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50 Cards in this Set
- Front
- Back
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classic signs of inflammation |
heat redness (increase in blood flow) swelling (fills with fluid) pain loss of function |
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difference between chronic and acute inflammation? |
acture: promotes repair, occurs within hours or days chronic = outlasts any repair process. Is no longer healing and causes further damage. lasts weeks, months, |
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what are the effects of vasodilation in acute inflammation? |
-increased blood flow -immune cells travel to the area |
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what are the effects of increased vascular permeability in acute inflammation? |
-blood cells become "leaky" -proteins leak out from the surrounding tissue, which changes the oncotic pressure -this causes fluids to follow the proteins -causes fluid and edema -also more leukocytes from increased permeability |
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what are some functions of immune cells? |
phagocytosis, clearance of cellular debris -regeneration and repair of tissue |
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what are some examples of inflammatory mediators? |
-enzymes -neuropeptides (neuronal signalling molecules) (ie substance P; stuff like GABA and ACh is also a neuropeptide tho not necessarily involved in immune response) -cytokines ( a cytokine is a category of cell signalling protein that includes growth factors, antibodies, immune and anti-immune response) |
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what do prostaglandins do? |
-they cause inflammation and pain -(lipid cells found in most body organs that do different things in different cells) |
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how are prostaglandins synthesized? |
through the oxidation (loss of electron/oxygen) of arachidonic acid -happens via 2 enzymes: COX-1 and COX-2 (cyclooxygenases) |
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cox 1 |
-always expressed throughout the body in relatively constant levels -involved in cell homeostasis (ie platelet function, cytoprotection (chemical protection) of GI tract, renal perfusion) |
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cox 2 |
induced, ie by injury -found in inflammed tissues -present only during inflammation or pain short half life -promotes inflammation and pain |
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what's the general cox pathway? |
arachidonic acid ---(COX 1 or 2)-> PGH2 -- PG(letter)S or TXS -----> PG(letter)2 or TXA2 ---> binds to (letter)P receptors letters are FITED |
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what is the effect of prostoglandins on smooth muscle? |
vasodilation, GI contraction |
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what is the effect of prostoglandins on platelets? |
aggregation (clotting) |
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what is the effect of prostoglandins on the kidneys? |
-increases renin (fluid retention from aldosterone in the kidney) -increases glomerular filtration rate |
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what is the effect of prostoglandins on the nervous system? |
peripheral and central sensitization |
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NSAIDs |
-nonsteroidal anti-inflammitory drugs -they inhibit COX 1 and COX 2 -ibuprofen, acetylsalicylic acid (aspirin), naproxen, diclofenac |
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how is Acetylsalicylic acid/aspirin different from other NSAIDs? |
-it's less potent -it has a longer half life -it has anti-platelet aggregation activities at low doses |
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what is the aspiring/acetylsalicylic acid starting dose? |
500 mg |
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what are typical aspirin doses? |
325-600mg every 4 hours as needed |
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what's the highest amount of aspirin you can take before it becomes toxic (typical people) |
4g/day |
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what dose of aspirin is used for anti-platelet activity/anti-clotting |
80mg |
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what are NSAID side effects? |
-high use/too much use leads to renal failure and GI damage (ulceration, bleeding) |
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What are advantages of using Coxibs vs. nonselective NSAIDs (and vice versa)? |
COXIBs have less renal and gut damage, and NSAIDs have less risks of clotting and cardiac risks |
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Coxibs mechanism of action |
-a type of NSAID -selectively inhibit COX2, preserving renal function and gastricmucosal integrity -reduce only inflammation prostaglandin production -but have more blood clot risk (recall COX1 causes clotting) |
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Coxibs - what do prescribe with it so it's safest for people with thrombotic (clotting) risk? |
-add 81 mg aspirin to reduce clotting potential -add a proton pump inhibitor to protect stomach from aspirin side effects (makes it less acidic) |
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what's the benefit of NSAID + opioid combinations? |
-less abuse potential than opioids -NSAID dose can only be raised so much -effective painkiller with less side effects than higher doses of NSAID (toxic) or opioids |
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vicoden composition |
500 mg acetaminophen + 5mg hydrocodone |
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vicoprofen composition |
200 mg ibuprofen + 7.5 mg hydrocodone |
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Topical diclofenac |
-used for arthritis pain primarily -target pain periphery therefore minimize central side effects, and have a higher safety margin and also more effective -come in a gel or a patch -side effect: local irritation |
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acetaminophen (paracetamol, tylenol) mechanism of action |
-deacetylated in the liver -converted to endocannadinoid in the brain -endocannabinoid reduces pain at CB1 (cannabanoid 1) receptor (not on slides: found in periaqueductal grey and dorsal horn layers 1 and 2 and block pain traveling through those areas) -it also reinforces descending serotonergic (5-HT) pathways that reduce pain |
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how much tylenol (acetaminophen) can you take before it's toxic? |
-up to 6 mg/day |
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what's acetaminophen used for? what are benefits? |
first line therapy for arthritis few drug interactions -lacks side effects of aspirin |
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what are tylenol adverse effects? |
few side effects -overdose: liver toxicity (hepatoxicity), kidney death (necrosis) |
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TRP channels (transient receptor potential) |
-pain, temperature, taste |
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TRP A |
garlic, cinnamon, horseradish |
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TRP MH |
mint, spearmint, 10-15 degrees celcius -why mint tastes cool (M for mint?) |
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TRP V1: what does it do |
garlic, hot chili peppers (capsaicin), heat above42 degrees celcius -v stands for vanillanoid (capsaicin is a type of vanillanoid) |
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Where are TRP V1 receptors located? |
-Where pain receptors are: -expressed on C fibers and A Delta fibers-in -laminella I and II of the dorsal horn of the spinal cord |
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-TRYPV1 therapeutic potential |
-peripheral neuropathic pain - |
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strength of capsaicin for topical creams |
-0.025-0.075% |
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strength of capsaicin for the patch (more intense one) |
-8% -30-60mins at a time |
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DMARD methotrexate (folex) |
-anti-rheumatoid drug -inhibits folic acid metabolism -which reduces immunocytes (white blood cells producing antibodies) -also reduces inflammatory cytokines |
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Adverse effects |
-highly toxic -loss of appetite, nausea, gastrointestinal hemorrhaging -liver disease |
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TNF alpha (tumour necrosis factor alpha) |
-part of the arthritis auto-immune response cytokine producing inflammation, pain, joint erosion -kills tumors |
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what are the two isoforms of TNF alpha? |
-membrane bound TNF (mTNF) -soluble TNF (sTNF) |
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what are the two TNF receptors? |
TNF - R1 TNF - R2 (TNF receptor 1, TNF receptor 2) |
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TACE (TNF a converting enzyme) |
-cleaves membrane bound TNF (from the membrane?) so it becomes sTNF -cleaves TNF receptor 1 -binds to receptors in the blood stream, leading to pain and inflammation |
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TNFalpha blockers |
-soluble receptors that bind to TNF -or microclonal antibodies that bind to the TNF -in both cases binding prevents it from docking to receptors -decreases acute flares and pain, can reverse arthritis |
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TNF alpha blockers side effects |
fever, infection, cost |
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examples of TNF alpha blockers |
etanercept (50mg/wk) infliximab (5mg/wk) adalimimab (40mg/wk) |
