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131 Cards in this Set

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  • Back
Worm Drugs
-pyrantel pamoate
-pyrantel,levamisole,piperazine, and ivermectin interfere w/synaptic trsmissn
-uncouples oxidative metabolism
-tapweorm scolex releases from the intestinal wall
-opens calcium channel to cause muscle tetany
-spastic paralysis
-causes tegmental damage which activates the host immune system
albendazole and mebendazole
-inhibits synthesis of microtubules neede for glucaose uptake-> dec glycogen conc and ATP conc-> death
-inhibits mitochondrial fumarate reductase
-immobliizes microfilariae via decreased muscular activity
-also alters surface membranes to make organism more susceptible to host defenses
pyrantel pamoate and levamisole
-ganglionic nicotinic cholinergic agonists=muscular tetany
-a GABA agonist at chloirde channel in NMJ
-->a flaccid paralysis
-releases GABA and inc GABA binding-> facilitate opening of chloride channels in NMJ-> flaccid paralysis in helminths, insect and ectoparasites
-may also cause tonic paralysis of musculature in nematodes via glutamate-gated Cl- channels found only in invertebrates
DOC for Cestodes (tapeworms)
-DOC for cestodes is niclosamide on an exam
-DOC is praziquantal in the real world
-third possible drug is mebendazole
DOC for roundworm (Ascaris lumbricoides)
pinworm (Enterobius vermicularis)
-a safety "pin" has a "bend" in it
-pyrantel pamoate
hookworm (Necatur americanus)
whipworm (Trichuris trichiura)
threadworm (Strongyloides stercoralis)
-DOC is ivermectin (allen iverson "threads" his way to the basket)
trichinosis (Trichinella spiralis)
- Wucheria bancrofti
- Onchocerca volvulus
- Wucheria bancrofti = diethylcarbamazine

- Onchocerca volvulus = ivermectin is the DOC
-tx of onchocerciasis and strongyloidasis (threadworm), ectoparasites
Trematodes (flukes) = Schistosoma
-praziquantel is the DOC
patient passes tape worm segments (proglottids) - most likely Taenia saginata (beef tapeworm) or a patient who likes to eat sushi passes tapeworm segments - most likely to be Diphyllobothrium latum (fish tapeworm) - treat with?
-tx = niclosamide or
Fish tapeworm causes megaloblastic anemia because the worm takes up all the vitamin B12 in the gut
poopy pants
Always worry that patient may have Taenia solium, pork tapeworm, which may
produce cysticercosis (larval cysts) in the brain, orbit, muscles, liver and lungs. Tx?
-Tx cysticercosis w/ albendazole
Baby w anal itching (pruritis) and a postive “cellophane tape” test . Dx and Tx?
-pinworm infestation
-tx w/ mebendazole or pyrantel pamoate
Patient w mixed infestation = cestode (tapeworm) + trematode (fluke) . Tx?
-tx w/praziquantel
Antiprotozoal Drugs
-Pentamidine isethionate
-DOC For?
-etro is DOC for Giardia, Trichomonas and C. dificile infections
-also active against?
-active against anaerobic protozoa and bacteria
-Entamoeba histolytica (amebiasis)
-MOA: reduced to active nitroderivative that inhibits DNA replication
-S/E = disulfiram-like reaction w EtOH Headache, n/v, flushing: teratogenic
Pentamidine isothionate
-MOA unknown
-second line drug for PCP (or PJP as we now call it...good job on staying up w/ the lit keeton...ass)
-DOC for PCP/PJP in AIDS pts
Antimalarial Drugs
-acute hemolysis in a pt tx w/primaquine. why?
-glucose-6-phosphate dehydrogenase deficiency
Antimalarial Drugs
-principal drawback of chloroquine for tx of malaria?
-wide-spread occurrence
of resistant strains
Antimalarial Drugs
-S/E's of chloroquine?
-S/E's of chloroquine = tinnitus, headache
Antimalarial Drugs
-DOC for prophylaxis for areas with chloroquine-resistant strains?
-mefloquine = DOC for prophylaxis for areas with chloroquine-resistant strains
Antimalarial Drugs
-DOC for tx of chloroquine-resistant malaria? and why?
-sulfadoxine - pyrimethamine is DOC for tx of chloroquine-resistant malaria b/c it has a different MOA than chloroquine
Antimalarial Drugs
-chloroquine = MOA: blocks DNA/RNA synthesis

-sulfadoxine = MOA: inhibits dihydropteroate synthase

-pyrimethamine = MOA: inhibits DHF reductase, can cause megaloblastic anemia
Antiviral Drugs
-HIV protease inhibitors = saquinivir
-used to tx herpes simplex virus (HSV)
-acyclovir (acycloguanosine) is converted to acyclovir-monophosphate by
thymidine kinase.

-Other enzymes convert it to acyclovir-triphosphate (acyclo-GTP)
which inhibits viral DNA polymerase.
-Why isn't acyclovir toxic to host cells?
-Why isn’t acyclovir toxic to the host cells?
-mammalian cells phosphorylate acyclovir
at 1/30-1/00 the rate of the HSV, and acyclo-GTP is 1/10-1/30 less active in inhibiting
mammalian DNA polymerase.
-What causes resistance of HSV to acyclovir?
-What causes resistance of HSV to acyclovir?
-a mutation which causes a
deficiency of thymidine kinase
-immunocompromised patient w/ mucocutaneous HSV infection. tx?
-patient w HSV encephalitis.tx?
-you guessed it...acyclovir
-patient w/ genital HSV infection. TX?
Keratoconjunctivitis caused by HSV. TX?...oh...what could it be?!?
-Keratoconjunctivitis caused by HSV is treated w/...

-trifluridine (trifluororthymidine)
-used to tx CMV
-phosphorylated to a triphosphate which inhibits DNA polymerase (triphosphate
a competitive substrate w/ deoxyguanosine triphosphate for incorporation into DNA –
stops DNA chain elongation to inhibit DNA synthesis
immunocompromised pt. w/CMV infxn. Tx?
-tx cmv w/ganciclovir!
Idoxuridine (resembles thymidine)
-MOA: triphosphate inhibits viral DNA polymerase.
-medical use?
-Used to tx HSV keratitis
interesting fact...
-When HSV becomes resistance to idoxuridine, it will be resistant to trifluridine
because both drugs are thymidine derivatives which inhibit DNA polymerase.
-MOA: inhibits the membrane coat ion channel that allows the acid-mediated
dissociation of ribonucleoprotein complex early in replication.
-This inhibition of
uncoating prevents the transfer of viral RNA into the cytoplasm of the mammalian cell
-medical uses?
-inhibits uncoating of influenza A and rubella viruses
-used prophylactically to prevent infx w/fluA
-tx of flu
-MOA: inhibition of viral neuraminidase
Zidovudine (AZT=azidothymidine)
-MOA:converted to an active triphosphate which either inhibits viral DNA polymerase
(reverse transcriptase) or is incorporated into DNA in the place of thymidine to stop DNA chain elongation.

-S/E = bone marrow depression and anemia
HIV protease inhibits=saquinivir
-MOA: inhibit HIV aspartic protease which converts polyproteins into functional core proteins and viral enzymes
1.MOA: causes protein synthesis:
-2,5 adenine synthetase makes adenylate oligomers which activate RNAse to
degrade viral RNA
-protein kinase phosphorylates elongation factor 2 to prevent peptide viral chain initiation
-PDEase degrades terminal nucleotide of t-RNA to inhibit viral peptide chain
-Net effects?
-interferes w viral penetration, uncoating, assembly and release

-interferes w the synthesis of viral mRNA

-inhibition of the translation of viral mRNA
Antifungal Drugs
-Amphoterecin B
Amphoterecin B
-MOA: binds to ergosterol in fungal membranes to form pores which increases the
permeability of the fungal membrane, cells lose ions and macromolecules; enhances
penetration of other antifungal drugs such as flucytosine
Amphoterecin B
-Resistance from decreased membrane ergosterol or altered structure of ergosterol
Amphoterecin B
-DOC for?...
-DOC for Coccidioides immitis and Aspergillus infections
Amphoterecin B
-also effective against?
-Also effective against Candida.
Amphoterecin B
-clinical usefulness is limited by its nephrotoxicity
-histological damage to renal tubules w/ cell necrosis

-renal tubular acidosis (a defect of renal function that produces systemic acidosis because bicarbonate ion cannot be reabsorbed in the PT or DT).

-hyperchloremic metabolic acidosis
Amphoterecin B
-how to avoid renal tox?
-renal toxicity can be avoided by giving MANNITOL to induce a high rate of urinary flow
-MOA: inhibits fungal CYP450 which prevents the demethylation of lanosterol to ergosterol, so blocks cell wall synthesis
-why is ketoconazole contraindicated in a patient receiving tx w/ amphoterecin B?
-because ketoconazole will BLOCK the antifungal actions of amphoterecin B
-medical uses?
-Used to tx Candida infections

-also effective against Coccidioides immitis
-bad S/E?
-inhibits CYP450 to inc the plasma conc of other drugs, esp. cyclosporine in transplant patients

-fluconazole also inc [cyclosporine] by MOA is unknown
-more S/E?
-inhibits adrenal 17-alpha & scc CYP450’s = adrenal insufficiency and dec[testosterone] & [estradiol]

-= gynecomastia & dec libido & potency in males; menstrual irregularities in females
-converted to fluorouracil which inhibits thymidylate synthesis and thus inhibits
DNA synthesis
-Fungal resistance to flucytosine develops rapidly and limits its clinical effectiveness,so amphoterecin B is used to treat systemic fungal infections

-OR flucytosine and
amphoterecin B are given together
-Ampho B enhances the penetration of flucytosine: synergistic antifungal activity
-S/E = bone marrow depression, limits clinical usefulness
-Which drug is selectively toxic to fungi because mammalian cells are unable to
catalyze its deamination? ...duh?
Trim-sulfa is DOC for tx of PCP (PJP)
megan is nice
-MOA: disrupts mitotic spindle by interacting w/ polymerized microtubules-> fungal mitosis is inhibited
-medical uses?
-used to tx dermatophytes w/hyphae...
-other use?
-Can also tx athlete’s foot w miconazole.

-MOA: Inhibit fungal CYP450 to block the synthesis of ergosterol
-USMLE vs. Real World
-on USMLE DOC for ringworm is griseofulvin
-in real world use a -conazole
Antibiotic Drugs
-penicillins (G+ bugs)
-Macrolides=eythromycin, clarithromycin, azithromycin =b-static
-TB tx="RIPE"=rifampin, isoniazid, pyrazinamide, ethambutalol
-Drugs that inhibit DNA gyrase=nalidixic acid and quinolones
Mostly affect G+ organisms
-MOA: interact w penicillin-binding proteins to inhibit transpeptidation and peptidoglycan synthesis; cell wall synthesis is inhibited.
-Eliminated by renal tubular secretion
-Probenecid increases the t1/2 by inhibiting renal
secretion (clearance).
-The [PCN] in serum inc whereas the [PCN] in the urine dec
-drugs that inhibit bacterial beta-lactamases (penicillinases)
1.clavulanate, sulbactam & tazobactam inhibit bacterial beta-lactamases (penicillinases)
2.PCN's resistant to beta-lactamse - primary use is beta-lactamase producing Staph.
-acid-labile: methcillin, nafcillin
-acid-stable = oxacillin, cloxacillin, dicloxacillin
-relationship b/t imipenem and cilastatin (spicy!!!)
-imipenem, which is resistant to beta-lactamase, is metabolized by renal tubular dihydropeptidases

-Cilastatin inhibits these renal peptidases to decrease the renal clearance of imipenem->increased half-life of imipenem
-rxns are common to all PCNs
-Cephalosporin MOA?
-same as penicillin
-MOA: interact w penicillin-binding proteins to inhibit transpeptidation and peptidoglycan synthesis; cell wall synthesis is inhibited.
pt w/gonorrhea. tx w/pcn for 8wks. returns with similar symptoms, but no diplococci in urine...what is the effin deal?
-patient has Chlamydia infection
-tx w/ tetracycline unless patient is a PREG female, then tx w/ erythromycin
pt has Streptococcus but is allergic to pcns...what to do?
-tx w/erthromycin
Vancomycin (a glycopeptide)
-MOA: blocks cell wall synthesis by preventing the release of sugar-glycan
pentapeptide linked to a phospholipid in the cell wall
Vancomycin and method of administration?
-Vancomycin is given i.v. for bacterial infections bx it is not absorbed when given p.o.
Vancomycin and C.diff. this is some wild stuff!!
-If Clostridium difficile occurs w i.v. vancomycin, p.o. vancomycin will still cure it.
-b/c po vanc is not absorbed (remember)
-MOA: binds to 30S subunit = interfere w initiation complex of peptide formation,
causes misreading of mRNA and break polysomes into non-functional monosomes.
-dec GFR inc the t1/2 of gentamicin
-PCN’s enhance the cellular penetration of aminoglycosides = synergistic effects
-drug accumulates in cells of PT and causes necrosis so urinary excretion of brush
border enzymes increases - effect usually reversible since cells of PT can regenerate
-get defect of renal concentrating mechanism because gent acts on DT and CD to decrease the sensitivity to ADH
-decreased GFR, mild proteinuria, hyaline and granular casts in urine
-net effect = mild increase in serum creatinine, hypokalemia, hypocalcemia and hypophosphatemia
-MOA:blocks sequential enzymes
-dihydropteroate synthase inhibited by Sulfa
-DHF reductase inhibited by trim
-mammal vs bacteria
-trimethoprim 100,000 X more active against bacterial enzyme vs mammalian enzyme
-issues w/bilirubin?
-sulfonamides can displace bilirubin from plasma protein binding sites and can cause kernicterus in neonates
pt w/AIDS develops PCP (PJP)...tx?
-tx w/ Trim-Sulfa
-MOA: bind to 30S subunit to block aminoacyl t-RNA binding to the acceptor (A) site
-acts against?
-acts against gram (+) and (-) organisms
-Rickettsiae, Mycoplasma, Chlamydia and amebas
-can it be used for pneumococcal pneumonia?
-Not used for pneumococcal pneumonia - tx w/ penicillins, cephalosporins or erythromycin
-Chelates Ca++ - adverse effect on formation of teeth and bones - fetus and babies

-severe rash w sunlight
-Chelates Ca++
-bioavailability decreased by milk and food in GI tract
-MOA: binds to 50S subunit and blocks aminoacyl translocation of peptide chain
pt tx w/ develops pseudomembranous colitis cause by C.diff...tx?
-tx w/oral metro or oral vancomycin
pt. w/pneumonia, but bug does not gram stain->atypical bug. tx?
-tx w/macrolide like eythromycin

-NB:if gram (+) pneumonia, probably Streptococcus
pneumoniae - tx w/ cephalosporin
erythromycin and the GI tract...?
-erythromycin causes stomach cramping bx it stimulates motilin receptors in stomach

-can be used to increase stomach motility in patients with diabetic gastroparesis
DOC for community acquired pneumo (CAP)???
tx of TB
-tx of TB= "RIPE"

-rifampin, isoniazid, pyrazinamide & ethambutol

-isoniazid (INH) causes hepatic damage; rifampin induces CYP450
Drugs that inhibit DNA gyrase
--->forms negative DNA supercoils
-nalidixic acid & fluoroquinolones (ciprofloxacin et al.)
Protein synthesis inhibitors
-buy AT 30, CELL at 50
buy AT 30, CELL at 50
A=aminoglycosides(cidal)+spectinomycin(static)-use for pcn-resistant gonorrhea
T=tetracyclines (static)

chloramphenicol, macrolides and clindamycin
-Since chloramphenicol, macrolides and clindamycin work at the same site, do NOT use them together because they will interfere w/ each other
Bactericidal Drugs
-PCN's, cephalosporins, aztreonam, imipenem
-aminoglycosides = gentamicin, etc.
-polymixin, colistin
-fluoroquinolones= norfloxacin, etc.
-nalidixic acid
Bacteriostatic Drugs
Bacterial Resistance
-NB: plasmid-mediated resistance is easily transferred by transduction to other species of bacteria
-beta-lactams = PCN's, cephalosporins, monobactams, carbapenems

-NB: the transpeptidase enzymes which are inhibited by the beta-lactams are called penicillin-binding proteins (PBP's) because they are the target site for these drugs
resistance to beta-lactams in G+ bugs
1.production of bacterial beta-lactamases

2.altered PBP's with decreased affinity for beta-lactams. Synthetic PCN's which are resistant to the beta-lactamases may not be effective if if the bug also has altered PBP's

3.MRSA = mutations change the binding sites of the PBP = no beta-lactam can bind to
the PBP = MRSA is resistanct to all beta-lactams (PCN's, cephs, imipenem, aztreonam)
-Tx MRSA w clindmycin, trim-sulfa or possibly doxycycline
resistance to beta-lactams in G- bugs
1.production of bacterial beta-lactamases (penicillinases) which may be inducible

2.reduced permeability -beta-lactams gain access to the periplasmic space (the site of the peptidoglycan wall in G- bugs) by passing through channels(called porins)in the outer bacterial membrane.
-A mutation which decreases the number of porins reduces the entry of the beta-lactams to their site of action.Thus a beta-lactam
could resistant to beta-lactamases,and yet not be able to inhibit bacteria growth because it could not reach the PBP's
resistance to Vancomycin
-vancomycin inhibits cell wall synthesis by binding to the terminal D-ala of the nascent peptidoglycan side chain
-this action inhibits transglycosylation, so both the elongation and the cross-linking of the peptidoglycan chain are inhibited
-Resistance occurs when a mutation changes the terminal D-ala to a D-lactate->vancomycin can no longer bind
-a single point mutation alter the binding of FQs to the active site of DNA gyrase
Aminoglycoside resistance
-plasmid-mediated enzymes are transferases which destroy the antibacterial effect of AG's by altering their structure

->the altered drug is inactive in inhibiting bacterial protein synthesis

-Enzymatic alterations include acetylation of amine groups and phosphorylation of hydroxyl groups
Macrolides and clindamycin resistance
Macs=ethryo,clarithro, and azithro
-bacterial enzymes methylate the 23S ribosomal component of the bacterial 50S ribosome
->this methylation prevents the binding of erthyromycin and clindamycin to the bacterial ribosome
tetracycline resistance
-tetracyclines (e.g., doxycycline) are pumped into susceptible bugs by an energy-dependent transport system in their cellular membranes
-Plasmids carry resistance genes which decrease the intracellular accumulation and code for efflux pumps which extrude the drug from the cell
folate synthesis inhibitors
-trim-sulfa resistance
-a plasmid-coded gene synthesizes a form of dihyropteroate synthetase which does not bind sulfonamides even though it still binds PABA
->bacterial folate synthesis cotinues unabated.
rifampin resistance
-mutation causing a single amino acid substitution in the beta-subunit of the DNA-directed RNA polymerase reduces the binding of rifampin
chloramphenicol resistance

-involves the production of acetyltransferases which inactivates the drug