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Chapter 5
Non-Opioid analgesics and antagonists
| Term | Definition |
|---|---|
| Perception | The physical components of pain |
| Reaction | The psychologic component of pain |
| Antipyretic | Ability to reduce fever: affect the hypothalamus(controls the body temperature) |
| Anti-inflammatory | Ability to reduce inflammation |
| Uricosuric | Ability to increase the excretion of uric acid in the urine |
| Anti-platelet | Ability to inhibit the aggregation(clumping) of platelets in the blood |
| Analgesic | ability to reduce or relieve pain |
| PGE | Prostaglandins, which are lipids produced by cells during inflammation and can sensitive the pain receptors |
| TNF-alpha | A cytokine that is released by cells during the inflamatory response in periodontal disease |
| Pain | The sensation of main is the means by which the body is made urgently aware of the presence of tissue damage. |
| Salicylate drugs | asprin (Bayer, Bufferin) |
| Nonsalisylate/ Nonnarcotic drugs | Acetaminophen (Tylenol) |
| NSAIDs | -ibuprophen(Advil) -naproxen(Aleve) -diclofenac(cataflam) -nabumetone(Relafen) -meloxicam(Mobic) -celecoxib(Celebrex) |
| Antigout drugs | -colchicine(Colcrys, Mitigare) -allopurinol(Zyloprim) |
| Arthritis drugs | -DMARD/Antimetabolite: methotrexate(Otrexup) -DMARD/TNF-a inhibitor: adalimumab(Humira) -DMARD/TNF-a inhibitor: etanercept(Enbrel) -NSAIDs: celecoxib (Celebrex) -DMARD/Antimalaria: hydroxychloroquine(Plaquenil) |
| A decrease in pain threshold is associated with: | Emotional instability, anxiety, fatigue, youth, certain nationalities, female gender, fear and apprehension |
| Where is the site of action for nonopiods? | The peripheral nerve endings. |
| Where is the site of action for opiods? | Within the CNS. |
| Salicylate classification | Indicated for pain/fever/inflammation/ myocardial infraction |
| NSAIDs classification | Indicated for pain/fever/inflammation |
| Nonsalicylate/Nonnarcotic classification | Indicated for pain only |
| COX-1 | Expressed in all tissues, catalyzes prostaglandins |
| COX-2 | Is activiated in damaged and inflamed tissues and catalyzes the formation of inducible prostaglandin(PGE2) associated with intensifying the inflammatory response |
| PGE2 | Stimulates nociceptors in peripheral nerves to send signals for pain to the CNS. PGE can lower the pain threshold to more painful stimuli, cause inflammation, fever, and edema |
| Asprin mechanism of action | Irriversibly inhibits the COX enzyme, thereby blocking the production of prostaglandins |
| Asprin uses | Pain relief, anti-inflammatory, fever reduction, cardiovascular protection. |
| Asprin side effects | Gastrointestinal effects, allergic reactions, bleeding risks |
| Non-selective NSAIDs | Inhibit both COX1 and COX2 |
| Selective NSAIDs | inhibit primarily COX2 (often prefered due to reduced risk of gastrointestinal side effects) |
| NSAIDs mechanism of action | Inhibits COX1 and COX 2 which are involved in the production of prostoglandins. |
| NSAIDs uses | Pain relief, anti-inflammatory, menstrual pain, some in prevention of cardiovascular events |
| NSAIDs side effects | Gastrointestinal issues, kidney problems, cardiovascular risks |
| Acetaminophen toxic effects | can cause liver damage or kidney disease |
| What does not mix well with acetaminophen? | Alcohol, it stimulates the oxidizing enzymes that metabolize acetaminophen to its toxic metabolite. |
| Acetaminophen mechanism of action | isnt fully understood, believed to inhibit prostoglandin synthesis in the CNS. |
| What is gout? | The over production of uric acid, or reduced excretion of uric acid. Primarily occurs in men and usually involves onee joint. |
| Gout treatments | NSAIDs and colchicine |
| What reduces the synthesis of uric acid | probenecid and allopurinol |
| What is arthritis? | An autoimmune disorder characterized by chronic inflammation to the body's joints. |
| What drugs are prescribed first for arthritis? | NSAIDs |
| What drugs slow and can stop the progression of arthritis? | DMARDs |
| In periodontal disease, what is responsible for the bone loss? | PGE (Prostaglandins) |
| What causes mass destruction in the tissue? | TNF-a |
| aspirin (Bayer, Bufferin) classification | Salicylate |
| aspirin (Bayer, Bufferin) indication | Pain, fever, inflammation |
| acetaminophen (Tylenol) classification | nonsalicylate |
| acetaminophen (Tylenol) indication | pain |
| ibuprofen (Advil) classification | NSAID |
| ibuprofen (Advil) indication | Pain, fever, inflammation |
| naproxen (Aleve) classification | NSAID |
| naproxen (Aleve) indication | Pain, fever, inflammation |
| diclofenac (Cataflam) classification | NSAID |
| diclofenac (Cataflam) indication | Pain, fever, inflammation |
| nabumetone (Relafen) classification | NSAID |
| nabumetone (Relafen) indication | Pain, fever, inflammation |
| meloxicam (Mobic) classification | NSAID |
| meloxicam (Mobic) indication | Pain, fever, inflammation |
| colchicine (Colcyrs, Mitgare) classification | antigout agent |
| colchicine (Colcyrs, Mitgare) indication | gout |
| allopurinol (Zyloprim) classification | antigout agent |
| allopurinol (Zyloprim) indication | gout |
| methotrexate (Otrexup) classification | DMARD/ antimetabolite |
| methotrexate (Otrexup) indication | arthritis/ cancer |
| hydroxychloroquine (Plaquenil) classification | DMARD/ antimalaria |
| hydroxychloroquine (Plaquenil) indication | Arthritis/malaria |
| adalimumab (Humira) classification | DMARD/ TNF-a inhibitor |
| adalimumab (Humira) indication | Arthritis/Ulcerative Colitits |
| etanercept (Enbrel) classification | DMARD/TNF-a inhibitor |
| etanercept (Enbrel) indication | Arthritis |
| celecoxib (Celebrex) classification | NSAID |
| celecoxib (Celebrex) indication | arthritis |