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Acetaminophen APAP paracetamol Analgesic antipyretic very weak anti inflammatory No gastric erosion bleeding no effect on platelets bleeding or urate excretion no effect on CV or respiratory systems Useful for patients intolerant to ASA who need analgesic or antipyretic effect Synergistic analgesia combined with opioid o Oxycodone APA codeine APAP Acetaminophen Toxicity Allergic skin rash Hypersensitivity unrelated to ASA Dose dependent potentially fatal hepatic or renal necrosis Highly reactive metabolite depletes hepatic glutathione and reacts with hepatic proteins leading to hepatic necrosis Max daily APAP dose is 1500 mg 48k overdoses annually in US Leading cause of acute liver failure in hospitalized patients Gold A DMARD Aurothioglucose gold sodium thiomalate usually IM Auranofin oral Toxicity o Skin mucous membranes esp mouth blue grey pigmentation o Proximal tubule of kidney o Severe blood dyscrasias Contraindications o Renal and hepatic disease o Infectious hepatitis o Blood disorders Leflunomide Immunomodulatory agent unique mechanism of action Inhibits mitochondrial enzyme dihydroorotate dehydrogenase DHODH involved in de novo synthesis of pyrimidine ribonucleotide uridine Active metabolite has a half life of two weeks Reduces signs and symptoms of inflammatory arthritis delays radiologic progression Anti TNFa Drugs Etanercept Enbrel o Recombinant fusion protein with two receptors for TNF a o Approved to tx RA when other drugs fail Both delay radiographic progression of RA High affinity and structural complementarily Mop up TNF alpha in extracellular fluid binding with no action consequences to the TNF alpha cannot bind to the receptors that are in the host Interleukin 1 Receptor Antagonists Anakinra Kineret Recombinant form of human IL 1 receptor antagonist Approved for tx of RA IL 1 is a primary pro inflammatory cytokine and is involved in cartilage damage and bone resorption in RA Requires S C administration Drugs to Treat Gout Colchicine Allpurinol Probenecid drugs that increase urinary excretion of uric acid Sulfinpyrazone Drugs to Reduce Uric Acid Levels Allopurinol Inhibits xanthine oxidase to reduce uric acid formation The immediate two steps just above the uric acid in pathway uses the same enzyme Inhibits two enzymes in a series in a pathway it is most effective Prevents relapses of gouty arthritis and complications of urate nephropathy Uricosuric Agents o Probenecid blocks tubular reabsorption of uric acid o Uric acid is only excreted through urination o Glomerular filtration in renal tubule then the reabsorption uptake pump lumen of renal tubule back into circulation o To increase rate of secretion inhibit active transport process Colchicine Anti inflammatory specific to gout but is not analgesic or uricosuric Used to tx acute gouty attack and reduces frequency of attacks FDA approved to tx familiar Mediterranean fever mechanism o Inhibits activity of leukocytes by decreasing their migration to the site of inflammation thereby reducing inflammation High toxicity o N V GI pain diarrhea chronic myopathy agranulocytosis aplastic anemia alopecia Old drug shuts down gouty attack NSAID can be effective to shut down gouty attack but most cause uric acid to go up or down Terms Infection invasion and multiplication of microorganisms in body tissues Localized UTI prostatitis otitis media meningitis wounds Systemic throughout the body such as a blood borne infection Colonization formation of population groups of the same microbe o May refer to normal flora or presence of pathogens in a particular tissue o May be an active infectious disease or just potential for infection Bacteremia presence of living bacteria in blood o Puncture wounds cuts scrapes dental work Septicemia a systemic infection caused by bacteria living and growing in bloodstream Sepsis multiple organs infected and damaged due to microbes and their toxins in the blood o Maladaptive reaction to severe infection including inflammation Sub Groups of Anti Infective Agents Antimicrobial Agents narrow spectrum extended spectrum broad spectrum Antiviral Agents Antifungal Agents Antiparasitic Agents o Antimycobacterial agents o Antiprotozoal agents o Anthelminthic agents General Mechanisms of Antimicrobial Agents Enzyme inhibition anti metabolite o Drug inhibits enzyme and the substrate cannot produce a product o Drug inhibits enzyme and used by enzyme to produce a phony product resulting in an antimicrobial effect o Sulfonamids trimethoprim bacterial enzymes inhibit enzyme o Acyclovir saquinavir viral enzymes inhibit viral enzymes tetracycline macrolides chloramphenicol Cell Wall Synthesis Inhibition o Beta lactams vancomycin Protein Synthesis Inhibition o Aminoglycosides antibacterial Nucleic Acid Synthesis Inhibition o Fluoroquinolones Cell Wall Permeability Disruption o Polyene and imidazole antifungals polymixins o PBN antifungal agent and punches holes in wall of fungal cells to kill them Bacteriostatic vs Bacteriocidal Bacteriostatic Agents o Only inhibit microbial growth o More dependent upon host immune defense mechanism to eradicate infection than bacteriocidal agents o Depends on status of patient s immune system bring numbers of bacteria down to a low value that the immune system can destroy Sulfonamides and trimethoprim Most protein synthesis inhibitors o Chloramphenicol o Clindamycin o Macrolides erythromycin o Tetracyclines Nitrofurantoin protozal infections Ethambutol parasites Bacteriostatic vs Bacteriocidal Bacteriocidal Agents kill bacteria o Cell wall synthesis inhibitors time dependent killing must finish treatment o Beta Lactams penicillin cephalosporins o Vancomycin Aminoglycosides only protein synthesis inhibitor that is cidal concentration dependent killing above minimal concentration to be effective very serious infections hospital setting Quinolones concentration dependent killing Bacitracin polymyxins Metronidazole MIC vs MBC MIC minimum concentration that inhibits cell growth MBC minimum concentration that will kill 99 9 of initial inoculum Complications of Antimicrobial Therapy Hypersensitivity reactions o Minor skin rash fever itching chills o Major anaphylaxis peripheral vasodilation redness color Stevens Johnson syndrome toxic epidermal necrolysis Hematologic Effects get baseline data from patient for bone marrow function Nephrotoxicity cause damage to kidney water insolubility dangerous VIIIth cranial nerve damage impairs balance and or hearing Superinfection secondary


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NU PHSC 4340 - Notes

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