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Cell wall synthesis inhibitors

الكلية كلية الطب     القسم  الادوية     المرحلة 3
أستاذ المادة نسرين جلال محمد البياتي       6/7/2011 9:26:01 PM

cell wall synthesis inhibitor

antimicrobial therapy:

drugs that have ability to injure or kill the invading mo without harming the

drugs that have ability to injure or kill the invading mo without harming the

host cells

antimicrobial drug: antibacterial , antiviral , antifungal

anti-parasitic drug: anti-protozoal , antihelmenthic

classification:

according to its effect

according to its effect

* bactericidal ds that kill bacteria

*bacteriostatic inhibit bacterial growth

acording to spectrum:

a- narrow – spectrum antibiotics

b- extend- spectrum antibiotics

c- broad- spectrum antibiotics .{candida albicans ( super infection ) }

according to targets ( mechanism of action ):

1- cell wall inhibitor

2-cell mem inhibitor

3-pr. synthesis inhibitor

4-dna synthesis inhibitor

5-metabolism inhibitors

combination:

single treatment used to:

single treatment used to:

1- reduce super infection

2- decrease emergencies of resistance

3-minimize toxicity

advantages of combination:

1- synergism ( ?-lactams & amino glycoside )

2- in infection with unknown origin

disadvantages of combination: -interfering with the action of each other

cell wall synthesis inhibitor

- cell wall not found in mammilian cells

-peptidoglycan is main component

- need proliferate cells

nam -nag nam nag namnam

-nag nam nag nam-

- cidal due to inhibition of trans peptidation by inhibiting pbp (enzyme

catalyze the formation of cross linkage between peptidoglycan chain so

changes in cw & morphology death due osmolarity or autolysis)

penicillin:

- include beta-lactam ring in their structure

- reach bone, csf, cns in inflam (meningitis), pass placenta & breast milk

- excreted actively (probenecid)

include:

*natural p :

1- benzyl p (p g)

1- benzyl p (p g)

-(g + cocci, g- cocci , g+bacilli , spirochetes)

- i/m , depot

2- phenoxymethyl p (p v)

-more acid stable

-spectrum samepg + some anaerobic microorganism

- orally

*anti staphylococcal penicillins

methicillin , nafcilin, oxacillin, dicloxacillin

-penicillinase resistant p

-staphylococci

-methcillin used in lab only ,toxic

- absorption decreased by food in stomach

- destructed by acid so given 30-60 min before meal

- nafcilin biliary exc

*extend spectrum p

ampicillin , amoxicillin

-are acid stable

- spectrum same pg + g- bacilli

-ampicillin choiced for g+bacilli( listeria monocytogens)

-treatment of respiratory infection

-combination with beta lactamase inhibitor (clavulanic acid +amoxicillin &

sulbactam+ ampicillin) protect them from enzymatic hydrolysis & extend

spectrum

- sulbactam+ ampicillin (i/v, i/m)

- amoxicillin ,clavulanic acid +amoxicillin (oral)

*anti pseudomonal p

-carboxy p (carbenicillin, ticarcillin)

-uridop ( piperacillin)

- against p. aeruginosa , g-bacilli (but not klebsiella)

- piperacillin most potent

-all are acid stable

-ticarcillin, piperacillin combined with ((clavulanic acid & tazobactam))

respectively increase spectrum to include pencillinase producing mo

- the combination given i/v , i/m because they acid unstable

adverse effect:

- hypersensitivity (due to its metabolite)

- diarrhea (changes in normal balance of intestinal mo)

- nephritis

- neurotoxicity ( irritate neuronal tissue)

- hematologic toxicities: decrease coagulation with antipseudomonal

- cation toxicity ps administered as na or k salts high conc of them cause

toxicity

uses of pen g:

preparation as procaine , benzathine to delay absorption

preparation as procaine , benzathine to delay absorption

- pneumonia

- syphilis

- gonorrhea

- clostridium ( anaerobic)

- anthrax

- diphtheria

- endocarditis

uses of amoxicillin:

-uti

-otitis

-meningitis

-pen resistant pneumococci

uses of ampicillin:

-shigellosis

-shigellosis

-listeria monocytogens

-e coli

-haemophilus influenzae

- salmonella typhi

uses of antipseudomonal

-e coli

-haemophilus influenzae

-enterobacter spp

-proteus ( indol positive)

cephalosporin:

- arebeta-lactam antibiotic, semi synthetic

- structurally & functionally related to pen

- same moa

- more resistant to beta-lactamase

- all pass placenta

1st generation:

cephalexin (oral, in pharyngitis,uti, respiratory infection )

cefazoline (parenteral , penetrate bone ) cefadroxil (oral, uti)

spectrum: s aureus , s epidermidis streptococcus pneumonia ,

st pyogenes anaerobic streptococci e coli klebsiella pneumoniae proteus

morabilis

2nd generation: weak against g+ cocci

-cefaclor oral

-cefprozil

-cefuroxime na ( parenteral, pass bbb, used in community acqin uired

pneumonia, in septicaemia )

-cefuroxime axetil: (oral, against ?-lactamase producing mo)

-cefoxitin: parenteral, in pelvic inflammatory disease, in gynecologic sepsis,

intra-abdominal sepses

streptococcus pneumonia , st pyogenes, anaerobic streptococci n gonorrheae

g- cocci, g- rods haemophilus influenzae

klebsiella pneumoniae , proteus morabilis, enterobacter aerogenes

3rd generation ceftriaxone , cefotaxime, ceftazidime ceftizoxime , cefdinir ,

ceftibuten, cefixime

-g- rods +neiseria gonorrhea+ enteric mo+ serratia

*ceftriaxone or cefotaxime :1st choice for meningitis

*ceftazidime: act against p aurogenosa ,reach csf cefdinir ,

cefixime: oral

cefotaxime : parenteral , reach csf,

other beta - lactam antibiotic

a-carbapenems

*imipenem

-imipenem combined with cilastatin to prevent metabolism by renal

dehydropingingingingeptidase

-combination cause n, v ,diarrhea

-against beta-lactamases mo, g+,- ,anaerobes, p au

uses: septicaemia, abdominal infection, pneumonia

*meropenem

-similar but not metabolized by kidney enzymes

-pass csf

b-monobactams

*aztreonam

-against g- & aerobic, but not g+& anaerobes

-safe alternative for patient sensitive to pencillin

uses:

septicaemia, complicated uti, gonorrhea

c-beta-lactamase inhibitor

clavulanic acid, salbactam, tazobactam

- contain beta-lactam ring but don’t have sig antimicrobial activity

- act after combination, protect pen from beta-lactamase

other cell wall synthesis inhibitor:

vancomycin

- g+ staph, clostridia, enterococci

-inhibit transglycosylation step

-given parenteraly , not absorbed from gut

uses:

-with cefotaxim & ceftriaxone for meningitis

-with aminoglycoside for enterococcal endocarditis

-orally for enterocolitis (closteridium)

se:

tinnitus, nephrotoxicity, phlebitis, chill & fever

daptomycin (90% pr binding)

- cidal

-g+, vancomycin resistant enterococci

- induce rapid depolarization of cell mm, disrupting mm function& inhibit

i/celular synthesis of dna , rna

uses:

-complicated skin infection, bacteremia due s aureus

se:

constipation, insomnia


المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .