Farmakologija - skripta

Farmakologija - Osječka skripta

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BIOTRANSFORMACIJA LIJEKA (Diana Kova!i")

Ljudi su svakodnevno izlo #eni stranim tvarima- ksenobioticima koji se apsorbiraju putem ko#e,di$nog ili probavnog sustava!

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Za!to je nu"na biotransformacija lijeka? Farmakolo$ki aktivne organske organske molekule- nastoje biti lipofilne i neionizirane. Lipofilni ksenobiotici transformiraju se u polarnije produkte – lak $e se izlu!uju! Da ne prolaze metaboli!ku konverziju u topljivije produkte imali bi puno du #i poluvijek eliminacije i produ#eno djelovanje. Metaboli!ki produkti : 1) farmakodinamski manje aktivni od izvornog lijeka 2) inaktivni 3) neki imaju poja !anu aktivnost ili toksi !nost • • •

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Uloga biotransformacije u raspolo "ivosti lijeka Biotransformacija se ve"inom doga %a izme%u apsorpcije u krv te eliminacije bubrezima. Manjim dijelom obavlja se ve " u lumenu ili stijenci crijeva. Postoje dvije faze reakcija biotransformacije: •

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Reakcije prve faze pretvaraju izvorni lijek u polarniji metabolit uvo%enjem ili otkrivanjem funkcionalne skupine (-OH, -NH2, -SH). Ako su ti metaboliti dovoljno polarni brzo se izlu !uju ali mnogi se ne izlu !uju brzo nego prolaze kroz drugu fazu reakcija - endogeni se supstrat (glukuronska, sulfurna,octena kiselina ili aminokiselina) povezuje s funkcionalnim skupinama metabolita. Nastaju konjugati velike polarnosti. U nekim slu!ajevima ve" izvorni lijek mo#e imati funkcionalne skupine i izravno stvarati konjugate (bez spajanja sa supstratima). Reakcije druge faze katkad mogu prethoditi reakcijama prve faze. •

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Gdje se obavlja biotransformacija lijeka? Jetra - glavni organ metabolizma lijekova! Neka druga tkiva kao $to su plu"a, probavni sustav, ko #a, bubrezi i mozak isto mogu metabolizirati. Mnogi lijekovi nakon oralne primjene nepromijenjeni se apsorbiraju iz tankog crijeva i transportiraju putem portalnog krvotoka u jetru - opse #an metabolizam = U#INAK PRVOG PROLASKA - mo#e naru$iti bioraspolo#ivost oralno primijenjenih lijekova! Neki se nakon oralne primjene vi$e metaboliziraju u crijevima nego u jetri Neki podlije#u zna!ajnom intestinalnom metabolizmu (50%) - va #no u osoba s o$te"enom funkcijom jetre. Lijekove mogu metabolizirati i mikroorganizmi u ni#im dijelovima crijeva, #elu!ana kiselina te probavni enzimi. • •

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downloaded from www.perpetuum-lab.com.hr

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Ve"inu biotransformacija kataliziraju specifi!ni stani!ni enzimi (smje$teni u ERu,mitohondrijima, citoplazmi, lizosomima ili !ak u jezgri)

Sustav mikrosomskih oksidaza mje!ovite funkcije i reakcije I.faze Enzimi (monooksigenaze ili oksidaze mje$ovite funkcije)- nalaze se u lipofilnoj membrani ER-a u jetri i drugim tkivima. Pri izolaciji membrana prilikom razdvajanja stani!nih frakcija reorganiziraju se u mjehuri"e - MIKROSOME (zadr #avaju obilje# ja ER-a, grubi retikul- s ribosomima, sinteza bjelan!evina, glatki retikul- oksidacijski metabolizam lijekova). Za aktivnost enzima potrebni su reduciraju"i agens (NADPH) i molekularni kisik- po molekuli supstrata utro$i se molekula kisika- jedan atom ide u produkt, drugi u vodu. •

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Klju!ni enzimi u oksidacijsko-redukcijskim procesima: 1. Flavoprotein NADPH-citokrom P450-reduktaza 2. Hemoprotein citokrom P450 (CYP) Mikrosomska membrana sadr #i vi$estruke oblike citokroma- niz izoformi! *Reakcije prve faze : a) Oksidacije ovisne o citokromu P450 - aromatska hidroksilacija, alifatska hidroksilacija, epoksidacija, oksidacijska dealkilacija (N,O,S), N-oksidacija, S-oksidacija, deaminacija, desulfuracija i deklorinacija b) Oksidacije neovisne o citokromu P450 - flavinmonooksigenaze, aminske oksidaze, dehidrogenacija, redukcije- azo,nitro i karbonilne te hidrolize estera i amida (* = vi$e o reakcijama u tablicama na stranici 56 i 57) • •

REAKCIJE I.FAZE: Mikrosomska oksidacija lijeka: 1. Oksidirani P450 (Fe3+) udru#uje se s lijekom supstratom - kompleks 2. NADPH donira elektron za P450 reduktazu- ona reducira oksidirani kompleks (Fe3+)P450- lijek) 3. Drugi elektron dolazi iz NADPH posredovanjem P450 reduktaze i slu #i za redukciju molekularnog kisika - nastaje kompleks “aktivirani kisik-P450lijek“ 4. Taj kompleks prenosi kisik do lijeka supstrata i stvara oksidirani produkt (drugi atom kisika prijelazi u vodu) P450 su spori katalizatori i reakcije koje kataliziraju su spore. •

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Najva#nije izoforme su CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2D6, CYP2E1, CYP3A4 - one kataliziraju ve"inu metabolizma lijekova i ksenobiotika! CYP3A4- vi $e od 50% svih lijekova koji se metaboliziraju u jetri. Doprinos pojedinih izoformi u metabolizmu nekog lijeka mo #e se ispitati in vitro(biljezima, P450-inhibitorima te protutijelima) i in vivo (neinvazivnim biljezima, analizom metabolita u izdahnutom zraku ili urinu nakon primjene lijeka selektivnog za pojedini enzim)

Indukcija enzima Razli!iti supstrati (kemikalije,one!i$"iva!i okoli$a) i lijekovi mogu inducirati izoforme P450 (pove "a sintezu ili smanji razgradnju)- dolazi do ubrzanog metabolizma


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supstrata i smanjenog djelovanja,ali u slu!aju lijekova koji se pretvaraju u reaktivne metabolite- pogor $anje toksi!nih u!inaka Receptori koji ve "u inducibilne supstrate: supstrate: 1. Receptor za policikli$ke aromatske ugljikovodike (AhR- aryl hydrocarbon )citoplazmatski, kompleks induktor-receptor prelazi u jezgru-aktivira regulacijski element gena CYP1A- indukcija citokroma. 2. Receptor X za pregnan (PXR) - U jezgri- indukcija CYP3A razli !itim spojevima - deksametazon, rifampin, mifepriston, fenobarbital, atorvastatin, i hiperforin (sastojak gospine trave) 3. Konstitutivni receptor za androstan (CAR- constitutive androstane receptor ))- u jezri,receptor siro!i"- indukcija CYP2B6, CYP2C9, CYP3A4 4. Receptor za aktivator proliferacije peroksisoma tip alfa (PPAR % peroxisome proliferator-activated receptor alfa) - jezgrin receptor siro!i" ,ligandi su mu lijekovi za snizivanje razine lipida (fenofibrat, gemofibrozil) zato $to je receptor za slobodne masne kiseline - indukcija CYP3A4 5. Receptor za retinoide X (RXR-retinoid x receptor )

Inhibicija enzima Odre%eni supstrati inhibiraju aktivnost enzima citokroma P450! Lijekovi koji imaju imidazolski prsten (cimetidin,ketokonazol) ve #u se za kompetetivnom inhibicijom reduciraju metabolizam supstrata. #eljezo u hemu P450 i kompetetivnom Neki supstrati ireverzbilno inhibiraju jer tvore kovalentne veze s hemom ili apoproteinom P450 -tako fragmentiraju ili modificiraju citokrome. • •

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REAKCIJE II.FAZE: •

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Konjugacijske reakcije s nekom endogenom supstancom - konjugati lijeka - polarne su molekule,tipi!no inaktivne i lako se izlu !uju. Za stvaranje konjugata potrebni su me%uprodukti i prijenosni enzimi (transferaze)nalaze se u mikrosomima ili u citoplazmi. Br #e su od reakcija kataliziranih s P450 ( reakcije prve faze).

Transferaze i reakcije: 1. UDP-glukuronozil - glukuronidacija uz UDP glukuronsku kiselinu kao endogeni reaktant 2. sulfotransferaza (SULT) - sulfatacija uz fosfoadenozil fosfosulfat 3. glutation transferaza transferaza (GSH-S transferaza )- konjugacija s glutationom N-acetiltransferaza (NAT )- acetilacija uz acetil-CoA kao supstrat 4. N-acetiltransferaza 5. metil transferaza (MT)- metilacija uz S-adenozilmetionin 6. epoksid-hidrolaze epoksid-hidrolaze (EH)- konjugacija s vodom 7. acil-CoA glicintransferaza - konjugacija s glicinom


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BIOTRANSFORMACIJA LIJEKOVA U TOKSI#NE METABOLITE BIOTRANSFORMACIJA metabolizam lijekova nije uvijek ne$kodljiv proces detoksikacije i eliminacije spoja neki se lijekovi metaboliziraju u reaktivne toksi$ne ili karcinogene me%uprodukte To se doga %a kada su zagu$eni alternativni detoksikacijski mehanizmi i kad su endogeni detoksikacijski supstrati iscrpljeni (glutation,glukuronska kiselina…) Primjer : Paracetamol (acetaminofen) - analgetik,antipiretik siguran je u terapijskim dozama, kada se doza prema$i glukuronidacijski i sulfatacijski putevi biotransformacije se zasite i put ovisan o P450 postaje izuzetno va#an. Kada se i on iscrpi akumulira se reaktivni toksi!ni metabolit - (N-acetilbenzoiminokinon) - reagira sa stani!nim proteinima - hepatotoksi !nost! Antidot protiv predoziranja je cisteamin i N-acetilcistein

KLINI#KO ZNA#ENJE METABOLIZMA LIJEKOVA Postoje individualne razlike u distribuciji i brzini metabolizma i izlu!ivanja lijekova. Odre%ene su geneti!kim te okoli $nim !imbenicima - dob (vrlo stari i vrlo mladi),spol (primje"eno u nekih supstrata kao $to je etanol- br #e metaboliziraju mu$karci),veli!ina jetre,dnevni ritam, tjelesna temperatura,prehrana (hrana s ro$tilja i povr "e iz porodice krsta$ica mogu inducirati enzime CYP1A,a sok od grejpa mo#e inhibirati metabolizam lijekova koji su supstrati CYP3A) ,izlo#enost induktorima i inhibitorima lijekova… Geneti $ki $imbenici : postoje spori i brzi acetilatori (smanjena ili pove"ana sinteza transferaza i brzina metabolizma) Prisutni su i polimorfizmi transferaza (UGT,GST)- o $te"ena konjugacija i eliminacija lijekova. • •

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POLIMORFIZMI reakcije I.faze: 1. Polimorfizam tipa oksidacije debrisokina-sparteina , naslje%uje se autosomno recesivno,smanjena je oksidacija debrisokina i drugih lijekova ovisnih o CYP2D6. Dolazi do pogre $ne ekspresije proteina P450- nastaju izoforme male ili nikakve aktivnosti. Nedavno opisan i polimorfizam koji uzrokuje vrlo brz metabolizam ovih lijekovazbog vi$estrukih genskih kopija CYP2D6 u nizu. 2. Polimorfizam aromatske hidroksilacije antikonvulziva mefenitoina koju katalizira CYP 2C19 -gubi se hidroksilazna aktivnost, oba se enantiomera (S) i (R)-mefenitoina demetiliraju u nirvanol koji se nakuplja u mnogo ve "im koncentracijama - znakovi duboke sedacije i ataksije. 3. Polimorfizam CYP2C9- rizik od $tetnih u!inaka lijekova koji se metaboliziraju navedenim citokromom - varfarin(krvarenja), fenitoin, losartan, tolbutamid, nesteroidni protuupalni lijekovi. 4. Polimorfizam CYP3A4 5. Polimorfizam CYP3A5 6. Polimorfizam CYP2A6 - odgovoran za oksidaciju nikotina (pu $a!i s niskom aktivno$"u ovog citokroma konzumiraju manje cigareta i imaju ni #u u!estalost raka plu"a) Stalno se otkrivaju novi polimorfizmi u metabolizmu lijekova…


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INTERAKCIJE IZME&U LIJEKOVA NA RAZINI METABOLIZMA Mnogi se supstrati zbog visoke lipofilnosti zadr #avaju ne samo na aktivnim mjestima enzima nego ostaju i vezani na lipidnu membranu ER-a - mogu inducirati mikrosomske enzime i kompetetivno inhibirati metabolizam istodobno primjenjenog drugog lijeka. U induktore enzima ubrajamo razne sedative-hipnotike,antipsihotike, antikonvulzive, lijek protiv tuberkuloze rifampin i insekticide. Razni lijekovi mogu istodobnom primjenom do"i u interakcije i ireverzibilno inaktivirati zajedni!ki metaboli!ki enzim. (Tijekom svog metabolizma inaktiviraju enzim pa je onda usporen i njihov vlastiti metabolizam kao i metabolizam istovremeno primjenjenog lijeka.) Npr.tako sok od grejpa inaktivira CYP3A4 u crijevnoj sluznici- pove"ava se bioraspolo#ivost lijekova koje metabolizira taj citokrom - felodipin,nifedipin,verapamil,ciklosporin A… •

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INTERAKCIJE IZME&U LIJEKOVA I ENDOGENIH TVARI Da bi se inaktivirali neki lijekovi moraju konjugirati s endogenim supstratima kao $to je glutation,sulfat ili glukuronska kiselina - zato se razli !iti lijekovi moraju natjecati za isti supstrat. Lijek koji br #e reagira mo#e iscrpiti supstrat i oslabiti metabolizam drugog lijeka. •

BOLESTI KOJE UTJE#U NA METABOLIZAM LIJEKA Bolesti koje zahva 'aju jetru - hepatitisi, ciroza, hemokromatoza, bilijarna ciroza… One o$tete jetrene metaboli!ke enzime i poremete eliminaciju lijeka (poluvijek eliminacije i trajanje u!inka klordiazepoksida i diazepama jako su produljeni u bolesnika s cirozom ili hepatitisom- u prosje!nim dozama mogu"a koma) Neki se lijekovi toliko brzo metaboliziraju da !ak ni redukcija jetrene funkcije ne "e bitno produ #iti njihovo djelovanje - ali sr$ane bolesti mogu smanjiti perfuziju jetre i ograni!iti njihovu dostavu u jetru pa im se eliminacija smanji. Tako%er plu'ne bolesti, hipotireoza, poreme 'ena funkcija hipofize, kore nadbubre#ne #lijezde te gonada smanjuje metabolizam lijekova u jetri $takoravjerojatno i ljudi. Upalni medijatori, citokini, du$ikov oksid u infekcijama,tumorima i upalama mogu o$tetiti metabolizam inaktivacijom i degradacijom P450 enzima. • •

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7.

Agonisti kolinergi!kih receptora i inhibitori kolinesteraze

Agonisti kolinergi!kih receptora mogu biti: 1.izravni (esteri kolina i alkaloidi) -djeluju na muskarinske i nikotinske receptore 2.neizravni= inhibitori acetilkolinesteraze (kratkodjeluju"i, srednjedugodjeluju"i, dugodjeluju"i)

1.IZRAVNI AGONISTI KOLINERGI "KIH RECEPTORA 1.ESTERI KOLINA (acetilkolin, metakolin, karbakol, betanekol )! netopljivi u lipidima, slabo se apsorbiraju iz probavnog trakta i oskudno dospijevaju u S#S Acetilkolin- jako osjetljiv na acetilkolinesterazu, djeluje na muskarinske i nikotinske receptore Metakolin i betanekol djeluju na muskarinske 2.ALKALOIDI : (muskarin, nikotin, pilokarpin, lobelin) ! nikotin, pilokarpin i lobelin su liposolubilni i dobro se apsorbiraju U"INCI IZRAVNIH AGONISTA NA ORGANSKE SUSTAVE: Oko: kontrakcija sfinktera pupile!mioza (M3 receptori) Kontrakcija cilijarnog mi$i"a! akomodacija (M3 receptori) Srce: negativni inotropni (% kontraktilnost), kronotropni (% frekvencija), dromotropni (% provo&enje) u!inak (M2) Krvne #ile: ako je endotel neo$te"en, agonisti M3 receptora "e potaknuti stvaranje NO (u endotelnim stanicama) koji difundira u glatke mi$i"ne stanice krvih 'ila i aktivira gvanilat ciklazu koja povisuje koncentraciju cGMP! relaksacija Respiracijski sustav : bronhokonstrikcija, poja!ano lu!enje bronhalnih 'lijezda (M3) Probavni sustav : poja!ana peristaltika i relaksacija sfinktera (M3) Mokra$ni sustav: poti!u pra'njenje mjehura; kontrakcija detruzora, relaksacija sfinktera Egzokrine #lijezde: poti!u sekraciju termoregulacijskih znojnica, suzne 'lijezde S%S: &4'2 receptor!nikotinski acetilkolinski receptor, izlaganje nikotinu dovodi do aktivacije tog receptora i poja!anog otpu$tanja dopamina $to dovodi do razvoja ovisnosti Visoke doze nikotina: tremor, povra"anje, stimulacija respiracijskog centra, konvulzije, koma Periferni #iv!ani sustav: nikotinski acetilkolinski receptori smje$teni u autonomnim ganglijima! njihovom aktivacijom u kardiovaskularnom sustavu prevladavaju u!inci simpatikusa, a u probavnom i mokra"nom parasimpatikusa %iv!anomi(i$na spojnica: agonisti nikotinskih receptora dovode do depolarizacije (zbog utoka Na i K) ! stalno izlaganje agonistu mo'e dovesti do depolariziraju"eg bloka


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NEIZRAVNI KOLINOMIMETICI = INHIBITORI ACETILKOLINESTERAZE 1.KRATKO DJELOVANJE: edrofonij 2.SREDNJE DUGO DJELOVANJE(esteri karbamata): neostigmin, piridostigmin, fizostigmin 3. DUGO DJELOVANJE (organofosfati): ekotiopat, paration, malation, soman, sarin

Kratkodjeluju"i i srednje-dugodjeluju"i su slabo liposolubilni i slabo se apsorbiraju iz probavnog trakta, oka, ko'e, plu"a i slabo se raspodjeljuju u S#S Iznimka je fizostigmin !ija je apsorpcija dobra bez obzira na mjesto primjene i raspodjeljuje se u S#S Svi organofosfati (osim ekotiopata!) se odli!no apsorbiraju kroz ko'u, plu"a, probavni sustav, spojnicu oka; prodiru u S#S (oni su insekticidi) Ekotiopat ne prodire u S#S jer je polaran MEHANIZAM DJELOVANJA INHIBITORA ACETILKOLINESTERAZE Ina!e se acetilkolin ve'e za aktivno mjesto na acetilkolinesterazi te dolazi do hidrolize! nastaju slobodni kolin i acetilirani enzim. U sljede"em koraku se uz dodatak vode (hidracija) raskida veza izme&u acetilne skupine i enzima Kratkodjeluju"i inhibitori acetilkolinesteraze( npr.edrofonij): ve'u se za aktivno mjesto enzima i prije!e vezanje acetilkolina (veza je jako slaba pa je u!inak inhibicije kratak, do 10 min) Srednjedugodjeluju"i inhibitori acetilkoliesteraze (npr.neostigmin) : ve 'u se za aktivno mjesto na enzimu, dolazi do hidrolize i nastaje karbamilirani enzim !ija je veza otpornija na hidraciju (u!inak do 6 sati) Dugodjeluju"i (organofosfati): isti mehanizam kao srednjedugodjeluju"i, samo $to nastaje fosforilirani enzim !ija je veza stabilna,a proces traje jako dugo U"INCI NEIZRAVNIH AGONISTA NA ORGANSKE SUSTAVE S%S: visoke koncentracije uzrokuju konvulzije, komu, zastoj disanja OKO, DI)NI, PROBAVNI, MOKRA *NI: isto kao izravni agonisti KARDIOVASKULARNI : negativni inotropni, kronotrpni, dromotropni u!inak Blago povi$enje perifernog otpora i krvnog tlaka zbog djelovanja na simpati!ke ganglije %IV"ANO-MI)I*NA SPOJNICA: umjerene doze poja!avaju u!inak acetilkolina (primjena u lije!enju miastenije gravis), a visoke doze mogu uzrokovati fibrilaciju mi$i"nih vlakana i fascikulaciju

KLINI"KA PRIMJENA: 1. lije!enje glaukoma ! jer se kontrakcijom sfinktera sfinktera pupile i cilijarnog mi$i"a olak $ava otjecanje o!ne vodice iz prednje o!ne sobice,a to dovodi smanjenja o!nog tlaka -lijekovi koji se primjenjuju: karbakol, pilokarpin, prije ekotiopat 2. lije!enje postoperativnog i neurogenog ileusa te retencije mokra $e -lijekovi koji se primjenjuju: betanekol, neostigmin


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3. dijagnostika i lije !enje miastenije gravis : primjenjuju se samo inhibitori acetilkolinesteraze edrofonij- dijagnostika i akutno lije!enje neostigmin, piridostigmin, fizostigmin 4. lije!enje trovanja antimuskarinskim lijekovima fizostigmin- jer prodire u S#S 5. lije!enje Sjogrenova sindroma- pilokarpin, cevimelin (jer poti!u lu!enje sline pa sprje!avaju suho"u usta) 6. odvikavanje od pu (enja- nikotin jer je izravni agonist nikotinskih &4'2 receptora i poti!e otpu$tanje dopamine (u obliku transdermalnih naljepaka I 'vaka"ih guma) -vareniklin: parcijalni agonist (4)2 receptora ($tetni u!inak-dovodi do suicidalnih misli) 7. paration,malation- insekticidi! toksi!ni za !ovjeka sarin! bojni otrov

)TETNI U"INCI 1.izravni agonisti muskarinskih receptora: -$tetni u!inci posljedica pretjerane posljedica pretjerane stimulacije muskarinskih receptora: mu!nina, povra"anje, poja!an nagon na mokrenje, salivacija, znojenje, bronhospazam - $tetni u!inci se poni$tavaju atropinom 2.izravni agonisti nikotinskih receptora: a) akutna toksi!nost nikotinom: konvulzije, koma, zastoj disanja, depolariziraju"i blok neuromuskularne spojnice, hipertenzija, sr !ane aritmije b) kroni!na toksi!nost: razvoj ovisnosti (lije!enje obja$njeno u kl.primjeni)

3. inhibitori kolinesteraze: - $tetni u!inci nastaju zbog trovanja pesticidima (organofosfatima)! mioza, salivacija, znojenje, bronhospazam, povra"anje, proljev, konvulzije, koma, depolariziraju"i neuromuskularni blok


13


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43. BETA-LAKTAMSKI I DRUGI ANTIBIOTICI KOJI DJELUJU NA STANI! NU STIJENKU I MEMBRANU (Marin Kuhari")

Penicilini i cefalosporini su glavni antibiotici koji inhibiraju sintezu stani #ne stijenke bakterija. Nazivaju se beta-laktami zbog specifi#nog #etvero#lanog prstena u svojoj strukturi. Ove dvije velike skupine beta-laktama uklju #uju neke od naju #inkovitijih, naj $ire primijenjenih i najbolje toleriranih lijekova za lije#enje mikrobnih infekcija. Vankomicin, fosfomicin i bacitracin tako%er inhibiraju sintezu bakterijske stijenke, ali iz razli#itih razloga nisu toliko va &ni kao $to su beta-laktami.

Pojava mikrobne rezistencije predstavlja izazov primjeni antimikrobnih lijekova. Mehanizmi nastanka mikrobne rezistencije uklju#uju: a) produkciju enzima koji inaktiviraju antibiotike b) promjene u strukturi ciljnih receptora c) smanjenje permeabilnosti membrane za antibiotike

Slika 1. Podjela beta-laktamskih antibiotika


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1. PENICILINI

A. KLASIFIKACIJA 6-aminopenicilanske kiseline i sadr &e beta-laktamski prsten koji je Svi su penicilini derivati 6-aminopenicilanske klju#an za njihovo antimikrobno djelovanje. Podskupine penicilina sadr &e dodatne kemijske supstituente koji odre %uju temeljna farmakolo$ka i antibakterijska svojstva nastalih spojeva. Minimalna inhibicijska koncentracija (MIC) bilo kojeg penicilina izra&ava se u µg/mL. Ve"ina se penicilina proizvodi u obliku natrijevih ili kalijevih soli slobodne kiseline. B. FARMAKOKINETIKA Penicilini se razlikuju po rezistenciji na &elu#anu kiselinu te im zbog toga oralna bioraspolo&ivost varira. Izlu#uju se nepromijenjeni u urinu putem glomerularne filtracije (10%) i tubularne sekrecije (90%), koja se mo &e inhibirati probenecidom (vidi 36. poglavlje). Ampicilin i nafcilin se djelomi#no izlu#uju putem &u#i. Poluvijek eliminacije ve"ine penicilina iznosi od 30 minuta do jednog sata. Prokainski Prokainski i benzatinski oblici penicilina G imaju produ&enu prisutnost lijeka u krvi jer se primjenjuju intramuskularno, $to dovodi do sporog osloba %anja lijeka u krv. Ve "ina penicilina prelazi krvno-mo&danu barijeru tek u slu#aju upale mo &danih ovojnica. C. MEHANIZAM DJELOVANJA i REZISTENCIJA Beta-laktami su baktericidni lijekovi. Inhibiraju sintezu stani#ne stijenke na nekoliko na #ina: (1) vezanjem na PBP-ove ( protein binding proteins), koji su smje$teni u citoplazmatskoj membrani bakterije; (2) inhibicijom transpeptidaze, enzima koji inhibira transpeptidaciju (popre#no povezivanje linearnih lanaca peptidoglikana koji #ine dio stan. stijenke); (3) aktivacijom autoliti#kih enzima koji o $te"uju stijenku. !etiri su glavna mehanizma rezistencije na peniciline (ali i druge beta-laktame): (1) inaktivacija antibiotika beta-laktamazama (penicilinazama); (2) modifikacija ciljnog PBP-a; (3) smanjeni prodor lijeka do ciljnog PBP-a i; (4) izbacivanje lijeka iz stanice (efluks). U primjeni su inhibitori beta-laktamaza (npr. klavulanska kiselina, sulbaktam, tazobaktam), koji se koriste u kombinaciji s penicilinima. D. KLINI!KA PRIMJENA 1. Penicilini uskog spektra, podlo &ni beta-laktamazi: Penicilin G je prototip ove podskupine. Koriste se u terapiji infekcija uzrokovanim streptokokima, meningokokima, enterokokima, G+ bacilima i spirohetama. Iako vi $e nije prikladan u terapiji gonoreje, penicilin G se i dalje koristi u lije#enju sifilisa. Aktivnost protiv enterokoka poja #ava se uz primjenu aminoglikozida. Penicilin V primjenjuje se oralno, i to kod orofaringealnih infekcija. 2. Penicilini izrazito uskog spektra, rezistentni na beta-laktamazu: Ova podskupina uklju#uje meticilin, nafcilin i oksacilin. Primarna im je upotreba u lije#enju infekcija uzrokovanih stafilokokima. Listerija, enterokoki i MRSA su rezistentni na ove peniciline. 3. Penicilini pro$irenog spektra, podlo &ni beta-laktamazi: Ovdje pripadaju ampicilin, amoksicilin, piperacilin i tikarcilin. Ampicilin i amoksicilin imaju


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sli#ne indikacije kao i penicilin G, uz infekcije uzrokovane enterokokima, L. enterokokima, L. monocytogenes, E. coli, P. mirabilis, H. influenzae i M. catarrhalis. catarrhalis. S druge strane, piperacilin i tikarcilin su aktivni protiv G- bakterija kao $to su pseudomonas, enterobacter i klebsiella.

Slika 2. Stani #na stijenka G- bakterija i mjesta djelovanja beta-laktama.

E. TOKSI ! NOST Penicilini su izrazito netoksi#ni. Najve"i broj ozbiljnih ne &eljenih $tetnih u#inaka posljedica je preosjetljivosti na penicilin. Izme%u svih penicilina postoji i ukri &ana preosjetljivost. Alergijske reakcije uklju#uju anafilakti#ki $ok (vrlo rijetko), reakcije tipa serumske bolesti (urtikarija, groznica, edemi oko zglobova, angioneurotski edem, intenzivan svrbe & i respiracijske smetnje) te raznoliki ko&ni osipi. Mogu se pojaviti lezije u ustima, groznica, intersticijski nefritis, eozinofilija, hemoliti#ka anemija, vaskulitis. Velike doze oralnog penicilina mogu uzrokovati GI smetnje, a ampicilin dovesti do pseudomembranoznog pseudomembranoznog kolitisa. Naficilin mo&e uzrokovati neutropeniju, oksacilin hepatitis, a metcilin intersticijski nefritis.

2. CEFALOSPORINI

A. KLASIFIKACIJA Cefalosporini su sli#ni penicilinima, ali su otporniji na mnoge beta-laktamaze te zbog toga imaju $iri spektar djelovanja. Nisu djelotvorni protiv enterokoka i L. i L. monocytogenes. monocytogenes. Rije# je 7-aminocefalosporanske kiseline. Mogu se podijeliti u #etiri glavne skupine o derivatima 7-aminocefalosporanske (generacije), uglavnom ovisno o spektru antimikrobne aktivnosti. Aktivnost prema G+ se smanjuje, a prema G- pove "ava idu"i od prve prema tre "oj generaciji.


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B. FARMAKOKINETIKA Nekolicina cefalosporina dostupna je za oralnu primjenu, ali se ve"ina primjenjuje parenteralno. Glavni mehanizam eliminacije je bubre&na ekskrecija putem tubularne sekrecije. Cefoperazon i ceftriakson se izlu#uju putem &u#i. Ve"ina cefalosporina I. i II. generacije ne prelazi krvno-mo&danu barijeru, #ak ni u slu #aju meningitisa. C. MEHANIZAM DJELOVANJA i REZISTENCIJA Cefalosporini se ve&u na PBP-ove na bakterijskoj citoplazmatskoj membrani i inhibiraju sintezu stani#ne stijenke. Baktericidni su, a strukturne razlike ih #ine manje podlo &nim razgradnji beta-laktamazama od penicilina. Me%utim, mnoge su bakterije razvile rezistenciju produkcijom drugih beta-laktamaza koje mogu inaktivirati cefalosporine. Rezistencija mo&e nastati i zbog smanjenja u membranskoj permeabilnosti te u promjenama na PBP-ovima. D. KLINI!KA PRIMJENA 1. Cefalosporini prve generacije: Cefazolin (parenteralno) i cefaleksin (oralno) su primjeri ove skupine. Aktivni su protiv G+ koka (stafilo- i strepto-). Osjetljivi su i mnogi sojevi E. sojevi E. coli i coli i K. K. pneumoniae. pneumoniae. Osim lije#enja infekcije ovim organizmima, lijek su izbora i za kirur $ku profilaksu. Minimalno su u#inkoviti protiv G- koka, enterokoka i MRSA-e, kao i ve "ine G- $tapi"a. 2. Cefalosporini druge generacije: Lijekovi u ovoj skupini uglavnom su slabije aktivni protiv G+ bakterija od prve generacije, ali su zato u #inkovitiji protiv G bakterija. Primjenjuju se kod infekcija B. infekcija B. fragilisom (cefotetan, cefoksitin ), H. influenzae ili influenzae ili M. M. catarrhalis ( catarrhalis (cefuroksim, cefaklor ). U ovu skupinu pripadaju i cefamandol, cefonicid, cefprozil i lorakarbef , dok se cefoksitin, cefmetazol i cefotetan zajedni#ki nazivaju cefamicinima. 3. Cefalosporini tre"e generacije: Glavne su im karakteristike poja#ana aktivnost protiv G- bakterija i sposobnost prelaska krvno-mo&dane barijere. Naju#inkovitiji su protiv enterobactera, providencije, serratiae i najserije. Ceftazidim i cefoperazon jedina su dva lijeka djelotvorna protiv P. protiv P. aeruginosa. aeruginosa. Ceftizoksim i moksalatam djelotvorni su protiv B. protiv B. fragilis. Ceftriakson (parenteralno) i cefiksim (oralno) se primjenjuju u lije #enju gonoreje. Tre"a se generacija cefalosporina upotrebaljava za lije#enje raznih ozbiljnih infekcija uzrokovanih organizmima koji su rezistentni na ve "inu drugih lijekova. 4. Cefalosporini #etvrte generacije: Cefepim je primjer ove podskupine. Djelotvoran je protiv P. protiv P. aeruginosa, aeruginosa, enterobakterija, S. aureus i aureus i S. S. pneumoniae, a izrazito je djelotvoran protiv hemofilusa i najserije. Dobro prodire u cerebrospinalnu teku"inu. E. TOKSI ! NOST Cefalosporini mogu dovesti do razli #itih reakcija preosjetljivosti, jednakih onima na peniciline. U#estalost ukri&ane reakcije izme%u penicilina i cefalosporina je niska, no ipak, bolesnicima s anafilaksijom na penicilin u povijesti bolesti ne smiju se davati cefalosporini. Lokalna iritacija mo&e prouzro#iti jaku bol nakon intramuskularne i tromboflebitis nakon


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intravenske injekcije. Mogu"a je bubre&na toksi#nost (intersticijski nefritis, tubularna nekroza). Cefalosporini s metiltiotetrazolnom skupinom (npr. cefoperazon, cefotetan) mogu uzrokovati hipoprotrombinemiju i poreme "aje krvarenja.

3. OSTALI BETA-LAKTAMSKI BETA-LAKTAMSKI ANTIBIOTICI

A. MONOBAKTAMI Spojevi s monocikli #kim beta-laktamskim prstenom. Njihov je spektar djelovanja ograni #en na aerobne G- $tapi"e (uklju#uju"i pseudomonas, klebsijelu i seraciju). Nisu djelotvorni protiv G+ bakterija ili anaeroba. Aztreonam je trenuta#no jedini dostupan monobaktam na tr &i$tu. Preferencijalno se ve&e na PBP3 i inhibira sintezu bakt. stijenke, ima sinergisti #ki u#inak s aminoglikozidima. Eliminira se tubularnom sekrecijom u bubregu. 'tetni su u#inci GI pote$ko"e s mogu"om superinfekcijom, vrtoglavica i glavobolja, glavobolja, te, vrlo rijetko, hepatotoksi#nost. Nemaju ukri&ane reakcije s penicilinima. B. INHIBITORI BETA-LAKTAMAZA Klavulanska kiselina, sulbaktam i tazobaktam. Imaju vrlo slabu antibakterijsku djelotvornost. Potentni su inhibitori mnogih, ali ne i svih bakterijskih beta-laktamaza i na taj na#in mogu peniciline podlo &ne hidrolizi za$tititi od inaktivacije. C. KARBAPENEMI U njih ubrajamo doripenem, ertapenem, imipenem i meropenem. Imipenem ima $irok spektar i dobru djelotvornost protiv mnogih G- $tapi"a (uklju#uju"i pseudomonasa), anaeroba i G+ koka. Rezistentan je na ve "inu beta-laktamaza. Primjenjuje se parenteralno, a zbog brze inaktivacije u bubregu djelovanjem dehidropeptidaze, primjenjuje se zajedno s inhibitorom tog enzima - cilastatinom. Doripenem i meropenem su sli #ni imipenemu, ali su ne $to djelotvorniji protiv G- $tapi"a i manje djelotvorni protiv G+ bakterija. Tako %er, bubre&na ih dehidropeptidaza ne inaktivira.

4. OSTALI LIJEKOVI LIJEKOVI KOJI DJELUJU DJELUJU NA STANI STANI!NU STIJENKU/MEMBRANU STIJENKU/MEMBRANU

A. GLIKOPEPTIDI Glavni je predstavnik vankomicin, koji je djelotvoran samo protiv G+ bakterija. Baktericidni je antibiotik koji se #vrsto ve&e na D-alanil-D-alanin zavr $etak nascentnog peptidoglikanskog pentapeptida i inhibira transglikozilazu. Rezistencija se razvija smanjenim afinitet om za vezno mjesto promjenom D-Ala s D-laktatom. Nedavno su se pojavili i VRE (vankomicinrezistentni enterokoki). Vankomicin ima uzak spektar djelovanja i koristi se u lije #enju ozbiljnih infekcija, glavni uzro #nik protiv kojeg se koristi jest MRSA, ali i protiv penicilinrezistentnog pneumokoka i C. difficile. difficile. Kada se primjenjuje oralno, ne apsorbira se iz GI trakta pa se mo&e koristiti u lije#enju bakt. enterokolitisa. Pri parenteralnoj primjeni, nepromijenje se eliminira bubrezima. U pacijenata s o$te"enjem bubrega nu &na je modifikacija doziranja. Toksi#ni su u #inci nefrotoksi#nost i ototoksi#nost, a rapidna


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intravenska infuzija mo&e uzrokovati "red man syndrome" (izrazito crvenilo kao posljedica osloba%anja histamina). Ostali su glikopeptidi teikoplanin, za kojega je specifi#no da se mo &e primijeniti i intramuskularno, te dalbavancin i telavancin, semisintetski lipoglikopeptidi. B. FOSFOMICIN Analog fosfoenolpiruvata i antimetabolitni inhibitor citosolne enolpiruvat-transferaze - ve &e se kovalentno na cisteinske ostatke u aktivnom mjestu i blokira vezanje fosfoenolpiruvata. Rezistencija se razvija putem smanjenja unutarstani#ne akumulacije lijeka. Izlu#uje se bubrezima. Manje je u#inkovit pri davanju pojedina #ne doze nego kod sedmodnevne primjene s fluorokinolonima. Sinergisti#ki djeluje s beta-laktamima i kinolonima. Koristi se u lije#enju nekompliciranih infekcija donjeg urinarnog trakta u &ena. C. BACITRACIN Peptidni antibiotik koji interferira kasni stadij sinteze stani#ne stijenke kod G+ bakterija. Izrazito je nefrotoksi#an pri sistemnoj primjeni, zbog #ega se primjenjuje samo lokalno. Slabo se apsorbira. Indiciran je za supresiju mije$ane bakterijske flore povr $inskih lezija ko&e, rana ili sluznica. D. CIKLOSERIN Inhibira mnoge G- i G+ organizme, ali se gotovo isklju #ivo koristi za lije#enje tuberkuloze uzrokovane M. uzrokovane M. tuberculosis. tuberculosis. Strukturni je analog D-alanina i inhibira ugradnju D-alanina u peptidoglikanski pentapeptid. Uzrokuje o dozi ovisne ovisne ozbiljne toksi #ne reakcije u CNS-u s glavoboljom, tremorom, akutnom psihozom i konvulzijama. E. DAPTOMICIN Novi cikli#ni lipopeptid. Antibakterijski spektar mu je sli #an vankomicinu, samo $to in vitro mnogo br &e djeluje baktericidno i djelotvoran je protiv VRE i S. aureusa. aureusa. Ve&e se za stani#nu membranu umetanjem svog lipidnog repa postupkom koji je ovisan o kalciju, $to uzrokuje depolarizaciju stanice, efluks kalija te brzu smrt stanice. Izlu#uje se bubregom.

Slika 3. Mehanizam djelovanja daptomicina


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43. BETA-LAKTAMSKI I DRUGI ANTIBIOTICI KOJI DJELUJU NA STANI! NU STIJENKU I MEMBRANU 1. Primarni mehanizam antibakterijskog djelovanja penicilina uklju"uje inhibiciju: a) beta-laktamaza b) sinteze N-acetilmuraminske kiseline c) ukri!enog vezanja peptidoglikana d) sinteze stani"ne mebrane e) transglikozilacije PITANJA 2 i 3. 33-godi #nji mu#karac. $ali se na disuriju i %uti gnoj iz uretre. Imao je bezbolan ulkus na penisu... Uglavnom, Uglavnom, ima gonoreju. 2. Najbolja terapija za gonoreju kod ovog pacijenta je: a) ampicilin oralno tijekom 7 dana b) ceftriakson intramuskularno, intramuskularno, jedna doza c) prokainski penicilin G intramuskularno, jedna doza plus probenecid probenecid oralno d) tetraciklin oralno tijekom 5 dana e) vankomicin intramuskularno, jedna doza 3. Imunofluorescentnom mikroskopijom teku &ine iz ulkusa je dokazana treponema. S obzirom na to da vjerojatno ima infekciju T. pallidum, najbolji postupak bio bi: a) dati jednu dozu fosfomicina, oralno b) ne dati nijedan drugi antibiotik jer terapija gonoreje pokriva i sifilis c) dati intramuskularni benzatinski penicilin G d) lije"iti oralnim tetraciklinom 7 dana e) lije"iti vankomicinom 4. Koja je tvrdnja o imipenemu to "na? a) U"inkovit protiv MRSA-e b) Ima uzak spektar antibakt. djelovanja c) Kod renalne disfunkcije, redukcija doze je potrebna da se sprije "e konvulzije d) Izrazito je podlo%an beta-laktamazama koje proizvode Enterobacteri e) Koristi se fiksno u kombinaciji sa sulbaktamom 5. 36-godi#nja %ena, nedavno lije "ena zbog leukemije, primljena u bolnicu zbog vrtoglavice, groznice i visoke temperature. Gramovim bojanjem dokazana prisutnost G- bacila u krvi. Inicijalna dijagnoza je bakterijemija, indicirani su parenteralni antibiotici. Povijest bolesti okriva da je prije 6 mjeseci imala urtikarije, hipotenziju i respiratorne smetnje nakon primjene oralnog penicilina V. Najprimjereniji lijek za empirijsko lije"enje bio bi: a) Aztreonam b) Cefazolin c) Imipenem d) Nafcilin e) Tikarcilin + klavulanska kiselina


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PITANJA 6-8. 52-godi #nji mu#karac (70 kg), doveden u hitnu u konfuznom stanju i deliriju. Ima povi #enu temperaturu vi #e od 24h. U tom se periodu %alio na te#ku glavobolju, imao je i vrtoglavicu i povra &ao je. Lumbalnom punkcijom uzima se uzorak likvora, nalazi pokazuju povi #ene proteine, sni%enu glukozu, neutrofiliju. Gramovim bojanjem dokazani G+ diplokoki, preliminarna dijagnoza je purulentni meningitis. 6. Lije"enje ovog pacijenta treba odmah zapo "eti intravenskom primjenom: a) ampicilina-sulbaktama b) cefazolina c) cefotaksima + vankomicina d) nafcilina e) tikarcilina 7. Rezistencija pneumokoka na penicilin G se razvija zbog: a) produkcije beta-laktamaze b) promjene u kem. strukturi ciljnih PBP-ova c) promjene u strukturi porina d) promjene u gra'i D-Ala-D-Ala gra'. jedinice peptidoglikanskog prekursora e) smanjene unutarst. akumulacije penicilina G 8. Da pacijent ima 82 godine i da su u likvoru prona 'eni G+ #tapi&i nalik na difteroide, empirijsko lije"enje bi uklju"ivalo koji antibiotik? a) Ampicilin b) Aztreonam c) Cefazolin d) Fosfomicin e) Meropenem 9. Pacijent treba antibiotik zbog enterokokalnog endokarditisa. Povijest bolesti otriva te#ku anafilakti"nu reakciju na penicilin G tijekom pro #le godine. Najbolji pristup bio bi lije"enje: a) amoksicilinom-klavulanatom b) aztreonamom c) cefazolinom + gentamicinom d) meropenemom e) vankomicinom 10. Koja je tvrdnja o vankomicinu to "na? a) U"inkovit protiv MRSA-e b) Bakteriostatki antibiotik c) Ve%e se za PBP d) Metabolizira se u jetri e) Oralna bioraspolo%ivost 11. Koja je od sljede&ih tvrdnji o biodispoziciji penicilina i cefalosporina najto"nija? a) Oralna bioraspolo%ivost je pogo 'ena metabolizmom u jetri b) Samo 3. generacija cefalosporina prelazi krvno-mo %d. barijeru c) Prokainski penicilin G je naj "e#&e kori#teni intravenski oblik antibiotika d) Renalna tubularna reapsorpcija beta-laktama je inhibirana probenecidom


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e) Nafcilin i ceftriakson se primarno izlu "uju putem !u"i

12. Stariji pacijent ima vru&icu, vjeruje se zbog infekcije. Ima mnogo lezija na ko %i, te se u njima dokazuje prisutnost G+ koka. Najprikladnija terapija je kojim lijekom? a) Amoksicilin b) Aztreonam c) Moksalaktam d) Nafcilin e) Penicilin G 13. Koja je od sljede&ih tvrdnji o cefotetanu to "na? a) U"inkovit protiv MRSA-e b) Lijek izbora u domicilnoj pneumoniji c) Cefalosporin 4. generacije d) Smanjuje protrombinsko vrijeme e) Antibakterijski Antibakterijski spektar uklju "uje B. fragilis 14. Ovaj lijek je u"inkovit protiv mnogih sojeva pseudomonasa. Me 'utim, kada se primjenjuje samostalno, pojavljuje se rezistencija. Ne smije se primijeniti na pacijentima koji su alergi"ni na penicilin. Njegova u "inkovitost protiv G- #tapi&a se pove&ava kada je primijenjen u kombinaciji s tazobaktamom. Rije " je o? a) Amoksicilinu b) Aztreonamu c) Imipenemu d) Piperacilinu e) Vankomicinu 15. Koja je od sljede&ih tvrdnji o ampicilinu NETO ! NA? a) U"inkovitost mu je poja "ana sulbaktamom b) Uzrokuje makulopapularne osipe c) Lijek je izbora za infekciju L. monocytogenes d) Eradicira ve#inu MRSA sojeva e) Mo%e uzrokovati pseudomembranozni kolitis


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45. AMINOGLIKOZIDI I SPEKTINOMICIN (Dunja !ojat) AMINOGLIKOZIDI (streptomicin, gentamicin, tobramicin, neomicin, kanamicin, amikacin, sisomicin, netilmicin)

-topljivi u vodi, aktivni u alkalnom mediju MEHANIZAM DJELOVANJA:

1. Pasivna difuzija kroz porine na vanjskoj membrani 2. Prijenos kroz stani" stani"nu membranu u citoplazmu ovisan o kisiku (pobolj# (pobolj #an vankomicinom ili penicilinom; inhibiran anaerobnim uvjetima) 3. Vezanje za 30S ribosoma unutar stanice ! INHIBICIJA SINTEZE PROTEINA: a) Sprje" Sprje"avaju stvaranje inicijacijskog kompleksa peptida b) Pogre# Pogre#no o" o"itavanje mRNA " krive AK " nefunkcionalni proteini c) Raspadanje polisoma na neu" neu "inkovite monosome MEHANIZMI REZISTENCIJE:

1. TRANSFERAZE inaktiviraju aminoglikozide (naj" (naj "e#$i na"in) #$i na" 2. Poreme$ Poreme$en ulazak u stanicu zbog MUTACIJE PORINA 3. Mutacija receptora na 30S podjedinici FARMAKOKINETIKA:

Oralno " slaba apsorpcija u intaktnom probavnom sustavu; u cijelosti se izlu "i stolicom Intramuskularno " dobra apsorpcija Intravenski " naj" naj"e#$e #$e se koristi *U% *U%INAK UBIJANJA BAKTERIJA OVISAN O KONCENTRACIJI – ve $a koncentracija lijeka ubija vi# vi#e bakterija i pove$ pove $anom brzinom *POSTANTIBIOTSKI U% U %INAK – antibakterijska aktivnost traje i nakon vremena u kojem je razina lijeka mjerljiva Izlu" Izlu"ivanje: BUBREZIMA (potrebna prilagodba kod bubre &nih bolesnika) NE ulaze u stanice " ne idu u S' S 'S (osim u upali) i u oko t (= 2-3 h NE!ELJENI "TETNI U#INCI:

OTOTOKSI% OTOTOKSI% NOST I NEFROTOKSI% NEFROTOKSI% NOST (pri dugoj terapiji, velikim dozama, starijih osoba); primjena sa diureticima Henleove petlje i drugim nefrotoksi" nefrotoksi "nim lijekovima pogor #ava nefrotoksi" nefrotoksi"nost. Ototoksi" Ototoksi"nost (o# (o#te$ te$enje sluha ili vestibularno o# o #te$ te$enj: vrtoglavica, gubitak ravnote& ravnote&e, ataksija).


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U jako visokim dozama (reverzibilno: neostigmin)

"

NEUROMUSKULARNA BLOKADA

"

prekid disanja

Rijetke reakcije preosjetljivosti! KLINI#KA PRIMJENA:

G – crijevne bakterije; sa beta-laktamskim antibioticima da se pro# pro#iri spektar djelovanja na G+; sa Pen " enterokokni endokarditis i br &e djelovanje protiv stafilokoknog i streptokoknog endokarditisa 1. STREPTOMICIN

-lijek druge linije za tuberkulozu (samo u kombinaciji s drugim lijekovima); kuga, tularemija, bruceloza, enterokokni endokarditisa i streptokokni endokarditis (sa penicilinom); enterokokne infekcije NE' NE'ELJENI U% U%INCI: alergijske reakcije, osipi, POREME) POREME)AJ VESTIBULARNE FUNKCIJE (mo& (mo&e biti ireverzibilan) ; kontraindiciran u trudno$ trudno $i 2. GENTAMICIN

-protiv G+ i - ; naj" naj "e#$e #$e se kombinira sa vankomicinom i penicilinom da se pove $a djelovanje; OZBILJNE INFEKCIJE G- (pseudomonas, enterobakter, proteus) ; LOKALNA PRIMJENA (inficirane opekline, rane, prevencija infekcija kod intravenskih katetera); INTRATEKALNA PRIMJENA (meningitis uzrokovan G- bakterijama " danas se uglavnom ne koristi) NE' NE'ELJENI U% U%INCI: NEFROTOKSI% NEFROTOKSI % NOST reverzibilna; OTOTOKSI% OTOTOKSI% NOST mo& mo&e biti ireverzibilna 3. TOBRAMICIN

-sli" -sli"an spektar kao gentamicin ; za lije" lije"enje infekcija donjih di# di #nih puteva P.aeruginosa; daje se i.v. NE' NE'ELJENI U% U%INCI: ototoksi" ototoksi"nost i nefrotoksi" nefrotoksi"nost 4. AMIKACIN - Daje se i.v. ; kod rezistencije na gentamicin i tobramicin; Mycobactrium tuberculosis; nefrotoksi" nefrotoksi"nost i ototoksi" ototoksi "nost 5. NETILMICIN 6. NEOMICIN I KANAMICIN - Slaba apsorpcija; primjenjuje se LOKALNO (inficirane povr #ine, u zglobove, #upljine u kojima je gnoj) i ORALNO (preoperativna priprema crijeva, hepatalna koma) - Protiv G + i -; ne djeluje protiv Pseudomonasa i streptokoka - Zna" Zna"ajna nefrotoksi" nefrotoksi"nost i ototoksilnost (gluho$ (gluho $a); mo& mo&e do$ do$i do neuromuskularne blokade; kod dugotrajne loklne primjene primjene " alergijske reakcije SPEKTINOMICIN

Sli" Sli"an AG po strukturi, protiv gonokoka rezistentnih na lijekove ili kod bolesnika alergi" alergi"nih na pencilin, intramuskularno, na mjestu primjene bol, nekad mu "nina i groznica; rijetko nefrotoksi" nefrotoksi"nost


190


PITANJA – 45.cjelina 1. Koja od navedenih tvrdnji o mehanizmu djelovanja aminoglikozida je pogre !na? a) Induciraju pogre!no "itanje mRNA b) Uzrokuju nestabilnost polisoma c) Inhibiraju peptidil transferazu d) Blokiraju stvaranje inicijacijskog kompleksa e) Inhibiraju sintezu proteina 2. Pacijent te#ak 70 kilograma sa klirensom kreatinina ve $im od 90mL/min ima gramnegativnu infekciju. Primjenjen je amikacin intramuskularno (doza: 5mg/kg svakih 8 sati) i dolazi do odgovora na terapiju. Nakon dva dana, klirens kreatinina smanjen je na 30mL/min. Uzimaju$i u obzir da nemamo podatke o koncentraciji amikacina u plazmi kako biste postupili? a) Smanjiti dnevnu dozu na ukupno 100 mg b) Smanjiti doziranje na 120 mg svakih 8 h c) Zadr #ati trenutnu terapiju i testirati sluh u pacijenta d) Primjeniti 5mg/kg svakih 12 h e) Prekinuti terapiju amikacinom i uvesti terapiju gentamicinom 3. Koja od navedenih tvrdnji o klini "koj uporabi aminoglikozida je pogre !na? a) Obzirom na njihovu polarnost n e mogu se aporbirati nakon oralne primjene b) %esto se koriste u kombinaciji sa cefalosporinima u lije "enju te!kih po #ivot opasnih bakterijskih infekcija c) Netilmicin je djelotvorniji od streptomicina za lije"enje bolni"ke infekcije Serratiom d) Spektar djelovanja aminoglikozida uklju"uje Bacteroides fragilis e) Gentamicin se koristi sa ampicilinom u lije"enju enterokoknog endokarditisa 4. Koja je od sljede$ih tvrdnji o bakterijskoj rezistenciji aminoglikozida to"na? a) Rezistencija ovisi o produkciji peptidil transferaza b) Bakterije otporne na aminoglikozide imaju karakteristi "ne promjene u putu sinteze folne kiseline c) Pojava rezistentnosti tijekom terapije je "esta d) Rezistencija se obi"no prenosi plazmidom a uzrokuje stvaranje enzima transferaze e) MRSA su osjetljivi na aminoglikozide

5. Koji od navedenih antibiotika je najvi !e djelotvoran protiv enterokoka u kombinaciji sa Pen G a) Amikacin b) Gentamicin c) Netilmicin d) Streptomicin


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e) Tobramicin

6. Promatraju$i antibakterijsku djelotvornost gentamicina, koja od navedenih tvrdnji je to"na? a) Efikasnost je proporcionalna sa vremenom u kojem je koncentracija lijeka u plazmi ve$a nego MIK b) Antibakterijska djelotvornost je neovisna o koncentraciji c) Gentamicin ookazuje antibakterijske u"inke i nakon !to se koncentracija lijeka snizi ispod mjerljivih razina u plazmi d) Antibakterijska djelotvornost je obi "no smanjena prisutno !$u inhibitora sinteze stani"nog zida e) Antibakterijska djelotvornost gentamicina je ovisna o vremenu

7. Odrasli pacijent (70kg) bakterijemiju najvjerojatnije izazvanu gram negativnim !tapi$ima. Tobramicin se koristi jednom dnevno, a doza mora dose $i maksimalnu koncentraciju u plazmi od 20mg/L. Pretpostavljamo da pacijent ima normalnu bubre#nu funkciju. Farmakokineti "ki parametri: Vd= 20L; t1/2=3 sata; CL= 80mL/min. Koju dozu trebamo dati? a) 100 mg b) 200mg c) 300mg d) 400mg e) 800mg

8. Koji od nabrojanih lijekova je naju "inkovitiji protiv otpornih sojeva M.tuberculosis, uklju"uju$i rezistentne na streptomicin? a) Amikacin b) Klaritromicin c) Gentamicin d) Meropenem e) Spektinomicin

9. 57 godina star mu !karac#ali se na bolove u i iza desnog uha. Fizikalni prekled ukazuje na edem vanjskog slu !nog kanala sa gnojnim iscjetkom i slabo !$u mi!i$a na desnoj strani lica. Nema znakova sistemne infekcije. Pacijent je dijabeti"ar, svakodnevno uzima glipizide, ali ne inzulin. Tako &er svakodnevno uzima i Aspirin 100mg. Ne uzima nikakve druge lijekove. U gnoju na &eni polimorfonukleari i gram negativni !tapi$i. Radna dijagnoza je upala vanjskog uha. Koju terapiju biste prepisali?


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a) Analgetici za bol, antibiotici se trebaju odabrati prema rezultatima (obrada kuluture) b) Pacijent treba biti otpu!ten ku$i ; oralno cefaclor c) Pacijent treba biti hospitaliziran a lije"enje treba po"eti gentamicinom + tikarclinom d) Pacijent treba biti hospitaliziran a lije"enje treba po"eti i.v. imipenem + cilastatin e) Pacijent treba biti hospitaliziran a lije"enje treba po"eti spektinomicinom.

10. Obzirom na toksi "nost gentamicina koja od sljede $ih tvrdnji nije to"na? a) Ototoksi"nost je smanjena ako se koriste diuretci petlje da bi se olak !ala ekskrecija gentamicina b) Sistemski neomicin je sigurniji nego gentamicin c) Gentamicin $e "e!$e uzrokovati ototoksi "nost nego renotoksi "nost d) Kod primjene uobi "ajenih doza prvi znak nefrotoksi"nosti je smanjeni klirens kreatinina e) Ototoksi"nost je ireverzibilna i o"ituje se kao vestibularna disfunkcija

11. Koja od sljede$ih tvrdnji o neomicinu je to "na? a) Koristi se kao dodatna terapija protiv tuberkuloze b) Lijek izbora u Rocky Mountain spotted fever c) Najmanje nefrotoksi"ni aminoglikozid d) Metabolizira se jetrenim enzimima e) Koristi se u jetrenoj komi

12. Streptomicin nema koristi u terapiji protiv? a) Bubonske kuge b) Bruceloze c) Lyme disease d) Tuberkuloze e) Tularemije

13. Koji lijek ima spektar aktivnosti i farmakokineti"ka svojstva gotovo identi "na gentamicinu? Pokazuje lo!u aktivnost u kombinaciji sa Pencilinom protiv enterokoka. a) Amikacin b) Eritromicin c) Netilmicin d) Spektinomicin e) Tobramicin


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14. Pacijentica stara 23 godine je trudna i ima gonoreju. Javljala se anafilaksija na terapiju amoksicilinom. Za lije"enje jednokratnom dozom odabrat $ete? a) Cefeksim b) Ceftriakson c) Ciprofloksacin d) Spektinomicin e) Tetraciklin

15. U terapiji nekoliko bakterijskih infekcija , ovaj lijek , kori!ten u kombinaciji sa aminoglikozidima, osigurava djelotvornost protiv mnogih stafilokoka. a) Amoksicilin b) Klavulonska kiselina c) Eritromicin d) Nafcilin e) Tetraciklin 16. Koja od sljede$ih tvrdnji o jednokratnom dnevnom doziranju aminoglikozida je pogre!na? a) Prikladno je za izvanbolni "ku terapiju b) Prilagodba doze je manje bitna kod bubre #nog zatajenja c) Potrebno je manje vrijeme njege d) Obi"no je manje toksi "no nego uobi "ajena vi!ekratna terapija e) Poddoziranje je manji problem

1.c; 2.b;3.d;4.d;5.d;6.c;7.d;8.a;9.c;10.e;11.e;12.c;13.e;14.d;15.d 2.b;3.d;4.d;5.d;6.c;7.d;8.a;9.c;10.e;11.e;12.c;13.e;14.d;15.d;16.b; ;16.b;


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Farmakologija - skripta

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