Unit 5 NURS 316 Test Questions and
Correct Answers
Normal Microbes Beneficial Effects ✅competing for nutrients
produced substances that affect invading microbes
affecting growth conditions
Inhibition of cell wall synthesis ✅penecillins
cephalosporins
carbapenems
misc.
Inhibition of protein synthesis (Translation) ✅Aminoglycosides
Tetracyclines
Oxazolidinones
Macrolides
Disruption of plasma membrane ✅azoles and polyenes
Inhibition of nucleic acid synthesis (replication/transcription) ✅floroquinolones
rifampicin
inihibition of metabolic pathways ✅sulfonamides
trimethoprim
Action of B-lactam antibiotics ✅b-lactam group of penicillin binds to inactivated
transpeptidases preventing peptidoglycan synthesis leading to cell destruction
Penecillin G ✅natural penicillin, required injection
Penicillin V ✅natural penicillin oral admin
Cephalosporins ✅sephalothin, cefixime
Oxacillin and Methacillin ✅semisynthetic penecillin
modification to prevent cleavage by B-lactamases
Chloramphenicol MOA ✅Blocks peptidyltransferase at 50S ribosomal subunit and
inhibitor peptide bond
Tetracycline ✅interferes with attachment of tRNA to mRNA-ribosome complex
, Streptomycin ✅changes shape of the 30S potion causing code on mRNA to be read
incorrectly
Quinolone and fluoroquinolones ✅inhibit DNA gyrase required for DNA replication
Trimethoprim/Sulfamethoxazole ✅inhibits bacteria enzyme dihydropteroate synthetase
that is essential for bacterial metabolism
Pharmacotherapy of TB ✅Initial phase - active cells are killed
continuation phase - dormant mycobacteria are killed and may last for 6 to 12 months
Isoniazid Función ✅M. Tuberculosis prophylaxis and treatment
first line drugs
Isoniazid MOA ✅inhibit synthesis of mycelia acid, better for rapidly dividing organisms
bactericidal and bacteriostatic for dormant mycobacteria
persister cells ✅microbes with genetic characteristics allowing for their survival when
exposed to an antibiotic
Superbugs ✅bacteria that are resistant to large numbers of antibiotics
Major mechanisms of antibiotic resistance ✅-drug inactivation or modification
-prevention of access to the drug target site
-alteration of the drug target side
-increasing active efflux to pump the drugs out of cells
Transformation ✅bacteria takes up DNA from environment
Transduction ✅donor DNA packaged in bacteriophage infects bacterium
Conjugation ✅donor bactéria transfer DNA to recipient by mating
Methicillin resistant bacteria mechanism ✅altered transpeptidased which are still active
for cross-linking but no longer recognized by beta-lactam
Vancomycin MOA ✅last line antibiotic for serious gram negative infections and binds
to the terminal amino residues of the NAM/NAG=peptide subunits
Vancomycin mechanisms of resistance ✅alteration to the terminal amino acid residues
of the NAM/NAG peptide subunits that vancomycin normally binds to
viral replication steps ✅-attachment
Correct Answers
Normal Microbes Beneficial Effects ✅competing for nutrients
produced substances that affect invading microbes
affecting growth conditions
Inhibition of cell wall synthesis ✅penecillins
cephalosporins
carbapenems
misc.
Inhibition of protein synthesis (Translation) ✅Aminoglycosides
Tetracyclines
Oxazolidinones
Macrolides
Disruption of plasma membrane ✅azoles and polyenes
Inhibition of nucleic acid synthesis (replication/transcription) ✅floroquinolones
rifampicin
inihibition of metabolic pathways ✅sulfonamides
trimethoprim
Action of B-lactam antibiotics ✅b-lactam group of penicillin binds to inactivated
transpeptidases preventing peptidoglycan synthesis leading to cell destruction
Penecillin G ✅natural penicillin, required injection
Penicillin V ✅natural penicillin oral admin
Cephalosporins ✅sephalothin, cefixime
Oxacillin and Methacillin ✅semisynthetic penecillin
modification to prevent cleavage by B-lactamases
Chloramphenicol MOA ✅Blocks peptidyltransferase at 50S ribosomal subunit and
inhibitor peptide bond
Tetracycline ✅interferes with attachment of tRNA to mRNA-ribosome complex
, Streptomycin ✅changes shape of the 30S potion causing code on mRNA to be read
incorrectly
Quinolone and fluoroquinolones ✅inhibit DNA gyrase required for DNA replication
Trimethoprim/Sulfamethoxazole ✅inhibits bacteria enzyme dihydropteroate synthetase
that is essential for bacterial metabolism
Pharmacotherapy of TB ✅Initial phase - active cells are killed
continuation phase - dormant mycobacteria are killed and may last for 6 to 12 months
Isoniazid Función ✅M. Tuberculosis prophylaxis and treatment
first line drugs
Isoniazid MOA ✅inhibit synthesis of mycelia acid, better for rapidly dividing organisms
bactericidal and bacteriostatic for dormant mycobacteria
persister cells ✅microbes with genetic characteristics allowing for their survival when
exposed to an antibiotic
Superbugs ✅bacteria that are resistant to large numbers of antibiotics
Major mechanisms of antibiotic resistance ✅-drug inactivation or modification
-prevention of access to the drug target site
-alteration of the drug target side
-increasing active efflux to pump the drugs out of cells
Transformation ✅bacteria takes up DNA from environment
Transduction ✅donor DNA packaged in bacteriophage infects bacterium
Conjugation ✅donor bactéria transfer DNA to recipient by mating
Methicillin resistant bacteria mechanism ✅altered transpeptidased which are still active
for cross-linking but no longer recognized by beta-lactam
Vancomycin MOA ✅last line antibiotic for serious gram negative infections and binds
to the terminal amino residues of the NAM/NAG=peptide subunits
Vancomycin mechanisms of resistance ✅alteration to the terminal amino acid residues
of the NAM/NAG peptide subunits that vancomycin normally binds to
viral replication steps ✅-attachment
