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78 Cards in this Set
- Front
- Back
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why where opioids formally know as narcotics?
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b/c sedation is a side effect
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what are the uses for opioids?
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pain
cough suppressant component of anesthesia decrease GI motility adjunct for pulmonary edema abuse |
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name 3 endogenous opioids
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Endorphins
Enkephalins Dynorphins |
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which opioid receptor is most important for analgesia?
what are its side effects? |
Mu
decreased RR, constipation, dependence |
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what are the side effects of drugs binding to kappa receptors?
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sedation
psychological effects/ hallucinations |
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what side effects do drugs binding to delta receptors have
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increases in hormonal releases
(minor side effects) |
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what is a mixed opioid
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a drug that is an agonist to one receptor but an antagonist to another
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in what mechanism do opioids inhibit pain transmission in ascending pathways
what is an example of a pathway which may be effected |
drugs that bind to g-protein coupled receptors
spinothalamic tract |
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how do opioids that bind to g-protein receptors work presynapticly?
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G proteins inhibit Ca entry and cAMP release, causing less neurotransmitter release
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how to opioids that bind to g-protein receptors work postsynapticly?
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G proteins open K channels (lose K) & hyper-polarize the membrane making it harder to excite the neuron
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how do drugs that bind to g-protein couple receptors in the CNS (and possibly the PNS) work?
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inhibit afferent transmission in ascending pain pathways
activates descending pain control pathways via disinhibition (pariaquaductal grey) |
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what are possible routes of administration for opioids?
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oral
IV epidural intrathecal transdermal |
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where does metabolism of opioids occur?
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mainly liver
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what is important for effective treatment of pain when using opioids?
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route and dosing schedule
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why is it important to get pts off opioid IV pumps ASAP
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d/t dependence issues especially with Mu receptor drugs
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what is an example of a strong agonist opioid
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morphine
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what is an example of a mild-to-moderate agonist opioid
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codeine
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how do mixed agonist-antagonist opioids work and when would they be used
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they normally stimulate kappa or delta receptors and block or only partially activate mu receptors
used when recovering from or decreasing the likelihood of dependence |
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when are opioid antagonist drugs used?
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to help in relief of dependence
could reverse adverse side effects |
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what receptors does codeine bind to
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all but at a lower affinity
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opioids' adverse effects
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sedation
possible euphoria respiratory depression possible additional cardiovascular problems GI distress/constipation |
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what is addiction
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compulsive drug use; psychological dependence
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what is tolerance?
what are 2 ways it occurs? |
when pt needs increased dose for the same functional response
caused by: a change in recptors (down regulation) enzyme induction |
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what is physical dependence
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the onset of withdrawal Sx when the drug is removed from the system
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what are opioid withdrawal Sx?
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flu-like symptoms
irritability tachycardia uncontrollable yawning muscle aches |
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what is methadone?
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a strong opioid agonist with milder withdrawal Sx
a pharmacological treatment of opioid addiction |
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what is buprenophine (Buprenex)?
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a partial mu agonist and a kappa antagonist
a pharmacological treatment of opioid addiction |
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what are the uses/effects of NSAIDs?
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decrease inflammation
decrease fever relieve mild-to-moderate pain anticoagulant |
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what is the mechanism of NSAIDs?
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anti-inflammatory and analgesic effects are d/t inhibition of eicosanoid synthesis
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what are eicosanoids and their definitions?
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prostaglandins: endogenous lipidlike compounds that help regulate a wide array of cell functions; pro-inflammatory
Thromboxanes; vasoconstriction and platelet aggregation Leukotrienes; pro-inflammatory esp in airway |
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what is the effect when eicosanoids are not working properly
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pain, fever, thrombus, menstrual problems
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What does the Lox pathway form?
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leukotrienes
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what do the Cox pathways form?
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prostaglandins
thromboxanes |
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what does the COX-1 pathway do?
where is it produced |
maintains homeostasis
protective in GI tract lining normally produced in normal cells |
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what does the COX-2 pathway do?
where is it produced |
is an emergency pathway
results in good effects of inflammation produced in injury pathways |
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what cox pathway(s) does aspirin effect
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COX 1 & 2
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what are the uses of aspirin (acetylsalicylic acid; ASA)?
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treat mild to mod musculoskeletal, joint and dysmenorrheal pain
treat fever in adults treat vascular disorders (low doses) prevent colorectal CA |
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What are adverse effects of aspirin?
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GI problems
renal and liver problems if pre-existing condition or decreased body water Reye syndrome ASA intolerance |
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what are O/D signs/Sx of aspirin?
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HA
decreased hearing confusion GI distress possibly metabolic acidosis & dehydration |
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what are "other" examples of NSAIDs and their brand names
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ibuprofen (Advil, Motrin)
Naproxen (Naprosyn) Naproxen sodium (Aleve) |
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what is Reye Syndrome?
what causes it? |
high fever, vomiting, liver dysfunction; leads to unresponsiveness and possibly death.
aspirin, flu, chicken pox |
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what is an example of a COX-2 selective inhibitor?
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Celecoxib (Celebrex)
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What are adverse effects of COX-2 selective inhibitors?
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risk of MI and ischemic CVA
shifts to favor increases platelet activity & increased risk of clotting in coronary and carotid arteries |
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what are differences of NSAIDs and acetominophen?
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acetominophen=
-no anti-inflammatory or anticoagulant effects in oral doses -no GI irritation or Reye Syndrom -high doses can cause liver toxicity -most transformation occurs in liver not bloodstream -less is bound to plasma protiens |
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when may tylenol be used for early Tx of OA or other musculoskeletal condidtions?
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if no inflammation
if have GI co-morbitity |
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what are the pharmacokinetics of NSAIDs?
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-most bound to plasma protiens while other is hydrolized to active matabolite
-biotransformation occurs in blood stream -further break down occurs in liver -excreted |
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what is vicodine composed of?
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acetominophen & hydrocodine
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what is tylonol 3?
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tylonol and codine
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what are pros of a PCA?
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pain control with decreased drug, leads to decreased side effects
tighter control of drug (stays in therapeutic range) |
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what are cons of PCA?
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the general opioid cons
user error (does not push) operater error (set wrong) mechanical error (clog) |
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What is the PT's roll in PCA pumps?
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can recognize when pts won't use d/t cognitive issues or when pt is no longer A&O d/t drug
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what is the loading dose?
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initial large dose to bring concentration into therapeutic range
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what is the demand dose?
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dose given when pt clicks button
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what is a lock out interval in relation to PCAs?
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min time b/w demand doses
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what is the background infusion rate in relation to PCAs?
what is a possible adverse effect? |
amount of drug given continuously
harder to contol side effects b/c pt does not control |
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what is succesful vs total demand and what can it tell you?
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dose given v. dose requested
can give you insight into pain control |
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what are drugs used in PCAs?
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opioids
opioid + nonopiod opioid + local anesthetic anesthetic |
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what are possible ways to administer PCAs
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IV
epidural intrathecal transdermal (patch) |
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when would you use a PCA long term?
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chronic pain
cancer |
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what is the definition of RA?
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chronic, systemic d/o primarily characterized by synovitis & acticular tissue distruction
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What are the S/S of RA.
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pain and inflammation of multiple joints
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What is the typical course of RA?
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progressive disease with possibility of remission
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What is the etiology of RA?
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somewhat unknown. An autoimmune response occurs, with end result of synovitis and articular distruction
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What is the Tx (pharmacological) of RA.
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decrease inflammation (NSAIDs gluco corticosteroids)
stop progression (DMARDs) |
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what are DMARDs?
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Disease-modifying antirheumatic drugs
-heterogeneous group that seem to slow or stop the RA disease process |
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how long do DMARDs take to work
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6 wks to 6 months
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what are examples of DMARD drug types?
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anticancer drugs
immune suppressants anti-inflammatory anti-inflammatory (via TNF inhibition) |
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What is an example of an anticancer drug for RA, when is it normally used and how do they work.
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Methotrexate (Rhematrex)
often first choice the don't allow cell to rapidly divide |
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What is an example of immune suppressants used for RA. When is it used? What are side effects?
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Azathioprine (Imuran)
Used for severe & active RA flu like Sx decreased immune fx fatigue |
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what is a category of anti-inflammatory drugs used for RA?
When are they normally used |
gold compounds
gold compounds are normally used in combo if other drugs are ineffective |
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What is TNF alfa's role in RA?
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binds to joint tissue to cause inflammation
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How do TNF inhibitors work?
What is an example of one? |
generally used as a combo
drug binds to TNF to not allow it to bind to receptor Infliximab (Remicade) |
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What are non-pharmaceutical treatments of OA?
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PT
joint replacement Sx |
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What are some OA pharmaceutical treatments?
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NSAIDs
acetaminophen viscosupplementation supplements |
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What is the administration of viscosupplementation?
How long can it last? What are the adverse effects? |
injection of hyluronan into the joint
transient but can last up to 6 months local pain and inflammation |
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What are two precursors to joint tissue constituents?
what are they thought to do? |
glucosamine
chondroitin sulfate possible increase in synovial fluid |
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What are the pros and cons of precursors to joint tissue constituents?
how long would you expect to see an effect? |
Pros: may decrease pain/inflammation
Cons: may cause GI problems may or may not work takes weeks to see an effect |
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what are three classes of RA drugs
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NSAIDs
glucocorticoids DMARDS |
