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201 Cards in this Set
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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? |
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? |
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 |
peptidoglycans |
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Antimicrobial Tx -- Mechanism of Action: These drugs block the 50s ribosomal subunit |
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 |
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 |
Sulfonamides (e.g. Bactrim), trimethoprim |
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Antimicrobial Tx -- Mechanism of Action: These drugs block DNA topoisomerases |
Quinolones (e.g. Cipro) |
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Antimicrobial Tx -- Mechanism of Action: Which drug blocks mRNA synthesis |
rifampin |
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Antimicrobial Tx -- Mechanism of Action: Which are the bacteriacidal Abx |
Penicillin, cephalosporin, vancomycin, aminoglycosides, fluoroquinolones, metronidazole |
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Antimicrobial Tx -- Mechanism of Action: These drugs disrupt the bacterial/fungal cell membranes |
polymyxins |
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Antimicrobial Tx -- Mechanism of Action: These specific disrupt fungal cell membranes |
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 |
Unknown |
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Penicillin: Which is the IV form and which is the oral form |
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 |
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 |
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? |
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 |
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 |
TRUE |
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Methicillin, nafcillin, dicloxacillin: Are these drugs penicillinase resistant? If so why? |
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? |
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 |
TRUE |
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Ampicillin and amoxicillin: Which has greater oral bioavailability? |
amOxicillin (O for Oral) |
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Ampicillin and amoxicillin: What do you use these for? |
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? |
Yes, they are penicillinase sensitive |
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Ampicillin and amoxicillin: Why not give these drugs with a penicillinase inhibitor. Name one. |
clavulanic acid |
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Ampicillin and amoxicillin: What should you watch out for when giving these drugs? |
Hypersensitivity rxn (ampicillin rash), pseudomembranous colitis |
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Carbenicillin, piperacillin, ticarcillin: Why are these considered to have an extended spectrum? |
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? |
Hypersensitivity rxn |
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Carbenicillin, piperacillin, ticarcillin: Why does concomitant administration with clavulanic acid increase the efficacy of these drugs? |
Because they are penicillinase sensitive. (only piperacillin and ticarcillin) |
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Cephalosporins: What is the mechanism of action of Cephalosporins? |
inhibit cell wall synthesis |
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Cephalosporins: How are they similar/different from penicillin? |
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? |
2nd gen has extensive gram neg coverage but weaker gram pos coverage |
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Cephalosporins: 1st gen covers what bugs? |
gram positives (staph and strep), Proteus mirabilis, E. coli, Klebsiella (PEcK) |
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Cephalosporins: 2nd gen covers what bugs? |
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? |
Cross the blood brain barrier |
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Cephalosporins: What are some other benefits of 3rd gen? |
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)? |
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? |
Aminoglycosides (increases nephrotoxicity) and ethanol (causes a disulfiram-like rxn -- headache, nausea, flushing, hypotension) |
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Aztreonam: When would you use aztreonam? |
Only to treat Klebsiella, Pseudomonas and Serratia sp. |
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Aztreonam: Is it beta-lactamase resistant? |
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? |
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? |
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? |
broad spectrum beta-lactamase-resistant abx |
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Imipenem/cilastatin: What do you always administer it with and why? |
cilastatin -- it decreases inactivation of imipenem in renal tubules |
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Imipenem/cilastatin: What do you use it for? |
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? |
Enterobacter |
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Imipenem/cilastatin: What are its side-effects |
GI distress, skin rash, seizures at high conc. |
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Vancomycin: Is it bactericidal or bacteriastatic and why? |
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? |
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? |
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? |
generally NOT many problems except, Nephrotoxicity, Ototoxicity and Thrombophlebitis |
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Vancomycin: What can happen with rapid infusion of vanco? |
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? |
Buy AT 30, CELL at 50 |
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Protein Synthesis Inhibitors: What does AT stand for? |
A = Aminoglycosides (streptomycin, gentamicin, tobramycin an damikacin. And T = Tetracyclines |
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Protein Synthesis Inhibitors: What does CELL stand for? |
C = Chloramphenicol, E= Erythromycin, L= Lincomycin and L= cLindamycin |
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Protein Synthesis Inhibitors: Which of the above are bactericidal? |
Only the aminoglycosides are, the rest are bacteriostatic |
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Aminoglycosides: Name some aminoglycosides? |
Gentamicin, neomycin, amikacin, tobramycin and streptomycin |
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Aminoglycosides: How do these drugs work? |
They inhibit formation of the initiation complex in mRNA translation |
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Aminoglycosides: Why are they ineffective against anaerobes? |
They require oxygen for uptake into bacteria |
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Aminoglycosides: When would you use aminoglycosides? |
against severe gram-negative rod infections |
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Aminoglycosides: What drugs can you use aminoglycosides with for synergy? |
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? |
Neomycin |
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Aminoglycosides: What are the two major toxicities? |
Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp. when used with loop diuretics). amiNOglycosides |
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Tetracyclines: Name some tetracylcines |
Tetracycline, doxycycline, demeclocycline, minocycline |
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Tetracyclines: How does it work? |
Blocks t-RNA attachment to 30S subunit |
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Tetracyclines: Which tetracycline can you use in patients with renal failure and why? |
Can use doxycycline because its elimination is fecal |
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Tetracyclines: Should you take these drugs with a glass of milk? |
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? |
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 |
GI distress, teeth discoloration, inhibition of bone growth in children, Fanconi's syndrome and photosensitivity |
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Macrolides: Name some macrolides? |
Erythromycin, azithromycin, clarithromycin |
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Macrolides: How do these drugs work? |
inhibit protein synthesis |
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Macrolides: What are they used for? |
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? |
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? |
GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes |
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Macrolides: What is the most common cause for non-compliance to macrolides? |
GI discomfort |
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Chloramphenicol: How does this drug work? |
inhibits 50S peptidyltransferase |
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Chloramphenicol: Main use? |
Meningitis (H. influenzae, N. meningitides, S. pneumo). Used conservatively b/c of toxicity |
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Chloramphenicol: What are the main toxicities? |
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? |
blocks peptide bond formation at 50S |
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Clindamycin: When do you use it? |
Anaerobic infections (e.g. Bacteroides fragilis and C.perfringens) |
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Clindamycin: Toxicities? |
Pseudomembranous colitis, fever, diarrhea |
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Sulfonamides: Name some sulfonamides |
Sulfamethoxazole (SMX), sulfisoxazole, triple sulfa and sulfadiazine |
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Sulfonamides: How does it work? |
Inhibits bacterial folic acid synthesis from PABA by blocking dihydropteroate synthase. |
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Sulfonamides: What are its uses? |
Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas and SMX for simple UTIs |
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Sulfonamides: Toxicities? |
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? |
inhibits folic acid pathway by blocking dihydrofolate reductase which humans have as well |
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Trimethoprim: What are its uses? |
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? |
Megaloblastic anemia, pancytopenia (may be alleviated with suplemental folinic acid) |
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Fluoroquinolones: What the most famous floroquinolone? |
Ciprfloxacin (treatment for Anthrax) |
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Fluoroquinolones: How does it work? |
inhibits DNA gyrase (topoisomerase II) |
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Fluoroquinolones: What are its uses? |
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? |
pregnancy and children |
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Fluoroquinolones: What are its toxicities? |
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? |
forms toxic metabolites in the bacteria. Bactericidal. |
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Metronidazole: What are its uses? |
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? |
Used as part of triple therapy: bismuth, amoxicillin and metronidazole |
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Metronidazole: Main toxicity? |
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 |
anaerobes above diaphram: Clindamycin, and anaerobes below diaphram: metronidazole |
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Polymyxins: How does it work? |
disrupts osmotic properties of bacteria, acts like a detergent |
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Polymyxins: What is it used for? |
resistant gram negative infections |
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Polymyxins: Toxicities? |
neurotoxicity, ATN |
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Isoniazid: How does it work? |
decreases synthesis of mycolic acid |
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Isoniazid: What is it used for? |
MTB (mycobacterium tuberculosis). The only agent used as solo prophylaxis against TB |
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Isoniazid: Toxicities? |
Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicitiy, drug induced SLE. INH, Injures Neurons and Hepatocytes |
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Isoniazid: What vitamin prevents neurotoxicity |
Vitamin B6 (pyridoxine) |
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Isoniazid: Why are toxicities particularly important to monitor in patients taking INH? |
INH half-lives are different in fast versus slow acetylators! |
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Rifampin: How does it work? |
inhibits DNA-dependent RNA polymerase |
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Rifampin: What is it used for? |
MTB, meningococcal prophylaxis |
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Rifampin: Toxicities? |
Minor hepatotoxicity and increases P-450 |
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Rifampin: How can it be used for leprosy? |
rifampin delays resistance to dapsone when used for leprosy |
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Rifampin: What would happen if you used rifampin alone? |
get rapid resistance |
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Rifampin: What does it do to bodily fluids? |
makes them red/orange in color |
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Rifampin: What are the 4 R's of Rifampin |
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? |
Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH) -- RESPIre |
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Anti-TB Drugs: What do you use for TB prophylaxis? |
INH |
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Anti-TB Drugs: What toxicity is common to all? |
hepatotoxicity |
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Anti-TB Drugs: AUTHOR |
Michael Shino |
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for penicillins / cephalosporins. |
Beta-lactamase cleavage of beta-lactam ring. |
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for aminoglycosides. |
Modification via acetylation, adenylation, or phosphorylation. |
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for vancomycin. |
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. |
Modification via acetylation. |
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for macrolides. |
Methylation of rRNA near erythromycin's ribosome-binding site. |
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for tetracycline. |
Decrease uptake or increase transport out of cell. |
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Resistance mechanisms for various antibiotics: Most common resistance mechanism for sulfonamides. |
Altered enzyme (bacterial dihydropteroate synthetase), decrease uptake, or increase PABA synthesis. |
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Nonsurgical antimicrobial prophylaxis: Drug of choice for meningococcal infection. |
Rifampin (drug of choice), minocycline. |
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Nonsurgical antimicrobial prophylaxis: Drug of choice for gonorrhea. |
Cefriaxone. |
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Nonsurgical antimicrobial prophylaxis: Drug of choice for syphilis. |
Benzathine penicillin G. |
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Nonsurgical antimicrobial prophylaxis: Drug of choice for history of recurrent UTIs. |
TMP-SMX. |
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Nonsurgical antimicrobial prophylaxis: Drug of choice for Pneumocystis carinii pneumonia. |
TMP-SMX (drug of choice), aerosolized pentamindine. |
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Anti-fungal therapy: Mechanism of action of the anti-fungal therapy polyenes. |
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. |
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. |
Blocks the production of purines from the precurors. |
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Anti-fungal therapy: Mechanism of action of the anti-fungal therapy griseofulvin. |
Disrupts microtubles. |
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Amphotericin B: Mechanism of action of Amphotericin B. |
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. |
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. |
Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias ("amphoterrible"). |
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Nystatin: Mechanism of action of Nystatin. |
Binds to ergosterol, disrupting fungal membranes. |
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Nystatin: Clinical use of Nystatin. |
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. |
Inhibits fungal steroid (ergosterol) synthesis. |
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Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Clinical uses of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole. |
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. |
Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills. |
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Flucytosine: Mechanism of action of Flucytosine. |
Inhibits DNA synthesis byconversion to fluorouracil, which competes with uracil. |
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Flucytosine: Clinical uses of Flucytosine. |
Used in sytemic fungal infections (e.g. Candida, Cryptococcus). |
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Flucytosine: Symptoms of Flucytosine toxicity. |
Nausea, vomitting, diarrhea, bone marrow supression. |
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Caspofungin: Mechanism of action for Caspofungin. |
Inhibits cell wall synthesis. |
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Caspofungin: Clinical use of Caspofungin. |
Invasive aepergillosis. |
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Caspofungin: Symptoms of Caspofungin toxicity. |
GI upset, flushing. |
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Terbinafine: Mechanism of action of Terbinafine. |
Inhibits the fungal enzyme squalene epoxidase. |
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Terbinafine: Clinical use of Terbinafinel. |
Used to treat dermatophytoses (especially onychomycosis). |
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Griseofulvin: Mechanism of action of Griseofulvin. |
Interfers with microtubule function; disrupts mitosis. Deposits in keratin-contianing tissues (e.g. nails). |
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Griseofulvin: Clinical use of Griseofulvin. |
Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm). |
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Griseofulvin: Symptoms of Griseofulvin toxicity. |
Teratogenic, carcinogenic, confusion, headaches, increase warfarin metabolism. |
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Antiviral chemotherapy: Viral adsorption and penetration into the cell is blocked by ---------. |
Gama-globulins (non-specific). |
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Antiviral chemotherapy: Uncoating of the virus after its penetration into the cell is blocked by --------. |
Amantadine (influenza A). |
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Antiviral chemotherapy: Early viral protein synthesis is blocked by --------. |
Fomivirsen (CMV). |
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Antiviral chemotherapy: Viral nuclei acid synthesis is blocked by --------. |
Purine, pyrimidine analogs; reverse transcriptase inhibitors. |
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Antiviral chemotherapy: Late viral protein synthesis and processing is blocked by --------. |
Methimazole (variola); protease inhibitors. |
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Antiviral chemotherapy: Packaging and assembly of new viron is blocked by --------. |
Rifampin (vaccinia). |
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Amantadine: Mechanism of action of Amantadine. |
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. |
Prophylaxis for influenza A; Parkinson's disease. |
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Amantadine: Symptoms of Amantadine toxicity. |
Ataxia, dizziness, slurred speech. (Rimantidine is a derivative with fewer CNS side effects.) |
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Zanamivir: Mechanism of action of Zanamivir. |
Inhibits influenza neuraminidase. |
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Zanamivir: Clinical use of Zanamivir. |
Both influenza A and B. |
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Ribavirin: Mechanism of action of Ribavirin. |
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase. |
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Ribavirin: Clinical use of Ribavirin. |
RSV (respiratory syncytial virus). |
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Ribavirin: Symptoms of Ribavirin toxicity. |
Hemolytic anemia. Severe teratogen. |
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Acyclovir: Mechanism of aciton of Acyclovir. |
Perferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase. |
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Acyclovir: Clinical use of Acyclovir. |
HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in immunocompromised patients. |
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Acyclovir: Symptoms of Acyclovir toxicity. |
Delirium, tremor, nephrotoxicity. |
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Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Mechanism of action of Ganciclovir. |
Phosphorlation by viral kinase; perferentially inhibits CMV DNA polymerase. |
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Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Clinical use of Ganciclovir. |
CMV, especially in immunocompromised patients. |
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Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Symptoms of Ganciclovir toxicity. |
Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir. |
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Foscarnet: Mechanism of action of Foscarnet. |
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. |
CMV retinitis in immunocompromised patients when ganciclovir fails. |
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Foscarnet: Symptoms of Foscarnet toxicity. |
Nephrotoxicity. |
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HIV therapy: Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are example of this type of anti-HIV drug. |
Protease inhibitor. |
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HIV therapy: Mechanism of action of protease inhibitors. |
Inhibit assembly of new virus by blocking protease enzyme. |
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HIV therapy: Symptoms of protease inhibitor toxicity. |
GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities, thrombocytopenia (indinavir). |
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HIV therapy: Reverse transcriptase inhibitors: |
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. |
Nucleoside. |
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HIV therapy: Nevirapine, delavirdine, and efavirenz are examples of --------- reverse transcriptase inhibitors. |
Non-nucleoside. |
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HIV therapy: Mechanism of action of reverse transcriptase inhibitors. |
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. |
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 -----------. |
Protease inhibitors, reverse transcriptase inhibitors. |
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HIV therapy: When should HIV therapy be initiated? |
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. |
AZT. |
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Interferons: Mechanism of action of Interferons. |
Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis. |
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Interferons: Clinical use of Interferons. |
Chronic hepatitis B and C, Kaposi's sarcoma. |
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Interferons: Symptoms of Interferon toxicity. |
Neutropenia. |
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Antiparasitic drugs: Clinical uses of Ivermectin. |
Onchocerciasis "rIVER blindness treated with IVERmectin". |
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Antiparasitic drugs: Clinical uses of Mebendazole / thiabendazole. |
Nematode/roundworm (e.g., pinworm, whipworm) infections. |
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Antiparasitic drugs: Clinical uses of Pyrantel pamoate. |
Giant roundworm (Ascaris), hookworm (Necator/Ancylostoma), pinworm (Enterobius). |
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Antiparasitic drugs: Clinical uses of Praziquantel. |
Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis) and cysticercosis. |
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Antiparasitic drugs: Clinical uss of Niclosamide |
Cestode/tapeworm (e.g., Diphyllobothrium latum, Taenia species) infections except cysticercosis. |
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Antiparasitic drugs: Clinical uses of Pentavalent antimony. |
Leishmaniasis. |
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Antiparasitic drugs: Clinical uses of Chloroquine, quinine, mefloquine, atovaquone, proguanil. |
Malaria. |
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Antiparasitic drugs: Clinical uses of Primaquine. |
Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P.ovale). |
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Antiparasitic drugs: Clinical uses of Metronidazole. |
Giardiasis, amebic dysentery (Entamoeba histolytica), bacterial vaginitis (Gardnerella vaginalis), Trichomonas. |
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Antiparasitic drugs: Clinical uses of Pentamidine. |
Pneumocystis carinii pneumonia prophylaxis. |
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Antiparasitic drugs: Clinical uses of Nifurtimox. |
Chagas' disease, American trypanosomiasis (Trypanosoma cruzi). |
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Antiparasitic drugs: Clinical uses of Suramin. |
African trypanosomiasis (sleeping sickness). |