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64 Cards in this Set
- Front
- Back
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Where do Pain medications work related to the Gate Control Theory? |
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Which opiods are Natural, Semi-synthetic, and Full Synthetic? |
Natural- Morphine & Codeine Semi-synthetic-Oxycodone & Hydrocodone Synthetic-Meperidine & Fentanyl |
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What type of drug is codeine, what metabolizes it, and what is its metabolite? |
A pro-drug (needs to be metabolized to be active) Metabolized by CP450-2D6 Morphine |
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What are other opioid pro-drugs that are metabolized by CP450-2D6 and what are their active metabolites? |
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How does Lipophilicity affect the spread of spinal epidural opioid medications? |
Greater spread of medication (risk of high block) with lower lipophilicity. |
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Which part of the pain pathway do local, regional, and systemic opioids work on? |
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How do enkephalins modulate pain? |
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How do opioids reduce pain? |
Mimic endorphins by binding to opioid receptors activating pain modulation system thought to block the release of Substance P. Work Centrally and do not have a ceiling effect. There is an antagonist. |
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What type of receptor is an Opioid receptor and what is the cellular response? |
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What are the three type of receptors and what effect do they have on the body? |
Mu: Responsible for supraspinalanalgesia, euphoria, respiratorydepression, bradycardia and physicaldependence. Delta: Modulate mu receptor activity. Kappa: Analgesia with little or norespiratory depression. |
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What is the affinity of medications and the receptors they affect? |
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What are examples of partial agonists & Agonist/antagonists, what type of pain are they effective for, and advantages/disadvantages? |
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What are examples of a weak agonists, what type of pain are they effective for, and advantages/disadvantages? |
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Describe Tramadol. |
Ultram® 50mg & Ultracet® 37.5/325mg Actions: Binds weekly to mu opioid receptors and inhibits re-uptake of serotonin and norepinephrine.
Disadvantages: Expensive and appears to be no more effective than APAP with codeine. Seizures have been reported. |
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Codeine/Hydrocodone/Oxycodone
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Profile:Mild to moderate to severe pain. Advantages: Good first line agent if nonsteroidalineffective and good agents forbreakthrough pain.
Disadvantages: Opioid side effects, CodeinePO is very nauseating, Watchacetaminophen. |
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Morphine Sulfate
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Actions: Onset 5-10min, peak 30min, andduration 3-4 hr. when given IV.
Advantages: Good analgesic, positive effects on preload for post-MI Disadvantages: Long onset, opioid side effectsand morphine-6 glucronide metaboliteaccumulation, histamine release |
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Methadone |
Use Advantages: Good analgesic, long half life beneficial in chronic pain, d-isomer has NMDA antagonist effects lowers tolerance Disadvantages: Accumulates and opioid side effects. Causes 1/3 of Narcotic Overdose-Difficult Pharmacodynamics |
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Meperdine |
Actions Advantages: May be given to morphine allergic patients, may have less effect on biliary spasm, and very efficacious for chills. Disadvantages: Long onset, Nor-meperdine metabolite may accumulate, and opioid side effects. MAOIs can cause Seratonin Syndrome |
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Fentanyl |
Actions Advantages: Rapid onset, may be used for morphine allergies, and very effective analgesic Disadvantages: Opioid side effects, and chest wall rigidity following rapid IV administration. |
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Narcan (Naloxone)
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Pharmacology: Competitiveinhibitor of opioids at the mu, kappa, and deltareceptors.
Actions: Onset 1-2 min, & duration 30-90 min Dose: Naloxone - 0.05-0.1 mg IV repeated every2-3 min. titrate dose up depending on clinicalresponse. Cautions: Maycause severe hypertension, ventriculardysrythmias and acute, sometimes fatalpulmonary edema. |
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How do you dose a medication if there is a cross sensitivity? |
Incomplete Cross tolerance- Need to reduce dose (~1/3) & titrate up
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How do NSAIDs work? |
Inhibit the enzyme cyclooxygenase,resulting in a decreased synthesis & release of prostaglandin
Work primarily peripherallyrather than centrally
Have a “ceiling effect”. |
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What is sensitization of pain receptors? |
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NSAIDs |
Examples: Ibuprofen, Naproxen, ASA,indomethacin
Profile: Treatment of mild pain Advantages: Help to reduce inflammation,low CNS side effects, no physicaldependence Disadvantages: Hematological, renal andhepatic adverse effects. |
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What are possible renal effects of NSAIDs? |
Long-term administration of NSAIDs has resulted inrenal papillary necrosis and other renal injury.
Renal toxicity has been seen in patients that rely onrenal prostaglandins for maintenance of renalperfusion. Both Cox 2 selective inhibitors and nonselectiveinhibitors may cause this effect. |
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What are risk factors that increase the risk of renal effects of NSAIDs? |
Impaired renal function
Heart failure Liver dysfunction Taking diuretics and ACE inhibitors Elderly |
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How to calculate Creatinine Clearance. |
CrCl=(140-age)*Wt/(Cr*72) For women multiply by 85% |
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What is the difference between Cox-1 & Cox-2? |
Cox-1 is found throughout the body, it is found in the GI tract, where it producesprostaglandins that are considered cytoprotective, is also found in the kidneys and inplatelets.
Cox-2 derived prostaglandins were considereddeleterious because they are found mainly at thesites of inflammation. |
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What is the Cardiovascular ToxicityHypothesis for why Cox-2 inhibitors cause more clotting issues? |
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What medications have the risk of life-threatening skin reactions potentially these include:Steven-Johnson SyndromeToxic epidermal necrolysis?
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NSAIDS, Abx (sulfonamides), Allopurinol, Anticonvulsants |
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Acetaminophen
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Mechanism: Similar to nonsteroidal, however: Effect more via central mechanism. No clinical effect on inflammation. Essentially no clinical effect on platelets.
Disadvantages: Potentially fatal hepatic necrosis. |
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Tylenol Metabolism |
CYP metabolism to a reactive metabolite which depletesglutathione and covalently binds to proteins
Mitochondrial permeability transition occurring with additionaloxidative stress, loss of mitochondrial membrane potential,and loss of the ability of the mitochondria to synthesize ATP |
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When is IV Tylenol most appropriate? |
For first dose to get it in faster, subsequent dose should be give by a different route to save money and is as effective.
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What is the summary of NSAIDs |
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What is the difference between an ester and an amide local anesthetic? |
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What are the effects of Cocaine? |
Blocks reuptake of Norepinepherine. |
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What are examples of Ester Local Anesthetics? |
Cocaine Procaine Tetracaine Benzocaine |
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What are examples of Amide Local Anesthetics? |
Lidocaine Mepivacaine Bupivacaine Etidocaine Prilocaine Ropivacaine |
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How do Local Anesthetics block pain transmission? |
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Where do Local Anesthetics work on the cell membrane? |
Has to be an activated channel to get the action of the local, inactivated gate blocks local from reaching receptor
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What does frequency dependence mean related to Locals? |
Frequency dependant block-nerve that fires faster is easier to block than one that fires slowly
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What are Important Factors affecting Anesthetic Action in general?
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Type of fiber
Small nerve fibers are more susceptible than large Degree of myelination Fiber length Fiber placement Frequency dependency |
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What are the different Nerve fibers and susceptibility to Local Anesthetics? |
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For mylenated nerves how many nodes need to be blocked? |
Need 2-3 nodes to block
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What is the order that sensation is blocked? |
1. pain
2. cold 3. warmth 4. touch 5. deep pressure 6. motor |
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Procaine (Novacaine)
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Type Ester (prototype)
Profile Slow onset, Short duration, Low toxicity Use Local infiltration, Spinal |
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Chloroprocaine
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Type Ester
Profile Very Fast onset, Short duration, Very Low toxicity Use Local infiltration, Nerve Blocks, Epidural |
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Tetracaine
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Type Ester
Profile Slow onset, Long duration, Moderate toxicity Use Spinal |
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Lidocaine
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Type Amide (prototype)
Profile Fast onset, Moderate duration, Moderate toxicity Use Most frequently used local anesthetic for all types of regional anesthesia |
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Bupivacaine
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Type Amide
Profile Slow onset, V long duration, High toxicity Use Most local and regional anesthesia where long duration is desired. Bupivacaine Liposome is a different formulation and is restricted use. |
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Etidocaine
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Type Amide
Profile Fast onset, Very long duration, Moderate toxicity Use Nerve blocks, Epidural |
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Ropivacaine
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Type Amide
Profile Slow onset, Very long duration, Moderate toxicity Use Similar to bupivacaine, less cardiac toxicity |
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What are factors that affect distribution of Local Anesthetics? |
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How many mg of lidocaine per CC is 1%? |
1% LIDOCAINE SOLUTION CONTAINS 10 MG OF LIDOCAINE PER ML.
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How many mcg of Epinephrine per CC in 1:100,000 1:200,000 or 1:400,000?
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A 1:100,000 solution contains 10 micrograms per ml.
A 1:200,000 solution contains 5 micrograms per ml. A 1:400,000 solution contains 2.5 micrograms per ml. |
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What are precautions for using Epinephrine with Local Anesthetics? |
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Where are ester and amide LA metabolized? |
Esters in the plasma Amides in the liver |
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What are signs of Lidocaine Toxicity? |
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Which class of medication is likely to have an true allergic reaction? |
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