Cell wall inhibitors
Clavulanic acid
B-Lactamase inhibitors
Teicoplanin
Sulbactam
Tazobactam
Monobactams
Cephalosporins
Penicillins
Cycloserine
Cabapenems
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It occurs in the cytoplasm & involves a racemase enzyme which converts the D-alanine to L-alanine, and ligase which couples two D-alanines together.
They have found major applications in the treatment of infections
They can blocked forming the stem peptide .
Interferes with the early stage of synthesis of peptidoglycan involving the assembly of the dipeptide D-alanine-D-alanine
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Vancomycin is active against G+ve bacteria
Vancomycin is inactive against G-ve bacteria
Vancomycin isn't inactive against MRSA
Vancomycin is active against Streptococci
Vancomycin isn't active against Enterococcus faecalis
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Can penetrate through the outer membrane of Gram-negative bacteria
The large molecule size of Gram-negative bacteria
Can't penetrate through the outer membrane of Gram-negative bacteria
The large molecule size of vancomycin
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Can treat infection of gram +ve and -ve
Its similar to vancomycin in does and all things
Its similar to vancomycin in chemical structure but vancomycin posses more fatty acid side chains
Can treat infection of gram +ve and cant of -ve
All answer correct except 1 opition
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 Vancomycin posses less fatty acid side chains than Teicoplani
 Vancomycin more acidic than Teicoplani
Vancomycin given IV and IM while Teicoplani given at one of site when Vancomycin is given
Vancomycin more lipophilic than Teicoplani
Vancomycin more effect than Teicoplani
Vancomycin administered per 12 hours while Teicoplani administered per 6 hours
Vancomycin are a slightly higher potency against most target organisms and a better toxicity profile rather thanTeicoplanin
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All answer is not correct
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The process of formation of Peptidoglycan take place in cytoplasm
Peptidoglycan is a macromolecule composed of sugar (glycan)^NAM and NAG ^ ( bound with b-1,4-glycosidic bond ) cross-linked by short peptide chains.
Each (NAM) contains a short peptide substituent made up of four amino acids (the stem peptides).
In the stem peptides there are the D-isomers of some amino acids (particularly D-alanine and D-glutamic acid) and unusual amino acids such as meso-diaminopimelic acid which are not found in proteins
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The crosslinking of the stem peptides : a direct peptide bond between the fourth amino acid on one chain and the third amino acid on an adjacent chain (NOT same amino acids )
The crosslinking of the stem peptides :may involve a short peptide bridge between the same amino acids on the stem peptides.
The functions of peptidoglycan: Responsible for maintaining the shape AND Act as a mechanical strength of the bacterial cell.
If it is damaged in any way, or its synthesis is inhibited, then the shape of the cells becomes distorted and they will eventually burst (lyse) due to the high internal osmotic pressure.
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Mammalian cells do not possess a cell wall
Mammalian contain no other macromolecules resembling peptidoglycan.
Mammalian cells possess a cell wall
Mammalian contain other macromolecules resembling peptidoglycan.
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L-alanine converts to D-alanine in present of ligase
Couples two D-alanines together occur in present of racemase
Transglycosylase enzyme Form glycosidic bond between the new monomer and the existing Peptidoglycan
The final stage of peptidoglycan assembly is the cross-linking of the linear glycan strands assembled by transglycosylation to the existing peptidoglycan in the cell wall occur without penicillin binding protein
The transfer new monomer (NAM and NAG) to the existing Peptidoglycan does not need carrier
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Work in the stage when the transglycosylase enzyme work.
Does not penetrate the cell membrane of bacteria but must cross the cell wall to reach the outer face of the cell membrane
It has been suggested that two vancomycin molecules from a back-to-back dimer which bridges between pentapeptides on separate glycan chains, thus preventing further peptidoglycan assembly
Glycopeptides prevent Form peptidoglycan
Bind to the enzyme itself, but do not to the disaccharide peptidoglycan precursor (disaccharide-pentapeptide )
They are not active against G-ve organisms due to the presence of the outer membrane.
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Naturally occurring: produced by fermentation of moulds such as Penicillium notatum and P. chrysogenum.
The most important examples of Semisynthetic penicillins : benzylpenicillin and phenoxymethylpenicillin
Benzylpenicillin is (penicillin G) while phenoxymethylpenicillin is (penicillin V).
In Semisynthetic Penicillins 6-aminopenicillanic acid (6-APA) is needed
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Anti-staphylococcal penicillins
Broad Spectrum Penicillins
Extended penicillins
Anti-pseudomonal penicillins
Natural penicillins
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G+ve strains of streptococci
Staphylococci
Meningococcus
All G-ve bacteria
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The group contain Methicillin, Carbenicillin, ticarcillin, piperacillin, and dicloxacillin
The group effect in Methicillin - resistant strains of Staphylococcus aureus
This group isn’t targets a specific group of bacteria which produces the β-lactamase enzyme/penicillinase-producing Staphylococci
The group contain Ampicillin and amoxicillin
The group isn't effect in (MRSA)
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It isn't extended penicillins
They are susceptible to activation by b-lactamases
They are susceptible to inactivation by penicillinase-producing pseudomonal
It isn't has an activity against Pseudomonas aeruginosa
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Have an antibacterial spectrum similar to Penicillin G but more effective against G+ve bacteria
Resistance to these antibiotics is a major clinical problem because of activation by penicillinase
Formulations are made by combining these compounds with β-lactamase inhibitors such as Cephalexin acid because it inactivation β-lactamase enzyme
Have an antibacterial spectrum similar to Penicillin V but more effective against G-ve bacteria
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All answer isn't correct
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They are drug of choice for such infections caused by Streptococcus
They are good drug active against MRSA
They are active against EKP G-ve Bacteria
This group can cross BBB so it can treat meningitis
They are susceptible to inactivation by b-lactamases
Active against P. aeruginosa
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More activity against G-ve compared with 1st generation.
Same activity against G+ve compared with 1st generation.
More resistant to b-lactamase compared with 1st generation.
More resistant to Escherichia coli , Klebsiella and Proteus compared with 1st generation.
Same activity against P. aeruginosa. compared with 1st generation.
Less resistant to meningitis than 4th generation
Same activity against P. aeruginosa. compared with 3rd generation.
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Extended spectrum of activity against G+ve organisms.
They have a greater resistance to beta-lactamases than the Fourth generation cephalosporins.
Can't reach the central nervous system (CNS).
They aren't susceptible to inactivation by b-lactamases
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Ceftazidime has more activity against P. aeruginosa compared with Cefpirome and Cefquinome
Cefadroxil and Cefazolin has same activity against P. aeruginosa compared with cafaclor and cefprozil
Cephradine and cephapirin has less activity against P. aeruginosa than Ceftazidime
Cephradine and cephapirin has less activity against P. aeruginosa than cafaclor and cefprozil
Cephradine and cephapirin has less activity against P. aeruginosa than cafaclor and cefprozil
Cephalexin and Cephalothin has less activity against P. aeruginosa than Ceftazidime
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Cefazolin can't cross BBB while cefepime it can
Cefuroxime can't cross BBB while ceftazidime it can
Cefozopran can cross BBB while cefaclor it can't
Cefoxitin can't cross BBB while Ceftriaxone it can
Cefuroxime can't cross BBB while ceftazidime it can
Cefuroxime can't cross BBB while ceftazidime it can
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Ceftriiaxone can't treat MRSA while cefaclor it can
Cefepime can't treat MRSA while ceftiraxone it can
Cefozopran can't treat MRSA while cefiquinome it can
Cefprozil can't treat MRSA while cefoxitin it can
Cefuroxime can't treat MRSA while ceftobiprole it can
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Cephalexin can't treat it
Ceftaroline can't treat it
Ceftobiprole can't treat it
Ceftriaxone can't treat it
Cephalothin can't treat it
Cephalothin can't treat it
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Cephapirin , cephalxin , cephalothin , cephradine , cefazolin and cefadroxil
Cefaclor , cefprozil , cefoxitin and cefuroxime
Ceftazidime & ceftriaxone
Cefotaxime
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Carbapenems is superior to Cephalosporins in resistant to b-lactamase enzymes.
Ceftazidime has best effectiveness against Pseudo. aeruginosa compared with CarbapenemsÂ
4th generation cephalosporins has less activate against +Ve bacteria than CarbapenemsÂ
Carbapenems has more activate against +Ve bacteria than Ceftazidime
Carbapenems is superior to Cephalosporins in broader antibacterial spectrum EXCEPT 3rd generation is superior than CarbapenemsÂ
Ceftazidime has best effectiveness against Pseudo. aeruginosa compared with CarbapenemsÂ
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Carbapenems haven't broader antibacterial spectrum compared to other b-lactam classes such as penicillins and cephalosporins.
Imipenem doesn't work without cilastatin because cilastatin is consider good antibiotic
Ertapenem has more activity than Meropenem , so Ertapenem administered once daily while Meropenem twice
Meropenem doesn't work without cilastatin because cilastatin enhances stability of Meropenem
Thienamycin is one of it and it isn't consider Natural
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Cilastatin is renal peptidase inhibitor
Enhances stability of impenem
Enhances stability of Meropenem
Cilastatin is consider inhibitor to Dehydropeptidase Enzyme
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Aztreanam is administered by intravenous injection
Aztreanam can be used for patients with allergies to penicillins and cephalosporins
Aztreanam has no activity against G+ve or aerobic bacteria
Aztreanam is active against G-ve aerobic bacteria e.g. Ps. aeruginosa
Aztreanam limited to use in hospitals.
Aztreanam limited to use in hospitals.
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Work in final stage of peptidoglycan synthetic (cross-linking of the linear glycan strands)
Work in transglycosylation through transpeptidase enzymes
B-Lactam antibiotics act by inhibiting the carboxy/transpeptidase or penicillin-binding proteins (PBPs) involved in the late stages of peptidoglycan biosynthesis.
The β-lactam antibiotics inhibit transpeptidases by acting as alternative substrates
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Resistance to many b-lactam agents is common and is most often caused by b-lactamases or by mutation in the PBPs resulting in reduced affinity
Mycoplasma Bacteria has Resistance to b-lactam antibiotics because it hasn't cell wall to attack by b-lactam antibiotics
Pseudomonas aeruginosa has Resistance to b-lactam antibiotics because it hasn't porins to allowed to drug to enter to it
Acquired Resistance can develop when patient negligent complete does for the drug
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It isn't antibiotics ( It hasn't any method to kill the bacteria )
May be chromosomal or plasmid - borne, inducible or constitutive.
B-lactamase inhibitors including clavulanic acid, sulbactam and tazobactam have been developed
Sulbactam has a similar spectrum of activity aganist b-lactamases compared with clavulanic acid, but is more potent
Clavulanic acid has more protection against enzymes that are primarily active against penicillins compared with its activity against cephalosporins
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Isolated from streptomyces species
It cant used alone
Clavulanic acid + Amoxicillin given orally
Ticarcillin+ Clavulanic acid given parenterally
We cant make combination of Meropenem with Clavulanic acid because Meropenem isn't need it
No answer is correct
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Penicillin
Clavulanic acid
Sulphone
Sulbactam
Tazobactam
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Ophthalmic administration
Nasal administration
Oral administration
Parental administration
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Ophthalmic
Nasal
Orally
Parenterally
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Fermentation from Penicillium mould
Fermentation from Penicillium yeast
Fermentation from Penicillium mould and yeast
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7-ACA are orally active
6-ACA are orally active
7-ACA are orally inactive
6-ACA are orally inactive
No answer is correct
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