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62 Cards in this Set
- Front
- Back
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Penicillin
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Binds penicillin binding proteins
blocks transpeptidase cross linking of cell wall Activate autolytic enzymes Use for gram + cocci, gram + rods, gram - cocci, and sphirocetes Not penicllinase resistant, bactericidal Toxicity- hypersensitivity, hemolytic anemia |
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Methicillin, nafcillin, dicloxacillin
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penicillinase resistant pencillins
Same mechanism as peniccilin, pencillinase resistant due to bulky R group. used for S. aureus (except MRSA, altered penicilin binding protein target site. Toxicity = hypersensitity reactions Methicillin can cause intersitital nephritis. "use naf for staph" naficillin is hepatically cleared, sso would have a problem with P450 induction/inhibition |
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Ampicillin, amoxicillin
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aminopenicillins. Mechanism is same as penicllin. Wider spectrum, but penicillinase sensitive. Combine with clavulanic acid (penicllinase inhibitor) to enchance spectrum.
amOxicllin has greater oral bioavailability than ampicillin. Use- HELPS - rods - Haemophilus, E. coli, Listeria monocytogenes, Proteus, Salmonella, enterococci. Toxicity - hypersensitivty reactions, ampicllin rash; pseudomembranous colitis. |
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Ticarcillin, carbenicclin, piperacillin
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Antipseudomonals
Same mechanism as penicllin. Used for pseudomanas and gram negative rods. Susceptible to pencillinase; use with clavinc acid. Toxicity - hypersensitivity reactions |
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1st generation cephalosporins
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cefazolin, cephalexin
B-lactam drugs that inhibit cell wall synthesis, less susceptible to to pencillinases, Bactericidal. Use - gram + cocci, Proteus mirabilis, E. coli, Klebsiella. Toxicity - hypersensitivity, cross hypersensitivity with pencillin 5-10% of patients. Increased nephrotoxicity with aminoglycosides, disulfram like reaction with ethanol. Pharmacokinetics – very water soluble, so none enter CNS. |
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2nd generation cephalosporins
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cefoxitin, cefaclor, cefuroxime
HEN PEcKS - Haemophilus, Enterobacter aerogenes, neisseria, proteus, E.coli, Klebseialla, Serratia marcescens. Can enter CNS |
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3d generation cephalosporins
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ceftriaxone, cefotaxime, ceftazimide
use - for serious gram negative infections resistant to other B lactams, meningitis (can penetrate BBB). Pseudomonas, ceftriaxone Ceftriaxone largely bile elimanted. Can use for everything except for LAME - listeria, atypicals,MRSA, enterococci. |
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4th generation
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cefepime - increased activity against pseudomnas, gram + organisms
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Azteronam
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monobactam resistant to B-lactamases. Inhibits cell wall synthesis (binds to PBP3).
Synergestic with aminoglycosides, no cross allergencitiy with penicillins Used for gram - rods - klebseilla, pseudomonas, serratia. No activity against gram +, anerobes. For peicllin allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides. Nontoxic, occasional GI upset. No cross sensitivity. |
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Impenem/cilastatin, meropenem
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impenem is broad spectrum, B lactamase resistant carbapenem. Always administered with cilastatin (inhibitor of renal dihyrdropeptidas I), to decrease inactivation in renal tubules.
Used for gram positive cocci, gram negative rods, and anaerobes. Drug of choice for enterobacter. Signifcant side effects limit use to life threatining infections, or after other drugs have failed -only given as last resort when all drugs have failed. Meropenem has reduce risk of seizures, stable to dihydropeptidase I. Toxicity - GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels. |
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Vancomycin
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inhibits cell wall synthesis by D-ala D-ala portion of cell wall.
Resistance = D-ala D-lac Nephrotoxicity, ototoxicity, thrombophlebitis (red man syndrome) |
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Gentamicin, neomycin, amikcin, tobramycin
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aminoglycosides - mean GNATS cannot kill anerobes
Only bacteriocidal protein synthesis inhibitor. Mech - inhibit formation of initiaion complex and cause misreading of mRNA. Require O2 for uptake, so ineffective against anaerobes. block 30S subunit at position 1 Use - Severe gram negative rod infections. Nephroxoic, ototoxic, teratogen. Notice they have glyco in their name, so extremely water soluble, renally cleared. Neomycin=neosporin...only topically used. Can cause contact dermatitis. Neomycin for bowel surgery. resistance=formation of enzymes that inactivate drugs via conjugation reactions that transfer actyl, phosphoryl, or adenylyl groups. Nephrotoxicity, Ototoxicicty, and Teratogenic. |
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Tetracycline, doxycycline, democylycline, minocycline
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binds to 30s, prevents attachment of aminoacyl tRNA. Limited CNS penetration.
Doxycyline is fecal eliminated - use for pateints with renal failure. Do not take with milk, antacids or iron containing preps because divalent cations inhibit its absorption in gut. Use - VACUUM THe BR Vibrio, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma, Tularemia, H. Pylori, Borrelia, Ricketttsia Toxicity - GI distress, discoloration of teeth, bone growth inhibition, photosenstitivy. Do not use in pregnancy a) Doxycyline =prostates – drug of choice for prostaitis – so think of chlaymdia/gonarrhea – it is very lipid soluble b) Minocycline – in saliva and tears because it is so water soluble. Used in meningococcal carrier state – also rifampin! (3rd generation cephalosporins in treatment of neisseria meningitits c) Demeclocycline – used in syndrome of SIADH – blocks its…it’s an endocrine use. Side effect would be diabetes insipidus. c) Resistance – bacterium methylates bases by methyltransferases, so then macrolides can’t bind. Resistance – they get pumped out of cell. This is pretty drastic for bacteria. The cell actually develops a transport system that gets out any chemical that is foreign. This tends to be non-selective, so it would be resistant to many drugs. P-glycoprotein is an example of pump – need Ca and energy…verapamil might help a little |
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Macrolides
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Macrolides – bind to 23S of 50S subunit and interfere with transolcation. MACRO so huge molecules and lipid soluble. Erythromycin, azithromycin, clarithromycin. If “thro” means it has color. These are wide spectrum antibiotics – also applies to teracyclines.
Works on gram +, atypicals, but usually associated with Legionalla and camplybacter. Azihtromycin – used in respiratory infection including mycobacterium avium intracellulare/ Would benefit more with a bacteriocidal drug (because HIV can’t clear em out). To use it in HIV, would have to use huge doses. Clarithromycin – greater activity against M. Avium and H. pylori a) Pharmacokinetics – erythromycin and clarehtromycin are metabolized by the liver. Inhibit P450’s and not safe in pregnancy…wouldn’t want to use this in HIV patients because of drug interactions.. Azithromycin is excreted by the kidney and does not inhibit cytochrome P45-…safer in pregnancy. b) Side effects – macrolides stimulin motilin receptors (gut peptide responsible for peristalsis in between meals) macrolides bind to this and mechanically stimulate the gut to cause diarrhea. So not only are you killing these bugs, you are now worsening diarrhea. The least GI distressing is Clarithromycin. Macrolides can cause reversible deatness. Erythromycin estolate (salt of it) causes cholestatis by obstructive jaundice…it makes a sludge. c) Resistance – bacterium methylates bases by methyltransferases, so then macrolides can’t bind. |
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Choramphenicol
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inhibits 50S peptidyltransferase activity. Bacteriostatic.
Use for meningitis - H. influenza, nesseria, strep pneumonia. Tox - anemia, aplastic anemia (dose independent), gray baby syndrome (in premature infants because they lack liver UDP glucuronyl transferase anything with phen it’s name has aromatic. Anything that has aromatic goes to liver and is lipid soluble. Everytime you see phen, think lipid soluble. Very wide spectrum, but toxic so not really used. |
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Clindamycin
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blocks peptide formation at 50S.
Treat aneraboes above diaphragm - bacteriodes, Clostridium not a macrolide, but same mechanism and mode of resistance. Very marrow spectrum – good for some gram + and some aerobes. Distrubutes to bone tissue and is pretty active – used in osteomyelitis – staph aureus (unless salmonella for sickle cell). First known drug to cause pseudomembranous colitis – results in superinfection of C. difficile (need to use vancomycin or metraniadazole). |
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Sulfonamides
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SMX- inhibit purine synthesis by inhibiting dyhydropteroate synthetase. (pterdine+ PABA)
Use - Nocardia, Chlamydia, UTI's Tox - hemolysis if G-6PD deficient, nephrotoxicity, photosensitivity, kernicterus. cotrimoxazole – DOC for nocardia, mycobacteria. Used for gram negative infections for complicated UTi’s - E coli samlmonalla, shigella, staph, strep, H. influenzae. Fungus – pneumocystisis carinii Protozoa: toxoplasma gondii – sulfadiaozome and pyrimethamine (works a) Pharmockinetics – hepatically acetetylated – metabolites are less water soluble than parent drug – renally excreted metabolites can cause crystalluria. It is high protein binding – has drug interaction by competition of protein binding. In neonates, there is a lack of conjugation, so it billirubin will stay attached to albumin, sulfonamides require conjugation and bind attach to albumin instead, displacing it. This can cause kernicturus. Remember that E. coli is very common cause of meningitis, so it is an issue here. b) Side effects – hypersensitivity, steven johnson’s syndrome. Phototxicitiy, GI distress, hemolysis in G-6PD deficiency. These drugs can acute distress by oxidation (fava beans, primaquine). |
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Trimethoprim
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TMP
Mechanism - inhibits becaterial dihydrofolate reducatse. Combined with TMP-SMx causing sequential block of folate synthesis. Use - Recurrent UTI's, shigella, Salmonall, Pneumocytsis |
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ciprofloxacin, norfloxiacin, ofloxacin, sparfloxacin, moxfloxacin, gatifloxacin, enoxacin, nalidixic acid
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Flouroquinolones
inhibit topoisomomerase II and topoisomerase IV (separates replicated DNA during cell division)….prevents supercoiling and negative coiling. Replication inhibitors. Resistance is increasing with these. a) activity – UTI’s when resistant for cotrimoxazole (TMP) STD’s/pelvic inflammatory diseases: gonorrhea, Chlamydia (ofloxacin)/ Skin soft tissue and bone infections by gram –‘s (except norfloaacin). Diarrhea to shigella, salmonella, E. Coli, campylobacter (any quinolone), drug resistant pneumococi (leveofloxacin). Salmonella is extremely sensitive to acid (so if person is taking antacid, they would be prone to it!) pharmacokinetics – chelators, iron and calcium limit absorption. Eliminated by kidney, reduce dose in renal dysfunction c) side effects – GI, phototoxicity, rashes, tendonitis and tendon rupture – might interfere with bone formation in growing kids and pregnancy. CNS effect, but all can increase QT interval and cause arrythmias. Contraindicated in pregnancy and in children |
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Metronidazole
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mechanism - forms toxic metabolites in the bacterial cell that damage DNA.
Clinical use - GET GAP on the Metro! Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteriodes, Clostridium). Used with bismuth with amoxicillin for "triple therapy" against H. Pylori. Tox - disulfiram like raection with alcohol, headache, metallic taste.Will discolor patients urine in reddish brown color. Get burning pee. Cam get peripheral neuropathy. |
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polymyxins
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bind to cell membranes of bacteria and disrupt their osmotic properties.
Resistant gram negative infections Tox - neurotoxic, acute renal tubular necrosis. |
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Anti TB
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. TB drugs – combination drug therapy – primary drugs are isonizid, firampin, ethambutol and pyrazinamide.
Prophlaxis is usually INH, but use rifampin if intolerant…if drug resistance is supescted use both. a) Isoniazid – inhibits myocolic acid synthesis…high level resistance – it is actually a prodrug – it requires a catalase to be turned on…some bugs have a deleted katGene, which is would make the drug not work. Low level resistance= deletions in inhA gene encodes acyl carrier protein (the target) Iso NI=nitrogen. Has a lot of nitrogen and nitrogen tends to get metabolized in liver, so this is what causes hepatotoxicity. Transaminases transport ammonia, so this is why you get high AST’s. Transaminases require vitamin B6…if you upregulate transaminase, you’ll need B6. If no B6, you’ll get an anemia from not making heme…iron will pile up in body – get a sideroblastic anemia. Increased iron. Isoniazid is most common cause of sideroblastic anemia..also get peripheral neuropathy, so need B6. Can also cause lupus. b) Rifampin – inhibits DNA dependent RNA polymerase – transcription inhibitor. Resistance occurs in changes in enzyme…induces cytochrome P450, so additive hepatotoxicity and drug interactions. Red-orange metabolites – all biological fliud turns bright red orange – everything is red with rif. Doesn’t clean up well, would even stain contacts. Which metabolite causes these colors? – desmethyl rifampin is one of the main metabolites. c) Ethambutol – inhibits synthesis of arabinogalactan – cell wall compenent. Patients can’t see red and green here. d) Pyrazinamide – unknown, but requires bacteria to be turned on – adds on to hepatoxicity – long lists of side effects, but increases porphyrin synthesis….increased cytochrom P-450 synthesis..it’s a p450 inducer just like rifampin e) streptomycin – aminoglycocide – neurotoxicity with deafness, vestibular dysfunction and nephrotoxicity Remember that all these drugs will be used for 6 months to a year….for avium – use high dose macrolides! Rifambutin is used too, which is similar to rifampin. |
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isoniazid
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decreases synthesis of mycolic acids
Use is TB prophlaxis Can cause hemolysis if G-6-PD deficient, SLE, vit B6 can prevent neurotoxicity. |
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Rifampin
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inhibits DNA dependent RNA polymerase
used for TB, delays resistance to dapsone when used for leprosy, H. influenza prophylaxis 4R's - RNA pol inhibitor, revs up P450, red body fluids, rapid resistance if used alone. |
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Jarisch-Herxhimer reaction
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this is due to release of toxin release in syphillus treatment (penicclin G). Get general malaise
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H. pylori treatment
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H. pylori – BMT – bismuth (pepto bismol, antacid and coating), metronidzole, tetracycline. This is cheap
Clarithromycin and omeprazole (proton pump inhibitor). Works good but really expensive. |
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Amphoterecin B
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Amphoterecin B (nyastatin only used topically due to toxicity)
a) mechanism – INTERACTS with ergosterol in fungal membranes to form artifical pores – this is a non-specific reaction, fluids and salts go through bugs. Resistant fungal strains have low ergosterol content in their cell membranes (use another sterol). c) Activity/use – any severe systemic fungal infection – aspergillus, candida, Cryptococcus, histoplasma, mucor, sporothrix. Can be added with flucytosine in candidiasis and crytopotoccous. d) Extremely water soluble so hard to cross CNS – administered directly into CNS by IV– intrathecal…slow clearance – it’s half life is over 2 weeks.. Can release histamine, use NSAIDs. The real worry is dose dependent renal toxicity – get decrease in GFR, tubular acidosis, decreased potassium and Mg2+. Can decrease erythropoietin -> get an anemia. Want to infuse slowly and support with fluids. |
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ketaconazole/flucoanazole, itraconazole
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a) mech – fungicidal and interfere with the synthesis of ergosterol by inhibiting 14 a demethylase, which is a fungal P450 (converst lanosterol to ergosterol). These drugs are also inhibitors of human P450’s. Resistance occurs via decreased intracellular accumulation (pumps – move drugs out).
Ketoconazole is the prototype – systemically, but doesn’t distribute in CNS Floconazole is the drug of choice, less toxic and very well distributed in brain tissue – both for prophylaxis and suppression of cryptococcos. Itraconazole – DOC in blastomycosis, sporotrichoses Clotrimazole/miconazole – used topically for jock itch, athletes foot. These drugs are effective orally – so antacids will decrease drug absorption or food. Only flucconazole goes to CNS – most HIV patients will use this for cryptococcous c) metabolism – inhibition of hepatic P450’s – drug interactions. d) Side effects – decrease synthesis of steroids including cortisol and testosterone. Elevated liver function tests and rare hepatotoxicity. |
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Flucytosine
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cytosine” a base – base analog, so is a pro-drug. Uracil is precursor of cytosine and thyrmine…flucytosine needs to be deaminated
Activated by fungal cytosine deaminase to 5-FU which after triphosphorylation is incorporated into fungal RNA and stops RNA synthesis 5-FU forms 5-Fd-UMP inhibits thymidylate synthase -> decreases thymine. Intereferes with DNA too. Does this well in humans, so toxic to bone marrow. Used in combination with amphotericin B for severe candidal and cryptococcal infections – enters CSF. Does cross BBB. |
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Griseofulvin
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used systemically for topical fungal infection – works on dermatophytes. Goes wherever keratin is- inteferes with microtubule structure (M phase specific) – side effects – headache, thrush peripheral neuritis, potentiates ethanol (shuts down acetylaldehyde dehydrogenase). Avoid with history of porphyria. Used orally
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Terbinafine
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inhibits squalene epoxidase and decreases ergosterol syntheis, only on dermatophytes – possible hepatotoxicity.
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Acyclovir
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nucleoside analog, so has to be phosphyrlated. The very first phosphate is placed by viral thymidine kinase, and then the other 2 are added by any kinase, even host cell. You would expect anti-neoplastic effects here, since it interferes with DNA synthesis, but remember, acyclovir needs to be turned on by the virus! The only place it can be turned on is where the virus is, and herpes doesn’t infect in the bone marrow, so not hepatotoxic! Once it has it’s 3 phosphate, it will inhibit viral DNA polymerase…it is a chain terminator because it lacks the 3’ hydroxyl group.
a) Resistance – virus can change the thymidine kinase. Strains of herpes that do not even have the enzyme. This is a TK – strain – completely resistant to acyclovir. More than 50% of herpes strains are TK- now. B) use HSV and VZV (not CMV, has no TK) c) side effects – minor with oral use. Crystallurai, not hematotoxic. d) new analogs – famciclovir and valcyclovir, more active on resistant strains, but still won’t work on TK- strains |
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Ganciclovir
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similar to that of acyclovir. Frist phosphorylation is viral specific to phosphotranserase (UL97) in CMV. Can also be used in HSV, so uses thymidine kinase. Resistance mechanisms similar to acyclovir. Any kinase can turn on this one….mostly used in CMV, but can use in HSV, VZV. Used for prophylaxis.
a) side effects – dose limiting bone marrow suppression (so if immunosuppressed, this is dangerous). Seizures. |
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Foscarnet
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expensive and needs IV. It is not an antimetabolie, but still inhibits viral DNA and RNA polymerases. Uses are identical to gnagciclyovir, plus greater activity versus acyclovir resistant strains of HSV. Get nephrotoxicity with acute tubular necrosis, electrolyte imbalance with hypocalcemia (tremors and seizures. Avoid pentamidine IV – very nephrotoxic…never use it with this.
Use this drug if you’re trying to avoid bone marrow suppression, unless it’s so severe that they were using pentamidine…need to use ganciclovir despite bone marrow suppression. |
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AZT
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Nucleoside reverse transcriptase inhibitor, can also inhibit regular DNA polymerase at enough doses, so can get bone marrow suppression. Zidovudine, so thiamine analog – phosphrylation to be turned on – nonspecifically. Resistance occurs by mutations in genes that codes for RT. Interefers with biding sites.
Drug interactions – azole, antifungals, cimetidine, indomethacin, probenecid, TMP-SMX – additive myelosuprressive affect (pneumocystis carinii). Rifampin would induce p450’. Side effects – hematotoxicity can be severe enough to warrant blood transfusion. Headache, asthenia, myalgia, myopathy, peripheral neropathy, rare, but ponteinally fatal lactic acidosis. Other NRTI’s work the same way – not complete cross resistance, all bind to slightly different spots – all other drugs have less bone marrow suppressing than AZT. |
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Didanosine
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DDI - Nucleoside reverse transcriptase inhibitor
inosine analog (precursor of adenine/guanine) – major drug to know of pancreatitis (valproic acid too!). Peripheral neuropathy. |
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Zalcitabine
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Nucleoside reverse transcriptase inhibitor
DDC - peripheral neuropathy, pancreatitis, cytoxsine analog. Probably not a good idea to combine with DDI. |
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Stavudine
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D4T - Nucleoside reverse transcriptase inhibitor
– exact analog of AZT, so don’t use it with them because they’d compete for same binding site, but less myelosupressive |
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Lamivudine
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3TC - Nucleoside reverse transcriptase inhibitor
least toxic, but least efficient. Some GI effects, usesd in hep B. Too weak to be used on their own.Didanosine |
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idinavir, ritonavir
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Part of HAART Therapy -
Proteaes inhibitors aspartate protease (pol gene) encoded is a viral enzyme that cleaves precursor polypeptides in HIV buds to form the proteins of the mature virus core. The enzyme cointains a dipeptide structure not seen in mammalian proteins, so PI’s bind to this dipepetide inhibiting it. Reisstance occurs via specific point mutations in the pol gene, so there is not complete cross resistance between different PI’s. This protease cleaves the precursor peptides (propeptides) and turns them on….these drugs inhibit this activity. Has nothing to do with DNA replication, so no bone marrow suppression. Different mode of action…can only be synergistic with other drugs. Structure of aspartate protease doesn’t exist in us….but selectivity is in dose. Resistant strains are emerging fast…single changes in pol gene…drugs won’t last for long, but resistance isn’t complete, so you can switch it. Clinical uses – ….used with two NRTI’s to give HAART. Side effects – neprholithiassis, GI, thrombocytopenia…inhibition of P450 – 3A4 isozyme which is the major isozyme (2/3rds of drugs). Might cause lipid/CHO metabolism disorders – proteases in our body might get shut down (proinsulin to insulin, chymotrypsin to trypsin). Might give diabetes. |
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delavirdine, nevirapine, efavirenz
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non-nucleoside analogs - don't need to be turned on. Reverse transcriptase inhibitors.
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Enfurvitide
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– fusion inhibitor – binds to gp41 (transmembrane protein, other is gp120- both are important for attachment – gp120 recognizes CD4, while gp41 recognizes chemokines). Once bound, gp41/gp120 retract and form a channel for HIV to get in. This drug binds to gp41 and prevents fusion of HIV to CD4 cells. Costs 20 G’s.
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Amantadine
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blocks attachment, penetration, and uncoating of influenza A virus. Use is prophalyix….causes atropine-like peripheral effects and livedo reticularis
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Zanamivir/Oseltamivir
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inhibit neouraminidases of influenzae A and B…use is prophlaxis. Both cause nausea and vomting and Zanamivir via inhalation causes nasal and throat irritation.
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Ribavarin
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– uses nucleoside analagos – monophosprylated form inhibits IMP dehydrogenase (inosine – precursor of purines) – inhibits purine synthesis, so no DNA or RNA. Triphosphate inhibits viral RNA polymerase and end capping of viral RNA
Can be used for RSV, Influenzae A and B, Lassa fever, hantavirus, adjunt to alpha interforons in hep C. Side effects= hematotoxic (all of them are except acyclovir), upper airway irritation, teratogenic. |
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Interferons
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boost our inflammatory response, help lymphocytes do their jobs better. Can be used for hep B, C, D. Antitumor – kaposie sarcoma, CML, multiple myeoloma, renal carcinoma and multiple sclerosis – doesn’t treat, but might manage and delay issues with that.
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mebendazole
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use for worms, decreases glucose uptake so worm can't eat. Will become paralyzed and detached.
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Cyclosporines
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Bind to cyclphilins. Complex blocks the differentiation and activation of T cells by inhibiting calcinuerin, which prevents production of IL-2 and its receptor
Used after translplantation, autoimmune tx. Predisposes patients to infections, lymphoma. Nephrotoxic (use mannitol) |
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Tacromilus
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binds to FK binding protein, inhibits secretion of IL-2
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Azthioprine
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precurosor of 6-mercaptopurine that inteferes with the metabolism and synthesis of nucleic acids. Toxic to lymphocytes.
Used for tranplants, autoimmune disorders Toxic to bone marrow, metabolized by xanthine oxidase |
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Muromonab-CD3
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binds ot CD3 on the surface of T cells.
Used after kidney transplants Used for cytokine release syndrome, hypersensitivity reactions |
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Sirolimus (rapamycin)
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binds to mTOR and inhibits T-cell proliferation in respnse to IL-2.
Used after kidney transplatnation. can lead to hyperlipidemia, thrombocytopenia |
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Mycophenolate mofetil
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inhibits de novo guanine synthesis and blocks lymphocyte production
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dacluzumab
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monclonal antibody with high affinity for the IL-2 receptor on activated T cell
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aldesluekin
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IL-2
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filgrastim
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granuloycte colony stimulating factor
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sargramostim
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macrophage colony stimulating factor
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Infliximab
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Anti TNF alpha - used for chrohn's disease
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Rituximab
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monclonal antibody against CD20 - used for NHL
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Trastuzumab (herecepton)
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Used for breast cancer
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Imatinib
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CML treatment - inhibits BCR/ABL tyrosine kinase
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Abciximab
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GPIIa/IIIa - inhibits this last step of platelet aggregation - used in angioplasties.
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