Pain/inflammation: Opioid Analgesics

Front 1

Name the 3 different forms of opioid analgesics

Back 1

Natural, semisynthetic, and synthetic forms

Front 2

What is the most common use for opioid analgesics?

Back 2

mod to severe pain control

Front 3

What are some other uses for opioid analgesics?

Back 3

cough suppression, component of anesthesia, decrease GI motility, adjunct for pulmonary edema, drugs of abuse

Front 4

What are the three endogenous opioids?

Back 4

endorphine, enkephalins, dynorphins

Front 5

Name the major types of opioid receptors in the CNS

Back 5

Mu, Kappa, Delta, Mixed

Front 6

What are the effects of Mu (both adverse and beneficial)?

Back 6

have strongest analgesic effect but cause most severe side effects such as respiratory depression, constipation, higher level of dependence

Front 7

What are the effects of Kappa (both beneficial and adverse)?

Back 7

has analgesic function and have less side effects but will cause sedation and psychotropic effects

Front 8

What are the effects of Delta?

Back 8

has an analgesic effect but side effects are minor

Front 9

What does it mean to have a mixed opiod receptor?

Back 9

some drugs will be agonist to 1 or more receptors and antagonist to the others

Front 10

What is the opiod mechanism of action?

Back 10

bind to opioid G-protein coupled receptors

Front 11

What is are the ways in which opioid affect pain pathways(2)?

Back 11

1. will inhibit afferent pain transmission in ascending pain pathways
2. Activate descending pain control pathways via disinhibition

Front 12

How do opioids inhibit afferent pain transmission in ascending pain pathways?

Back 12

Opioid will affect pre and post membranes: presynaptic G proteins inhibit calcium entry and cAMP release causing less NT release; postsynaptic G proteins open K channels and hyperpolarize the membrane making it harder to excite the neuron

Front 13

What are the possible effects on peripheral nerve terminals?

Back 13

causes decreased excitability and thus decreased transmission of that axon

Front 14

What are the routes of administration for opioids?

Back 14

some oral, some parenteral (intrathecal, epidural, transdermal)

Front 15

Where are opioids primarily metabolized?

Back 15

in the liver

Front 16

Name the 4 types of opioids

Back 16

strong agonists
mild-moderate agonists
mixed agonist-antagonists
antagonists

Front 17

Give an example or mechanism of action for each type of opioid

Back 17

1. strong agonist - morphine gives the strongest pain control
2. mild to mod - codeine, binds to each receptor at a lower affinity, lower efficacy will result
3. Mixed - stimulate kappa or ddelta but block or only partially stimulate Mu
4. Antagonists - binding to one of opioid receptor but not causing functional effects; used for dependence; Mu anta could reverse resp depression

Front 18

What are the adverse effects of opioid use?

Back 18

sedation, possible euphoria, respiratory depression, possible additional cardiovascular problems, GI distress

Front 19

Name some of the problems associated with opioid use over a period of time?

Back 19

Addiction, tolerance, physical dependence, opioid withdrawal symptoms

Front 20

Describe opioid withdrawal symptoms

Back 20

flu like, insomnia, irritability, tachycardia, muscle aches, uncontrollable yawning, desire of the drug

Front 21

How would you pharmacologically treat opioid addiction?

Back 21

use of methadone, buprenophrine

Front 22

What are the advantages to using methodone?

Back 22

strong opiod agonist, milder withdrawal symptoms than other opioids, it is withdrawn slowly in conjuction with non-pharm tx

Front 23

Why use buprenophrine to treat opioid addiction?

Back 23

mixed agonist-antagonist, partially activates mu receptors and is stronger antagonist for kappa receptors, no hallucinogenic effects with some pain control

Front 24

What are some of the uses for NSAIDS?

Back 24

decrease inflammation
relieve mild to mod pain
antipiuretic
anticoagulant

Front 25

What is the mechanism of action for anti-inflammatories?

Back 25

inhibition of eicosanoid synthesis

Front 26

What are eicosanoids?

Back 26

drugs that have wide variety of effect on any system in the body

Front 27

Name the 3 eicosanoids and their functions

Back 27

1. Prostaglandins - are endogenous lipidlike compounds that help regulate a wide array of cell functions; and are pro-inflammatory
2. Thromboxane - cause vasoconstriction and platelet aggregation
3. Leukotrienes - are pro-inflammatory especially in the airway

Front 28

Describe eicosanoid synthesis pathway (briefly)

Back 28

made from phospholipids which are then converted into lipoxiginase which forms leukotrienes and coxiginase pathways which forms prostaglandins and thromboxanes.

Front 29

Which eicosanoid pathway does NSAIDS inhibit?

Back 29

will inhibit COX pathways

Front 30

Inhibition of COX pathway involves what?

Back 30

inhibition of PG and TX synthesis causing anti-inflammatory and analgesis effects

Front 31

What are the COX enzyme systems?

Back 31

COX 1 and COX 2

Front 32

Describe what each COX enzyme pathway does normally

Back 32

COX 1 is normally produced in functioning cells and it maintains homeostasis;
COX 2 is an emergency pathway produced by injured cells and it develops inflammation

Front 33

What does it mean then if NSAIDS are nonselective?

Back 33

will effect both COX pathways meaning that side effects occur in normal functioning cells

Front 34

What are the uses of aspirin?

Back 34

treat mild to mod pain and inflammation, treat fever in adults, treat vascular disorders such as MIs and CVAs, prevent colorectal CA

Front 35

What are the adverse effects of aspirin?

Back 35

GI problems, renal and liver problems if pre-existing disease or decreased body water, O/D signs and symptoms such as HA: decreased hearing, confusion,dehydration

Front 36

What are the adverse effects of aspirin in small children?

Back 36

reye syndrome included high fever, vomiting, liver dysfunction, unresponsiveness and possible death, ASA intolerance; not advisable use after fracture or bone symptoms

Front 37

Name NSAIDS that are aspirin-like and what the main differences are

Back 37

ibuprofen (Advil, Motrin), Naproxen(Naprosyn), and Naproxen sodium (Aleve) have no risk of reye syndrome and have differences in side effects and cost

Front 38

What is one COX-2 selective inhibitor?

Back 38

Celecoxib (Celebrex)

Front 39

What are the adverse effects of COX-2 selective inhibitor?

Back 39

MI and ischemic CVA, increased platelet activity and increased risk of clotting in coronary and carotid aa

Front 40

What are the key similarities between acetominophen (Tylenol) and NSAIDS?

Back 40

same analgesis and antipyretic effects, no apparent anti-inflammatory or anticoagulant effects in oral doses, no GI irritation or reye syndrome

Front 41

What could be problematic with Tylenol use?

Back 41

high doses can cause liver toxicity

Front 42

For what types of conditions is Tylenol used and when?

Back 42

first for early OA and other MS conditions, not to use when lots of inflammation is present

Front 43

What is the mechanism of action for Tylenol?

Back 43

not fully understood, inhibits COX probably inhibit PG, and may preferentially inhibit CNS prostaglandins (COX-3)

Front 44

Pharmacokinetics of ASA

Back 44

most is bound to plasma proteins and unbound drug is hydrolyzed to active metabolite where it is then further broken down in the liver

Front 45

Pharmacokinetics of acetaminophen

Back 45

absorbed rapidly, much less is bound to plasma proteins, biotransformation occurs mostly in liver, toxic metabolite must be conjugated for detoxification and excretion