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MED 2207-Antimicrobials Self-Assessment Answers
MED 2207-Antimicrobials Self-Assessment Answers
MED 2207-Antimicrobials Self-Assessment Answers
5.
6.
7.
8.
when treating a sore throat in a patient with a history of anaphylactic reaction to another
beta-lactam antibiotic.
C. Good choice. This is chemically different type of antibiotic (a lincosamide) that inhibts
protein synthesis, and is effective against beta-lactamase producing bacteria such as
group A strep. The objective of this question was for you to identify a drug that would
NOT cross-react with a beta-lactam in a patient with a history of beta-lactam induced
anaphylaxis.
D. This is a carbapenem. Carbapenems are structurally related to beta-lactams, and do
show asmall incidence (<1%) of cross-reactivity in those patients with a truely
confirmed sensitivity to beta-lactams. Treatment with a carbapenem is considered not
advisable (they are contraindicated) in patients with a history of anaphylatoid reactions to
beta-lactam antibiotics.
E. This is a type of penicillin resistant to beta-lactamases produced by most
staphlococci. Treatment with nafcillin is not advisable in a patient with a history of
anaphylatic reaction to a beta-lactam antibiotic.
A. Correct! Carbapenems (imipenem, meropenem, doripenem, ertapenem) currently
produce the best outcomes in terms of bacteriologic clearance. Carbapenems are one of
the "drugs of last resort" against bacteria resistant to multiple antibiotics. ESBLs are
resistant to the other answer options listed.
B. Not the best choice listed. These penicillins (ampicillin, amoxicillin, piperacillin) have
been given this classification based upon their ability to penetrate through the outer
membrane of gram-negative bacteria, providing greater activity against these organisms
compared to the natural (narrow spectrum) penicllins (Pen G & Pen V). The combination
of an extended pencillin plus a beta-lactamase inhibitor (e.g. piperacillin + tazobactam)
has been used to treat ESBL infections in the past, but due to the development of
resistance, the outcomes are not typically as favorable as when using another drug
option listed here.
C. ESBLs will inactivate all cephalosporins.
D. ESBLs will inactivate monobactams.
E. ESBLs will inactivate all narrow spectrum penicillins (e.g. Pen V & Pen G).
A. This penicillin is given orally, and would not be the most likely candidate for producing
this type of reaction. Possible, yes, but likely, no.
B. This monobactam can occassionally produce skin rashes, but this reaction sounds a
bit different. There is a more likely answer option.
C. This antibiotic is known for affecting skeletal muscle, producing myalgia & weakness
with increased CPK levels. But this is not what is being observed here.
D. Not likely. This drug can inhibit monoamine oxidase (MAO) and produce a serotoninexcess or tyramine-excess type reaction when drugs or foods are consumed that elevate
these compounds. However, this reaction would elevate blood pressure, and would not
cause the flushing type response.
E. Correct! The signs & symptoms described are those commonly referred to as "red
man syndrome" or sometimes "red neck syndrome". These symptoms result from
histamine release when vancomycin is infused too rapidly. Remember this one. Its a
classic side effect for a relatively commonly used drug.
A. Correct! Drug A has the largest "zone of inhibition". As the drug diffuses out of the
disc, the concentration decreases as a function of distance. A larger zone of inhibition
indicates that the antibiotic is inhibiting bacterial growth even at low concentrations.
Small zones of inhibition indicate relative resistance to the antibiotic. Absence of a zone
of inhibition indicates total resistance (lack of drug effect).
A. these drugs inhibit the 30 S ribosomal subunit at different locations.
B. No, these drugs are dissimilar and have different mechanisms of action, including
effects on the 50S ribosome (chloramphenicol), RNA polymerase (rifamycins), and DNA
gyrase (fluoroquinolones).
C. Correct! This mechanism of resistance is of great clinical relevance when considering
the appropriate therapy for infections by S. aureus, including MRSA.
D. No. These drugs have different mechanisms of action, including the bacterial cell
membrane (daptomycin & polymyxins) and folic acid synthesis (sulfonamides).
E. No. These drugs have different mechanisms of action including causing DNA strand
breaks (metronidazole), tRNA synthetase (mupirocin), and biosynthesis of mycolic acids
(isoniazid)
9. DF
10. A. Aminoglycosides are notorious for having 3 major types of side effects: 1)
Ototoxicity - both reversible auditory & irreversible vestibular toxicity due to damage of
hair cells; 2) nephrotoxicity - caused by damage to the renal proximal convoluted
tubule, and 3) neuromuscular blockade - more rare & most commonly seen in patients
with myasthenia gravis.
B. No. While fluroquinolones can cause QT prolongation, they are not protein synthesis
inhibitors, and aren't known for P-450 interactions.
C. Correct! These dose-dependent drug effects are more commonly observed with
erythromycin (especially when its given IV), followed by clarithromycin.
D. No. These drugs interfere with RNA polymerase, and are notorious inducers of P-450
(mainly rifampin). They don't inhibit P-450, and aren't known for their cardiac effects.
E. No. These drugs are known for their effects on bone and teeth, and for causing some
degree of increased photosensitivity.