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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.
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).