Micro Drugs

bananas's version from 2015-06-11 22:48

Penicillin Drugs

Question Answer
What is the mechanism of action of penicillin G, V? Binds penicillin-binding proteins (transpeptidases). Blocks transpeptidase cross-linking of peptidoglycan in cell wall. Activates autolytic enzymes
What is the clinical use of Penicillin G, V? Mostly used for gram positive organisms. Also gram negative cocci and spirocheters.
How does resistance develop to penicillin G, V? Pencillinase in bacteria cleaves B-lactam ring.
Mechanism of amoxicillin and ampicllin? Same as penicillin. WIder spectrum: penicllinase sensitive like penicillin
Clinical use of amoxicillin and ampicillin? grams +'s plus HHELPS (H. Flu, H. Pylori, E Coli, Listeria, Proteus, Salmonella, Shigella)
What is special about methicillin, nafcilllin, oxacillin?Only PENCILLIN TYPE THAT IS Penicillinase resistant because bulky R groups blocks access of B-lactamase to B-lactam ring. They are not active against MRSA however
What is the clinical use of piperacillin, tiracillin and carbenicillin? Pseudomonas and gram negative rods
What is the purpose of B-lactase inhibitors? To protect the antibiotic from destruction by B-lactamase (penicillinase)
What happens if you give a patient amoxicillin who has mono? Rash!
Penicillins are structural analogs ofD-Ala-D-Ala


Question Answer
Mechanism of actionB lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.
What happens as you increase in generation of cephalosporinsyou increase gram - coverage and decrease gram + coverage
What are the first generation cephalosporinscefazolin and cephalexin
What bugs do first generation coverPEcK (Proteus, E. coli, Klebsiella)
What bugs do second generation coverHENS PECK (H. Flu, Enterobacter, Neisseria, Proteus, E. coli, Klebsiella, Serratia)
What are the second generation cephalosporinscefoxtin, cefaclor, cefuroxime
What are the third generation cephalosporinscerftriaxone, cefotaxime, ceftazidime
What bugs do third generation coverserious gram negative infections (ceftazidime has pseudo coverage)
What is the 4th generation cephalosporincefepime
What bugs do 4th generation cephalosporins covergram negative organisms increased activity against pseudomonas and gram positive organisms.
What is the 5th generation cephalosporincepftraloine- broad gram positive and gram negative, including MRSA; does NOT include pseudomonas
What bugs do cephalosporins not coverthey are LAME against (listeria, atypicals, MRSA and enterococci). Remember ceftaroline covers MRSA
What is the mechanism of resistance against cephalosporinsstructural changes in penicillin binding proteins (transpeptidases)


Question Answer
Mechanism of action of carbapenemsimpinem is a broad specture, B-lactamse resistant carbapenem. Always administered with cilastin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules
What is the clinical use of carbapenemsgram positive cocci, gram negative rods and pseudomonas.
Toxicity of carbapenemsSignificant side effects limit to life threatening infections. CNS toxicity at high plasma levels
What is the mechanism of action of monobactams (aztreonam)less susceptible to B-lactamases. Prevents peptidoglycan cross linking by binding to penicillin binding protein 3. Synergistic with aminoglycosides
If someone has a penicillin allergy will they be allergic to aztreonamNO. There is no cross allergenicity with penicillins.
Clinical use of aztreonamgram negative rods only (including pseudomonas). No activity against gram-positive or anaerobes.
Mechanism of action of vancomycininhibits cell peptidoglycan formation by binding D-ala D-ala Portions of cell wall precursors. Not susceptible to B-lactamases.
Clinical use of vancomycingram positive bugs only
Toxicity of VancomycinRed man syndrome and remember NOT (Nephrotoxicity, Ototoxicity, Thrombophlebitis)
How can one prevent red man syndromeslow down infusion of vancomyci and pretreat with antihistamines
Mechanism of Resistance against VancomycinOccurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac

Protein Synthesis Inhibitors

Question Answer
Mnemonic for the Protein Synthesis InhibitorsBuy AT 30, CCELL at 50. (aminoglycosides, tetracyclines) (chloramphenicol, clindamycin, erythryomycin (macrolides), linezolid, lincomycin)
Mechanism of action of aminoglycosidesirreversible inhibition of initiation complex through binding of 30S complex. Can cause misreading of MRNA. Requires O2 for uptake ineffective against anaerobes.
Clinical use of aminoglycosidessevere gram negative rods infections
Toxicity of aminoglycosidesNOT (nephrotoxicity, NMJ blockage, Ototoxicity, Teratogen) don't confuse with NOT of vancomycin
What are the aminoglycosidesgentamicin, neomycin, amikacin, tobramycin, streptomycin
How do bugs become resistant to aminoglycosidesBacterial transferase enzymes inactivate the drug by acetylation, phosphorylation or adenylation. Mutation of genes that encode ribosomal proteins nencause tehy modify the ribosomal binding sites for drugs.
MOA of tetracyclinesBind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
Do not take tetracyclines withmilk or antacids because divalent cations inhibit drug's absorption in the gut
Clinical use of tetracyclinesBorrelia, M. Pneumoniae, Rickettsia, Chlamydia, Acne
Toxicity of tetracyclinesDiscoloration of teeth and inhibition of bone growth in children and photosensitivity
Mechanism of resistance of against tetracyclinesdecreased uptake or increased efflux out of bacterial cells by plasmid encoded transport pumps
Chloramphenicol toxicitygray baby syndrome in premature infants because the lack liver UDP glucuronyl transferase. Can give phenobarbital. Also causes aplastic anemia
Clindamycin clinical useanaerobic infections above the diaphragm
Toxicity of clindamycinPseudomembranous collitis
LinezolidMechanism of action specifically binds to 23S portion of 50S subunit.
Linezolid clinical usegram positive species including MRSA and VRE
Clinical use of macrolidesPUS (atypical Pneumonia, URI, STD)
Toxicity of macrolidesMACRO (gi Motlity, Arrhthymia, acute Cholestatic hepatisis, Rash, eOsinophilia)
Mechanism of resistance against macrolidesmethylation of 23S rRNA binding site

THF inhibitor pathway

Question Answer
MOA of trimpethopriminhibits bacterial dihydrofolate reductase
Toxicity of trimpethoprimmegaloblastic anemia
What drugs block dihydrofolate reductasetrimethoprim, methotrexate and primethamine
Mechanism of action of sulfonamidesinhibit folate synthesis. Inhibit dihydropteroate synthase.
Toxicity of sulfonamidesHemolysis if G6PD deficient, kernicterus, SJS, phototoxicity
What are the sulfa drugsSulfa Pills Frequently Cause Terrible Acute Symptoms (Sulfalazine, Probenecid, Furosemide, Celecoxib, Thiazides, Acetazolamide, Sulfonyureas)


Question Answer
Mechanism of fluroquinolonesinhibit prokaryotic enzyme topoisomerase II and topoisomerase IV
Toxicity of fluroquinolonesMay cause cartilage damage in children less than 18. May cause tendonitis in those over 60.
Mechanism of resistance against fluroquinoloneschromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps
Clinical use of daptomycinS. Aureus Skin infections
Toxicity of daptomycinmyopathy, rhabdomyolysis
Mechanism of Action of MetroForms toxic free radical metabolites in the bacterial cell that damage DNA.
Clinical use of metroGET GAP on the Metro (Giardia, Entamoeba, Trichomonas, Gardenerella, Anaerobes, h.Pylori)
Toxicity of metrodisulfram-like reaction with alcohol

General antivirals

Question Answer
Zanamivir, oseltamivir mechinhibit influenza neuraminidase - decreasing the release of progeny virus
Zanamivir, oseltamivir clinical usetx and prevention of both influenza A and B
Ribavarin mechInhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase
Ribavarin clinical useRSV, chronic hepatitis C
Ribarvirin toxhemolytic anemia. Severe teratogen
Acyclovir mechMonophophorylated by HSV/VZV thymidine kinase
Guanosine analog
Preferentially inhibits viral DNA polymerase by chain termination
Acyclovir clinical useHSV & VZV + weak activity against EBV
Valacyclovirprodrug of acyclovir w better oral bioavailability
Famciclovirrelated to acyclovir
for herpes zoster
Acyclovir mechanism of resistanceMutated viral thymidine kinase
Ganciclovir mech5'-monophosphate formed by a CMV viral kinase
Guanosine analog
Preferentially inhibits viral DNA polymerase
Ganciclovir clinical useCMV, esp in immunocompromised
Progdrug, valganciclovir, has better oral bioavailability
Ganciclovir toxLeukopenia
renal tox
Ganciclovir mech of resistancemutated viral kinase
Foscarnet mechViral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme
Does not require activation by viral kinase
Foscarnet clinical useCMV retinitis in immunocompromised patients when ganciclovir fails
acyclovir-resistant HSV
Foscarnet toxnephrotoxic. Lead to symptomatic hypocalcemia and hypomagensia
Cidofovir mechpreferentially inhibits viral DNA polymerase
does not require phosphorylation by viral kinase
Cidofovir clinical useCMV retinitis in immunocompromised patients when ganciclovir fails
acyclovir-resistant HSV
Cidofovir toxicitynephrotoxic - coadminister with probenecid and IV saline to reduce toxicity

Antimycobacterial drugs

Question Answer
IsoniazidDecreases synthesis of mycolic acids
Use: prophylaxis against TB (only drug used alone for TB ppx)
Neuro (prevented with B6), hepatotoxic, lupus
Inhibits P450
RifampinInhibits DNA-dependent RNA polymerase
Use: TB, leprosy, H. influenza
Tox: Revs up P-450, red/orange body fluids
Works within macrophage phagolysosomes - requires acidic environment
Tox: hyperuricemia, hepatotoxic
Ethambutol↓ carbohydrate polymerizaction of mycobacterium cell wall by blocking arabinosyltransferase
Tox: optic neuropathy (red-green color blindness)

Antimicrobial Prophylaxis

Question Answer
High risk for endocarditis and undergoing surgical or dental proceduresamoxicillin, cephalexin, amoxicillin
exposure to gonorrheaceftraxione
history of recurrent UTISTMP-SMX, nitrofurantoin, amoxicillin, cephalexin
Exposure to meningococcal infectionceftriaxone or ciprofloxacin or rifampin
Prevention of gonococcal conjunctivitis in newbornerythromycin ointment
Prevention of postsurgical infection due to S. aureuscefazolin
prophylaxis of strep pharyngitis in child with prior rheumatic feverpenicillin G or oral penicillin V
exposure to syphillispenicillin G
H. Flurifampin

HIV therapy

Question Answer
"navir"s mechinhibits HIV-1 protease (pol gene) → prevent cleaving of HIV mRNA into their functional parts
"navir"s toxHyperglycemia
GI intolerance (nausea/diarrhea)
Ritonavir toxinhibits P450
Indinavir toxNephropathy
NRTIs mechNucleoside analogs → activated via phosphorylation → competitively inhibit nucleotide binding to reverse transcriptase → terminate DNA chain d/t lack of 3' OH group
must be phosphorylated to be active (except tenofovir, a nucleoTide)
NRTIs toxBM suppression - can be reversed w G-CSF and erythropoietin
peripheral neuropathy
lactic acidosis (nucleosides)
rash (non-nucleosides)
Zidovudane (AZT) clinical use and toxNRTI used for general prophylaxis during pregnancy to reduce risk of fetal transmission
Tenovirnucleotide analog (NRTI) so it does not have to be activated
NNRTIs mechbind to reverse transcriptase at different site than NRTIs
Don't require phosphorylation to be active or compete with nucleotides
NNRTIs toxBM suppression - can be reversed w G-CSF and erythropoietin
peripheral neuropathy
lactic acidosis (nucleosides)
rash (non-nucleosides)
RaltegravirIntegrase inhibitor → inhibits HIV genome integration into host cell chromosome
Raltegravir toxrash, myopathy
Interferons mechglycoproteins synthesized by virus-infected cells
block replication of both RNA and DNA viruses
IFN-α clinical usechronic hep B and C
Kaposi's sarcoma
IFN-β clinical useMS
IFN-γ clinical useNADPH oxidase deficiency
Interferons toxneutropenia
enfuviritidebinds gp41 inhibiting viral entry
maravirocbinds CCR-5 on t cells inhibiting interaction with gp120

Rapid-fire categorization

Question Answer
Raltegravieintegrase inhibitor

chronic Hep C therapy

Question Answer
ribavirininhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase
simprevirHCV protease inhibitor
sofosbuvirinhibits HCV RNA dependent RNA polymerase acting as a chain terminator


Question Answer
amphotericin Bbinds ergosterol; forms membrane pores that allow leakage of electrolyes
clinical use of amphotericin Bserious, systemic mycoses
Toxicity of amphotericin Bfever, chills, hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis
nystatinswish and swallow for oral candidiasis
MOA of nystatinsame as amphtericin B. topical use only
flucytosine moainhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase
clinical use of flucytosinesystemic fungal infections
toxicity of flucytosinebone marrow suppresion
azoles moainhibit fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol
Clinical use of azolessystemic mycoses
Clinical use of fluconazolechronic suppression of cryptococcal meningitis in AIDS and candidal infections of all types
Clinical use of itraconazoleBlasto, Cocci, Histo, Sporothrix
Toxicity of azolesinhibits cytochrome P450
Mechanism of action of terbinafineinhibits funal enzyme squalene epoxidase which decreases ergosterol synthesis
MOA of echinocandinsinhibit cell wall synthesis by inhibiting synthesis of B-glucan leads to cell lysis and death
Clinical use of echinocandinsinvasive aspergillosis, Candida
What are echinocandinsandidulafungin, caspofungin, micafungin
MOA of griseofulvininterferes with microtubule functions; disrupts mitosis.
Tox of griseofulvininduces cytochrome P450 and warfarin
Electrolyte disturbances in amphotericin B therapyhypokalemia and hypomagnesia

Malaria therapy

Question Answer
Primaquinemust be used in addition to chloroquine to eradicate Vivax and Ovale from latent hepatic infections
Chloruqinetreatment of choice for uncomplicated malaria
Most serious side effect of cloroquine useretinopathy