antibiotics Flashcards
why are penicillins and cephalosporins called beta lactams? and what is their mechanism?
both antibiotics have a 4 member ring in their structure
they inhibit DD-transpeptidase (aka penicillin binding protein), an enzyme that is essential for cross linking peptidoglycan chains in the bacterial cell wall.
they are bacteriocidal
which enzyme is responsible for catalyzing peptidoglycan binding proteins that create cross links for peptidoglycan
a. transpeptidase
b. glycosyltransferase
c. Beta lactamases
d. transferase
transpeptidase
what is the mechanism of vancomycin?
a. its a beta lactam
b. its produced in nature by actinobacteria
c. it inhibits peptidoglycan formation
d. it inhibits peptidoglycan cross linking
vancomycin is NOT a beta lactam, its produced in nature by actinobacteria, it inhibits peptidoglycan cross linkages
what is the difference between beta lactamase and beta lactamase inhibitors?
beta lactamase is responsible for antibiotic reisstance. they are bacterial enzymes that hydrolyze the beta lactam ring of certin penicillins and/or cephalsporins, which enhance resistance
beta lactamase inhibitors (calvunic acid) prevent and protect penicillins and cephalsporins from being hydrolyzed to revent inactivation.
an enzyme that helps build the peptidoglycan chain
glycosyltransferase
what are the 3 common shapes for bacterium?
cocci, bacilli, and spiral
how is the peptidoglycan layer linked together?
linked by transferase and peptidoglycan is cross linked by peptides
explain the mechanism of aminoglycosides
- they block initiation of the ribosome complex
- they cause the ribosome to misread the mrna
- inhibit translocation (attatchment to a chromosome)
how do chloramphenicol, macrolides, and tetracyclines differ?
chloramphenicol and macrolides bind to the 50S subunit to block transpeptidation (elongation of protein)
tetracyclines bind to the 30S subunit and prevent binding of incoming trna
*note that all of these drugs are protein synthesis inhibitors
why is PABA necessary for bacterial DNA synthesis?
A) PABA is directly incorporated into bacterial DNA as a base.
B) PABA is used to produce purines and pyrimidines needed for DNA replication.
C) PABA modifies bacterial DNA to increase mutation rates.
D) PABA prevents DNA damage by neutralizing free radicals.
PABA is used to produce purines and pyrimidines needed for DNA replication.
Explanation: Bacteria convert PABA into dihydrofolic acid, which is further processed into tetrahydrofolic acid (THF), a key molecule for synthesizing DNA bases (thymidine, adenine, guanine).
How do beta-lactamase inhibitors help combat antibiotic resistance?
A) They bind to bacterial ribosomes, preventing protein synthesis needed for beta-lactamase production
B) They directly kill bacteria, making them more effective than beta-lactam antibiotics alone
C) They inhibit the bacterial enzyme beta-lactamase, preventing it from breaking down beta-lactam antibiotics
D) They increase the bacterial cell wall thickness, making bacteria more susceptible to beta-lactam antibiotics
They inhibit the bacterial enzyme beta-lactamase, preventing it from breaking down beta-lactam antibiotics
Explanation: Beta-lactamase inhibitors (e.g., clavulanic acid, sulbactam, tazobactam) bind irreversibly to beta-lactamases, preventing them from inactivating beta-lactam antibiotics. This restores the effectiveness of antibiotics like amoxicillin and piperacillin.
how does bacterial resistance to beta-lactam antibiotics develop most effectively?
A) By altering the target enzyme structure so that antibiotics cannot bind
B) By increasing the thickness of the bacterial cell wall
C) By reducing the production of peptidoglycan to avoid antibiotic detection
D) By using efflux pumps to remove antibiotics before they reach the cell wall
By altering the target enzyme structure so that antibiotics cannot bind
How do beta-lactamase inhibitors like clavulanic acid enhance the effectiveness of beta-lactam antibiotics?
A) By increasing the permeability of bacterial cell walls to antibiotics
B) By preventing bacterial enzymes from breaking down beta-lactam antibiotics
C) By binding directly to bacterial ribosomes to enhance protein synthesis inhibition
D) By increasing the concentration of peptidoglycan, making bacteria more susceptible
By preventing bacterial enzymes from breaking down beta-lactam antibiotics
What is the relationship between folic acid and PABA in bacterial metabolism?
A) PABA is a breakdown product of folic acid used for energy.
B) PABA is an essential precursor for bacterial folic acid synthesis.
C) PABA inhibits folic acid metabolism to prevent bacterial growth.
D) PABA and folic acid function independently in bacterial metabolism.
PABA is an essential precursor for bacterial folic acid synthesis.
Explanation: Bacteria synthesize folic acid from para-aminobenzoic acid (PABA), which is necessary for producing nucleotides used in DNA replication.
How do folic acid inhibitors like and trimethoprim and sulfonamides work?
A) They mimic PABA and dihydroflouric acid and alter metabolism of PABA
B) They bind directly to bacterial DNA, preventing replication.
C) They break down existing folic acid, depleting bacterial stores.
D) They prevent the absorption of dietary folic acid in bacterial cells.
both trimethoprim and sulfonamides have a similar structure to paba and dihydroflouric acid. these drugs interfere with paba metabolic pathways
a
How do bacteria gain resistance to beta-lactam antibiotics?
A) By modifying the structure of their ribosomes to prevent antibiotic binding
B) By producing enzymes that break the beta-lactam ring, making the antibiotic ineffective
C) By increasing the synthesis of peptidoglycan to counteract the antibiotic’s effects
D) By using efflux pumps to remove beta-lactam antibiotics before they reach their target
aome bacteria producte beta lactamases (penicillinase, cephalosporinase) whichc break the beta lactam ring and render antibiotic acitivities
b
Which of the following best explains how bacteria develop antibiotic resistance?
A) They mutate their DNA or acquire resistance genes, leading to reduced antibiotic effectiveness.
B) They become stronger over time by repeated exposure to antibiotics, similar to how muscles grow with exercise.
C) They store unused antibiotics in their cytoplasm to neutralize future drug effects.
D) They develop protective capsules that make them completely immune to all antibiotics.
They mutate their DNA or acquire resistance genes, leading to reduced antibiotic effectiveness.
Explanation: Bacteria develop resistance through genetic mutations or by acquiring resistance genes via horizontal gene transfer (conjugation, transformation, transduction). This can lead to efflux pumps, altered drug targets, or enzyme production (e.g., beta-lactamases) that inactivate antibiotics
What kind of antibiotics are trimethoprim and sulfonamides
they are folic acid inhibitors that mimic PABA and dihydroflouric acid
