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41 Cards in this Set
- Front
- Back
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Forms of opioids
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Natural (poppy seed), semisynthetic, synthetic
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Used for opioids?
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Moderate to severe pain
Cough suppression Component of anesthesia Dec GI motility Adjunct for pulmonary edema Drugs of abuse |
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3 families of endogenous opioids
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Endorphins, enkephalins, dynorphins
Released during times of stress |
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3 types of opioid reeptors and effects/side effects
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Mu - strongest anagelsic affect, but most severe side effects (Resp depression, constipation, dependence)
Kappa - Less effective, causes sedation, psychotic effects/hallucinations Delta - less effectve, minor side effects such as increased growth hormone release |
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Mixed agonist-antagonist (and example)
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Certain opioid drugs can stimulate certain receptors while blocking others
Buprenix (Buprenaphine) |
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How do opioids effect presnyaptic neurons?
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1. Opioids bind to receptors at pre-synaptic terminals
2. Binding stimulates G protein activity which inhibits opening of Ca2+ channels and release of cAMP 3. Dec Ca2+ influx results in less NT release from pre-synaptic terminal and less excitability of post-synaptic terminal |
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How do opioids effect postsynaptic neurons?
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1. Opioid binds to receptor on postsynaptic neuron
2. Binding activates G protein which opens K+ channels 3. Opening K+ channels causes hyperpolarization of the membrane, making it harder to excite the neuron |
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Where are G-coupled receptors for opioids locate?
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CNS and possibly PNS (at primary snesory nerve endings)
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2 general ways opioids block pain transmission
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1. Inhibit afferent pain transmission in ascending pain pathways
2. Activate descending pain control pathways via disinhibition |
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Explain disinhibition of desceding pathways
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Opioids inhibit interneurons that normally inhibit the ability of descneding pathways to mederate pain. So they inhibit an inhibitor, which allows the descending pathways to block pain
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How are opioids delivered?
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1. Oral (less effective for high pain)
2. Parenteral (IV) 3. Epidural, intrathecal, transdermal |
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What receptor do strong agonists of opioids use and give 2 examples
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Mu agonists
Morphine and Dilaudid |
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What are mild to moderate agonists and examples?
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Do not have as high an affinity or efficacy as strong agonists, but still treat moderate pain
Stimulate each of the receptros but at a lower affinity Codein, hydrocoone, OxyContin |
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When you a mixed agonist-antagonist?
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Treat dependence and less side effects if agonist for kappa instead of Mu
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5 general adverse effects of opioids
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Sedation
Euphoria (adverse?) Repsiratory depression CV problems GI distress/constipation |
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Opioid withdrawl symptoms
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Flu-like, insomnia, irritability, tachycadia, yawning, muscle aches
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Methadone
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Strong opioid agonist used to treat addiction b/c it has milder withdrawl symptoms than other opioids
Used in conjunction with non-pharm tx |
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Buprenophine
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Mixed agonist-antagonist that is a partial agonist for Mu and antagonist for Kappa
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Uses/effects of NSAIDs
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1. Dec inflammation
2. Relieve mild/mod pain 3. Dec body temp and fever (antipyresis) 4. Anti-coagulant (long-term use) 5. Tx vascular disorders 6. Prevent colorectal cancer |
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What are NSAIDs anti-inflammatory and analgesic effects due to?
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Inhibition of eicosanoid synthesis
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What are eicosanoids?
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20 carbon fatty acids that contain several double bonds
Prostaglandins, Thromboxanes, and Leukotrienes |
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What are prostaglandins?
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Endogenous lipidlike compounds that help regulate a wide array of cell functions; pro-inflammatory
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What are Thromboxanes responsible for?
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Vasoconstriction and platelet aggregation
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What are Leukotrienes responsible for?
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Pro-inflammatory, esp. in the airway
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2 enzyme systems that convert arachidonic acid into biologically active compounds
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Cyclooxygenase (COX) enzyme = Prostaglandins and thromboxanes
Lipoxygenase (LOX) enzyme - leukotrienes |
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What pathway do NSAIDs block?
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Cyclooxygenase (COX) pathway
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Mechanism of action for NSAIDs
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Anti-inflammatory and analgesic effects due to inhibition of PG and TX synthesis (inhibit COX enzyme)
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Cox-1 vs. Cox-2 pathways
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COX-1: Mediate normal cell activity and help maintain homeostasis. Protective prostaglandins responsible for stomach and kidney fxt (side-effects)
COX-2: Produced in injured cells; emergency pathway that is activated by cytokines |
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Aspirin (acetylsalicyclyic acid) uses
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Treat mild/mod pain and inflammation esp. MSK and joint, dysmenorrheal (Andrew Ross) pain
Anti-coagulant Treat fever in adults (not children) Treat vascular disorders Prevent colorectal CA |
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Adverse effects of aspirin
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GI problems (Main issue)
Renal and liver problems if pre-existing dx or dec body water |
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OD signs of aspirin?
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HA, dec hearing, confusion, GI distress, metabolic acidosis and dehydration
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Why is apirin not advisable to children?
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Reye syndrome: fever, vomiting, liver dysfxt; leads to unresponsiveness and possibly death. Usually after flu or chicken pox
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Why not use NSAIDs after fx or bone surgery (ie spinal fusion)?
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Certain prostaglandins appear to be IMP in stimulating early stages of bone formation
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Main difference between aspiring and aspirin-like NSAIDs?
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Main differences are in side effects and safety; but none appear more effective
Ibuprofen = less GI discomfot and less toxicity to organs but 5x more expensive than aspirin Many are Rx only (20x more expensive) No risk for Reye dx |
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Celecoxib (celebrex) mechanism of action and adverse effects
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Inhibits COX-2 only
Risk of MI and CVA Inc platelet activity and inc risk of clotting in coronary and carotid a. in some pts |
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Mechanism of action for acetominophen?
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Inhibits COX and prostaglandins, but may preferentially inhibit CNS prostaglands (COX-3?)
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When to use Acetominophen and not NSAIDs?
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Early OA and other MSK conditions when not associated with an inflammatory process
In children, b/c no risk of Reye syndrome |
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Similiarities/differences btw tylenol and NSAIDs
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Same analgesic and antipyretic effects
No anti-inflammatory or anticoagulant effects No GI irritaiton or Reye syndrome High doses can cause liver toxicity (don't use in at risk populations such as alcoholics) |
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Where are NSAIDs found in the body when ingested?
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80-90% bound to plasma proteins (albumin), but it is the 10-20% unnbound that is hydrolyzed to active metabolite in the bloodstream
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Where are NSAIDs hydrolyzed?
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Biotransformation occurs in the bloodstream, further breakdown occurs in the liver where it is excreted
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Where is acetaminophen located in the body?
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Much less bound to plasma proteins than NSAIDs
Biotransformation occurs in the liver Toxic metabolite (NAPQI) must be conjugated for detoxification and exretion |
