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VetMed Pharmacology8

Anti-Inflammatory Pharmacology

QuestionAnswer
Non-Steroidal Anti-Inflammatory Drug class of pharmaceutical that exerts an anti-inflammatory effect by inhibiting prostaglandin and/or leukotrienes but is not composed of a cholesterol "core"
COX-1 Function synthesizes "protective" prostaglandins like PGI2 in the GI mucosa and renal tubule epithelium
COX-2 Function synthesizes pro-inflammatory prostaglandins
Non-Selective NSAIDs MOA inhibit activity of COX-1 and COX-2 results in decreased PGG2 and PGH2 production
PGG2 and PGH2 precursors for general prostaglandin synthesis
Only NSAID that Permanently Inhibits COX aspirin (through acetylation) possibly phenylbutazone
NSAID General Properties most are organic acids high plasma protein binding ionized form more extensively excreted in urine
Pathophysiology of NSAID Action suppress inflammatory prostaglandin synthesis suppress WBC degranulation and diapedesis decrease injury/destruction from WBCs reduce tissue edema reduce visceral and musculoskeletal pain suppresses hyper-coagulation states reduces life-threatening p
Best NSAID for Visceral Abdominal Pain flunixin meglumine (Banamine)
Best NSAID for Musculoskeletal Pain phenylbutazone
Novel NSAID Uses tx certain neoplastic dz such as osteosarcoma maintain gestation closer of premature PDA diagnostic determination of bone marrow platelet production
NSAID Sequelae GI ulceration renal toxicity if co-administered w/ aminoglycosides increase risk of haemorrhage renal toxicity (pseudo-OD) if hypoproteinemic displacement of protein-bound pharmaceuticals
C/I for NSAIDs renal tubular dysfunction GI ulceration existing/ongoing haemorrhage
Non-Selective NSAIDs salicylic acid para-aminophenols indole/indene acetates heteroacryl acetic acid arylpropionoates anthranilic acid enolic acids alkanones phenylbutazone, flunixin meglumine
Selective COX-2 Inhibitor NSAID MOA inhibit inflammatory PG's but avoid PGI2 inhibition
Selective COX-2 NSAIDs diaryl-substituted furanones diaryl-substituted pyrazoles indole acetic acid suflonanilides misc - meloxicam, topoxalin, carprofen, deracoxib
Metabolization of NSAIDs glycine, either/phenolic glucuronide, ester/acyl glucoronide conjugation rxns in mitochondria and smooth-ER in hepatocytes
Metabolization of Aspirin hydrolyzed to salicylic acid in GI tract, plasma, liver, and RBC cytosol
Primary Excretion of NSAIDs glomerular filtration/tubular secretions
Decreases Renal Tubular Re-absorption NSAID conjugation high urinary flow
Dipyrone NSAID that is less likely to mask severe visceral pain requiring surgery
Leukotrienes generated by the biochemical conversion of membrane phospholipids to arachidonic acid with lipoxoygenases to leukotrienes
Proinflammatory Leukotrienes ("4-series") LTB4 LTC4 LTD4 LTE4
Anti-inflammatory Leukotrienes ("5-series") LTB5 LTC5 LTD5 LTE5
Zyleuton (Zyflo) orally active inhibitor of 5-lipoxygenase
Monteleukast (Singulair) leukotriene receptor antagonist
Zafirlukast (Accolate) oral leukotriene receptor antagonist
Cetirizine hydrochloride (Zyrtec) antihistamine and a racemic selective H1 receptor antagonist
Leukotriene MOA's (4) Anti-FLAP Agents LTB4 Receptor Antagonists 5-Lipoxygenase Inhibitor Agents LTC4, LTD4, LTE4 Receptor Antagonists
Advantages of Leukotriene Inhibitors suppress symptoms associated primarily with leukotriene over-production avoid side effects of anti-PG NSAIDs avoid CNS side effects of anti-histamines avoid side effects of glucocorticoids
Theophylline Analogs MOA inhibit cyclic nucleotide phosphodiesterase resulting in increased cAMP and increased cGMP --> bronchodilation
Antihistamine Fxn block histamine H1 receptors
Results of Stimulation of H1 Receptors vasodilation bronchoconstriction endothelial cell separation pain/itching
Cromolyn Sulfate antihistamine that suppresses degranulation of mast cells and leukotriene release used to prevent bronchospasms in feline asthma
Glucocorticoid anti-inflammatory agent that possess a cholesterol core structure highly bound to plasma proteins most are conjugated with sulfate or glucoronide
Glucocorticoid MOA inhibits phospholipase A2 --> reduces availability of arachidonic acid substrate --> decreased production of COX, leukotrienes, HETE, HPETE also stabilizes cellular membranes inhibition of PA2 inhibition of nuclear receptor complexes --> immunosuppress
Glucocorticoid Physiological Effects resist stressful scenarios stimulates gluconeogenesis, enhances glycogen deposition adipose tissue redistribution mediates lipolysis
Glucocorticoid Metabolism sequential addition of H+ or O atoms --> conjugation rxns
Synthetic Glucocorticoid Metabolism hepatic 11beta-hydroxysteroid dehydrogenase
Clinical Applications of Glucocorticoids anti-inflammatory vascular collapse cerebral edema immunosuppression renal disease hepatic disease lymphoreticular neoplasia
Antu-Inflammatory More Effective in Managing Visceral Pain NSAIDs over Glucocorticoids
Glucocorticoid Sequelae protein synthesis inhibition immunosuppression GI ulceration corneal ulcer exacerbation renal dysfunction degenerative joint disease
Steroid Hormone Inhibitors mitotane ketoconazole (Cushing's/Hyperadrenocorticism) aminoglutethimide (breast/prostate carcinoma) metyrapone (Cushing's) trilostane (cancer) cyproheptadine (PDH) pergolide (PDH)
Crysotherapeutics MOA suppress abnormal immune response by inhibiting macrophage and T-lymphocyte maturation
Crysotherapeutic Uses may cure auto-immune conditions Ex: pemphigus foliaceus, pemphigus vulgaris, rheumatoid arthritis, sjogren syndrome, lupus
Diagnostic Use of Corticosteroids and ACTH differentiating a pituitary tumor from an adrenal tumor in Cushing's syndrome
Ketoconazole (agent, fxn, sequelae) antifungal agent inhibits biosynthetic capacity of cytochrome P450, making it one of the most effective tx of Cushing's causes hepatic dysfxn and inhibits Rx activation
Created by: 26509889
 

 



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