Opiods and Pain Flashcards
1
Q
What’s the difference between pain and suffering? (Definition wise)
A
Pain - The physiologic reaction
Suffering - Psychologic aspect of pain
2
Q
A fibers transmit what kind of pain?
A
Sharp acute pain
3
Q
C fibers transmit what kind of pain?
A
Aching pain
4
Q
What is the prototypical drug in the opiate category?
A
Morphine
5
Q
Describe what sorts of pain Morphine can be used to treat
A
Both physiologic and psychologic aspects of pain; decreased perception and response to pain
6
Q
Where are opiate receptors located in the body?
A
Everywhere, but most concentrated along pain pathways (CNS) and GIT
This includes synapses at interneurons
7
Q
Stimulation of an opiate receptor causes what to cAMP?
A
G-protein coupled decrease in adenylate cyclase –> decreasing cAMP in cell
8
Q
With opiate induced low cAMP, what is the end result?
A
Increased K+ efflux and decreased Ca++ influx –> hyperpolarization and less neurotransmitter release
9
Q
Describe what is the suspected most important use of opiates in the body
A
Central nervous system analgesic; many opiate receptors in CNS
10
Q
What is substance P and how do opiates interact with it?
A
Substance P is an excitatory neurotransmitter for pain
Opiates decrease its release
11
Q
What non-opiate ways can one cause analgesia?
A
Electrical stimulation of enkephalinergic neurons, or acupuncture
12
Q
What are the three opiate receptors?
A
Mu, Kappa, Delta
13
Q
Of the three opiate receptors, which produces the best analgesic effects in spinal, supraspinal and peripheral body?
A
Mu
14
Q
Of the opiate receptors, which only produces analgesic effects spinally? Spinal and peripheral?
A
Delta and Kappa
15
Q
Which opiate receptor causes no respiratory depression?
A
Kappa
16
Q
Which opiate receptor causes no pupil constriction
A
Delta
17
Q
Which opiate receptors cause reduced GI motility, and which has the smallest effect on the GI motility?
A
All three (Mu, Delta, Kappa); Kappa has least GIT effects
18
Q
Which opiate receptor causes a sensation of euphoria?
A
Mu
19
Q
Which opiate receptor causes the sensation of dysphoria and psychotomimesis?
A
Kappa
20
Q
Which opiate receptor does not produce sedation?
A
Delta
21
Q
Which opiate receptors produce physical dependence when activated?
A
Mu and Kappa
22
Q
Opium comes from what natural soource?
A
Opium poppy
23
Q
Describe some of the beneficial actions of opium and opiates
A
No loss of consciousness
Less intense pain “cured”
Selective, does not affect other sensations
Euphoria (may become mental clouding)
24
Q
Describe some non-beneficial actions of opium and opiates
A
Drowsiness Nausea/vomiting Decreased VA Apathy Decreased concentration
25
Continuous dull aching pain is best relieved by?
Morphine (C fibers)
26
What happens if you give increasingly higher doses of opiates?
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Increased subjective effects to relieve pain
More euphoria/dysphoria
Decreased respiration
Possible mood alterations
(No incoordination)
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27
What is pinpoint pupil and what causes it?
Pronounced miosis from opiates acting on ANS at the level of Edinger-Westphal nucleus.
28
With enough opiate use, can tolerance be developed to pinpoint pupil? How do you treat pinpoint pupil? Does pinpoint pupil affect any diagnosing?
No tolerance to this
Treat with opiate antagonists (Atropine)
Lowers IOP in normal and glaucoma patients
29
What effect do opiates have on the respiratory system?
SEVERE respiratory depression; decreased responsiveness to pCO2 and depression of respiratory control centers in brain --> accumulating more CO2 and not breathing it out fast enough
30
Due to opiate effects on respiration, how would opiates affect a cough? What population groups may be severely affected by opiates?
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Antitussive effect (cough suppressive) directly acting on cough control centers
Elderly patients, Chronic Obstructive Pulmonary DIsease patients (COPD)
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31
The nausea and vomiting caused by opiates is a result of stimulating what area?
Chemoreceptor zone
32
In an untreated epileptic patient, what may happen with opiate administration?
Convulsions
33
What effect do opiates have on the cardiovascular system?
Dilating resistance and capacitance vessels (arteries/veins)
34
Describe some cautions and contraindications for opiates just based on the cardiovascular effects seen
Do not use in cases of higher intracranial pressure (head trauma)
Caution for patients in shock
35
What is the most significant effect opiates have on the GI tract?
Anti-diarrheal; increased smooth muscle tone, decreased propulsive movements throughout the entire GI tract
Action is local in the muscles and central in nervous system to decrease motility
36
What other side effects can result in the GI tract due to opiates?
Intense biliary/renal/ureteral/colic pain even with opiates in system due to constant contraction
Urinary urgency/difficulty
37
Describe the metabolism of Morphine
Rapid and significant first pass effect (75%) not effective orally
Is bound by glucuronide and is put into enterohepatic re-circulation loop.
Well absorbed subcutaneously, intramuscular or IV
38
Describe two uses for opioid receptor antagonists
Treating opioid overdose
| Severe respiratory depression of unknown cause (rule out or confirm opioid overdose)
39
Describe codeine and how it compares to morphine
Similar structure
1/10th potency subcutaneously, but is orally effective
Must be given in IV for severe pain
Same toxicities if given at same dose as morphine
40
How is codeine metabolized in the liver?
Turned into morphine
41
What is an 'off-label' use for codeine that isn't pain related?
Antitussive; cough suppressant
42
Describe detromethorphan's uses and effects
Non-narcotic anti-tussive
| Is a dextroisomer of levomethorphan
43
Will detromethorphan be blocked by naloxone (opiate receptor antagonist)?
No, believed to act on non-opioid receptor, might be blocking NMDA receptors instead
44
Describe the dangers of using detromethorphan in terms of toxicities, dependence and the efficacy as an antitussive compared to codeine.
No respiratory depression, analgesia or euphoria
No dependence, fairly safe and OTC
Same anti-tussive ability as codeine
45
How does hydromorphine compare to morphine?
Hydromorphine has five times the potency and a shorter duration of action
46
Describe oxycodone and how it compares to morphine
Same efficacy as morphine, but is orally effective --> highly abused
47
How does vicodin differ from oxycodone?
It's oxycodone with an OH group
48
What is the most frequently prescribed drug in the USA?
Vicodin (hydrocodone with acetaminophen)
49
What is the name of the first synthetic opioid developed?
Meperidine (Demerol)
50
Describe Mepieridine
Different structure than morphine
Higher convulsant risks
Originally thought to be obstetric (didn't cross placenta)
51
What is the use of mepiridine?
Only analgesic, less antitussive and less antidiarrheal effects
1/10th to 1/5th of morphine's potency but all the same side effects
52
Describe a major issue with meperidine
Crosses placenta and depresses fetal respiration
53
What is Diphenoxylate?
Synthetic opioid, often with atropine added to decrease abuse.
Schedule 5 drug and requires prescription
Used for anti-diarrheal
54
What is loperamide?
Completely synthetic opioid, very similar in structure to diphenoxylate but much less abuse
Used for anti-diarrheal effects and available OTC
Poor lipid solubility, cannot go into CNS and stays peripherally and in GI tract.
55
What is Methadone?
Synthetic opioid, excellent opioid but all the same side effects as other opioids
Same potency as morphine but much longer duration
56
What are some non analgesic uses for methadone?
Heroin addiction; flood receptors and negate heroin actions but still on an opioid.
LAAM may be better due to lasting 3 days not 1
57
What is Propoxyphene (Darvo)?
Synthetic opioid
Less potent than codeine (morphine too)
Very significant respiratory depression, especially if combined with CNS depressants.
58
What are the three partial agonist opioids?
Buprenorphine (Buprenex)
| Pentazocine (Talwin)
59
Describe Buprenorphine (Buprenex)
A partial agonist as an opioid.
Equally effective as morphine as an analgesic
Is a partial agonist at mu receptors; an antagonist at kappa receptors
60
Describe Pentazocine (Talwin)
Most frequently used of partial agonist opioids
Is a weak antagonist at mu receptors; gives good analgesic effect at kappa receptors
Low addiction, lower side effects compared to morphine
61
What is a great use for pentazocine?
Treating chronic pain
62
What are the opioid receptor antagonists?
Naloxone
Naltrexone
Tramadol
63
Describe the effects of naloxone and naltrexone
Short acting, reversing effects of endogenous or exogenous opiates in the body
No effects if there are no opiates already in the system
64
Describe Tramadol
Newer analgesic, weak mu receptor binding and inhibits reuptake of NE and 5-HT for some antidepressant effects too
Can cause some dependence, but has a low abuse potential
65
Describe some toxicities with Tramadol
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Dizziniess
Vertigo
CNS stimulation
Constipation
Pruritis (itching)
GI upset
Seizures
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66
Describe the contraindications for opioid use
Head Trauma - Higher pCO2 leading to vasodilation leading to higher pressure
Asthma/Chronic pulmonary disease - Decreased response to pCO2 and lower respiration rate more likely to cause hypoxia
Convulsive Disorders/CNS stimulants - Opioid convulsive action is enhanced in these situations
67
How does opioid tolerance develop?
Based on dose and frequency of dosing.
68
What tolerance develops rapidly in opioid use? What effects don't become tolerated?
Tolerance to respiratory depression is impressive
| Little tolerance to miosis and constipation
69
Describe physical dependence and how it works
The body needing the presence of the drug to operate normally; body has regulated normal function to the level of drug being in the body, removing it causes withdrawal
70
What causes the drug seeking behaviour seen?
Physiologic dependence on the drug and wanting to avoid withdrawal symptoms
71
What are the withdrawal symptoms seen with opioid withdrawal?
(Opposite of morphine's toxicities)
Diarrhea
Increased CNS activity not sedation
Aggression/anxiety
72
How to treat withdrawal symptoms in opioid withdrawal?
Give an opiate
Can resolve in time
Clonidine (Alpha 2 agonist) has some effects
73
Describe the NSAIDs and non-opioid analgesics (generally)
Diverse
Analgesic for mild/moderate pain
Antipyretic (lowers fever)
74
Describe how NSAIDs and non-opioid analgesics interact with inflammation
All except acetaminophen are also anti-inflammatory
75
How do NSAIDs and non-opioid analgesics related to prostaglandin synthesis?
All inhibit prostaglandin synthesis
| Specifically COX
76
Describe common features of aspirin
Most frequently used analgesic, anti-pyretic and anti-inflammatory
Can be used as an anti-platelet (blood thinner)
77
Describe ASA's method of action
Inhibiting prostagalndin synthesis via inhibition of COX substances.
Works in peripheral and central nervous systems
78
What is the suspected role of prostagalndins in pain?
May cause increased response to pain (Hyperaglesia)
79
Describe ASA's antipyretic actions
Decreases fever in therapeutic dose, but not in normals
Promotes vasodilation and sweating
Believed to affect PG synthesis in centrally located hypothalamus
80
Describe ASA's anti-inflammatory actions
Decreasing prostaglandin synthesis, prostaglandins believed to accent inflammatory response.
Will not affect phagocyte aggregation at sites of inflammation however
81
Of the anti-platelet drugs, how effective is ASA?
It is the most effective anti-platelet drug
82
Describe ASA's anti-platelet actions
Irreversible acetylation of COX enzyme inhibiting prostaglandin synthesis in platelets, normal cells not affected heavily as they can regenerate the enzyme
83
Describe ASA's GI actions
NSAIDs and the like cause GI upset to a degree. (Ulceration, perforation, bleeding)
Prostagalndins may have protective function in stomach, you're removing them with ASA
84
Describe ASA's effects on respiration
High doses can lead to respiratory alkalosis due to deeper breathing and faster respiration rate
85
Describe ASA's effects on metabolism.
Uncouples the oxidative phosphorylation
| See a higher heat production and higher oxygen consumption as a result
86
Describe the pharmacokinetics for ASA
Rapidly absorbed after oral administration
Turned to salicyclic acid which is also an active compound
Elimination is dose-dependent (zero-order)
87
What are some common toxicities with NSAIDs and ASA?
GI Tract are the most common (upset, nausea, vomiting, bleeding, ulceration, anemia, bloody stools)
Possible hypersensitivity reaction in those already sensitive to some NSAIDs
Little concentration can cause lethal overdose in children
Intoxication
88
Describe the intoxication that can be produced with ASA or NSAIDs
Continuum of effects
Mild at low doses - Tinnitus, dizziness, headache/confusion
Serious - Salicylism at high doses; nausea, vomiting, dairrhea, hypernea, hemorrhage, acid/base problems, lethality
89
What kind of treatment can be offered with ASA and NSAIDs?
Supportive, fix symptoms
90
What is Reye's Syndrome?
Aspirin given to a child after a flu/chicken pox/viral disease causing nerve and liver damage
91
How can you prevent Reye's Syndrome?
DO NOT give aspirin to children with fever from an undiagnosed disease
92
Describe the uses for acetaminophen and how well it can be used in place of ASA
Popular analgesic and anti-pyretic. Good substitute for ASA
No GI problems, or increased uric acid, no platelet inhibition
Very safe drug
93
How does acetaminophen interact with ASA?
No cross sensitivites
94
Can you use acetaminophen in a child's undiagnosed fever?
Yes, no Reyes syndrome
95
Describe acetaminophen's anti-inflammatory actions
Very little, doesn't work well in the periphery
96
Describe the method of action for acetaminophen
Weak inhibitor of COX enzymes, still inhibits prostaglandin synthesis but mostly centrally.
97
Describe the toxicities for acetaminophen
Minimal at therapeutic doses
Overdose can cause serious problems (hepatic necrosis, renal necrosis, hypoglycemia, coma, death)
See early symptoms of overdose in first 24 hours; Mild nausea, anorexia, pain, hepatic damage in first days, bleeding, jaundice leading to death
98
In the event of an acetaminophen overdose, how can you treat it?
Treat EARLY
| Give N-Acetyl cysteine (key piece for glutathione) to treat overdose
99
What is the aspirin triad?
Increased risk of aspirin sensitivity in patients with asthma or nasal polyps or chronic urtiacaria
Allergic conditions but in the absence of an actual aspirin allergy.
100
Describe the toxicity profile in chronic NSAID use
Higher risk of GI problems and fluid accumulation due to kidney effects
101
What is the ocular symptom that can occur with NSAIDs?
Diffuse retinal stromal deposits
EOM abnormalities
Color Vision Disturbances
Toxic amblyopia
Blurry vision when on medications requires eye exam
102
What is Indomethacin (Indocin)?
Most potent NSAID and used for last resort treatment
| More frequent toxicities; GI, HEADACHE, and all standard NSAID toxicities
103
What is the name of the new relatively selective COX-2 inhibitor?
Celecoxib
Little action on platelet aggregation or GI tract
Contraindicated in ASA sensitivity
104
Describe the contraindications of all NSAIDs
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Known allergic hypersensitivity
NSAID induced asthma or urticarial
Presence of Aspirin Triad
Pregnancy in 3rd term
Coronary Artery Bypass Grafting surgery (periop pain)
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