Pharmacology Ch 13 Antiinflammatory Drugs

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Pharmacology Ch 13 Antiinflammatory Drugs
2015-10-15 01:39:21
Antiinflammatory drugs

Pharm ch 13 Antiinflammatory
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  1. WBC at site of inflammation do 3 things...
    • 1) Destroy bacteria and direct other cells of the process 
    • 2) Start to clean up mess by removing dying cells
    • 3) Pave the way for healing process
  2. Main WBC involved in inflammation
    Neutrophils followed by lymphocytes
  3. WBC squeeze through a junction between endothelial cell
  4. How do corticosteroids work?
    Block action of phospholipase and stops the progression of inflammation
  5. 2 kinds of corticosteriods
    • Synthetic corticosteroids
    • Mineralcorticoids
  6. Synthethic corticosteroids naturally are called..
  7. Where are glucocorticoids released from?
    Zona fasciculata
  8. How do glucocorticoids work?
    • Inhibit phospholipase
    • Deposit glycogen in liver
    • Increase blood glucose levels
  9. Have little or no effect of inflammation, associated with water and electrolyte balance
  10. 3 types of corticosteroids
    • Short acting
    • Intermediate acting
    • Long acting
  11. Last less than 12 hours, hydrocortisone which is cortisone until it goes through biotransformation twice
    Short acting corticosteroid
  12. Lasts between 12 and 36 hours, Prednisone and Prednisolone.
    Intermediate acting corticosteroid
  13. Lasts longer than 48 hours, Dexamethasone. Called "methasones"
    Long acting corticosteroids
  14. 3 liquid forms of corticosteroids
    • Aqueous solution
    • Alcohol solution 
    • Suspension
  15. Combined with salt to make soluble in water
    • Aqueous solution 
    • EX: Sodium phosphate and sodium succinate
  16. No sallt and no additives
    • Alcohol solution
    • EX: Dexamethasone
  17. Suspended in diluent. Crystals suspension dissolve over several days and release small amounts of glucocorticoid each day and provide prolonged duration
  18. Corticosteroid effects
    • Reduce inflammation
    • Reduce capillary permeability 
    • Inhibit fibroblasts
    • Suppress T-lymphocytes
    • Catabolic effect on proteins
    • Causes abortions
    • Causes stress triad
  19. How do corticosteroids reduce inflammation?
    By blocking conversion of arachidonic acid to eicosanoids
  20. How do corticosteroids reduce capillary permeability?
    By reducing production of cell factors that cause increased vascular permeability of the capillaries and so help maintain integrity of the capillaries and reduce some of the mechanisms of swelling in injured tissues
  21. How do corticosteroids cause abortions?
    Due to exogenous corticosteroids. After 20 days of gestation the bitch will abort in 2-5 days after steroids.
  22. What is a stress triad?
    • Decreasing numbers of lymphocytes and eosinophils. Increase in neutrophils and thromboycytes. 
    • Lymphopenia, eosionopenia and neutrophilia
  23. Jugular is located between what two muscles?
    Sternocephalicus and brachiocephalicus
  24. Why do we not give a steroid shot before giving vaccines to patients who have reactions?
    Steroids suppress immune system and allows virus to replicate inside the animal
  25. Contraindications for steroids
    • Systemic or local fungal infection
    • Avoid vaccines 
    • Suppress immune system 
    • Increase platelets and neutrophils
    • Decrease lymphocytes, eosinophils and monocytes
  26. Iatrogenic diseases caused by steroids
    • Hyperadrenocorticism (Cushings)
    • Hypoadrenocorticism (Addisons)
  27. Cushings disease
    Can occur naturally or by parenteral or oral Rx of corticosteroids by clinician. Selegiline hydrochloride suppresses MOTB which suppresses dopamine and cortisol from zona fasciculata
  28. Symptoms of cushings disease
    Alopeica, muscle wasting, polyuria, polydipsia, polyphagia, pot belly and thin skin
  29. Addisons disease
    Results from animal being taken off steroids after years of administration can go from hyper to hypo over night
  30. How do NSAID stop inflammation?
    • By blocking activity of cyclooxygenase and subsequent production of prostaglandins
    • Inhibiting COX-1 and COX-2 to varying degrees
  31. Why are NSAID's not considered analgesics
    They reduce discomfort and pain associated with inflammation but not visceral or somatic pain at the CNS level
  32. Side effects of NSAID's
    • GI ulcers
    • Bone marrow suppression
    • Tissue necrosis
  33. What was used to combat pain before modern medicine?
    Willow bark, active ingredient is salicylic acid
  34. How did Bayer make aspirin?
    Added acetyl group to salicylic acid and created acetylsalicylic acid
  35. What happened in 1971 in regards to NSAID's?
    JR Vane discovered that NSAID's blocked production of prostaglandins from arachidonic acid, creating the Vane Model
  36. What happened in 1976 in regards to NSAID's?
    Prostaglandin synthase was identified as cyclooxygenase (COX) and showed NSAID exert their effects by inhibiting production of COX and prostaglandins
  37. NSAID examples
    • Phenylbutazone- inhibits COX
    • Acetylsalicylic acid (Aspirin) 
    • Acetaminophen (Tylenol) 
    • Flunixin Meglumine (Banamine)- cattle/horses
    • Carprofen (Rimadyl)- used for degenerative joint disease or postoperative pain of soft tissue
    • Ibuprofen (Advil)- dont use on dog/cats
    • Ketoprofen- Horses inflammation of muscoskeletal disorders
    • Naproxen- horse/humans 
    • Dipyrone- old NSAID horses for colic
  38. COX-1 plays a role in...
    Normal tissue function
  39. COX-2 plays a role in...
    With pain, fever, inflammation
  40. COX-2 Inhibitors
    Coxibs are compounds that target inhibition of COX-2, one of the main enzymes in inflammation pathway. Older NSAID targeted COX-1 as well causing gastric side effects.
  41. What year was COX-1 and COX-2 first discovered?
  42. Which COX has a larger active site?
  43. COX-1 is always present in many tissues and therefore...
    Enzymes are called “housekeeping” prostaglandins and are required for homeostatic activity in the GI tract, kidney, and platelets
  44. Which COX inhibitors are less toxic?
    COX-2 inhibitors
  45. Proinflammatory prostaglandins are produced by the induction of which COX?
    COX-2, drugs producing specific COX-2 effects would be more effective in producing analgesic, anti inflammatory and antipyretic effects.
  46. Functions of COX-1
    • Thromboxane A2 required for normal  platelet function
    • Prostaglandin E2 required for sodium homeostasis in kidneys
    • Endogenous prostaglandins function to protect GI tract
  47. Functions of COX-2
    • Embryo implantation
    • Apoptosis in cancer cells (shrinkage)
    • Cancer pain-reduction
    • Bone response to mechanical stress
    • Vasodilation 
    • Inflammation
    • Receptors for pain
  48. What happens if you inhibit COX-1 enzymes for a long time?
    • GI ulceration, erosion
    • Adverse effects on renal functions
    • Problems with homeostasis (platelets)
  49. Inhibition of COX-1 and COX-2 produces what 2 things?
    • Decrease in pain
    • Decrease of inflammation
  50. Joint injury and/or cartilage damage triggers inflammation and what...
    COX-2 functions with increased production of inflammatory eicosanoids, PGE2 from arachidonic acid
  51. PGE2 promotes production of what..?
    Matrix metalloproteinases (MMPs), enzymes that break down cartilage
  52. In regards to joint mobility inflammation promotes oxidative stress, what does that mean?
    Inflammation decreases tissue inhibitor of metalloproteinase (TIMP) which normally reduces impact of cartilage-damaging MMPs
  53. How does diet help with joint mobility?
    Diet encourages COX-2 to convert eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) into less inflammatory PGE3 resulting in less PGE2 and less cartilage damage
  54. What are chondroprotective agents?
    Medicines that slow the process of arthritis in joints by supporting the health of the joint cartilage
  55. Examples of chondroprotective agents
    • Polysulfated glycosaminoglycans (PSGAGs)
    • Hyaluronic acid 
    • Glucosamine and chondroitin sulfate
  56. How do PSGAGs work for the joints?
    • Trap water and act as a moisturizer for cartilage
    • Adequan injectable reduces activites of MMPs in joint fluid that degrade cartilage
  57. How does hyaluronic acid work for the joints?
    • Natural component found in synovial fluid and acts as a lubricant and suppresses PGE2
    • Legend or Hyalovet IV or injected into joint space
  58. How do glucosamine and chondroitin sulfate work on joints?
    • Increase efficiency of chondrocytes to repair cartilage 
    • Stimulates prodution of hyaluronic acid
    • Inhibit destructive MMP
    • EX: Cosequin
  59. IC50 Data
    • Used to differentiate activity of NSAIDs and their effects on COX-1 and COX-2
    • Value is a result of an in vitro test tube under controlled conditions
    • The higher the value indicates preference for inhibiting COX-2 over COX-1
  60. Coxib- class NSAIDs
    • Rimadyl
    • Ectagesic
    • Deramax
  61. Why not give cats or beagles aspirin?
    • The effect is on the liver metabolism, the alteration and number of RBCs, and the inability of the hemoglobin to carry oxygen and carbon dioxide.
    • Hemoglobin is converted to Methemoglobin which cannot carry oxygen or carbon dioxide.
  62. Examples of drugs that can be used pre operation
    • Acepromazine
    • Hydromorphine
    • Glycopyrrolate 
    • Carprofen
  63. Example of drugs that can be used post operation
    • Carprofen
    • Hydromorphine
    • Bupivacaine
  64. Group of adrenocorticosteroids associated with antiinflammatory response
  65. COX produced eicosanoids cause platelets to adhere to each other and thus contribute to the clotting mechanism
  66. Means loss of hair and clinical sign of Cushings disease
  67. Type of immunity provided by antibodies
    Humoral immunity
  68. Combination of NSAID use plus arterial hypotension can produce this kidney condition
    Renal papillary necrosis
  69. Lipoxygenase produced what eicosanoid
  70. Diseases caused by the bodys own defense mechanisms turning against its own tissues, example would be lupus
    Autoimmune reactions
  71. Increase in neutrophils
  72. Effect meaning that tissue is being destroyed or broken down
    Catabolic effects
  73. Type of cell that produces antibodies against invading pathogens
  74. Refers to the outer part of the adrenal gland
  75. Another name for hyperadrenocorticism
    Cushings syndrome
  76. Enzyme that produces prostaglandins and thromboxanes
  77. Collective term for all prostaglandins, leukotrienes, and thromboxanes produced by the arachidonic acid pathway
  78. Means low numbers of eosionphils
  79. Condition characterized by clinical signs consistent with insufficient amounts of glucocorticoids
    Addisons disease
  80. Production of glycogen in the liver
  81. Hormone released from the hypothalamus that stimulates pituitary to release ACTH
    Corticotropin-releasing factor
  82. Means decreased monocytes
  83. Means decreased size and seen in muscles and skin in animals with hyperadrenocorticism
  84. Means that the animal has an elevated level of either natural cortisol or exogenous corticosteroids
  85. Means the patient is exhibiting clinical signs consistent with low levels of corticosteroids
  86. Means disease or condition caused by the vet
  87. Hormone released by adrenal gland, is a mineralcorticoid
  88. Arachidonic acid is acted on by COX and this enzyme to produce the eicosanoids
  89. Group of adrenocorticosteroids affects mainly the electrolytes and water balance in the body with little or no antiinflammatory effect
  90. Creation of glucose from amino acids
  91. Decrease of lymphocytes in circulation
  92. Ibuprofen, ketoprofen, naproxen all belong to the same group of compounds charaterized by this chemical structure
    Propionic acid
  93. Type of body defense mechanism characterized by cells that attack pathogens or foreign proteins
    Cell-mediated immunity
  94. Thromboxanes and these inflammatory mediators are produced by COX
  95. Series of enzymes resulting in the production of eicosanoids after an injury
    Arachidonic acid pathway
  96. Cells involved in cell-mediated immunity, dont produce antibodies
  97. Hormone released by the pituitary gland that stimulates the adrenal gland to produce corticosteroids
    Adrenocorticotropic hormone (ACTH)
  98. NSAID that comes in a rapidly disintegrating tablet, called a dual-pathway NSAID
  99. Chondroprotective agent that is a component of the joint synovial fluid, acts a lubricant
    Hyaluronic acid
  100. Intermediate acting glucocorticoid that is not a pred
  101. Older NSAID used on horses for relief of inflammation associated with the musculoskeletal system
  102. First COX-2 selective inhibitor released for vet medical use in US
  103. Intermediate acting corticosteroid in active form
    Prednisolone, methylprednisolone, triamcinolone
  104. Antiinflammatory that works differently from NSAIDs or glucocorticoids
  105. Short acting glucocorticoid, topical
  106. Besides carprofen the other three COX-2 selective inhibitors used in vet medicine
    • Etodolac (EtoGesic)
    • Deracoxib (Deramaxx)
    • Meloxicam (Metacam)
  107. Long acting glucocorticoid that comes in aqueous solution, alcohol form, and suspension form
  108. Prototype drug for the salicylates, OTC, hits both COX-1 and COX-2
  109. Derivatives of propionic acid, OTC drug, high incidence of gastric ulcers when given to dogs
    Ibuprofen, ketoprofen, naproxen
  110. NSAID used primarily in horses for relief from colic, has more analgesic effect then phenylbutazone
    Flunixin meglumine
  111. Chondroprotective agent that mimics components of normal joint cartilage, traps water molecules and helps provide springy charateristics
  112. Intermediate acting corticosteroid, must pass through liver to be converted to its active form, prednisolone
  113. Nutriceutical chondroprotective agents, precursors for PSGAGs
    Glucosamine and chondroitin sulfate
  114. Human OTC drug used to relieve discomfort from pain but is not an NSAID
  115. TRUE OR FALSE. Long acting glucocorticoid drug combined with acetate, diacetate, pivalate or valerate would identify it as an aqueous solution
  116. TRUE OR FALSE. Vaccines should not be given to a dog that has been on prednisone for allergic skin reactions because the immune system will not be able to respond
  117. TRUE OR FALSE. Hypoalbuminemic animals the dose of NSAIDs may have to be increased to achieve same effect on tissues
  118. TRUE OR FALSE. Most common target organs for NSAID toxicity are the kidney and liver
    False, kidney and GI tract
  119. TRUE OR FALSE. NSAIDs should be able to provide enough analgesia to allow and animal with a broken leg to be positioned for a radiograph
  120. Are increased retention of sodium associated with glucocorticoid effects?
  121. Is maintain integrity of the capillaries associated with glucocorticoid effects?
  122. Are decreased fibroblast activity associated with glucocorticoid effects?
  123. Are decreased t-lymphocyte activity associated with glucocorticoid effects?
  124. Are decreased scar tissue formation associated with glucocorticoid effects?
    Yes, decreased fibroblasts
  125. Are increased b-lymphocyte activity associated with glucocorticoid effects?
  126. Is lymphocytosis associated with glucocorticoid effects?
    No, caused lymphopenia
  127. Are increased eosinophils and monocytes associated with glucocorticoid effects?
    No, cause eosinopenia and monocytopenia
  128. Are increased neutrophils associated with glucocorticoid effects?
  129. Are muscle wasting and atrophy associated with glucocorticoid effects?
  130. What effects do NSAIDs have on the stomach and intestinal mucus production?
    Decrease mucus production
  131. What effects do NSAIDs have on production of sodium bicarbonate by the GI tract wall?
    Decrease sodium bicarbonate secretion
  132. What effects do NSAIDs have on the repair of the GI epithelial cells?
    Slow healing of the GI tract wall

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