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Antibiotics that Act on Cell Membrane -More toxicity here, bactericidal & fungicidal A) Cationic Surface Active Agents o 1) Polymyxin MOA: detergent disru ting Cell Me!brane S ect: "arro#$ %&-) 'acilli Abs: "ot Absorbed %(, () in*ection +ist: "o CS, distriubtion -er!: Adverse: "e hrotoxic significant, .esistance is .A./ ') 0olyene %rou o 1) Nystatin MOA: S ect: Abs: used to ically, not absorbed %( +ist: -er!: Adverse$-ox: less otent as A ' but -oxic o 1) Amphotericin B MOA: fungicidal2 binds to sterol in CM er!its disru tion S ect: Abs: Most use () in*ection +ist: used for dee ,ungal infections of 'one, 3ung, Meningitis -er!: .enal /xcretion Adverse$-ox: ,ever, headache, Chills, .enal -oxic C) A4ole Antifungals o 1) (!ida4ole- is Kedonconozole 5 used less o 1) -ria4oles- used !ore no# Itraconazole MOA: decrease sterol synthesis faulty Cell Me!brane S ect: Abs: oral, () +ist: "o C"S -er!: ter! in liver Adverse$-ox: don6t use in co!bo #$ A! hotericin ' Fluconazole MOA: decrease sterol synthesis S ect: Abs: 7ell Absorbed %(, Oral +ist: C F! use "or "un#al Menin#itis -er!:

Adverse$-ox: no co!bo Clotrimazole- A'S: 8se -o ical +) Additional Antifungal Agents o $erbina"ine MOA: Bindes to %in! &air! Nails S ect: Abs: #ell absorbed %(, Oral, very good in fungal infections +ist: -er!: Adverse$-ox: o Flucytosine- later III. Antibiotics a""ectin# Nucleic Acids A) ,luoro9uionoloneso Cipro"loxacin ' (e)oFloxacin MOA: inhibit *NA $opoisomerases+ relieves tension by nic:$sealing S ect: bactericidal % &-) 'acili Abs: %( #ell Absorbed, Calciu! foods i! ede abs +ist: -er!: so!e liver, !ost .enal /xcretion Adverse$-ox: don6t give to re 1;yrs cartila#e dama#e+ %( u set, !ild nausea, diarrhea ') ,i"ampin MOA: bloc:s ."A synthesis S ect: so!e %&-) and !ost %&<) Abs: %( +ist: -otal 'ody #ater CS, -er!: 3iver !etabolis!, excrete in Bile ' Feces Adverse$-ox: (ncrease !eta, increase Cyt 0=>?, +ec @alf life of drugs2 $erato#enic- no reggers or of age regs2 %( u set Put oran#e $int into s-eat ' tears! non toxic C) Nitro"urantoin- urinary tract antise tic MOA: $reats .$I/s by being excreted in active for!2 !etaboli4ed to reactive inter!ediates, affefects +"A S ect:$ Selctive -ox-re9uires active !etabolis!2 'act A Ma!!als Abs: #ell absorbed %( +ist: -er!: .enal /xcretion in Active ,or! effective & .a id Adverse$-ox: %( u set, Pulmonary "ibrosis! nausea, vo!it, headache I0. Antibiotics that Inhibit Protein ynthesis A) +rugs acting on B?S .iboso!al Subunit- bloc:s "MS *unction o 1) Amino#lycosides-

MOA: cause !isreading %enetic code, #rong AA insertion$'-cidal S ect: %&-) 'acilli, Anaerobes+ use broadly vsC bacteria & tubercle Abs: 0oor %(, !ost () & (M +ist: "o C"S -er!: .enal /xcretion Adverse$-ox:renal tocix es #$ Cephalosporin+ hearing and )' toxicity unbalanced 8se of A!ino%6s li!ited to: -oxicity, .a ide develo !ent of resistance, 3ac: of Oral absorbation &not a 1st line dru#2 0enicillin cause synergistic effect on u ta:e of stre to!ycin in SC faecalis 12 3entamicin- older, sa!e MOA and -oxic, has !any resistances 42 Ami%acin- 8S/+ 1st, ne#er, large s ectru!, %-'acilli, vsC Central 52 $obramycin- !ore broad,better than last t#o for -ubercle 62 Netilmicin- ne#est, broad, reserved as 3ast @o e o 1) $etracyclines MOA: bind to B?S rece tor and slo# rotein syn$ 'acteriostatic S ect: very broad: G(+-), Actinomycetes, Rickettsiae, Mycoplasma, Chlamydia, Entamoeba Histolytica Abs: #ell absorbed %(, avoid (ron & Calciu! #hen ta:ing +ist: (n CS,, Bone ' $eeth -er!: .enal /xcretion$ +oxy in active for! .CCC Adverse$-ox: Mild %( u set, so!e liver tox2 su erinfectiondisru t nor!al flora, gives o ortunistic infections a chance &Pseudomonas2 0hototoxicity- s:in reaction to sulight +iscoloration of teeth, bro#ning -D0/S: 1) 7ral8Parenteral o $etracycline o 7xytetracycline- tendency to bind to teeth 1) 7ral o Minocycline- !etaboli4ed by liver, !uch in urine & feces is not active o *oxycycline- excrete in feces in acti)e "orm ') +rugs that act on >?S .iboso!al Subunit o 1) Chloramphenicol MOA: (nhibit 0e tide bond for!ation, bacteriostatic2 don6t use co!bo because it could cause co! etition S ect: broad, %&<-), ric:ettsia

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Abs: #ell absorbed, oral +ist: #ell CS, -er!: 3iver !etabolis! follo#ed by .enal /xcretion2 !ost bro:en do#n to %lucouridation and little deacetylation$dehalgoen: both go to tubular secretion2 all & add unchanged) is glo!erular filtration Adverse$-ox: Allergy, !ild %( u set, can be Su erinfection, don6t give to ne# borns & lo# !etabolis!) can be cardiotoxic2 reduce bone !arro# %reat against @C (nfluen4a cause !eningitis2 fights A!oxicillin reisitance used in co!bo #$ a!ox 'acteriostatic and 'acteriocidal can inhibit each other 'one !arro# toxicity 12 $oxic Bone Marro- uppressiono Marro#: "or!ocellular o 0eri heral 'lood: Ane!ia o +ose .es onse: +ose related o -i!e of a earance: during treat!ent o Co!!on Sy! : Ane!ia o 0rognosis: recovery 42 Aplastic Anemiao Marro#: @y o lastic$a lastic o 0eri heral blood- 0ancyto enia o +ose res onse- "ot dose related o -i!e of A earance: +ays$!onths later o Co!!on Sy! : 0ur ura or @e!!orhage o 0rognosis- Often fatal 1) Macrolides 4a2 erythromycin MOA: (nhibit 0e tide bond for!ation, bacteriostatic2 S ect: #ide range %<, fe# %-, !icro las!a Abs: #ell absorbed %(, +ist: CS, distribution -er!: 3iver !etabolis!, feces excreted Adverse$-ox: !ild in liver, !ild %( 8 set- nausea (f renal insufficiency, does ad*ust!ent not necessary because only drugs using :idney to ter! need dose ad*ust 4b2 Clarithromycin- sa!e MOA, slightly !ore broad s ectru!, !ore%<4c2 Acithromycin- increased oral absor tion, !ore broad for %B) Clindamycin MOA: S ect: si!ilar to 0en % but !ore effective for Anaerobes Abs: #ell in %(, oral

+ist: no CS, -er!: Adverse$-ox: !ild %( u set 1?E, nausea, diarrhea C) "e# +rugs inhibiting 0rotein Synthesis: ,or )anco!ycin-.esistant Organis! o 1) 9uinupristin8 *al"opristin MOA: bind to >?S and inhibits$bacteriostatic inhibit e bond S ect: %< &sta h, Stre , entero) and )anco!ycin .esistant Abs: not absorbed %(, () +ist: -er!: liver !etaboli4ed, excreted in bile Adverse$-ox ain, infla!!ation, ede!a, thro!bo hlebitis at infusion site & ;>E)2 arthralgia and !yalgias co!!on: :oint and muscle pain o 1) (inezolid MOA: binds to >?S bloc:s ;?s for!ation S ect: %<, sta h,stre , entero-vanco resistant: 'roader S ectru! Abs: #ell absorbed fro! %( +ist: -er!: liver !etaboli4ed, excreted in 8rine Adverse$-ox !ild %( u set, thro!bocyto enia &reversible), !onitor latelet count if ta:ing !eds for 1 #ee:s< 0. Antibiotics a""ectin# intermediary metabolism; Antimetabolites -all are co! etitive inhibitors, decrease roduct levels so it #ill beco!e li!iting in substrate level reactionsC 1) ul"onamides o MOA: analog of 0-a!inobenxoic acid &PABA Folic), re9uired for folic acid synthesis2 decrease availability i! ortant cofactor for 1 carbon trans"ers <."A, +"A, nucleotides) Actual: inhibits +ihydro teroic acid for!ation for! 0A'A o S ect$Selectivity: !a!!als re9uire ,olic acid in diet vsC 'acteria synthesi4e in diet : !ore %< less %o Abs: #ell absorbed fro! %( tract, bacteriostatic o +ist: o -er!: renal excretion a lot of active sulfa in urine o Adverse$-ox: safe, !ild liver tox2 occasional decrease in bone !arro# and !ild ane!ia Concern: 00- in urinary tract: ul"isoxazole used+ best solubility -8 p& =.= > ?.= 1) $rimethoprim-sul"amethoxazole MOA: inhibits +@, reductase bloc: reduction o" *&F to $&F2 :ee s lo# -@, thus oor carbon transfers 'y itself, -ri is #ea:ly antibacterial but used in co!bo #$ sulfa drugs

S ect$ selective: concentration re9uired to inhibit 'acteria >? ercent is very lo# co! ared to !a!!als: > vs 1F???? Abs: +ist: -er!: Adverse$-ox B) Flucytosine <=-F.2 MOA: !etaboli4ed by Fun#i to >-,8, bloc:s nucleic acid synthesis S ect$Selective: fungi have to !etaboli4e,!a!!alian cells lo# ca acity to !etaboli4e Abs: #ell absorbed %( +ist: total body #ater, thus CS, -er!: acti)e "orm /xcreted in 8rine, not metabolized Adverse$-ox: de ression of bone !arro#2 %( u set

Che!othera y of )iral (nfections A roaches to control )iral (nfections -viruses are intracellular arasites: level of success less for Antiviral vsC 'act$fung o 1) (!!unological 3evel of effectiveness: @igh S ectru!: "arro# +uration of /ffect: 3ong o 1) (nterferon - natural rotein inhibiting viral re lication 3evel of effectiveness: Moderate$@igh S ectru!: 'road +uration of /ffect: Short o B) Che!ical 3evel of effectiveness:3o#$!oderate S ectru!: "arro# +uration of /ffect: Short 0rocess of )iral (nfection o /ntry into host and release "A &adsor tion, 0enetration, 8ncoating) )iral %eno!e re lication asse!ble ne# viruses and release Antiviral +rugs &"on-.etroviral$+"A viruses) o A) Antiher es )irus o 1a) Acyclo)ir MOA: %uanosine anaolog effective vsC @er es & / stein 'arr )irusC Metabolites to !ononuc-0, inhibit +i & tri 06s for!ation )iral encoded rotein carries out 1st i! ortant ste

+rug +ecreases +"A syn by co! eting #$ guanosine nuc and gets incor orated so!e#hat S ect$ selective: @er es & /') Abs: #ell absorbed %( +ist: -er!: Adverse$-ox o 1a) 3anciclo)or MOA: guanosine nucleoside analog S ect$ selective: her es Abs: oral abso rtion +ist: -er!: Adverse$-ox: !ore toxic than Acyclo cause su ression of bone !arro# and tertogenic otential o Ba) Idoxuridine MOA: -hy!idine analog, inhibits +"A syn in her es S ect$ selective: @er es2 in /ye because eye has non re roducing cells Abs: -o ical use, used in /ye Con*uctiva +ist: -er!: Adverse$-ox: )ery -oxic, o =a) 0idarabine MOA: +"A synthesis inhibitor$ Adenosine Analog 8sed in co!bo #$ Acyclovir for @er es (nfection S ect$ selective: @er es Abs: +ist: -er!: Adverse$-ox o ') @e atitis ': o 1) Ade"o)ir *ipi)oxil MOA: +i i ovoxis inhibits )iral *NA Poly, not li!ited to @er es o C) Antiinfluen4a +rugs- li!ited s ectru! but good vsC (nfluen4a A -/ffective -reat!ent and 0ro hylaxis o 1) Amantadine- effective Orally o 1) 7seltami)ir- effective orally o B) @anami)ir- 0arentral .oute o +) Other Antivirals o 1) (ami)udine- good vsC @e atitis ' ((C +rugs for retroviral infections o @() slide- 1GHB first isolation of @()

@ido)udine- reverse transcri tase inhibitor used 1GH; aAuina)ir- rotease inhibitor 1GG> Ne)irapine- non nucleoside reverse transcri tase inhibitor 1GGF Bn"u)irtide- fusion inhibitor o C+= rece tor on - cells surfaces bind viral g 11? and g =1 o .everse transcri tase is highly error rone, allo#s @() to evolve o 8se drugs in co!bo because: 1) 'e effective vsC resistant viruses 1) cover your atient because ex ect resistance to develo o A) .everse -ranscri tase (nhibitors o 1) Nucleoside ,e)erse $ranscriptase Inhibitors- cause re!ature ter!ination by addening analog instead of hydroxyl: a2 @ido)udine <A@$2- viral rotein$ -hy!idine Anaolog2 !ust be !etaboli4ed to nucleoside tri hos hate b2 *idanosine- adenosine analog: !ust be !etaboli4ed also o 1) Non nucleoside re)erse transcriptase inhibitors a2 ne)irapine- inhibitors of en4y!es b2 B"a)irenz- inhibitors of en4y!e co! ared treat!ents: tri le nucleoside regi!en vs "on "uc < 1-B nucleosides found2 /faviren4 < 1-B #as su erior to *ust three nucleosides for initial treat!ent of @() better, !ore rolong ti!e #$ not having virologic failure in initial treat!ents #$n H #ee:s co!bo is better but resistances for both eventually develo o ') 0rotease (nhibitor o 1) Indina)ir- roteolytic cleavage of e tide needed first2 @as !a*or tox %( u set, liver tox, @y erglyce!ia, #orsen +iabetes, ,at redistribution to 'ac: "ec:, @y erli ide!ia o C) "e# +evelo !ent o 1) Bn"u)irtide- BF AA oly e tide binds to viral envelo e, inhibiting fusion of )iral Coat roteins rece tor #$ C+= bloc:s attach!ent ex ensive: 1? %6s$Dear "o#: use co!bo of fusion, rotease, and 1< reverse transcri tase inhibitors o ,usion inhibitors increase ti!e of lac: of virologic failure

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