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Pharm > L3: Opioids and non-opioid pain meds + tx of inflammation > Flashcards

L3: Opioids and non-opioid pain meds + tx of inflammation Flashcards

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1
Q

receptor classes

A

mu, delta, kappa

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2
Q

mu functions

A

analgesia, sedation, slow GI, inhibit respiration

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3
Q

endorphins

A

primary endogenous opioid affinity for mu

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4
Q

delta functions

A

analgesia

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5
Q

enkephalins

A

primary endogenous opioid affinity for delta

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6
Q

kappa functions

A

analgesia, slow GI

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7
Q

dynorphins

A

primary endogenous opioid affinity for kappa

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8
Q

morphine types

A

natural, semisynthetic, synthetic

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9
Q

primary use for morphine

A

manage acute, moderate to severe, constant pain

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10
Q

strong full agonists

A

morphine, methadone, fentanyl

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11
Q

mild to moderate (partial) agonists

A

codeine, hydrocodone, oxycodone

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12
Q

antagonists

A

nalaxone (Narcan)

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13
Q

mixed agonist-antagonists

A

buprenophrine

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14
Q

2 main mechanisms for opioid receptors

A

presynaptic and post synaptic

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15
Q

presynaptic opioid receptor mechanism

A

g proteins inhibit Ca2+ entry and CAMP release

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16
Q

what does a presynaptic opioid receptor mechanism result in

A

causes less neurotransmitter release which means its more likely to fire

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17
Q

post synaptic opioid receptor mechanism

A

g-proteins open K+ channels and hyper-polarize the membrane

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18
Q

what is the result of a post synaptic opioid receptor mechanism

A

harder to excite the post synaptic neuron

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19
Q

what is the effect on nociception

A

action in the ascending pathway result in a decrease in nociception transmission

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20
Q

what are the effects when opioids bind to primary sensory nerve endings

A

decreased excitability and transmission of nociceptive input

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21
Q

what determines whether exogenous opioid administration involves the first-pass effect?

A

the route of administration; oral route undergo first pass metabolism while others (IVs) bypass it

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22
Q

name alternative routes of opioid administration that bypass the first-pass effect

A

IV (PCA), rectal suppository, transdermal patch, intranasal, buccal transmucosal (lozenge)

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23
Q

what is the patient-controlled analgesia (PCA)

A

a type of IV opioid administration allowing patients to self-administer controlled doses

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24
Q

give examples of opioids used in transdermal and rectal administration

A

transdermal: fentanyl, buprenorphine. Rectal: morphine

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25
how are exogenous opioids distributed in the body
they rapidly leave the bloodstream and localize in well-vascularized tissues like skeletal muscle
26
what is the main site of metabolism for exogenous opioids
the liver, primarily via hepatic CYP450 enzymes
27
what factors affect opioid metabolism
genetic variability and drug-specific metabolism rates
28
why is cuation needed with opioid metabolites?
some are neuro-excitatory and some are more potent than the parent drug (codeine metabolized to morphine
29
how are opioids primarily excreted from the body
via the kidneys
30
primary uses
pain management
31
other uses for opioids
component of anesthesia, dec. GI motility, cough suppression, treat shivering, adjunct for acute pulmonary edema, drugs of abuse, manage opioid withdrawal
32
full agonists
morphine and fentanyl
33
which opioid analgesic is the most efficacious
full agonists
34
morphine
many forms of administration, prototypic opioid analgesic, very powerful - for most severe pain
35
fentanyl
many forms of parenteral administration, analgesics and adjunct for anesthesia, short duration
36
partial adonists are used for what kind of pain
mild to moderate
37
what are examples of partial agonists
oxycodone and codeine/hydrocodone
38
oxycodone
oral administration, analgesic, for moderate to severe pain
39
codeine/hydrocodone
oral administration, least powerful of opioids - for least severe pain - may be used in combo with acetaminophen
40
mixed agonist-antagonists
bupreorphine - used to treat opioid dependency/withdrawal
41
primary acute adverse effects
CNS issues, DI distress, pupil constriction, acute toxicity/overdose
42
how do opioid's acutely effect the CNS
sedation, respiratory depression, seizures (due to neuro-excitatory metabolites)
43
how do opioid's acutely effect GI distress
nausea/vomiting and constipation
44
what is the clinical name for pupil constriction
miosis
45
what does acute toxicity/overdose look like
extreme miosis, respiratory depression, coma
46
pharmacological treatment of opioid overdose (acute)
nalaxone (narcan)
47
what kind of treatment is nalaxone
full antagonist used for acute opioid overdose
48
other uses of nalaxone
treatment of respiratory and CNS depression
49
how is nalaxone administered
via IV, IM, or nasal spray
50
opioids primary chronic adverse effects
tolerance, hyperalgesia, impairment while driving, addiction, physical dependence (withdrawal effects)
51
acute withdrawal symptoms
rhinorrea/lacrimation, muscle aches, irritability, uncontrollable yawning, chills, sweating, vomiting
52
classic treatment of opioid dependency/withdrawal
methadone
53
newer treatment of opioid of opioid dependency/withdrawal
bupreophrine - mixed agonist-antagonist
54
neonate opioid dependency symptoms
ANS, GI, neuro, high-pitched cry
55
contraindications for opioid use
tendency for dependence, brain injury, pregnancy/lactation, liver/kidney disease, pulmonary disease, endocrine disease
56
what is a major caution when using opioids due to risk of habit-forming behavior
tendency for dependence - requires careful monitoring and ensuring adequate pain control
57
why should opioids be used with caution in patients with brain injury
they can increase intracranial pressure and mask neurologic changes
58
is opioid use safe during pregnancy and lactation
use with caution - may affect the fetus or nursing infant and can lead to neonatal withdrawal
59
why are liver and kidney diseases a concern with opioid use
these conditions impair drug metabolism and excretion, increasing the risk of toxicity
60
why is pulmonary disease a contraindication for opioids
opioids can suppress respiratory drive, worsening conditions like COPD or asthma
61
what endocrine conditions require caution with opioids
opioids may interfere with hormonal regulation and worsen endocrine diseases
62
what is a major class of drugs that can dangerously interact with opioids due to sedation
sedative, hypnotics - increases the risk of respiratory depression and overdose
63
name other drug classes that can interact with opioids
antipsychotics and certain antidepressants, especially MAO inhibitors (risk of serotonin syndrome or severe sedation)
64
patient-controlled analgesic (PCA)
pt can self-administer small doses of pain med relatively frequently for optimal pain control - usually via IV or intro spinal canal
65
what is a loading dose in PCA
a larger initial dose of medication given to quickly achieve therapeutic levels in the body
66
what is a demand dose in PCA
the amount of drug the patient receives each time they press the PCA button
67
what is the lockout interval in PCA
a set period of time during which no additional doses will be given after a demand dose, even if the button is pressed
68
what does "successful demands" mean in PCA use?
the number of times the patient presses the button, regardless of whether medication was delivered
68
what does "total demands" refer to in PCA use
the number of times the patient presses the button, regardless of whether medication was delivered
68
what does "successful demands" mean in PCA case
the number of button presses that actually resulted in a dose being delivered (i.e., not blocked by the lockout interval)
68
what are NSAIDs
NSAIDs stand for non-steroidal anti-inflammatory drugs
68
what are NSAIDs primary uses/effects?
anti-inflammatory, analgesic (mild to moderate pain), antipyretic (fever reduction), ASA (aspirin)
69
what does ASA inhibit
platelet aggregation which helps to decrease clotting
70
how do NSAIDs work
inhibit eicosanoid synthesis by blocked COX enzymes, COX-1, COX-2, most NSAIDs are nonselective
71
what are eicosanoids
prostoglandins, thromboxanes, leukotrienes, synthesis
72
what role do prostoglandins play (PGs)
pro-inflammatory; regulate pain, fever, inflammation
73
what role do thromboxanes (TXs) play?
vasoconstriction and platelet aggregation
74
what role do leukotrienes play?
pro-inflammatory (especially in airways)
75
what role does synthesis play
via COX (PGs/TXs) or lipoxygenase (leukotrienes)
76
what are the uses of aspirin
used for mild to moderate MSL/joint main and dysmenorrhea, fever reduction (for adults only), vascular disorders (antiplatelet effects)
77
what are teh adverse effects of aspirin?
GI irritation, Reye syndrome (in children), ASA intolerance, impaired bone healing
78
how do aspirin-like NSAIDs differ from aspirin?
no reye syndrome risk, fewer GI side effects, some are OTC
79
what is unique about COX-2 inhibitors (celecoxib)
targets only COX-2 (less GI irritation) and there is an increased MI/stroke (due to unopposed platelet activity)
80
how does acetominophen compare to NSAIDs
they are both analgesic and antipyretic but don't have anti-inflammatory or anticoagulent effects and no GI irritation or Reye syndrome
81
What is the mechanism for acetaminophen
likely inhibits CNS COX
82
what are glucocorticoids used for?
anti-inflammatory (autoimmune diseases, asthma/COPD) and prevent transplant rejection
83
what are the key side effects of glucocorticoids
muscle/bone/skin breakdown, growth retardation, hypertension, infection risk
84
which drug classes are anti-inflammatory
NSAIDs and glucocorticoids

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