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Pharmacology II > Opiods and Pain > Flashcards

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

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2
Q

A fibers transmit what kind of pain?

A

Sharp acute pain

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3
Q

C fibers transmit what kind of pain?

A

Aching pain

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4
Q

What is the prototypical drug in the opiate category?

A

Morphine

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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

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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

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7
Q

Stimulation of an opiate receptor causes what to cAMP?

A

G-protein coupled decrease in adenylate cyclase –> decreasing cAMP in cell

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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

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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

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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

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11
Q

What non-opiate ways can one cause analgesia?

A

Electrical stimulation of enkephalinergic neurons, or acupuncture

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12
Q

What are the three opiate receptors?

A

Mu, Kappa, Delta

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13
Q

Of the three opiate receptors, which produces the best analgesic effects in spinal, supraspinal and peripheral body?

A

Mu

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14
Q

Of the opiate receptors, which only produces analgesic effects spinally? Spinal and peripheral?

A

Delta and Kappa

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15
Q

Which opiate receptor causes no respiratory depression?

A

Kappa

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16
Q

Which opiate receptor causes no pupil constriction

A

Delta

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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

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18
Q

Which opiate receptor causes a sensation of euphoria?

A

Mu

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19
Q

Which opiate receptor causes the sensation of dysphoria and psychotomimesis?

A

Kappa

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20
Q

Which opiate receptor does not produce sedation?

A

Delta

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21
Q

Which opiate receptors produce physical dependence when activated?

A

Mu and Kappa

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22
Q

Opium comes from what natural soource?

A

Opium poppy

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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)

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24
Q

Describe some non-beneficial actions of opium and opiates

A 
Drowsiness
Nausea/vomiting
Decreased VA
Apathy
Decreased concentration
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25
Q

Continuous dull aching pain is best relieved by?

A

Morphine (C fibers)

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26
Q

What happens if you give increasingly higher doses of opiates?

A 
Increased subjective effects to relieve pain
More euphoria/dysphoria
Decreased respiration
Possible mood alterations
(No incoordination)
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27
Q

What is pinpoint pupil and what causes it?

A

Pronounced miosis from opiates acting on ANS at the level of Edinger-Westphal nucleus.

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28
Q

With enough opiate use, can tolerance be developed to pinpoint pupil? How do you treat pinpoint pupil? Does pinpoint pupil affect any diagnosing?

A

No tolerance to this
Treat with opiate antagonists (Atropine)
Lowers IOP in normal and glaucoma patients

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29
Q

What effect do opiates have on the respiratory system?

A

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

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30
Q

Due to opiate effects on respiration, how would opiates affect a cough? What population groups may be severely affected by opiates?

A 
Antitussive effect (cough suppressive) directly acting on cough control centers
Elderly patients, Chronic Obstructive Pulmonary DIsease patients (COPD)
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31
Q

The nausea and vomiting caused by opiates is a result of stimulating what area?

A

Chemoreceptor zone

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32
Q

In an untreated epileptic patient, what may happen with opiate administration?

A

Convulsions

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33
Q

What effect do opiates have on the cardiovascular system?

A

Dilating resistance and capacitance vessels (arteries/veins)

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34
Q

Describe some cautions and contraindications for opiates just based on the cardiovascular effects seen

A

Do not use in cases of higher intracranial pressure (head trauma)
Caution for patients in shock

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35
Q

What is the most significant effect opiates have on the GI tract?

A

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

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36
Q

What other side effects can result in the GI tract due to opiates?

A

Intense biliary/renal/ureteral/colic pain even with opiates in system due to constant contraction
Urinary urgency/difficulty

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37
Q

Describe the metabolism of Morphine

A

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

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38
Q

Describe two uses for opioid receptor antagonists

A

Treating opioid overdose

Severe respiratory depression of unknown cause (rule out or confirm opioid overdose)

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39
Q

Describe codeine and how it compares to morphine

A

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

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40
Q

How is codeine metabolized in the liver?

A

Turned into morphine

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41
Q

What is an ‘off-label’ use for codeine that isn’t pain related?

A

Antitussive; cough suppressant

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42
Q

Describe detromethorphan’s uses and effects

A

Non-narcotic anti-tussive

Is a dextroisomer of levomethorphan

43
Q

Will detromethorphan be blocked by naloxone (opiate receptor antagonist)?

A

No, believed to act on non-opioid receptor, might be blocking NMDA receptors instead

44
Q

Describe the dangers of using detromethorphan in terms of toxicities, dependence and the efficacy as an antitussive compared to codeine.

A

No respiratory depression, analgesia or euphoria
No dependence, fairly safe and OTC
Same anti-tussive ability as codeine

45
Q

How does hydromorphine compare to morphine?

A

Hydromorphine has five times the potency and a shorter duration of action

46
Q

Describe oxycodone and how it compares to morphine

A

Same efficacy as morphine, but is orally effective –> highly abused

47
Q

How does vicodin differ from oxycodone?

A

It’s oxycodone with an OH group

48
Q

What is the most frequently prescribed drug in the USA?

A

Vicodin (hydrocodone with acetaminophen)

49
Q

What is the name of the first synthetic opioid developed?

A

Meperidine (Demerol)

50
Q

Describe Mepieridine

A

Different structure than morphine
Higher convulsant risks
Originally thought to be obstetric (didn’t cross placenta)

51
Q

What is the use of mepiridine?

A

Only analgesic, less antitussive and less antidiarrheal effects
1/10th to 1/5th of morphine’s potency but all the same side effects

52
Q

Describe a major issue with meperidine

A

Crosses placenta and depresses fetal respiration

53
Q

What is Diphenoxylate?

A

Synthetic opioid, often with atropine added to decrease abuse.
Schedule 5 drug and requires prescription
Used for anti-diarrheal

54
Q

What is loperamide?

A

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
Q

What is Methadone?

A

Synthetic opioid, excellent opioid but all the same side effects as other opioids
Same potency as morphine but much longer duration

56
Q

What are some non analgesic uses for methadone?

A

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
Q

What is Propoxyphene (Darvo)?

A

Synthetic opioid
Less potent than codeine (morphine too)
Very significant respiratory depression, especially if combined with CNS depressants.

58
Q

What are the three partial agonist opioids?

A

Buprenorphine (Buprenex)

Pentazocine (Talwin)

59
Q

Describe Buprenorphine (Buprenex)

A

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
Q

Describe Pentazocine (Talwin)

A

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
Q

What is a great use for pentazocine?

A

Treating chronic pain

62
Q

What are the opioid receptor antagonists?

A

Naloxone
Naltrexone
Tramadol

63
Q

Describe the effects of naloxone and naltrexone

A

Short acting, reversing effects of endogenous or exogenous opiates in the body
No effects if there are no opiates already in the system

64
Q

Describe Tramadol

A

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
Q

Describe some toxicities with Tramadol

A 
Dizziniess
Vertigo
CNS stimulation
Constipation
Pruritis (itching)
GI upset
Seizures
66
Q

Describe the contraindications for opioid use

A

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
Q

How does opioid tolerance develop?

A

Based on dose and frequency of dosing.

68
Q

What tolerance develops rapidly in opioid use? What effects don’t become tolerated?

A

Tolerance to respiratory depression is impressive

Little tolerance to miosis and constipation

69
Q

Describe physical dependence and how it works

A

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
Q

What causes the drug seeking behaviour seen?

A

Physiologic dependence on the drug and wanting to avoid withdrawal symptoms

71
Q

What are the withdrawal symptoms seen with opioid withdrawal?

A

(Opposite of morphine’s toxicities)
Diarrhea
Increased CNS activity not sedation
Aggression/anxiety

72
Q

How to treat withdrawal symptoms in opioid withdrawal?

A

Give an opiate
Can resolve in time
Clonidine (Alpha 2 agonist) has some effects

73
Q

Describe the NSAIDs and non-opioid analgesics (generally)

A

Diverse
Analgesic for mild/moderate pain
Antipyretic (lowers fever)

74
Q

Describe how NSAIDs and non-opioid analgesics interact with inflammation

A

All except acetaminophen are also anti-inflammatory

75
Q

How do NSAIDs and non-opioid analgesics related to prostaglandin synthesis?

A

All inhibit prostaglandin synthesis

Specifically COX

76
Q

Describe common features of aspirin

A

Most frequently used analgesic, anti-pyretic and anti-inflammatory
Can be used as an anti-platelet (blood thinner)

77
Q

Describe ASA’s method of action

A

Inhibiting prostagalndin synthesis via inhibition of COX substances.
Works in peripheral and central nervous systems

78
Q

What is the suspected role of prostagalndins in pain?

A

May cause increased response to pain (Hyperaglesia)

79
Q

Describe ASA’s antipyretic actions

A

Decreases fever in therapeutic dose, but not in normals
Promotes vasodilation and sweating
Believed to affect PG synthesis in centrally located hypothalamus

80
Q

Describe ASA’s anti-inflammatory actions

A

Decreasing prostaglandin synthesis, prostaglandins believed to accent inflammatory response.
Will not affect phagocyte aggregation at sites of inflammation however

81
Q

Of the anti-platelet drugs, how effective is ASA?

A

It is the most effective anti-platelet drug

82
Q

Describe ASA’s anti-platelet actions

A

Irreversible acetylation of COX enzyme inhibiting prostaglandin synthesis in platelets, normal cells not affected heavily as they can regenerate the enzyme

83
Q

Describe ASA’s GI actions

A

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
Q

Describe ASA’s effects on respiration

A

High doses can lead to respiratory alkalosis due to deeper breathing and faster respiration rate

85
Q

Describe ASA’s effects on metabolism.

A

Uncouples the oxidative phosphorylation

See a higher heat production and higher oxygen consumption as a result

86
Q

Describe the pharmacokinetics for ASA

A

Rapidly absorbed after oral administration
Turned to salicyclic acid which is also an active compound
Elimination is dose-dependent (zero-order)

87
Q

What are some common toxicities with NSAIDs and ASA?

A

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
Q

Describe the intoxication that can be produced with ASA or NSAIDs

A

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
Q

What kind of treatment can be offered with ASA and NSAIDs?

A

Supportive, fix symptoms

90
Q

What is Reye’s Syndrome?

A

Aspirin given to a child after a flu/chicken pox/viral disease causing nerve and liver damage

91
Q

How can you prevent Reye’s Syndrome?

A

DO NOT give aspirin to children with fever from an undiagnosed disease

92
Q

Describe the uses for acetaminophen and how well it can be used in place of ASA

A

Popular analgesic and anti-pyretic. Good substitute for ASA
No GI problems, or increased uric acid, no platelet inhibition
Very safe drug

93
Q

How does acetaminophen interact with ASA?

A

No cross sensitivites

94
Q

Can you use acetaminophen in a child’s undiagnosed fever?

A

Yes, no Reyes syndrome

95
Q

Describe acetaminophen’s anti-inflammatory actions

A

Very little, doesn’t work well in the periphery

96
Q

Describe the method of action for acetaminophen

A

Weak inhibitor of COX enzymes, still inhibits prostaglandin synthesis but mostly centrally.

97
Q

Describe the toxicities for acetaminophen

A

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
Q

In the event of an acetaminophen overdose, how can you treat it?

A

Treat EARLY

Give N-Acetyl cysteine (key piece for glutathione) to treat overdose

99
Q

What is the aspirin triad?

A

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
Q

Describe the toxicity profile in chronic NSAID use

A

Higher risk of GI problems and fluid accumulation due to kidney effects

101
Q

What is the ocular symptom that can occur with NSAIDs?

A

Diffuse retinal stromal deposits
EOM abnormalities
Color Vision Disturbances
Toxic amblyopia

Blurry vision when on medications requires eye exam

102
Q

What is Indomethacin (Indocin)?

A

Most potent NSAID and used for last resort treatment

More frequent toxicities; GI, HEADACHE, and all standard NSAID toxicities

103
Q

What is the name of the new relatively selective COX-2 inhibitor?

A

Celecoxib
Little action on platelet aggregation or GI tract
Contraindicated in ASA sensitivity

104
Q

Describe the contraindications of all NSAIDs

A 
Known allergic hypersensitivity
NSAID induced asthma or urticarial
Presence of Aspirin Triad
Pregnancy in 3rd term
Coronary Artery Bypass Grafting surgery (periop pain)

Pharmacology II (10 decks)

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