| Term | Definition |
|---|
| ciprofloxacin | Fluoroquinolone antibiotic. Inhibits type II topoisomerases and; therefore, blocks DNA replication. Resistance by target gene modification and altered uptake/efflux |
| levofloxacin | Fluoroquinolone antibiotic. Inhibits type II topoisomerases and; therefore, blocks DNA replication. Can cause a prolonged QT interval and thus bradycardia. Resistance by target gene modification and altered uptake/efflux. |
| rifampin | Inhibits bacterial RNA polymerase. Induces CP450. Patient's urine turns bright orange. Can develop hepatotoxicity if used in patients with HIV protease inhibitors. Resistance by target gene mutation in rpoB subunit of RNA polymerase. |
| metronidazole | Produces compounds toxic to DNA. Can be used on obligate anaerobes. IV/PO penetrates the CNS! Can promote renal retention of Lithium... NOT TO BE USED W/ ALCOHOL. |
| sulfanilamide | analogue of PABA and bunks enzyme activity leading to failure to manufacture DHF and THF. DO NOT give to patients with a G6P or folate deficiency. Resistance by mutated target genes, high levels of PABA transforming enzyme, newly transferred genes w/ resistant enzymes, and altered uptake/efflux. |
| trimethoprim | Analogue of DHF (not mammalian DHF) and blocks formation of THF. Can be given concurrently with a sulfa drug (as TMP-SMX) to form an efficient double block on bacterial THF development. |
| dapsone | Analogue of PABA which blocks formation of DHF. Do not give to patients with G6P or folate deficiency. Resistance by mutated target gene, increased enzymes to act on PABA, newly transferred genes with resistant enzymes. Can lead to neutropenia and dematitis in HIV patients. (this sulfa drug begins with a "d") |
| penicillin | Binds transpeptidase and stops formation of crossbridges in the cell wall. Crosses the BBB with inflammation present. Drug possesses a beta lactam ring. Resistance by mutations in transpeptidases, beta lactamase presence, and latered uptake. This drug spawned a slew of additional drugs. |
| bacitracin | Blocks dephosphorylation of carrier molecules for cell wall componants; therefore, causes reduced availibility of parts to build the cell wall. Often given topically with neomycin and polymyxins (as neosporin). |
| vancomycin | Binds to D-Ala residues on the pentapeptides which form the cross bridges in the cell wall. IV or PO, but NOT absorbed through the GI... only for GI infections. Resistance by D-Ala-->D-Ser/Lactate. Rapid IV infusion can lead to a histamine related flushing called "Redman Syndrome." Nephrotoxicity can occur if taken with an aminoglycoside AB. |
| dioxacillin | Inhibits transpeptidases and stop cell wall formation. A penicillin: short half-life, beta lactam ring, and good bioavailibility. Resistance by mutations in transpeptidases, beta lactamase presence, and altered uptake. This drug begins with a "d." |
| ampicillin | Inhibits transpeptidases and stop cell wall formation. A penicillin: short half-life, beta lactam ring, and good bioavailibility. Resistance by mutations in transpeptidases, beta lactamase presence, and altered uptake. This drug begins with an "a." |
| amoxicillin | Inhibits transpeptidases and stop cell wall formation. A penicillin: short half-life, beta lactam ring, and good bioavailibility. Resistance by mutations in transpeptidases, beta lactamase presence, and altered uptake. This drug begins with an "a" and is a tasty pink, refrigerated goo. |
| nafcillin | Inhibits transpeptidases and stop cell wall formation. A penicillin: short half-life, beta lactam ring, and good bioavailibility. Resistance by mutations in transpeptidases, beta lactamase presence, and altered uptake. This drug begins with an "n." |
| cephalexin | A cephalosporin that inhibits transpeptidases and inhibits cell wall formation. This drug begins with a "cepha." |
| cefotaxime | A cephalosporin that inhibits transpeptidases and inhibits cell wall formation. This drug begins with a "cefo." |
| ceftazidime | A cephalosporin that inhibits transpeptidases and inhibits cell wall formation. This drug begins with a "ceft." |
| aztreonam | A monobactam that inhibits transpeptidases and inhibits cell wall formation. |
| imiperem/cilastatin | A carbapenem that inhibits transpeptidases and inhibits cell wall formation. It is delivered with a drug that prevents the breakdown of the carbapenem. "______/______" |
| tetracycline | A tetracycline AB that blocks protein synthesis by ribosomes by binding to the 30S subunit. IV/PO... good GI absorption and can diffuse into the CNS. Antagonistic beta lactam ABs. Resistance by efflux pumping, bacteria produce a protein that binds ribosomes and blocks the activity of the tetracycline. Not to be used in children or preggies because it causes long-term discoloration of teeth. |
| doxycycline | A tetracycline AB that blocks protein synthesis by ribosomes by binding to the 30S subunit. IV/PO... good GI absorption and can diffuse into the CNS. Antagonistic beta lactam ABs. Resistance by efflux pumping, bacteria produce a protein that binds ribosomes and blocks the activity of the tetracycline. Not to be used in children or preggies because it causes long-term discoloration of teeth. This drug begins with a "d." |
| tigecycline | A tetracycline AB that blocks protein synthesis by ribosomes by binding to the 30S subunit. IV/PO... good GI absorption and can diffuse into the CNS. Antagonistic beta lactam ABs. Resistance by efflux pumping, bacteria produce a protein that binds ribosomes and blocks the activity of the tetracycline. Not to be used in children or preggies because it causes long-term discoloration of teeth. This drug begins with a "t." |
| erythromycin | A macroglide AB, binds the 50S subunit of ribosomes and prevents protein synthesis. IV/PO. This macroglide has considerably more nausea associated along with a greater risk for prolonged QT interval. Resistance by methylation of ribosomes to block binding and efflux pumping. |
| azithromycin | A macroglide AB, binds the 50S subunit of ribosomes and prevents protein synthesis. IV/PO with a longer half-life than many macroglides. Usually given to preggies and children. Resistance by methylation of ribosome to block binding and efflux pumping. |
| clarithromycin | A macroglide AB, binds the 50S subunit of ribosomes and prevents protein synthesis. IV/PO. Begins with a"c." |
| streptomycin | An aminoglycoside AB that blocks protein synthesis by binding the 30S subunit of the ribosome. Initially penetrate the bacterium by interrupting the Mg crosslinks between LPS residues... this can be suppressed in vitro by acidic pH or and anaerobic environment. 2 effects: 1) PAE (post AB effect) - continued suppression of bacterial growth after the ABs are stopped. 2) Concentration Dependent Killing - more Aminoglycoside-->more bacteria death. Synergistic effect with beta lactam ABs. IV/IM (not PO). Resistance by efflux pumping, decreased uptake, and enzyme inactivation. Can cause nephrotoxicity, but especially ototoxicity. Still used as a first choice for bioterrorism agents. |
| gentamycin | An aminoglycoside AB that blocks protein synthesis by binding the 30S subunit of the ribosome. Initially penetrate the bacterium by interrupting the Mg crosslinks between LPS residues... this can be suppressed in vitro by acidic pH or and anaerobic environment. 2 effects: 1) PAE (post AB effect) - continued suppression of bacterial growth after the ABs are stopped. 2) Concentration Dependent Killing - more Aminoglycoside-->more bacteria death. Synergistic effect with beta lactam ABs. IV/IM (not PO). Resistance by efflux pumping, decreased uptake, and enzyme inactivation. Can cause nephrotoxicity and ototoxicity. Begins with a "g." |
| tobramycin | An aminoglycoside AB that blocks protein synthesis by binding the 30S subunit of the ribosome. Initially penetrate the bacterium by interrupting the Mg crosslinks between LPS residues... this can be suppressed in vitro by acidic pH or and anaerobic environment. 2 effects: 1) PAE (post AB effect) - continued suppression of bacterial growth after the ABs are stopped. 2) Concentration Dependent Killing - more Aminoglycoside-->more bacteria death. Synergistic effect with beta lactam ABs. IV/IM (not PO). Resistance by efflux pumping, decreased uptake, and enzyme inactivation. Can cause nephrotoxicity and ototoxicity. Begins with a "t." |
| clindamycin | A lincosamine that blocks protein synthesis by binding the 50S subunit of the ribosome. IV/PO, DOES NOT REACH THE CNS. |
| linezolid | An oxazolidinedione that blocks protein synthesis by binding to the 50S subunit of the ribosome. IV/PO. Resistance by mutation of 23s rRNA. Thrombocytopenia in long-term therapy. DO NOT GIVE WITH SSRIs. |
| chloramphenicol | Blocks protein synthesis by binding the 50s subunit of the ribosome. IV/PO. Resistance by acetylation and efflux pumping. Aplastic anemia, bone marrow suppression, and Gray Syn (circulatory collapse, coma, death) possible with use. |
| quinupristin/dalfopristin | Block protein synthesis by binding the 50S subunit of the ribosome. IV ONLY. These two drugs always given with one another because it minimizes prevalence of resistance. Resistance by methyation to alter the target of the ribosome and efflux pumping. Use can lead to arthralgias and myalgias. |
| mupirocin | Blocks protein synthesis by inhibiting the ile tRNA synthase on ribosomes. Topical. Resistance by target site mutation. |
| retapamulin | Block protein synthesis by binding the 50S subunit of the ribosome. Resistance by target site mutation. Topical; good for MRSA and group A strep. Newer drug. |
| polymyxins | Distrupt bacterial membranes by charge alteration. Topical, usually applied with bacitracin and neomycin (neosporin). IV/IM as well. |
| daptomycin | Lipopeptide that interferes with bacterial cell membrane function and pore formation. IV. Test for elevated liver enzymes and creatine phosphokinase. Discontinue if they elevate (not sure about this last part). |
| nitrofurantoin | Mechanism mimics radiation damage. PO; concentrates in urine for Tx of UTIs. Can cause a harmless brown color to the urine... can also cause lung problems. |
| isoniazid | Drug used to treat mycobacterial infections; especially TB. Less effective on diseases caused by atypical mycobacteria. Drug has widespread distribution in body fluids and tissues (even the CNS). |
| isoniazid | A prodrug that is activated by KatG (a mycobacterial catalase peroxidase) and hen exerts its effects by forming a covalent bond with an acyl carrier protein (AcpM) and KasA (carrier protein synthase)... this blocks the formation of mycolic acid and kills mycobacteria. |
| isoniazid | Resistance to this drug can be due to over-expression of inhA gene which encodes an acyl carrier protein reductase, a mutaion of the KatG gene, and mutations in KasA. |
| isoniazid | This drug can induce the development of jaundice in ~1% of patients which can be fatal if the drug is not discontinued. Alcoholics and preggies are at greater risk for this effect. Neuropathy can also develop in patients with a relative pyridoxine deficiency (which is more likely in slow acetylators and malnourished, alcoholic, diabetic, AIDS patients). CNS SEs include psychosis, memory loss, and seizures. |
| rifampin | A first line drug against TB that binds RNA polymerase and inhibits RNA synthesis. Typically administered with INH so as to decrease the incidence of a resistant emergency. Penetrates most tissues, but has no intrinsic ability to cross the BBB. Can be used as prophylaxis in the event of an INH resistant latent TB. |
| rifampin | SEs of this first-line TB drug incluse 1) light chain proteinuria 2) rash 3) jaundice 4) flu-like symptoms when used intermittently. The drug also is a potent inducer of P450 and causes the patient's secretions to harmlessly turn orange. |
| ethambutol | First line TB drug that inhibits mycobarterial arabiosyl transferases (encoded by emb genes) which inhibits the formation of arabinoglycan; an essential component of the mycob. cell wall. |
| ethambutol | Resistance to this drug is often caused by mutations that lead to over-experssion of emb genes. The most common SE is a retrobulbar neuritis resulting in the loss of visual acuity and red/green color blindness. Therefore, it is contraindicated in children too young to be evaluated for vision loss. |
| pyrazinamide | A first line drug in the treatment of TB. This is a prodrug converted to its active form by an enzyme encoded by pncA. It is a synthetic analogue of nicotinamide. |
| pyrazinamide | Resistance to this drug may occur due to mutations in pncA (blocking conversion to its active form) OR by decreased drug uptake. THe major SEs include hepatotoxicity, GI disturbances, and hyperuricemia (watch carefully in patients with gout!). Used with rifampin and INH in short course tx regimes. |
| streptomycin | A first line TB drug that has poor penetration into the cells; therefore, it is mostly effective against extra-cellular bacilli. It is always administered with other drugs. Resistance could be due to a point mutation in the rpsL or rrs genes that alters the ribosomal binding site. |
| second-line drugs | The agents are considered if resistance occurs to streptomycin, INH, rifampin, ethambutol, and pyrazinamide or failure of conventional therapy, possibly due to adverse effects which limit its course. |
| p-aminosalicylic acid | This second-line TB drug is a folate synthesis antagonist (not Dapsone/sulfonamides). |
| dapsone | Leprosy drug that inhibits folate synthesis by blocking formation of DHF (analogue of PABA). This drug, along with sulfonamides, concentrate in the skin of M leprae infected patients. Hemolysis possible especially in patients with a G6PD defeiciency. |
| clofazimine | Alternative treatment of leprosy. Erratic absorption rate and is stored in the skin where it can cause discoloration from red-brown-black. |
Combine with other sets
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