Pharm. Review V

Front 1

Worm Drugs

Back 1

-niclosamide
-praziquantal
-albendazole
-mebendazole
-thiabendazole
-diethylcarbamazine
-pyrantel pamoate
-levamisole
-piperazine
-ivermectin
-pyrantel,levamisole,piperazine, and ivermectin interfere w/synaptic trsmissn

Front 2

niclosamide

Back 2

MOA
-uncouples oxidative metabolism
-tapweorm scolex releases from the intestinal wall

Front 3

praziquantal

Back 3

MOA
-opens calcium channel to cause muscle tetany
-spastic paralysis
-causes tegmental damage which activates the host immune system

Front 4

albendazole and mebendazole

Back 4

MOA
-inhibits synthesis of microtubules neede for glucaose uptake-> dec glycogen conc and ATP conc-> death

Front 5

thiabendazole

Back 5

MOA
-inhibits mitochondrial fumarate reductase

Front 6

diethylcarbamazine

Back 6

MOA
-immobliizes microfilariae via decreased muscular activity
-also alters surface membranes to make organism more susceptible to host defenses

Front 7

pyrantel pamoate and levamisole

Back 7

MOA
-ganglionic nicotinic cholinergic agonists=muscular tetany

Front 8

piperazine

Back 8

MOA
-a GABA agonist at chloirde channel in NMJ
-->a flaccid paralysis

Front 9

ivermectin

Back 9

MOA
-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

Front 10

DOC for Cestodes (tapeworms)

Back 10

-DOC for cestodes is niclosamide on an exam
-DOC is praziquantal in the real world
-third possible drug is mebendazole
-TMI

Front 11

DOC for roundworm (Ascaris lumbricoides)

Back 11

-albendazole
-mebendazole
-pyrantelpamoate
-piperazine

Front 12

pinworm (Enterobius vermicularis)

Back 12

-Mebendazole
-a safety "pin" has a "bend" in it
-pyrantel pamoate

Front 13

hookworm (Necatur americanus)

Back 13

-albendazole
-mebendazole

Front 14

whipworm (Trichuris trichiura)

Back 14

-albendazole
-mebendazole

Front 15

threadworm (Strongyloides stercoralis)

Back 15

-DOC is ivermectin (allen iverson "threads" his way to the basket)
-albendazole
-thiabendazole

Front 16

trichinosis (Trichinella spiralis)

Back 16

-albendazole
-mebendazole

Front 17

Filariae
- Wucheria bancrofti
- Onchocerca volvulus

Back 17

- Wucheria bancrofti = diethylcarbamazine

- Onchocerca volvulus = ivermectin is the DOC

Front 18

ivermectin

Back 18

-tx of onchocerciasis and strongyloidasis (threadworm), ectoparasites

Front 19

Trematodes (flukes) = Schistosoma

Back 19

-praziquantel is the DOC

Front 20

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?

Back 20

-tx = niclosamide or
praziquantel

Front 21

Fish tapeworm causes megaloblastic anemia because the worm takes up all the vitamin B12 in the gut

Back 21

poopy pants

Front 22

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?

Back 22

-Tx cysticercosis w/ albendazole

Front 23

Baby w anal itching (pruritis) and a postive “cellophane tape” test . Dx and Tx?

Back 23

-pinworm infestation
-tx w/ mebendazole or pyrantel pamoate

Front 24

Patient w mixed infestation = cestode (tapeworm) + trematode (fluke) . Tx?

Back 24

-tx w/praziquantel

Front 25

Antiprotozoal Drugs

Back 25

-Metronidazole
-Pentamidine isethionate
-Trim-Sulfa

Front 26

Metronidazole
-DOC For?

Back 26

-etro is DOC for Giardia, Trichomonas and C. dificile infections

Front 27

Metronidazole
-also active against?

Back 27

-active against anaerobic protozoa and bacteria
-Entamoeba histolytica (amebiasis)
-Bacteroides

Front 28

Metronidazole
-MOA?

Back 28

-MOA: reduced to active nitroderivative that inhibits DNA replication

Front 29

Metronidazole
-S/E

Back 29

-S/E = disulfiram-like reaction w EtOH Headache, n/v, flushing: teratogenic

Front 30

Pentamidine isothionate

Back 30

-MOA unknown
-second line drug for PCP (or PJP as we now call it...good job on staying up w/ the lit keeton...ass)

Front 31

Trimethoprim-Sulfamethoxazole

Back 31

-DOC for PCP/PJP in AIDS pts

Front 32

Antimalarial Drugs
-acute hemolysis in a pt tx w/primaquine. why?

Back 32

-glucose-6-phosphate dehydrogenase deficiency

Front 33

Antimalarial Drugs
-principal drawback of chloroquine for tx of malaria?

Back 33

-wide-spread occurrence
of resistant strains

Front 34

Antimalarial Drugs
-S/E's of chloroquine?

Back 34

-S/E's of chloroquine = tinnitus, headache

Front 35

Antimalarial Drugs
-DOC for prophylaxis for areas with chloroquine-resistant strains?

Back 35

-mefloquine = DOC for prophylaxis for areas with chloroquine-resistant strains

Front 36

Antimalarial Drugs
-DOC for tx of chloroquine-resistant malaria? and why?

Back 36

-sulfadoxine - pyrimethamine is DOC for tx of chloroquine-resistant malaria b/c it has a different MOA than chloroquine

Front 37

Antimalarial Drugs
-MOAs?

Back 37

-chloroquine = MOA: blocks DNA/RNA synthesis

-sulfadoxine = MOA: inhibits dihydropteroate synthase

-pyrimethamine = MOA: inhibits DHF reductase, can cause megaloblastic anemia

Front 38

Antiviral Drugs

Back 38

-Acyclovir
-Ganciclovir
-Idoxuridine
-Amantadine
-Zanamivir
-Zidovudine
-HIV protease inhibitors = saquinivir
-Interferons

Front 39

Acyclovir

Back 39

-used to tx herpes simplex virus (HSV)

Front 40

Acyclovir
-MOA?

Back 40

-acyclovir (acycloguanosine) is converted to acyclovir-monophosphate by
thymidine kinase.

-Other enzymes convert it to acyclovir-triphosphate (acyclo-GTP)
which inhibits viral DNA polymerase.

Front 41

Acyclovir
-Why isn't acyclovir toxic to host cells?

Back 41

-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.

Front 42

Acyclovir
-What causes resistance of HSV to acyclovir?

Back 42

-What causes resistance of HSV to acyclovir?
-a mutation which causes a
deficiency of thymidine kinase

Front 43

Acyclovir
-immunocompromised patient w/ mucocutaneous HSV infection. tx?

Back 43

-acyclovir

Front 44

Acyclovir
-patient w HSV encephalitis.tx?

Back 44

-you guessed it...acyclovir

Front 45

Acyclovir
-patient w/ genital HSV infection. TX?

Back 45

-acyclovir

Front 46

Keratoconjunctivitis caused by HSV. TX?...oh...what could it be?!?

Back 46

-Keratoconjunctivitis caused by HSV is treated w/...

-trifluridine (trifluororthymidine)

Front 47

Ganciclovir

Back 47

-used to tx CMV

Front 48

Ganciclovia
-MOA?

Back 48

-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

Front 49

immunocompromised pt. w/CMV infxn. Tx?

Back 49

-tx cmv w/ganciclovir!

Front 50

Idoxuridine (resembles thymidine)
-MOA?

Back 50

-MOA: triphosphate inhibits viral DNA polymerase.

Front 51

Idoxuridine
-medical use?

Back 51

-Used to tx HSV keratitis

Front 52

interesting fact...

Back 52

-When HSV becomes resistance to idoxuridine, it will be resistant to trifluridine
because both drugs are thymidine derivatives which inhibit DNA polymerase.

Front 53

Amantadine
-MOA

Back 53

-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

Front 54

Amantadine
-medical uses?

Back 54

-inhibits uncoating of influenza A and rubella viruses
-used prophylactically to prevent infx w/fluA

Front 55

Zanamivir

Back 55

-tx of flu
-MOA: inhibition of viral neuraminidase

Front 56

Zidovudine (AZT=azidothymidine)

Back 56

-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

Front 57

HIV protease inhibits=saquinivir

Back 57

-MOA: inhibit HIV aspartic protease which converts polyproteins into functional core proteins and viral enzymes

Front 58

Interferons
-MOA?

Back 58

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
elongation

Front 59

Interferons
-Net effects?

Back 59

-interferes w viral penetration, uncoating, assembly and release

-interferes w the synthesis of viral mRNA

-inhibition of the translation of viral mRNA

Front 60

Antifungal Drugs

Back 60

-Amphoterecin B
-Ketoconazole
-Flucytosine
-Trim-Sulfa
-Griseofulvin

Front 61

Amphoterecin B
-MOA?

Back 61

-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

Front 62

Amphoterecin B
-resistance?

Back 62

-Resistance from decreased membrane ergosterol or altered structure of ergosterol

Front 63

Amphoterecin B
-DOC for?...

Back 63

-DOC for Coccidioides immitis and Aspergillus infections

Front 64

Amphoterecin B
-also effective against?

Back 64

-Also effective against Candida.

Front 65

Amphoterecin B
-toxicity?

Back 65

-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

Front 66

Amphoterecin B
-how to avoid renal tox?

Back 66

-renal toxicity can be avoided by giving MANNITOL to induce a high rate of urinary flow

Front 67

Ketoconazole
-MOA?

Back 67

-MOA: inhibits fungal CYP450 which prevents the demethylation of lanosterol to ergosterol, so blocks cell wall synthesis

Front 68

Ketoconazole
-why is ketoconazole contraindicated in a patient receiving tx w/ amphoterecin B?

Back 68

-because ketoconazole will BLOCK the antifungal actions of amphoterecin B

Front 69

Ketoconazole
-medical uses?

Back 69

-Used to tx Candida infections

-also effective against Coccidioides immitis

Front 70

Ketoconazole
-bad S/E?

Back 70

-inhibits CYP450 to inc the plasma conc of other drugs, esp. cyclosporine in transplant patients

-fluconazole also inc [cyclosporine] by MOA is unknown

Front 71

Ketoconazole
-more S/E?

Back 71

-inhibits adrenal 17-alpha & scc CYP450’s = adrenal insufficiency and dec[testosterone] & [estradiol]

-= gynecomastia & dec libido & potency in males; menstrual irregularities in females

Front 72

Flocytosine
-MOA?

Back 72

-converted to fluorouracil which inhibits thymidylate synthesis and thus inhibits
DNA synthesis

Front 73

Flocytosine
-resistance?

Back 73

-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

Front 74

Flocytosine
-synergy?

Back 74

-Ampho B enhances the penetration of flucytosine: synergistic antifungal activity

Front 75

Flocytosine
-S/E?

Back 75

-S/E = bone marrow depression, limits clinical usefulness

Front 76

Flocytosine
-Which drug is selectively toxic to fungi because mammalian cells are unable to
catalyze its deamination? ...duh?

Back 76

-flucytosine

Front 77

Trim-sulfa is DOC for tx of PCP (PJP)

Back 77

megan is nice

Front 78

Griseofulvin
-MOA?

Back 78

-MOA: disrupts mitotic spindle by interacting w/ polymerized microtubules-> fungal mitosis is inhibited

Front 79

Griseofulvin
-medical uses?

Back 79

-used to tx dermatophytes w/hyphae...
-Trichphyton
-Microsporum
-Epidermophyton

Front 80

Griseofulvin
-other use?

Back 80

-Can also tx athlete’s foot w miconazole.

-MOA: Inhibit fungal CYP450 to block the synthesis of ergosterol

Front 81

Griseofulvin
-USMLE vs. Real World

Back 81

-on USMLE DOC for ringworm is griseofulvin
-in real world use a -conazole

Front 82

Antibiotic Drugs

Back 82

-penicillins (G+ bugs)
-Vancomycin=bactericidal
-Aminoglycosides=bactericidal
-Trim-Sulfa=bacteriostatic
-Tetracyclines=bacteriostatic
-Lincosamides=clindamycin=b-static
-Macrolides=eythromycin, clarithromycin, azithromycin =b-static
-TB tx="RIPE"=rifampin, isoniazid, pyrazinamide, ethambutalol
-Drugs that inhibit DNA gyrase=nalidixic acid and quinolones

Front 83

Penicillins

Back 83

Mostly affect G+ organisms

Front 84

Penicillins
-MOA?

Back 84

-MOA: interact w penicillin-binding proteins to inhibit transpeptidation and peptidoglycan synthesis; cell wall synthesis is inhibited.

Front 85

Penicillins
-kinetics?

Back 85

-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

Front 86

Penicillins
-drugs that inhibit bacterial beta-lactamases (penicillinases)

Back 86

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

Front 87

Penicillins
-relationship b/t imipenem and cilastatin (spicy!!!)

Back 87

-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

Front 88

Penicillins
-Hypersensivity?

Back 88

-rxns are common to all PCNs

Front 89

Penicillins
-Cephalosporin MOA?

Back 89

-same as penicillin
-MOA: interact w penicillin-binding proteins to inhibit transpeptidation and peptidoglycan synthesis; cell wall synthesis is inhibited.

Front 90

pt w/gonorrhea. tx w/pcn for 8wks. returns with similar symptoms, but no diplococci in urine...what is the effin deal?

Back 90

-patient has Chlamydia infection
-tx w/ tetracycline unless patient is a PREG female, then tx w/ erythromycin

Front 91

pt has Streptococcus but is allergic to pcns...what to do?

Back 91

-tx w/erthromycin

Front 92

Vancomycin (a glycopeptide)
-bactericidal
-MOA?

Back 92

-MOA: blocks cell wall synthesis by preventing the release of sugar-glycan
pentapeptide linked to a phospholipid in the cell wall

Front 93

Vancomycin and method of administration?

Back 93

-Vancomycin is given i.v. for bacterial infections bx it is not absorbed when given p.o.

Front 94

Vancomycin and C.diff. this is some wild stuff!!

Back 94

-If Clostridium difficile occurs w i.v. vancomycin, p.o. vancomycin will still cure it.
-b/c po vanc is not absorbed (remember)

Front 95

Aminoglycosides=bactericidal
-MOA?

Back 95

-MOA: binds to 30S subunit = interfere w initiation complex of peptide formation,
causes misreading of mRNA and break polysomes into non-functional monosomes.

Front 96

Aminoglycosides
-gfr?

Back 96

-dec GFR inc the t1/2 of gentamicin

Front 97

Aminoglycosides
-synergy?

Back 97

-PCN’s enhance the cellular penetration of aminoglycosides = synergistic effects

Front 98

Aminoglycosides
-Toxicity?

Back 98

-ototoxic,nephrotoxic
-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

Front 99

Trim-Sulfa=bacteriostatic
-MOA?

Back 99

-MOA:blocks sequential enzymes
-dihydropteroate synthase inhibited by Sulfa
-DHF reductase inhibited by trim

Front 100

Trimethoprim
-mammal vs bacteria

Back 100

-trimethoprim 100,000 X more active against bacterial enzyme vs mammalian enzyme

Front 101

Sulfonamides
-issues w/bilirubin?

Back 101

-sulfonamides can displace bilirubin from plasma protein binding sites and can cause kernicterus in neonates

Front 102

pt w/AIDS develops PCP (PJP)...tx?

Back 102

-tx w/ Trim-Sulfa

Front 103

Tetracyclines=bacteriostatic
-MOA?

Back 103

-MOA: bind to 30S subunit to block aminoacyl t-RNA binding to the acceptor (A) site

Front 104

Tetracyclines
-acts against?

Back 104

-acts against gram (+) and (-) organisms
-Rickettsiae, Mycoplasma, Chlamydia and amebas

Front 105

Tetracyclines
-can it be used for pneumococcal pneumonia?

Back 105

-NO NO NO NO
-Not used for pneumococcal pneumonia - tx w/ penicillins, cephalosporins or erythromycin

Front 106

Tetracyclines
-S/E

Back 106

-Chelates Ca++ - adverse effect on formation of teeth and bones - fetus and babies

-severe rash w sunlight

Front 107

Tetracyclines
-Bioavailability?

Back 107

-Chelates Ca++
-bioavailability decreased by milk and food in GI tract

Front 108

Lincosamides=clindamycin=bacteriostatic
-MOA?

Back 108

-MOA: binds to 50S subunit and blocks aminoacyl translocation of peptide chain

Front 109

pt tx w/clindamycin...pt develops pseudomembranous colitis cause by C.diff...tx?

Back 109

-tx w/oral metro or oral vancomycin

Front 110

Macrolides=b-static
-DRUGS?

Back 110

-erythromycin
-clarithryomycin
-azithryomycin

Front 111

pt. w/pneumonia, but bug does not gram stain->atypical bug. tx?

Back 111

-tx w/macrolide like eythromycin

-NB:if gram (+) pneumonia, probably Streptococcus
pneumoniae - tx w/ cephalosporin

Front 112

erythromycin and the GI tract...?

Back 112

-erythromycin causes stomach cramping bx it stimulates motilin receptors in stomach

-can be used to increase stomach motility in patients with diabetic gastroparesis

Front 113

DOC for community acquired pneumo (CAP)???

Back 113

-MACROLIDES
-erythromycin
-clarithryomycin
-azithryomycin

Front 114

tx of TB

Back 114

-tx of TB= "RIPE"

-rifampin, isoniazid, pyrazinamide & ethambutol

-isoniazid (INH) causes hepatic damage; rifampin induces CYP450

Front 115

Drugs that inhibit DNA gyrase
--->forms negative DNA supercoils

Back 115

-nalidixic acid & fluoroquinolones (ciprofloxacin et al.)

Front 116

Protein synthesis inhibitors
-buy AT 30, CELL at 50

Back 116

buy AT 30, CELL at 50
A=aminoglycosides(cidal)+spectinomycin(static)-use for pcn-resistant gonorrhea
T=tetracyclines (static)

C=chloramphenicol(static)
E=erythromycin(static)
L=Lincomycin(static)
L=cLindamycin(static)

Front 117

chloramphenicol, macrolides and clindamycin

Back 117

-Since chloramphenicol, macrolides and clindamycin work at the same site, do NOT use them together because they will interfere w/ each other

Front 118

Bactericidal Drugs

Back 118

-PCN's, cephalosporins, aztreonam, imipenem
-vancomycin
-bacitracin
-cycloserine
-aminoglycosides = gentamicin, etc.
-methenamine
-polymixin, colistin
-rifampin
-isoniazid
-fluoroquinolones= norfloxacin, etc.
-nalidixic acid

Front 119

Bacteriostatic Drugs

Back 119

-spectinomycin
-chloramphenicol
-macrolides
-lincomycin
-clindamycin
-tetracycline
-nitrofurans=nitrofurantoin
-trim-sulfa

Front 120

Bacterial Resistance

Back 120

-NB: plasmid-mediated resistance is easily transferred by transduction to other species of bacteria

Front 121

Beta-lactams

Back 121

-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

Front 122

resistance to beta-lactams in G+ bugs

Back 122

1.production of bacterial beta-lactamases
(penicillinases)

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

Front 123

resistance to beta-lactams in G- bugs

Back 123

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

Front 124

resistance to Vancomycin
(VREs)

Back 124

-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

Front 125

Fluoroquinolones

Back 125

-a single point mutation alter the binding of FQs to the active site of DNA gyrase

Front 126

Aminoglycoside resistance
-gentamicin
-tobramycin
-amikacin

Back 126

-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

Front 127

Macrolides and clindamycin resistance
Macs=ethryo,clarithro, and azithro

Back 127

-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

Front 128

tetracycline resistance
-doxycycline

Back 128

-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

Front 129

folate synthesis inhibitors
-trim-sulfa resistance

Back 129

-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.

Front 130

rifampin resistance

Back 130

-mutation causing a single amino acid substitution in the beta-subunit of the DNA-directed RNA polymerase reduces the binding of rifampin

Front 131

chloramphenicol resistance

Back 131

-plasmid-mediated

-involves the production of acetyltransferases which inactivates the drug