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49 Cards in this Set

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(I hate to do this, but it was indicated as a question) What characterizes inflammation?
Redness (rubor) - Vasodilation
Heat (calor) - Vasodilation
Pain (dolor) - hyperalgesia
Swelling (Tumor) - increased vascular permeability
Loss of function (functio laesa)
What are the three distinct phases of the inflammatory response?
Acute Transient Phase - Local vasodilation and increased capillary permeability
Delayed Subacute Phase - infiltration of leukocytes and phagocytic cells (continued itching and swelling due to slowly migrating leukocytes)
Chronic Proliferative Phase - tissue degeneration and fibrosis
What are the various classes of inflammatory mediators (you probably can't name all of them because you are dumb... hehe J/K... It'd be too difficult... just name a few)
Vasoactive amines
Platelet Activating Factors
Complement system
Kinin System
Fibrinolytic Pathways
Nitric Oxide
Adhesion Molecules
Arachadonic Acid
With regards to vasoactive amines histamine and serotonin what are their functions and locations?
Histamine - abundant in granules of mast cells and function to regulate local immune responses as a potent vasodilator, gastric acid secretion, WBC chemotaxis, and decreases neutransmitter release
Serotonin - released by platelets after platelet aggregation or under the influence of PAF. Important inflammatory factor and neutransmitter similar actions to histamine
What is the function of Platelet Activating Factor (PAF)?
Released by mast cells and basophils to cause platelet degranulation
What is the active components of the complement system that affect inflammation?
C3a and C5a both degranulate mast cells and basophils.
C5a is also chemotactic
What are the inflammatory mediators of the kinin system?
Hageman factor (factor XIIa) - conversts prekallikrein to kallikrein a chemotactic factor which causes production of bradykinin. Factor XIIa also causes coagulation
What are the inflammatory cytokines?
IL-1, IL-2, TNF, and GMCSF
What are the effects of Nitric Oxide in the realm of an inflammatory mediator?
Relaxation of smooth muscle, inhibition of platelet aggregation, induction of cytokines (TNF-alpha and IFN-gamma), potent vasodilator, and pathogenesis of septic shock
What are the inflammatory mediators of Arachidonic Acid Metabolites?
Cyclooxygenase products - PGs and TXA2
Lipoxygenase products - HETEs and Leukotrienes
What are the three types of cyclooxygenases and what do they do?
COX-1: Produces Prostaglandins that mediate homeostatic functions (constitutively expressed) - role in gastric mucosa, kidney, platelets, and vascular endothelium
COX-2: produces prostaglandins that mediate inflammation, pain and fever - induced mainly in sites of inflammation but constitutively expressed in brain and kidney
COX-3: a splicing variant of COX-1
Describe the production of prostaglandins.
Phospholipase A2 cleaves membrane lipids into Arachadonic Acid which is cleaved by either COX or LIPOX to Prostaglandins and Thromboxanes or Leukotrienes through 5-HETE respectively
What are the products of COX-1?
PGE2, PGI2 - GI Protection
PGI2, TXA1 - Platelet function and Blood Flow Regulation
PGI2 - Kideny function
What are the role of the Prostaglandins?
Pain, Inflammation, Fever, and incrase in Mucus production or decrease in acid production
What are some various types of NSAIDS?
Propionic Acid Derivatives
Enolic Acids (Oxicams)
Arylacetic acid derivatives
Selective COX-2 Inhibitors
Inhibiting what enzyme that is a inflammatory mediator may reduce colon cancer by up to 50%?
What is the protype drug for the salicylates and how does it function?
Acetylsalicylic acid (Aspirin) most widely used and prescribed analgesic-antipyretic-anti-inflammatory drug.
Covalently and irreversibly modifies both COX-1 and COX-2 by acetlyating Serine-530 in the active site. Not a complete block of COX-2.
How does Aspirin affect platelets?
Aspirin inactivates COX-1 (the only one detected in platelets) leading to a decrease in production of TXA2 leading to a loss of platelet aggregation.
How many days are platelets inhibited by Aspirin?
Their entire lifespan of 8-10 days.
How is Aspirin eliminated from the body?
It is metabolized by glucouronidation
What does the Salicylate Salicymide do?
Analgesic action but lacks anti-inflammatory actions
What does the Salicylate Diflunisol (dolobid) do?
prolonged analgesic effect (2x longer than aspirin)
More potent anti-inflammatory than asirin but equal GI toxicity
Can be used for Rheumatoid and osteoarthritis
What does the Salicylate Fendosal do?
greater analgesic and anti-inflammatory activity than aspirin with less GI toxicity
How is Salicylates normally transported in the blood?
Mostly bound to the plasma protein albumin
What are the major side effects associated with salicylate intoxication?
Hyperthermia (due to inhibition and uncoupling of oxidative phosphorylation)
Gastric Irritation due to decrease in PGE2 and PGI2 which protects gastric mucosa
What is Reye's syndrome and what are the symptoms?
Aspirin given for fevers caused by viral infections (I forgot the mechanism of effects)
Acute onset of encephalopathy, liver dysfunction, and fatty infiltration fo the liver and other viscera
What are the proprionic Acid derivatives?
What is the utility of Ibuprofen?
Proprionic Acid Derivative:
Prescribed for Rheumatoid Arthritis and Osteoarthritis
99% bound to plasma proteins
Side Effects: Not recommended for pregnaant women, blurred visiona nd skin rashes, and GI effects
What is the utility of Naproxen?
Proprionic Acid Derivative:
20 times more potent than aspirin
99% bound to plasma proteins
Side Effects: GI discomfort, drowsiness and headache, Not recommended for pregnant or breast feeding women
What is the utility of Ketoprofen?
Proprionic Acid Derivative:
Orudis - effective in humans and animals
What is the utility of Oxaprozin?
Proprionic Acid Derivative:
Daypro - can be administered once daily
What are the arylacetic acid derivatives?
Indomethacin (Indocin)
Sulindac (Clinoril)
Ketorolac (Toradol)
Diclofenac (Voltaren)
Bromfenac (Duract)
Nabumetone (relafen)
What is the utility of Indomethacin?
Arylacetic Acid Derivative:
Stinky, Prescribed for Rheumatoid Arthritis and other arthritis
What is the utility of Sulindac?
Arylacetic Acid Derivatives:
8 times more effective than aspirin but less potent than indomethacin
What is the utility of Ketorolac?
Arylacetic Acid Derivative:
Potent Analgesic but only moderate anti-inflammatory
Greater analgesia only when used IM
What is the utility of Etodolac?
Arylacetic Acid Derivatives:
Shown to be selective for COX-2
Postoperative Analgesia for 6-8 hours
What is unique about Nabumetone?
Arylacetic Acid Derivative:
Prodrug - converted to active drug (6-methoxy-2-napthylacetic acid) in the liver.
What are the Enolic Acids (Oxicams)?
Piroxicam (Feldene)
Meloxicam (Mobic)
What is the utility of Piroxicam?
Enolic Acid:
Better tolerated than asprin or indomethacin
Once a day
Additive anti-inflammatory effect: inhibits migration of neutrophils
What is the ultility of Meloxicam?
Enolic Acid:
Osteoarthritis and Rheumatoid Arthritis
More selective COX-2 Inhibitor
How is that most if not all NSAIDS have the ability to increase the affects of Warfarin?
By competitively binding for plasma proteins the NSAIDS displace Warfarin allowing more to float freely in the blood increasing its effects.
How do NSAIDS affect Thiazides?
THey decrease the effectiveness of Thiazides by competing for excretion space in the proximal tubule
How do NSAIDS affect methotrexate?
May increase its toxicity by competing for tubular secretion
What effects do NSAIDS have on Lithium?
Causes increased toxic doses by competing with lithium for renal elimination
What are some up and coming COX-2 specific inhibitor drugs and what is so great about them?
Celecoxib (celebrix)
Refecoxib (VioXX)
Valdecoxib (Bextra)
Not better at treating symptoms but do not cause GI or renal side effects
There effectiveness is identified by their IC50 Cox2 to IC50 Cox1 ratio. (IC50 - Inhibitory COncentration 50%)
Want low Cox2 IC50 and High Cox1 IC50
What are the benefits of Acetaminophens and what are they?
provide analgesic and antipyretic activity possibly inhibiting COX-3 in the CNS and maybe weakly inhibiting other COX enzymes
What are the side effects of Acetaminophen compared to NSAIDS?
Little to no anti-inflammatory reaction
No gastric irritation or ulceration
No platelt function interference
Does not inhibit neutrophil activation
No effect on cardiovascular or respiratory systems
What is some general info on acetaminophen?
20-50% bound to plasma proteins
90-100% recovery in urine as hepatic conjugates from glucuronidation or sulfation after first day of therapeutic dose
Converted into N-acetylimidoquinone (NAPQI) - a toxic metabolite
Contraindicated with alcohol intoxication due to depletion of glutathione levels
What is an antidote for tylenol overdose?
N-acetyl-cysteine (mucomyst, mucosil) IV because it replenishes Glutathione