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79 Cards in this Set
- Front
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What is the mechanism of action, clinical uses, and toxicities? |
Mechanism: Bind penicillin-binding proteins; Blocks transpeptidase cross-linking of cell wall; Activates autolytic enzymes.
Use: Gram positive organisms and syphilis. Toxicity: Hypersensitivity reactions, hemolytic anemia |
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What is the mechanism of action, clinical uses, and toxicities?
Penicillinase-resistant penicillins (methicillin, nafcillin, dicloxacillin |
Mechanism: Bind penicillin-binding protein; blocks transpeptidase cross-linking of cell wall; activates autolytic enzymes (same as penicillin).
Use: S. aureus (except MRSA) Toxicity: Hypersensitivity reactions; methicillin - interstitial nephritis. |
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What is the mechanism of action, clinical uses, and toxicities?
Aminopenicillins (ampicillin, amoxicillin) |
Mechanism: Bind penicillin-binding proteins; block tranpeptidase cross-linking of cell wall; activate autolytic enzymes (same as penicillin).
Use: Extended-spectrum penicillin (certain gram-positive bacteria and gram-negative rods) HELPS - Haemophilus influenza, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, enteroccoi Toxicity: Hypersensitivity reactions, ampicillin rash; pseudomembranous colitis. |
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What is the mechanism of action, clinical uses, and toxicities?
Antipseudomonals/"carboxypenicillins" (Ticarcillin, carbenicillin, piperacillin, azlocillin) |
Mechanism: Binds penicillin-binding proteins; blocks transpeptidase cross-linking of cell wall; activate autolytic enzymes (same as penicillin).
Use: Extended-spectrum penicillin. Pseudomonas spp and gram-negative rods; susceptible to penicillinase (use with clavulanic acid) Toxicity: Hypersensitivity reactions |
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What are beta-lactamase inhibitors?
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Often added to penicillin antibiotics to protect the antibiotic form destruction by beta-lactamase (penicillinase). Ex. clavulanic acid, sulbactam, tazobactam.
Augmentin = clavulanic acid + amoxicillin |
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What are examples of antipseudomonals?
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Ticarcillin, carbenicillin, piperacilin, azlocillin
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What are the clinical uses?
1st generation cephalosporins (cefazolin, cephalexin) |
Use: PEcK - Proteus mirabilis, E. coli, Klebsiella pneumoniae
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What is the general mechanism of action and toxicities of cephalosporins?
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Mechanism: Beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.
Toxicity: Hypersensitivity reactions, vitamin K deficiency. Cross-hypersensitivity with penicillins occurs in 5-10%. Increased nephrotoxicity of aminoglycosides; disulfiram-like reactions with ethanol |
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What are the clinical uses?
2nd generation cephalosporins (cefoxitin, cefaclor, cefuroxime) |
Gram positive cocci.
HEN PEcKS - Haemophilus influenza, Enterobacter aerogenes, Neisseria spp. Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens |
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What are the clinical uses?
3rd generation cephalosporins (ceftriaxone, cefotaxime, ceftazidime) |
Serious gram negative infections resistant to other beta-lactams (broad spectrum).
Ceftriaxone - meningitis and gonorrohea Ceftazidime - Pseudomonas |
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What are the clinical uses?
4th generation cephalosporins (cefepime) |
Increased activity against pseudomonas and gram-positive organisms.
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What is the mechanism of action, clinical uses, and toxicities?
Aztreonam |
Mechanism: Monobactam resistant to beta-lactamases. Inhibits cell wall synthesis (binds to PBP3). Synergistic with aminoglycosides. No cross-allergenicity with penicillins.
Use: Gram negative rods ONLY. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides. Toxicity: Usually nontoxic; occasional GI upset. No cross-sensitivity with penicillins or cephalosporins. |
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What is the mechanism of action, clinical uses, and toxicities?
Imipenem/cilastatin, meropenem |
Mechanism: beta-lactamase resistant carbapenem.
Use: Broad-spectrum - gram positive cocci, gram negative rods, and anaerobes (does not cover MRSA). Toxicity: GI distress, skin rash, CNS toxicity (seizures) at high plasma levels. |
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What is the mechanism of action, clinical uses, and toxicities?
Vancomycin |
Mechanism: Inhibits cell wall mucopeptide formation by binding D-ala D-ala portions of cell wall precursors (muramyl pentapeptide)
Use: Gram positive ONLY. Serious mutlidrug-resistant organisms, including S. aureus, enterococci and C. difficile. Toxicity: Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing - 'red man syndrome'. Can largely be prevented by pretreatment with antihistamines and slow infusion rate (type I hypersensitivity) |
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What are examples of aminoglycosides?
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GNATS - Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin
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What are examples of antibiotics that work as 30S inhibitors?
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Aminoglycosides (bacteriocidal)
Tetracyclines (bacteriostatic) |
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What is the mechanism of action, clinical uses, and toxicities?
Aminoglycosides (Gentamicin, Neomycin, Amikacin, Tobramycin) |
Mechanism: Inhibit formation of initiation complex and cause misreading of mRNA. Require O2 for uptake (ineffective against anaerobes). Bactericidal.
Use: Severe gram negative rods. Synergistic with beta-lactam antibiotics. Neomycin for bowel surgery. Toxicity: Nephrotoxicity (especially when used with cephalosporins), Ototoxicity (especially when used with loop diuretics), Teratogen. |
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What is the mechanism of action, clinical uses, and toxicities?
Tetracyclines (Tetracycline, doxycycline, demeclocycline, minocycline |
Mechanism: Binds to 30S and prevent attachment of aminoacyl-tRNA. Bacteriostatic. Must NOT take with milk, antacids, or iron-containing preparations because divalent cations inhibit its absorption in gut.
Use: Borrelia burgdorferi (Lyme disease), H. pylori, M. pneumoniae. Can accumulate intracellularly (Rickettsia, Chlamydia, Vibrio, Treponema) Toxicity: GI distress, discolouration of teeth and inhibition of bone growth in children, photosensitivity, teratogen |
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What are examples of tetracyclines?
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Tetracycline, doxycycline, demeclocycline, minocycline
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What are examples of macrolides?
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Erythromycin, Azithromycin, Clarithryomycin
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What is the mechanism of action, clinical uses, and toxicities?
Macrolides (erythromycin, azithromycin, clarithromyin) |
Mechanism: Inhibit protein synthesis by blocking translocation; binds to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.
Use: Atypical pneumonias (Mycoplasma, chlamydia, legionella), URI, STDs, gram positive cocci (streptococcal infections in patients allergic to penicillin), and Neisseria Toxicity: Prolonged QT interval (especially erythromyin), GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis, eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral anticoagulants. |
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What is the mechanism of action, clinical uses, and toxicities?
Chloramphenicol |
Mechanism: Inhibits 50S peptidyltransferase activity. Bacteriostatic.
Use: Meningitis (Haemophilus influenza, Neisseria meningitidis, Streptococcus pneumoniae). Toxicity: Anemia (dose dependent), aplastic anemia (dose dependent), gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase). |
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What is the mechanism of action, clinical uses, and toxicities?
Clindamycin |
Mechanism: Blocks peptide bond formation at 50S ribosomal subunit. Bacteriostatic.
Use: Anaerobic infections (bacteroides fragilis, Clostridium perfringens) in aspiration pneumonia or lung abscesses. Treat anaerobes above the diaphragm (vs. metronidazole - anaerobic infections below diaphragm). Toxicity: Pseudomembranous colitis, fever, diarrhea |
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What is the mechanism of action, clinical uses, and toxicities?
Sulfonamides (Sulfamethoxazole - SMX, sulfisoxazole, sulfadiazine) |
Mechanism: PABA antimetabolites inhibit dihydropteroate synthetase. Bacteriostatic.
Use: gram positive, gram negative, nocardia, chlamydia. Triple sulfas or SMX for simple UTI Toxicity: Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (warfarin). |
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What is the mechanism of action, clinical uses, and toxicities?
Trimethoprim |
Mechanism: Inhibits bacterial dihydrofolate reductase. Bacteriostatic.
Use: In combination with sulfonamides (TMP-SMX), causing sequential block of folate synthesis. Combination used for recurrent UTI, Shigella, Salmonella, Pneumocystis jiroveci. Toxicity: Megaloblastic anemia, leukopenia, granulocytopenia. |
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What is the mechanism of action, clinical uses, and toxicities?
Fluoroquinolones (ciprofloxacin, levofloxacin, norfloxacin, ofloxacin, sparfloxacin, moxifloxacin, gatifloxacin, enoxacin, nalidixic acid) |
Mechanism: Inhibit DNA gyrase (topoisomerase II). Bactericidal. Must not be taken with antacids.
Use: gram negative rods of urinary and GI tracts (including pseudomonas), Neisseria, some gram positive organisms Toxicity: GI upset, superinfections, skin rashes, headache, dizziness, teratogen. Tendonitis and tendon rupture in adults; leg cramps and myalgias in kids |
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What is the mechanism of action, clinical uses, and toxicities?
Metronidazole |
Mechanism: Forms free radical toxic metabolites in the bacterial cell that damage DNA. Bactericidal, antiprotozoal.
Use: GET GAP - Giardia, Entamoeba, Trichomonas, Garderella vaginalis, Anaerobes (Bacteroides, Clostridium - pseudomonas colitis), h. Pylori (BMT regimen). Anaerobic infection below the diaphragm Toxicity: Disulfiram-like reaction with alcohol; headache, metallic taste, peripheral neuropathy. |
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What is the mechanism of action, clinical uses, and toxicities?
Polymyxins (polymyxin B, colistimethate/polymyxin E) |
Mechanism: Binds to cell membranes of bacteria and disrupt their osmotic properties. Polymyxins are cationic, basic proteins that act like detergents.
Use: Resistant gram negative infections. Toxicity: Neurotoxicity, acute renal tubular necrosis. |
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What are the anti-TB drugs?
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INH-SPIRE - Streptomycin, Pyrazinamide, Isoniazid (INH), Rifampin, Ethambutol
Note: important SE is hepatotoxicity (and red-green colour blindness for ethambutol) |
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What is the mechanism of action, clinical uses, and toxicities?
Isoniazid (INH) |
Mechanism: Decrease synthesis of mycolic acids. Bacteria catalase-peroxidase needed to convert INH to active metabolite.
Use: Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB. Toxicity: Neurotoxicity, hepatotoxicity, lupus. Pyridoxine (vit B6) can prevent neurotoxicity, lupus |
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What is the mechanism of action, clinical uses, and toxicities?
Rifampin |
Mechanism: Inhibits DNA-dependent RNA polymerase
Use: Mycobacterium tuberculosis; delays resistant to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenza type B. Toxicity: Minor hepatotoxicity and drug interactions (increase P450); orange body fluids (nonhazardous side effect) |
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What are the 4Rs of Rifampin?
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RNA polymerase inhibitor
Revs up microsomal P450 Red/orange body fluids Rapid resistance if used alone |
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What antimicrobial prophylaxis is given?
Meningococcal infection |
Rifampin (drug of choice), minocycline
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What antimicrobial prophylaxis is given?
Gonorrhea |
Ceftriaxone
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What antimicrobial prophylaxis is given?
Syphilis |
Benzathine penicillin G
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What antimicrobial prophylaxis is given?
History of recurrent UTIs |
TMP-SMX
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What antimicrobial prophylaxis is given?
Pneumocystis jiroveci pneumonia |
TMP-SMX (drug of choice), aerosolized pentamidine
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What antimicrobial prophylaxis is given?
Endocarditis with surgical or dental procedures |
Penicillins
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What antimicrobial prophylaxis is given?
Mycobacterium avium-intracellulaire |
Azithromycin
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What is the treatment for MRSA (methicillin resistant staphylococcus aureus)? For VRE (vancomycin resistant enterococci)?
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MRSA - vancomycin
VRE - linezolid and streptogramins (quinupristin/dalfopristin) |
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What is the mechanism of action, clinical uses, and toxicities?
Amphotericin B |
Mechanism: Binds ergosterol (unique to fungi) forms membrane pores that allow leakage of electrolytes.
Use: Serious, systemic mycoses (Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor). Intrathecally for fungal meningitis (does not cross BBB). Toxicity: Fever/chills, hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis. |
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What is the mechanism of action, clinical uses, and toxicities?
Nystatin |
Mechanism: Binds ergosterol; forms membrane pores that allow leakage of electrolytes (same as Amphotericin B).
Use: "Swish and swallow" for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis Toxicity: None mentioned in First Aid |
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What is the mechanism of action, clinical uses, and toxicities?
Azoles (Fluconazole, ketoconazole, etc) |
Mechanism: Inhibit fungal sterol (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to ergosterol.
Use: Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS (crosses BBB) and candidal infections of all types. Ketoconazole for Blastomyces, Coccidioides, Histoplasma, Candida albicans. Toxicity: Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills |
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What is the mechanism of action, clinical uses, and toxicities?
Flucytosine |
Mechanism: Inhibits DNA synthesis by conversion to 5-fluorouracil
Use: Systemic fungal infection (candida, cryptococcus) in combination with amphotericin B Toxicity: Nausea, vomiting, diarrhea, bone marrow suppression. |
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What is the mechanism of action, clinical uses, and toxicities?
Caspofungin, Micafungin |
Mechanism: Inhibits cell wall synthesis by inhibiting synthesis of beta-glucan.
Use: Invasive aspergillosis, candidiasis (HIV patients) Toxicity: GI upset, flushing |
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What is the mechanism of action, clinical uses, and toxicities?
Terbinafine |
Mechanism: Inhibits the fungal enzyme squalene epoxidase (decrease ergosterol)
Use: Used to treat dermatophytoses (especially onychomycosis - fungal infection of fingers or toe nails) Toxicity: None mentioned in FIrst Aid |
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What is the mechanism of action, clinical uses, and toxicities?
Griseofulvin |
Mechanism: Interferes with microtubule function, disrupts mitosis. Deposits in keratin-containing tissues (nails).
Use: Oral treatment of superficial fungal infections; inhibits growth of dermatophytes (tinea, ringworms) Toxicity: Teratogen, carcinogenic, confusion, headaches, increased P-450 and warfarin metabolism, disulfiram-like reaction |
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What is the mechanism of action and use?
Pyrimethamine |
Selectively inhibits plasmodial dihydrofolate reductase (best for P falciparum).
Use: Drug of choice for toxoplasmosis when combined with sulfadiazine. |
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What is the mechanism of action and use?
Sodium stibogluconate |
Mechanism: Inhibits glycolysis at PFK reaction.
Use: Leishmaniasis |
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What is the mechanism of action and use?
Nifurtimox |
Mechanism: Forms intracellular oxygen radicals which are toxic to the organism.
Use: Trypanosomiasis (Chagas disease) |
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What is the mechanism of action and use?
Chloroquine |
Mechanism: Blocks plasmodium heme polymerase, leading to accumulation of toxic hemoglobin breakdown products that destroy the organism.
Use: Anti-malarial prophylaxis. Note: Use quinine for chloroquine-resistant species when used in combination with pyrimethamine/sulfonamide. SE: hemolytic anemia in G6PD deficiency |
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What is the mechanism of action and use?
Mebendazole |
Mechanism: Inhibits glucose uptake and microtubule synthesis.
Use: Antihelminthic for nematodes |
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What is the mechanism of action and use?
Pyrantel pamoate |
Mechanism: Stimulates nicotinic receptors at neuromuscular junctions. Contraction occurs, followed by depolarization-induced paralysis.
Use: Roundworms (Ascaris lumbricoides) and Hookworms (Necator americanus). No effect on tapeworms (cestodes) or flukes (trematodes). |
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What is the mechanism of action and use?
Praziquantel |
Mechanism: Increases membrane permeability to calcium, causing contraction and paralysis of tapeworms and flukes.
Use: Cestodes (tapeworms) and Trematodes (flukes) |
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What is the mechanism of action, clinical uses, and toxicities?
Amantadine |
Mechanism: Blocks viral penetration/uncoating (M2 protein). Also causes the release of DA from intact nerve terminals.
Use: Prophylaxis and treatment for influenza A ONLY; Parkinson's disease. Toxicity: Ataxia, dizziness, slurred speech, atropine-like Note: Rimantidine is a derivative with fewer side effects. Does not cross BBB. 90% of all influenza A strains are resistant to amantadine (not used) |
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What is the mechanism of action, clinical uses, and toxicities?
Zanamivir, oseltamivir |
Mechanism: Inhibit influenza neuraminidase, decreasing the release of progeny virus.
Use: Both influenza A and B, H1N1, avian flu Toxicity: Nasal, throat irritation |
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What is the mechanism of action, clinical uses, and toxicities?
Ribavirin |
Mechanism: Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase (nucleoside analogue). Needs to be phosphorylated
Use: RSV (adult only), chronic HCV (adjunct to alpha-interferons) Toxicity: Hemolytic anemia. Teratogen |
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What is the mechanism of action, clinical uses, and toxicities?
Acyclovir |
Mechanism: Monophosphorylated by HSV/VZV thymidine kinase (requires kinase for activation). Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination (only works on replicating viruses).
Use: HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. |
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What is the mechanism of action, clinical uses, and toxicities?
Ganciclovir |
Mechanism: 5'-monophosphate formed by a CMV viral kinase or HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase.
Use: CMV (especially in immunocompromised patients - mostly prophylaxis). Toxicity: Leukopenia, neutropenia, thrombocytopenia, renal toxicity, mucositis, fever, rash, crystalluria. More toxic to host enzymes than acyclovir. |
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What is the mechanism of action, clinical uses, and toxicities?
Foscarnet |
Mechanism: Viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does not require activation by viral kinase.
Use: CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV. Toxicity: Nephrotoxicity (ATN) |
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What is HAART therapy?
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Highly active antiretroviral therapy. Initiated when patients present with AIDS-defining illness, low CD4 cell counts (<350), or high viral load. Regimen consists of 3 drugs to prevent resistance: 2 nucleoside reverse transcriptase inhibitors (NRTI) + 1 protease inhibitor OR 2 NRTIs + non-nucleoside reverse transcriptase inhibitor (NNRTI)
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What are examples of protease inhibitors?
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"navir"
Saquinavir, Ritonavir, Indinavir, Nelfinavir, Amprenavir |
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What is the mechanism of action, clinical uses, and toxicities?
Protease inhibitors |
Mechanism: Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
Use: Part of HAART therapy for HIV management Toxicity: Hyperglycemia (insulin resistance, central adiposity), lipodystrophy, thrombocytopenia (indinavir), drug interactions (ritonavir), crystalluria |
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What are examples of nucleoside reverse transcriptase inhibitors (NRTI)?
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Zidovudine (ZDV, formerly AZT - Azidothymidine), Didanosine (ddI), Zalcitabine (ddC), Stavudine (d4T), Lamivudine (3TC), Entricitabine (FTC), Abacavir (ABC)
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What is the mechanism of action, clinical uses, and toxicities?
NRTIs (nucleoside reverse transcriptase inhibitors) |
Mechanism: Competitively inhibit nucleotide binding to reverse transcriptase and terminate DNA chain (lack a '3-OH group). Must be phosphorylated by thymidine kinase to be active.
Use: Part of HAART therapy for HIV management. ZDV is used for general prophylaxis and during pregnancy to reduce risk of fetal transmission. Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV). |
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What are some examples of non-nucleoside reverse transcriptase inhibitors (NNRTI)?
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Nevirapine, Efavirenz, Declaviridine
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What is the mechanism of action, clinical uses, and toxicities?
NNRTI (non-nucleoside reverse transcriptase inhibitors) |
Mechanism: Bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides
Use: Part of HAART therapy for HIV management. Toxicity: Peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides). |
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What are examples of fusion inhibitors?
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Enfuvirtide, Maraviroc (blocks CCR5 protein on T cell surface to prevent viral entry), Raltegravir (integrase inhibitor)
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What is the mechanism of action, clinical uses, and toxicities?
Enfuvirtide |
Mechanism: Bind HIV viral gp41subunit, inhibit conformational change required for fusion with CD4 cells, blocking entry and replication.
Use: Used in HIV patients with persistent viral replication despite antiretroviral therapy. Toxicity: Hypersensitivty reactions, reaction at subcutaneous injection site, increased risk of bacterial pneumonia. |
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What is the mechanism of action, clinical uses, and toxicities?
Interferons |
Mechanism: Glycoproteins synthesized by virus-infected cells block replication of both RNA and DNA viruses
Use: IFN-a: Chronic HBV, HCV, Kaposi sarcoma; IFN-b: MS; IFN-g - NADPH oxidase deficiency Toxicity: Neutropenia |
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What antibiotics should be avoided in pregnancy?
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SAFE Moms Take Really Good Care
Sulfonamides (kernicterus), Aminoglycosides (ototoxicity), Fluoroquinolones (cartilage damage), Erythromycin (acute cholestatic hepatitis in mom, clarithromycin - embryotoxic), Metronidazole (mutagenesis), Tetracyclines (discoloured teeth, inhibition of bone growth), Ribavirin (teratogenic), Griseofulvin (teratogenic), Chloramphenicol (gray baby) |
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What 2 drugs make Augmentin?
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Amoxicillin + Clavulanic acid
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What 2 drugs make Timentin?
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Ticarcillin + Clavulanic acid
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What 2 drugs make Zosyn?
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Piperacillin + Tazobactam
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What are some common infections associated with Pseudomonas aeroginosa
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Pneumonia ( CF, immunocompromised), Burn would infections, Corneal infections (contact lens), Osteomyelitis (Diabetes, IV drug use), Sepsis (high mortality), External otitis (elderly diabetes), Hot tub folliculitis, Endocarditis (IV drug), UTI (IDC)
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What are the clinical used for tetracyclines?
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VACUUM THe BedRoom
Vibrio, Acne, Chlamydia, Ureaplasma Urealyticum, Mycoplasma pneumonia, Tularemia, H. pylori, Borrelia, Rickettsia |
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What causes Gray Man syndrome?
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Amiodarone
Note: Gray baby synrome = chloramphenicol |
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What are the clinical uses for TMP-SMX?
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MRSA skin infections, PCP pneumonia, UTI, Salmonella, Shigella
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What drugs are effective against Pseudomonas?
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Polymyxins, Fluoroquinolones, Cefepime, Aztreonam, Aminoglycosides, Extended spectrum penicillins (piperacillin)
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