This document summarizes various classes of antibiotics including their mechanisms of action, resistance mechanisms, pharmacokinetics and uses. It discusses β-lactam antibiotics such as penicillins that inhibit bacterial cell wall synthesis, aminoglycosides that inhibit protein synthesis, fluoroquinolones that inhibit DNA replication, sulfonamides that inhibit folate synthesis, and others. Each antibiotic class is described in terms of its antibacterial spectrum, route of administration, and common side effects. The document provides a comprehensive overview of major antibiotic classes and properties.
Dear students, you can watch the Complete chapter of antibiotics in these videos as per PCI syllabus
1)Antibiotics-History & Introduction
https://www.youtube.com/watch?v=xdKch...
2)Easy Learning Of Chapter - β-Lactam antibiotics-Cephalosporin
https://www.youtube.com/watch?v=D7b5g...
3)Learn Complete Topic -β-Lactam antibiotics(Penicillin) in Medicinal Chemistry
https://www.youtube.com/watch?v=qXQ3S...
Dear students, you can watch the Complete chapter of antibiotics in these videos as per PCI syllabus
1)Antibiotics-History & Introduction
https://www.youtube.com/watch?v=xdKch...
2)Easy Learning Of Chapter - β-Lactam antibiotics-Cephalosporin
https://www.youtube.com/watch?v=D7b5g...
3)Learn Complete Topic -β-Lactam antibiotics(Penicillin) in Medicinal Chemistry
https://www.youtube.com/watch?v=qXQ3S...
The all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
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https://pubrica.com/academy/case-study-or-series/how-many-patients-does-case-series-should-have-in-comparison-to-case-reports/
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1. M.A.A.Al-Maqrashi
Antibiotic
MOA & Resistance
mechanism
Pharmacokinetics & Uses A.E
InhibitorsofCellWallSynthesis
β-Lactam
[Penicillins]
Natural
penicillin G
penicillin V
±
cidial
interfere with the last step of
bacterial cell wall synthesis
(transpeptidation or cross-
linkage), resulting in less stable
membrane:
- covalently bind to the active
site of PBPs → inhibit the
transpeptidation reaction
and stop peptidoglycan
synthesis.
Penicillin-binding proteins
[PBP]:
- are membrane proteins that
cross-link peptidoglycan.
- removes the terminal
alanine in the process of
forming a cross-link with a
nearby peptide.
Resistance:
- β lactamase
- modification of PBP
[MRSA+MRSE]
- Impaired penetration of
drug to target PBPs [G-
]
- antibiotic efflux
- Penicillin G:
- inactivated by gastric juice
& low oral absorbtion.
- IV
- Depot forms: IM
[e.g. Procaine penicillin G
and benzathine penicillin G]
- Penicillin V: orally
- incompletely absorbed after oral
administration, and they reach
the intestine in sufficient amounts
to affect the composition of the
intestinal flora.
- cross the placental barrier
- no penetration into bone or CSF
[unless they are inflamed]
- Penicillin levels in the prostate &
eye are insufficient
- excreted in urine & breast milk
- effective against rapidly growing
organisms that synthesize a
peptidoglycan cell wall.
- hypersensitivity
[maculopapular rash,
angioedema, anaphylactic
shock etc.]
- GIT upsets
[nausea, vomiting, diarrhea,
pseudomembranous colitis.]
- Nephritis
- Neurotoxicity [even
epilepsy]
- Hematologic toxicities
[neutropenia]
Anti-staphyl.C
penicillins
methicilli,
cloxacillin
+
- IM or IV
- Penicillinase-producing S.
aureus.
- Penicillinase-producing S.
epidermis.
Broad spectrum
Aminopenicillins
(e.g. amoxicillin)
-
- Orally
- Similar to that of penicillin G
– e.g. Haemophilus
influenzae, Escherichia coli,
and Proteus mirabilis
Anti-
pseudomonal
piperacillin
-
- IM or IV
- against Pseudomonas
aeruginosa [Bacilli]
[Cephalosporins]
1st
g.: cephalexin
±
cidial
- have same mode of action as
penicillins and they are
affected by same resistant
methods.
- IV or IM
- Higher generations increase efficiency against gram -ve
- Ceftaroline: 5th gen. against MRSA (S. aureus)
- Allergy
- Thrombophlebitis [after IV
injection]
- Renal toxicity.
- Hypo-prothrombinemia and
bleeding disorders
2nd
g.: cefoxitin
3rd
g.:
Cefotaxime
4th
g.: Cefopime
[β-lactamase inhibitors]
Clavulanic acid
tazobactam
- Resemble β-lactam molecules but very weak antibacterial action.
- Available only in a fixed-dose combination with penicillins and cephalosporins.
- potent inhibitors of most of bacterial β lactamases → protect hydrolyzable penicillins from inactivation
Penicillin-β-lactamase inhibitor combinations:
- empiric therapy for infections caused by a wide range of potential pathogens.
- treatment of mixed aerobic and anaerobic infections, such as intra-abdominal infections.
- Amoxicillin + clavulanic acid [o-amoxiclav]
- Piperacillin + Tazobactam: the combination is must
2. M.A.A.Al-Maqrashi
Cont.ICWS
[Glycopeptides]
Vancomycine
+
cidial
- Binds to the terminal two D-
alanine residues of
pentapeptide → inhibiting
peptidoglycan backbone
elongations.
Resistance:
- Replacement of D-Ala by D-
lactate in resistant
organisms.
- Given by slow IV infusion (not absorbed orally) for systemic
infections
- Oral vancomycin is limited to treatment for antibiotic-associated
colitis by Clostridium difficile [anaerobic bacteria]
- Used in the treatment of MRSA, MRSE, enterococcal infections
- Red Man Syndrome
- shock from histamine
release associate with rapid
infusion.
- Ototoxicity
- Nephrotoxicity
Inhibitorsofproteinsynthesis
[Macrolides]
Erythromycin
+
static
- Bind irreversibly to a site on
the 50S subunit of the
bacterial ribosome → inhibits
the translocation step
- against many of the same organisms as penicillin G
- An alternative to penicillin in allergic individuals
- GIT disturbance.
- Cholestatic jaundice.
- Ototoxicity.
[Aminoglycosides]
Gentamycin
-
cidial
- irreversible inhibitors of
protein synthesis.
- Passive diffusion via porin
channels across the outer
membrane.
- Actively transported across
the cell membrane into the
cytoplasm by an oxygen-
dependent process.
- they bind the 30S subunit:
- interfere with assembly of
the functional ribosomal
- misread the genetic code
- Block of translocation on
mRNA.
- Concentration dependent.
- has postantibiotic effect.
- mostly used against aerobic G-
bacteria including Pseudomonas
aeruginosa.
- Their structure prevents adequate oral absorption.
- Must be given parenterally to achieve adequate serum levels.
- Mostly, Combined with a β-lactam antibiotic to:
- extend coverage to include potential gram-positive pathogens.
- take advantage of the synergism between these two classes of
drugs.
- Streptomycin is used as a second-line agent for treatment of
tuberculosis.
- Ototoxicity:
- deafness.
- vertigo and loss of
balance.
- Nephrotoxicity.
- Neuromuscular paralysis
[decrease in release of Ach.]
[Tetracyclines]
Tetracycline
±
static
- Bind reversibly to the 30S
subunit:
- Blocking the binding of
aminoacyl-tRNA to the
acceptor site on the
mRNA-ribosome complex.
- This prevents addition of
amino acids to the growing
peptide.
- broad-spectrum antibiotics
- Against Rickettsia, Chlamydia, Mycoplasma.
- used in combination regimens to treat gastric and duodenal ulcer
disease caused by Helicobacter pylori
- GIT upsets
[nausea, vomiting and
diarrhea.]
- Discoloration of teeth in
growing children.
- Phototoxicity
[sunburn occurs when a
patient receiving a
tetracycline is exposed to
sun.]
- Nephrotoxicity.
- Superinfections
[overgrowth with Candida or
resistant staphylococci]
3. M.A.A.Al-Maqrashi
Cont.IPS
[Chloramphenicol] ±
static
- potent inhibitor of microbial
protein -synthesis.
- binds reversibly to the 50S
subunit of the bacterial
ribosome and inhibits
peptide bond formation
(step 2).
- broad-spectrum antibiotic: against both aerobic and anaerobic
- Against Rickettsiae
- toxic: it is restrictly used.
- GIT upset:
[nausea, vomiting, diarrhea.]
- Anemia: [aplastic anemia.]
- Gray baby syndrome in
neonates:
[newborn infants lack an
effective glucuronic acid
conjugation mechanism for
the degradation and
detoxification of
chloramphenicol.]
- Inhibits hepatic microsomal
enzymes.
ActingonNucleicAcid
[Fluoroquinolones]
1st
g.: Nalidixic acid
±
cidial
- Enter the bacteria by passive diffusion through porins in the outer membrane.
- They inhibit the replication of bacterial DNA by interfering with the action of DNA gyrase
(topoisomerase II) and topoisomerase IV during bacterial growth and reproduction.
- Binding of the quinolone to both enzymes and the DNA forms a complex that can cause cell death by
inducing cleavage of the DNA.
Resistance:
- mutation of the target
- ↓porin molecules
- active transport out.
- Higher generations increase efficiency against gram +ve
- GIT upset:
[nausea, vomiting, diarrhea.]
- CNS:
[headache, dizziness, light-
headedness.]
- Phototoxicity.
- Connective tissue problems:
[tendinitis or tendon
rupture.]
2nd
g.:
Ciprofloxacin
Norflaxacin
Oflaxicin
3rd
g.: Cefotaxime
4th
g.: Cefopime
[Sulfonamides]
Sulfadiazine
±
static
- inhibit the synthesis of
bacterial dihydrofolic
Acid ← compete with PABA for
dihydropteroate synthase.
- synthetic analogs of PABA.
- Only organisms that synthetize their folate requirements de novo
are sensitive to the sulfonamides.
- inhibit Nocardia sp, Chlamydia trachomatis, and some protozoa.
- Crystalluria:
[sulfonamides can precipitate
in urine, especially at neutral
or acid pH. ]
- Hypersensitivity.
- Hemopoietic disturbances:
[hemolytic anemia in G6PD
deficiency.]
- Kernicterus:
[occur in newborns,
sulfonamides can displace
bilirubin from binding sites on
serum albumin → Bilirubin
pass into the CNS (BBB is not
fully developed) ]
4. M.A.A.Al-Maqrashi
Cont.ANA
[Trimethoprim]
static
- Selectively inhibits bacterial
dihydrofolic acid reductase
- less efficient inhibitor of mammalian dihydrofolic acid reductase.
- Sulfonamide (PABA competitor) + Trimethoprim (dihydrofolate reductase inhibitor) = bactericidal
synergistic activity: treating UTI and respiratory tract infections.
[Metronidazole]
cidial
- inflicts breaks in the DNA
itself.
- active against a wide range of anaerobes. [e.g. Clostridium difficile]
- a second antimicrobial (eg, β-lactam) is usually added to cover aerobic and facultative bacteria.
[Rifampin] ±
cidial
- Inhibits the synthesis of RNA
from DNA by inhibiting RNA
polymerase.
- Active against most Gram-positive bacteria and selected Gram-negative organisms.
- Used to treat tuberculosis.