant
analgesic
euphoric
sedative effects
92
If someone is given opioids but has a respiratory rate of less than 8-10, what do you do?
Hold the mediation and CONTACT PROVIDER!
| Cannot give something different without provider approval
93
is morphine sulfate a high alert medication
yes, it has a heightened risk of causing significant patient harm
94
drug class: fentanyl
Opioid agonist
95
route of fentanyl
Parenteral
Transdermal
Transmucosal
epidural , intrathecal
96
Potency of fentanyl
High potency: 100 times that of morphine
97
is fentanyl a high alert medication
yes
98
indiction of parenteral fentanyl
used in combination with other agents for induction & maintenance of surgical anesthesia
99
indication of transdermal fentanyl
life-threatening respiratory depression is a special concern with transdermal patch because of delayed onset of effects
100
fentanyl should only be used with patents who are
opioid tolerant and should not be used to in patients who are not opioid tolerant
101
drug class of pentazocine
Opioid agonist-antagonist; analgesic
102
pentazocine is ____ of kappa receptor and ____ of mu receptor
agonist of kappa receptors; weak antagonist of MU receptor
103
Indication for pentazocine
moderate pain
104
Route for pentazocine
PO only
105
what can pentazocine do to a patient who is physically dependent on a pure opioid agonist?
can precipitate withdraw symptoms
106
lidocaine is a
Topical analgesic, local anesthetic
107
Route for lidocaine
aerosol spray, cream, gel, lotion, ointment, patch, solution
108
MoA: lidocaine
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
Only NSAID given via IV
Ketorolac
110
Opioid antagonists
Brind strongly to opioid receptors without receptor activation
- -- Block effects of narcotics
- --useful in reversing narcotic respiratory depression or hypotension
111
Acute narcotic abstinence syndrome
```
Nausea/vomiting
Sweating
Tachycardia
Hypertension
Tremors
Anxiety
```
112
Opioid antagonists indications
Reverses the effects of narcotics, manages known or suspected narcotic overdose
113
Naltrexone
used orally in the management of alcohol or narcotic dependence
114
Naloxone route
Iv, Im, SQ, via ETT
115
Naloxone acts as
a competitive antagonist at opioid receptors ---> blocking opioid actions
116
Naloxone reverses adverse side effects of opioids like
Respiratory depression, sedation, euphoria, coma, analgesia
117
Naloxone has a _____ metabolism
High first pass metabolism (give IV)
118
Naoloxone must be given in ___ doses
Small doses until adequate response is recieved
119
Half life of naloxone
short, will require repeat dosing
120
Sedation scale 1
Awake and alert
121
Sedation scale 2
Slightly drowsy, easily aroused
122
Sedation scale 3
frequently drowsy, arousable, drifts off to sleep during conversation
123
Sedation scale 4
somnolent, minimal or no response to physical stimulation
124
Tolerance
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
Physical dependence
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
Addiction
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
Pseudoaddiction
drug seeking behavior caused by need for better pain relief
128
Is acetaminophen anti-inflammatory?
No!
129
What to avoid when giving acetaminophen
Individuals who drink and have a toxic liver
130
Acetaminophen is "good for" individuals who
- Have peptic ulcer
- Hemophilia
- Children with viral infection
-Good alternative for NSAIDS to decrease risk of bleeding
131
does acetaminophen cause GI problems
Rarely, but can still happen!
132
NSAIDs are not good for individuals with
- Renal failure
- Peptic ulcers
- Asthma
- Hypertension
- taking anticoagulants
133
In general, NSAIDS moA
Inhibit cyclooxyenase (COX)
134
Inhibiting COX 1 can cause
Vasoconstriction
Bronchoconstriction
Decrease in renal and GI protection
Deceased platelet aggregation
135
Non-selective non-salicylates
Ibuprofen
Meloxicam
Ketorolac
136
Although ketorlac is a non-selective non salicylate, which COX are they more "drawn to"
Cox 1
137
Cox 2 decreases or prevents
Inflammation and fever
138
Does cox 2 cause decrease platelet aggregation?
No, COX 2 normally inhibits platelet aggr. but since celecoxib inhibits COX 2, it may promote it rather than inhibit
139
Inhibiting Cox 2 causes an increase risk of
Myocardial infarction/stroke
140
Inhibiting COX 2 causes
- Decrease inflammation and fever
- Decrease pain sensitivity
- Inhibits the decreasing of platelet aggregation
141
Opioid antagonists reverse
Hypotension and respiratory depression
142
Side effects of opioid antagonist
Hypertension
tachycardia
sweating
anxiety
143
Opioids =
low and slow vitals
Decreased HR, BP, RR, Brain
144
Opioids should be avoided for
Old individuals
pregnant
hypotension
hepatic or renal failure
145
high risk for death and how to prioritize
- advanced age 70<
- pulmonary disease
- Post surgery
Choose patient that is oldest and then the most recent surgery
146
Do opioids have any fever/inflammation reduction effects?
NO
147
Common side effects of opioid agonists that does not cause alert
- burning when injecting
- Itching
- Nausea/vomitting
148
What side effects call for opioid antagonist
Respiratory rate <12
Unarousable
Falling asleep while talking
149
What should you do before giving a new fentanyl patch?
Remove the first before adding the second
150
Pain is classifies in terms of
- Onset and duration
- source
- disease or other conditions that cause it
151
nociception
sensation of perception of pain; processing of pain signals
152
Nocireceptors
- 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
Nociceptors respond to
Noxious stimuli
154
Examples of noxious stimuli
thermal, chemical, mechanical
155
How do nociceptors perform a protective function
identifying changes that may endanger the body
156
A-delta and A-beta fibers are
Afferent nerve fibers
157
A delta fibers are
most myelinated, large diameter
| FAST
158
A delta fibers are responsible for
Acute, sharp pain
159
A-beta fiber is the second most
myelinated, 2nd fastest, and second in diameter
160
A beta fiber are
Sensitive
161
Stimulation of A-beta fibers can
prevent nociceptive fibers from reaching high center in the brain, which reduce pain
162
are C-fibers myelinated?
No they are unmyelinated with a small diameter and slow
163
C-fiber is responsible for
Fibromyalgia, aching, and chronic pain
164
Most numerous type of nociceptor
C-fiber
165
How can A-delta or C-fiber be overridden?
Stimulation of A-beta can override stimulus
166
Gating mechanism is located in the
Dorsal horn of the spinal cord
167
Opening/closing of the spinothalamic response to C fiber activity can be induced by
- Stimulating mechanoreceptive afferent
| - Efferent stimulation from the brain, which inhibit transmission
168
When nerves receive non-painful signals such as vibration or cold,
the brain closes the gate on the pain signals
169
If gate is open, then
Pain impulses reach the brain
170
gate is closed by incoming impulses from large fibers or from the brain, how is gate opened?
impulses from smaller fibers
171
Nociception involves 4 basic processes
Transduction
Transmission
Perception
Modulation
172
Acute inflammation characterized by
Localized signs: redness, swelling, pain and loss of function
173
Systemic signs of acute inflammation
Pyrexia and leukocytosis (Increase WBC)
174
Intracellular cation, Potassium, causes
increase sensitivity to pain
175
Serotonin (5HT) causes
Capillary vasodilation and increase permeability
| - warmth and localized swelling
176
Bradykinin (BK) results in q
Increase sensitivity to pain
177
Histamine (H)
Capillary vasodilation and increase permeability
| - warmth and localized swelling
178
Prostaglandins (PG) results in
Increase sensitivity to pain and vasodilation
179
Substance P )SP results in
Transmit pain to higher brain centers
