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Complementary and Alternative Medicine (CAMs)
natural supplements that are classified as “dietary” supplements so they are not subject to FDA testing
potential effects of CAM use with conventional medicine
additive effects, opposite effects, enzyme induction
legal classification of marijuana
schedule 1: high potential for abuse and no accepted medical use
common cannabinoids of marijuana
THC (psychoactive) and CBD (medicinal)
neuromuscular indications of marijuana
pain, MS, resistant seizures, nausea, appetite stimulant, anxiety
mechanism of marijuana
takes advantage of the endogenous cannaboid system in humans: bind to CB1 and CB2 receptors to modulate pain and provide immunosuppression and anti-inflammation and are then broken down by enzymes
systemic side effects of marijuana
increase HR/BP, airway inflammation and obstruction, higher doses cause nausea
CNS side effects of marijuana
giddiness/euphoria, confusion, paranoia, decreased cognition, decreased balance and coordination
symptoms of cannabis use disorder
tolerance and withdrawal, great deal of time spent to obtain and use, failure to fulfill obligations, social problems, used despite knowledge of problems
polypharmacy
more than 5 medications taken or at least 1 unnecessary medication taken
characteristics of polypharmacy
no reason for drug, duplicates, contraindicated drugs, interacting drugs, inappropriate dose, treating adverse reaction
pharmokinetic changes in older adults
decreased liver function slows metabolism, decreased kidney function slows excretion, decreased absorption, decreased distribution
pharmacodynamic changes in older adults
receptor binding and intracellular response changes, decline in homeostatic mechanisms (circulatory, posture, cognitive, muscles)
side effects in the elderly
2-3x more likely and more severe, more at risk because of age/fragility/organ dysfunction
why is acetaminophen the first choice in treating OA
anti-inflammatory of other NSAIDs is not needed
why are NSAIDs (specifically COX-2 inhibitors) more helpful in the later stages of OA
anti-inflammatory effect and reduce pain
mechanism of traditional DMARDs (rheumatoid arthritis medication)
non-selective inhibition of cytokine synthesis and cellular activation (auto-immune response)
mechanism of newer DMARDs (rheumatoid arthritis medication)
target specific responses like tumor necrosis factors and interleuken receptor blockers
side affects of DMARDs (rheumatoid arthritis medication)
toxicity, GI problems, hematological disorders, fevers, rashes
mechanism of centrally acting antispasm drugs
work in CNS (sedation): increase GABA-mediated inhibition which decreases excitability of alpha motor neurons, increase serotonin to inhibit outgoing information
benefits of muscle relaxants
more difficult to excite the muscle, decreases anxiety
benefits of intraethecal delivery of muscle relaxants
injected directly into the neural tissue which decreases side effects
other mechanisms of muscle relaxants
inhibition of calcium and acetylcholine release