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Flashcards in Micro 14 - Other Cell Wall Inhibitors Deck (22)
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What is the mechanism of action of Aztreonam?

A monocylic beta-lactam; inhibtis cell synthesis by binding to penicillin-binding protein 3.


What are the clinical uses for Aztreonam?

Use for patients with penicillin-allergies and those with renal insufficiency. Synergistic with Aminoglycosides. Covers a lot of G(-), E.coli, Klebsiella, Pseudomonas, Serratia. No activity against G(+) or anaerobes. Pretty nontoxic and no cross-sensitivity with penicillins.


What are the 4 big carbapenems?

Imipenem/cilastatin, meropenem, ertapenem, doripenem.


What is the mechanism of action of carbapenems?

They work by binding to penicillin-binding proteins.


What is the mechanism of cilastatin and why is it that any carbapenem is always given in conjunction with it?

Because it inhibits renal dehydropeptidase-1; this causes decrease inactivation of carbapenem in the renal tubules.


What are the clinical uses for carbapenems?

It is a broad spectrum; G(+ and -) anaerobes, pseudomonas. It is used in empiric treatment of life-threatening infections. However, it does not cover MRSA (combine with vancomycin).


What are the benefits of using Meropenem compared to other carbapenems?

It decreases risk of seizures, and it is not inactivated in the renal tubules.


What are three side effects of carbapenems?

GI distress, Skin rash, some CNS toxicity (imipenem).


What is the mechanism of action of vancomycin?

It inhibits cell wall synthesis by inhibiting cell wall mucopeptide formation by binding to the D-ala D-ala moieties of the cell wall precursors; inhibiting cell wall glycopeptide polymerization. It is also bacteriocidal.


What are the clinical uses of vancomycin?

Only covers G(+). Very effective in MRSA and some enterococci. Can be used orally against clostridium difficile. Staph epidermidis as well.


What are the side effects of Vancomycin?

Nephrotoxicity, Ototoxicity, Thrombophlebitis.


What is Red Man syndrome?

Caused by vancomycin, It is diffuse flushing of the whole body, caused by non-specific mast cell degranulation. Treatment is pretreat with antihistamines, slow down the infusion and restart the vancomycin once the syndrome is gone.


Lewis Notes. Match the following to Aztreonam, Carbapenems, Vancomycin: Bind D-ala D-ala, PBP-3, PBP, G(-) only, MRSA & enterococci, No renal involvement, Nephrotoxicity, Thrombophlebitis, Broad spectrum.

Aztreonam: PBP-3, G(-) only, No renal involvement. Carbapenems: PBP, Broad spectrum. Vancomycin: Bind to D-ala D-ala, MRSA & enterococci, Nephrotoxicity, Thrombophlebitis.


What cell wall inhibitor can cause "red man" syndrome?



What cell wall inhibitor is the "aminoglycoside pretender"?



What cell wall inhibitor is the inpatient treatment for MRSA?



What cell wall inhibitor is used in hospitalized patient with new G(+) cocci clusters in blood?



What cell wall inhibitor is used in the treatment for C.diff colitis?



What cell wall inhibitor is used in broad spectrum coverage for appendicitis?

Imipenem/cilastatin or meropenem.


What cell wall inhibitor is effective against Pseudomonas?

Cefepime, Aztreonam, Carbapenems, Carboxpenicillins (eg. ticarcillin).


How does an organism develop resistance to vancomycin?

Change in the aminoacid sequence. When the original (D-ala D-ala) changes to D-ala D-lac.


A patient is receiving an IV infusion of an antibiotic and the nurse calls you when his face becomes flushed 15 minutes after the infusion started. What is the treatment for this patient?

Stopping the vancomycin and giving an antihistamine (diphenhydramine). Then restart the infusion at a slower rate.