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201 Cards in this Set
- Front
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Antimicrobial Tx -- Mechanism of Action: The penicillin type drugs work by blocking ------ synthesis, specifically by inhibiting this molecule from cross-linking?
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blocks bacterial cell wall synthesis by inhibition of peptidoglycan synthesis.
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Antimicrobial Tx -- Mechanism of Action: Which other drugs (aside from penicillin) have this same mechanism of action?
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Imipenem, aztreonam and cephalosporins
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Antimicrobial Tx -- Mechanism of Action: Bacitracin, vancomycin and cycloserine block the synthesis of this molecule, preventing cell wall synthesis
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peptidoglycans
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Antimicrobial Tx -- Mechanism of Action: These drugs block the 50s ribosomal subunit
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clindamycin, chloramphenicol, erythromycin, lincomycin, linezolid, streptogramins "Buy AT 30, CELL at 50"
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Antimicrobial Tx -- Mechanism of Action: These drugs block the 30s ribosomal subunit
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Aminoglycosides and tetracyclines "Buy AT 30, CELL at 50"
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Antimicrobial Tx -- Mechanism of Action: These drugs block nucleotide synthesis by interfering with the folate pathway
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Sulfonamides (e.g. Bactrim), trimethoprim
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Antimicrobial Tx -- Mechanism of Action: These drugs block DNA topoisomerases
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Quinolones (e.g. Cipro)
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Antimicrobial Tx -- Mechanism of Action: Which drug blocks mRNA synthesis
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rifampin
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Antimicrobial Tx -- Mechanism of Action: Which are the bacteriacidal Abx
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Penicillin, cephalosporin, vancomycin, aminoglycosides, fluoroquinolones, metronidazole
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Antimicrobial Tx -- Mechanism of Action: These drugs disrupt the bacterial/fungal cell membranes
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polymyxins
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Antimicrobial Tx -- Mechanism of Action: These specific disrupt fungal cell membranes
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amphotericin B, nystatin, fluconazole/azoles (FAN the fungal cell membranes)
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Antimicrobial Tx -- Mechanism of Action: What is the mechanism of action of Pentamidine
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Unknown
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Penicillin: Which is the IV form and which is the oral form
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G = IV, V=oral
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Penicillin: Which of these is not a mechanism of penicillin action: (1) binds penicillin-binding protein, (2) blocks peptidoglycan synthesis, (3) blocks transpeptidase catalyzed cross-linking of cell wall and (4) activates autolytic enzymes
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Penicillin does not block peptioglycan synthesis, bacitracin, vancomycin and cycloserine do that
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Penicillin: T or F: penicillin is effective against gram pos and gram neg rods
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False: penicillin is used to treat common streptococci (but not staph), meningococci, gram pos bacilli and spirochetes (i.e. syphilis, treponema). Not used to treat gram neg rods.
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Penicillin: What should you watch out for when giving penicillin?
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Hypersensitivity rxn (urticaria,severe pruritus) and hemolytic anemia
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Methicillin, nafcillin, dicloxacillin: These drugs are used mainly for what type of infection
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Staphlococcal infection (hence very narrow spectrum)
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Methicillin, nafcillin, dicloxacillin: T or F: these drugs have the same mechanism of action as penicillin
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TRUE
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Methicillin, nafcillin, dicloxacillin: Are these drugs penicillinase resistant? If so why?
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Bulkier R group makes these drugs resistant to penicillinase
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Methicillin, nafcillin, dicloxacillin: What should you watch out for when giving these drugs?
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Hypersensitivity rxn (urticaria,severe pruritus); methicillin can cuase interstitial nephritis
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Ampicillin and amoxicillin: T or F: these drugs have the same mechanism of action as penicillin
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TRUE
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Ampicillin and amoxicillin: Which has greater oral bioavailability?
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amOxicillin (O for Oral)
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Ampicillin and amoxicillin: What do you use these for?
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Ampicillin/amoxicillin HELPS to kill enterococci (H. influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella)
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Ampicillin and amoxicillin: Can penicillinase effect these drugs efficacy?
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Yes, they are penicillinase sensitive
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Ampicillin and amoxicillin: Why not give these drugs with a penicillinase inhibitor. Name one.
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clavulanic acid
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Ampicillin and amoxicillin: What should you watch out for when giving these drugs?
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Hypersensitivity rxn (ampicillin rash), pseudomembranous colitis
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Carbenicillin, piperacillin, ticarcillin: Why are these considered to have an extended spectrum?
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Because they are effective against pseudomonas and other gram neg rods (enterobacter and some species of klebsiella)
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Carbenicillin, piperacillin, ticarcillin: What should you watch out for when giving these drugs?
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Hypersensitivity rxn
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Carbenicillin, piperacillin, ticarcillin: Why does concomitant administration with clavulanic acid increase the efficacy of these drugs?
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Because they are penicillinase sensitive. (only piperacillin and ticarcillin)
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Cephalosporins: What is the mechanism of action of Cephalosporins?
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inhibit cell wall synthesis
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Cephalosporins: How are they similar/different from penicillin?
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both have a beta-lactam ring structure but cephalosporins are less susceptible to penicillinases
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Cephalosporins: What are the main similarities/difference between 1st and 2nd generation cephalosporins?
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2nd gen has extensive gram neg coverage but weaker gram pos coverage
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Cephalosporins: 1st gen covers what bugs?
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gram positives (staph and strep), Proteus mirabilis, E. coli, Klebsiella (PEcK)
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Cephalosporins: 2nd gen covers what bugs?
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gram positives (staph and strep) though less so, H. influenzae, Enterobacter aerogenes, Neisseria, Proteus mirabilis, E. coli, Klebsiella (HEN PEcK)
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Cephalosporins: What can 3rd generation drugs do that 1st and 2nd generation can't?
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Cross the blood brain barrier
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Cephalosporins: What are some other benefits of 3rd gen?
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better activity against gram neg bugs resistant to beta-lactam drugs. Ceftazidime for Pseudomonas and ceftriaxone for N. gonorrhea
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Cephalosporins: What are the benefits of 4th gen (e.g. Cefipime)?
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increased activity against Pseudomonas, gram pos organisms and more beta-lactamase resistant (i.e. 4th gen combines 1st gen and 3rd gen characteristics into super drug)
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Cephalosporins: What drugs should you avoid taking with cephalosporins?
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Aminoglycosides (increases nephrotoxicity) and ethanol (causes a disulfiram-like rxn -- headache, nausea, flushing, hypotension)
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Aztreonam: When would you use aztreonam?
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Only to treat Klebsiella, Pseudomonas and Serratia sp.
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Aztreonam: Is it beta-lactamase resistant?
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Yes, this is one of the huge benefits of the drug, and it is not cross-reactive with PCN!
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Aztreonam: Which population of pt. is this drug good for?
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The PCN-allergic patient that can't take aminoglycosides b/c of renal insufficiency
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Aztreonam: Are there any toxicity issues with this drug?
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Not really. Generally well tolerated with occasional GI upset. Vertigo, Headache and rare hepatotoxicity have been reported.
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Imipenem/cilastatin: What is imipenem?
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broad spectrum beta-lactamase-resistant abx
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Imipenem/cilastatin: What do you always administer it with and why?
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cilastatin -- it decreases inactivation of imipenem in renal tubules
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Imipenem/cilastatin: What do you use it for?
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Gram pos cocci, gram neg rods and anaerobes (broad spectrum)
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Imipenem/cilastatin: What bug is it the drug of choice for?
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Enterobacter
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Imipenem/cilastatin: What are its side-effects
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GI distress, skin rash, seizures at high conc.
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Vancomycin: Is it bactericidal or bacteriastatic and why?
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Bactericidal because it blocks cross linkage and elongation of peptidoglycan by binding D-ala D-ala protion of cell wall.
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Vancomycin: How does resistance to Vanco occur?
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D-ala D-ala is replaced with D-ala D-lactate which vanco does not block
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Vancomycin: What is it used for?
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Used for serious infection that is resistant to other drugs (e.g. gram pos multi-drug resistant organisms like S. aureus and C. difficile, methicillin resistant staph (MRSA))
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Vancomycin: What are the important toxicities of vanco?
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generally NOT many problems except, Nephrotoxicity, Ototoxicity and Thrombophlebitis
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Vancomycin: What can happen with rapid infusion of vanco?
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Red man's syndrome. Diffuse flushing which can be controlled by pretreatment with anti-histamines and with slow infusion rate
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Protein Synthesis Inhibitors: Which drugs target bacterial protein synthesis by blocking the 30S unit vs 50S unit?
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Buy AT 30, CELL at 50
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Protein Synthesis Inhibitors: What does AT stand for?
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A = Aminoglycosides (streptomycin, gentamicin, tobramycin an damikacin. And T = Tetracyclines
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Protein Synthesis Inhibitors: What does CELL stand for?
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C = Chloramphenicol, E= Erythromycin, L= Lincomycin and L= cLindamycin
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Protein Synthesis Inhibitors: Which of the above are bactericidal?
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Only the aminoglycosides are, the rest are bacteriostatic
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Aminoglycosides: Name some aminoglycosides?
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Gentamicin, neomycin, amikacin, tobramycin and streptomycin
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Aminoglycosides: How do these drugs work?
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They inhibit formation of the initiation complex in mRNA translation
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Aminoglycosides: Why are they ineffective against anaerobes?
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They require oxygen for uptake into bacteria
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Aminoglycosides: When would you use aminoglycosides?
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against severe gram-negative rod infections
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Aminoglycosides: What drugs can you use aminoglycosides with for synergy?
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the drugs that inhibit cell wall synthesis (e.g. penicillin and cephalosporins -- the beta-lactam antibiotics). Presumably this allows the drug to get in with out reliance on oxygen transport
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Aminoglycosides: What drug in this class is commonly used for bowel surgery?
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Neomycin
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Aminoglycosides: What are the two major toxicities?
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Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp. when used with loop diuretics). amiNOglycosides
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Tetracyclines: Name some tetracylcines
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Tetracycline, doxycycline, demeclocycline, minocycline
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Tetracyclines: How does it work?
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Blocks t-RNA attachment to 30S subunit
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Tetracyclines: Which tetracycline can you use in patients with renal failure and why?
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Can use doxycycline because its elimination is fecal
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Tetracyclines: Should you take these drugs with a glass of milk?
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NO, because it intereferes with absorption in the gut as does antacids and iron-containing preparations
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Tetracyclines: What are tetracyclines used for?
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VACUUM your Bed Room -- Vibrio cholerae, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi, Rickettsia, tularemia
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Tetracyclines: What are the common toxicities
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GI distress, teeth discoloration, inhibition of bone growth in children, Fanconi's syndrome and photosensitivity
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Macrolides: Name some macrolides?
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Erythromycin, azithromycin, clarithromycin
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Macrolides: How do these drugs work?
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inhibit protein synthesis
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Macrolides: What are they used for?
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URIs, pneumonias, STDs -- gram pos cocci in patients that are allergic to PNC --- Mycoplasm, Legionella, Chlamydia, Neisseria.
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Macrolides: Pneumonic for macrolide use?
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Eryc's Niple is at his Mid Clavicular Line (Eryc is brand name for erythromycin). Mycoplasm, Legionella, Chlamydia, Neisseria.
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Macrolides: What are the major toxicities?
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GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes
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Macrolides: What is the most common cause for non-compliance to macrolides?
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GI discomfort
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Chloramphenicol: How does this drug work?
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inhibits 50S peptidyltransferase
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Chloramphenicol: Main use?
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Meningitis (H. influenzae, N. meningitides, S. pneumo). Used conservatively b/c of toxicity
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Chloramphenicol: What are the main toxicities?
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Anemia and aplastic anemia (both dose dependent), gray baby syndrome (in premes b/c they lack UDP-glucoronyl transferase)
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Clindamycin: How does it work?
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blocks peptide bond formation at 50S
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Clindamycin: When do you use it?
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Anaerobic infections (e.g. Bacteroides fragilis and C.perfringens)
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Clindamycin: Toxicities?
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Pseudomembranous colitis, fever, diarrhea
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Sulfonamides: Name some sulfonamides
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Sulfamethoxazole (SMX), sulfisoxazole, triple sulfa and sulfadiazine
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Sulfonamides: How does it work?
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Inhibits bacterial folic acid synthesis from PABA by blocking dihydropteroate synthase.
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Sulfonamides: What are its uses?
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Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas and SMX for simple UTIs
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Sulfonamides: Toxicities?
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hypersensitivity rxn, hemolysis if G6PD deficient, nephorotoxicity (tubulointerstitial nephritis), kernicterus in infants, displace other drugs from albumin (e.g. warfarin)
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Trimethoprim: How does it work?
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inhibits folic acid pathway by blocking dihydrofolate reductase which humans have as well
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Trimethoprim: What are its uses?
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used in combo with Sulfamethoxazole (TMP-SMX) causing a sequential block of folate synthesis. Used for recurrent UTIs, Shigella, Salmonella, and prophylaxis for PCP in AIDS patients
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Trimethoprim: Toxicities?
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Megaloblastic anemia, pancytopenia (may be alleviated with suplemental folinic acid)
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Fluoroquinolones: What the most famous floroquinolone?
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Ciprfloxacin (treatment for Anthrax)
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Fluoroquinolones: How does it work?
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inhibits DNA gyrase (topoisomerase II)
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Fluoroquinolones: What are its uses?
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Gram neg rods or urinary and GI tract (incl. pseudomonas), Neisseria, some gram pos sp
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Fluoroquinolones: What population is contraindicated for use?
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pregnancy and children
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Fluoroquinolones: What are its toxicities?
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GI upset, superinfection, skin rashes, headache, dizziness and tendonitis and tendon rupture in adults. FluoroquinoLONES hurt attachment to BONES.
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Metronidazole: How does it work?
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forms toxic metabolites in the bacteria. Bactericidal.
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Metronidazole: What are its uses?
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anti-protozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, anaerobes (bacteroides, clostridium)
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Metronidazole: What is the role of Metronidazole in H. pylori infection?
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Used as part of triple therapy: bismuth, amoxicillin and metronidazole
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Metronidazole: Main toxicity?
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disulfiram-like (antabuse) reaction to alcohol and headache
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Metronidazole: Which drug do you use to treat anaerobic infections above the diaphram and below the diaphram
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anaerobes above diaphram: Clindamycin, and anaerobes below diaphram: metronidazole
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Polymyxins: How does it work?
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disrupts osmotic properties of bacteria, acts like a detergent
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Polymyxins: What is it used for?
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resistant gram negative infections
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Polymyxins: Toxicities?
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neurotoxicity, ATN
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Isoniazid: How does it work?
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decreases synthesis of mycolic acid
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Isoniazid: What is it used for?
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MTB (mycobacterium tuberculosis). The only agent used as solo prophylaxis against TB
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Isoniazid: Toxicities?
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Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicitiy, drug induced SLE. INH, Injures Neurons and Hepatocytes
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Isoniazid: What vitamin prevents neurotoxicity
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Vitamin B6 (pyridoxine)
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Isoniazid: Why are toxicities particularly important to monitor in patients taking INH?
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INH half-lives are different in fast versus slow acetylators!
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Rifampin: How does it work?
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inhibits DNA-dependent RNA polymerase
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Rifampin: What is it used for?
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MTB, meningococcal prophylaxis
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Rifampin: Toxicities?
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Minor hepatotoxicity and increases P-450
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Rifampin: How can it be used for leprosy?
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rifampin delays resistance to dapsone when used for leprosy
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Rifampin: What would happen if you used rifampin alone?
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get rapid resistance
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Rifampin: What does it do to bodily fluids?
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makes them red/orange in color
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Rifampin: What are the 4 R's of Rifampin
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RNA polymerase inhibitor, Revs up microsomal p-450, Red/Orange body fluids, Resistance is rapid
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Anti-TB Drugs: What are the anti-TB drugs?
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Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH) -- RESPIre
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Anti-TB Drugs: What do you use for TB prophylaxis?
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INH
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Anti-TB Drugs: What toxicity is common to all?
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hepatotoxicity
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Anti-TB Drugs: AUTHOR
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Michael Shino
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for penicillins / cephalosporins.
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Beta-lactamase cleavage of beta-lactam ring.
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for aminoglycosides.
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Modification via acetylation, adenylation, or phosphorylation.
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for vancomycin.
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Terminal D-ala of cell wall component replaced with D-lac; decrease affinity.
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for Chlorampenicol.
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Modification via acetylation.
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for macrolides.
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Methylation of rRNA near erythromycin's ribosome-binding site.
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for tetracycline.
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Decrease uptake or increase transport out of cell.
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for sulfonamides.
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Altered enzyme (bacterial dihydropteroate synthetase), decrease uptake, or increase PABA synthesis.
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Nonsurgical antimicrobial prophylaxis: Drug of choice for meningococcal infection.
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Rifampin (drug of choice), minocycline.
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Nonsurgical antimicrobial prophylaxis: Drug of choice for gonorrhea.
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Cefriaxone.
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Nonsurgical antimicrobial prophylaxis: Drug of choice for syphilis.
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Benzathine penicillin G.
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Nonsurgical antimicrobial prophylaxis: Drug of choice for history of recurrent UTIs.
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TMP-SMX.
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Nonsurgical antimicrobial prophylaxis: Drug of choice for Pneumocystis carinii pneumonia.
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TMP-SMX (drug of choice), aerosolized pentamindine.
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Anti-fungal therapy: Mechanism of action of the anti-fungal therapy polyenes.
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Form artificial pores in the cytoplasmic membrane.
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Anti-fungal therapy: Mechanism of action of the anti-fungal therapies terbinafine and azoles.
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Terbinafine blocks the conversion of squalene to lanosterol. Azoles block the conversion of lanosterol to ergosterol.
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Anti-fungal therapy: Mechanism of action of the anti-fungal therapy flucytosine.
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Blocks the production of purines from the precurors.
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Anti-fungal therapy: Mechanism of action of the anti-fungal therapy griseofulvin.
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Disrupts microtubles.
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Amphotericin B: Mechanism of action of Amphotericin B.
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Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes and disrupt homeostasis. "Amphotericin 'tears' holes in the fungal membrane by forming pores."
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Amphotericin B: Clinical uses of Amphotericin B.
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Used for a wide spectrum of sytemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier.
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Amphotericin B: Symptoms of Amphotericin B toxicity.
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Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias ("amphoterrible").
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Nystatin: Mechanism of action of Nystatin.
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Binds to ergosterol, disrupting fungal membranes.
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Nystatin: Clinical use of Nystatin.
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Swish and swallow for oral candidiasis (thrush).
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Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Mechanism of action for fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
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Inhibits fungal steroid (ergosterol) synthesis.
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Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Clinical uses of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
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Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, coccidioides, Histoplasma, Candida albicans; hypercortisolism.
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Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Symptoms of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole toxicity.
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Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills.
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Flucytosine: Mechanism of action of Flucytosine.
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Inhibits DNA synthesis byconversion to fluorouracil, which competes with uracil.
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Flucytosine: Clinical uses of Flucytosine.
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Used in sytemic fungal infections (e.g. Candida, Cryptococcus).
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Flucytosine: Symptoms of Flucytosine toxicity.
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Nausea, vomitting, diarrhea, bone marrow supression.
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Caspofungin: Mechanism of action for Caspofungin.
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Inhibits cell wall synthesis.
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Caspofungin: Clinical use of Caspofungin.
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Invasive aepergillosis.
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Caspofungin: Symptoms of Caspofungin toxicity.
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GI upset, flushing.
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Terbinafine: Mechanism of action of Terbinafine.
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Inhibits the fungal enzyme squalene epoxidase.
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Terbinafine: Clinical use of Terbinafinel.
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Used to treat dermatophytoses (especially onychomycosis).
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Griseofulvin: Mechanism of action of Griseofulvin.
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Interfers with microtubule function; disrupts mitosis. Deposits in keratin-contianing tissues (e.g. nails).
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Griseofulvin: Clinical use of Griseofulvin.
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Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).
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Griseofulvin: Symptoms of Griseofulvin toxicity.
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Teratogenic, carcinogenic, confusion, headaches, increase warfarin metabolism.
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Antiviral chemotherapy: Viral adsorption and penetration into the cell is blocked by ---------.
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Gama-globulins (non-specific).
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Antiviral chemotherapy: Uncoating of the virus after its penetration into the cell is blocked by --------.
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Amantadine (influenza A).
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Antiviral chemotherapy: Early viral protein synthesis is blocked by --------.
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Fomivirsen (CMV).
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Antiviral chemotherapy: Viral nuclei acid synthesis is blocked by --------.
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Purine, pyrimidine analogs; reverse transcriptase inhibitors.
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Antiviral chemotherapy: Late viral protein synthesis and processing is blocked by --------.
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Methimazole (variola); protease inhibitors.
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Antiviral chemotherapy: Packaging and assembly of new viron is blocked by --------.
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Rifampin (vaccinia).
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Amantadine: Mechanism of action of Amantadine.
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Blocks viral penetration/uncoating; may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals. "Amantadine blocks influenza A and rubellA and causes problems with the cerebellA."
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Amantadine: Clinical uses of Amantadine.
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Prophylaxis for influenza A; Parkinson's disease.
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Amantadine: Symptoms of Amantadine toxicity.
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Ataxia, dizziness, slurred speech. (Rimantidine is a derivative with fewer CNS side effects.)
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Zanamivir: Mechanism of action of Zanamivir.
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Inhibits influenza neuraminidase.
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Zanamivir: Clinical use of Zanamivir.
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Both influenza A and B.
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Ribavirin: Mechanism of action of Ribavirin.
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Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
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Ribavirin: Clinical use of Ribavirin.
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RSV (respiratory syncytial virus).
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Ribavirin: Symptoms of Ribavirin toxicity.
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Hemolytic anemia. Severe teratogen.
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Acyclovir: Mechanism of aciton of Acyclovir.
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Perferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.
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Acyclovir: Clinical use of Acyclovir.
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HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in immunocompromised patients.
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Acyclovir: Symptoms of Acyclovir toxicity.
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Delirium, tremor, nephrotoxicity.
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Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Mechanism of action of Ganciclovir.
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Phosphorlation by viral kinase; perferentially inhibits CMV DNA polymerase.
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Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Clinical use of Ganciclovir.
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CMV, especially in immunocompromised patients.
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Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Symptoms of Ganciclovir toxicity.
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Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.
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Foscarnet: Mechanism of action of Foscarnet.
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Viral DNA polymerase inhibitor that binds to the pyrophophate binding site of the enzyme. Does not require activation by viral kinase. "FOScarnet = pyroFOSphate analog."
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Foscarnet: Clinical use of Foscarnet.
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CMV retinitis in immunocompromised patients when ganciclovir fails.
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Foscarnet: Symptoms of Foscarnet toxicity.
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Nephrotoxicity.
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HIV therapy: Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are example of this type of anti-HIV drug.
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Protease inhibitor.
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HIV therapy: Mechanism of action of protease inhibitors.
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Inhibit assembly of new virus by blocking protease enzyme.
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HIV therapy: Symptoms of protease inhibitor toxicity.
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GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities, thrombocytopenia (indinavir).
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HIV therapy: Reverse transcriptase inhibitors:
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0
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HIV therapy: Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC), stavudine (d4T), lamivudine (3TC), and abacavir are examples of --------- reverse transcriptase inhibitors.
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Nucleoside.
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HIV therapy: Nevirapine, delavirdine, and efavirenz are examples of --------- reverse transcriptase inhibitors.
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Non-nucleoside.
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HIV therapy: Mechanism of action of reverse transcriptase inhibitors.
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Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of viral genome into host DNA.
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HIV therapy: Symptoms of reverse transcriptase inhibitor toxicity.
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Bone marrow supression (neutropenia, anemia), periphral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).
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HIV therapy: Highly active antiretroviral therapy (HAART) generally entails combination therapy with ---------- and -----------.
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Protease inhibitors, reverse transcriptase inhibitors.
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HIV therapy: When should HIV therapy be initiated?
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When patients have low CD4 counts (<500 cells/mm3) or high viral load.
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HIV therapy: -------- is used during pregnancy to reduce risk of fetal transmission.
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AZT.
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Interferons: Mechanism of action of Interferons.
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Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis.
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Interferons: Clinical use of Interferons.
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Chronic hepatitis B and C, Kaposi's sarcoma.
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Interferons: Symptoms of Interferon toxicity.
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Neutropenia.
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Antiparasitic drugs: Clinical uses of Ivermectin.
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Onchocerciasis "rIVER blindness treated with IVERmectin".
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Antiparasitic drugs: Clinical uses of Mebendazole / thiabendazole.
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Nematode/roundworm (e.g., pinworm, whipworm) infections.
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Antiparasitic drugs: Clinical uses of Pyrantel pamoate.
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Giant roundworm (Ascaris), hookworm (Necator/Ancylostoma), pinworm (Enterobius).
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Antiparasitic drugs: Clinical uses of Praziquantel.
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Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis) and cysticercosis.
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Antiparasitic drugs: Clinical uss of Niclosamide
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Cestode/tapeworm (e.g., Diphyllobothrium latum, Taenia species) infections except cysticercosis.
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Antiparasitic drugs: Clinical uses of Pentavalent antimony.
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Leishmaniasis.
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Antiparasitic drugs: Clinical uses of Chloroquine, quinine, mefloquine, atovaquone, proguanil.
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Malaria.
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Antiparasitic drugs: Clinical uses of Primaquine.
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Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P.ovale).
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Antiparasitic drugs: Clinical uses of Metronidazole.
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Giardiasis, amebic dysentery (Entamoeba histolytica), bacterial vaginitis (Gardnerella vaginalis), Trichomonas.
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Antiparasitic drugs: Clinical uses of Pentamidine.
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Pneumocystis carinii pneumonia prophylaxis.
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Antiparasitic drugs: Clinical uses of Nifurtimox.
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Chagas' disease, American trypanosomiasis (Trypanosoma cruzi).
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Antiparasitic drugs: Clinical uses of Suramin.
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African trypanosomiasis (sleeping sickness).
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