FA Antimicrobials

Start Studying!

Terms

undefined, object

copy deck

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

Start Studying!

Deck Info

Number of cards 201