Infectious Diseases - Meds Flashcards

Question

How does penicillin work?

Answer 1

1. penicillins penetrate outer cell layer 2. gets into inner layer that has transpeptidases which build cell walls 3. penicillin's b-lactam ring binds to and inhibits competitively the transpeptidase enzyme (b/c competitive, can overcome intermediate resistance with higher drug dose). 4. cell wall synthesis stopped 5. holes in cell wall, bacteria die (bactericidal) bacteria can create enzymes that break down pencillins - that is why you hear about penicillinase-resistant penicillin = beta lactamase enzymes of bacteria cleave penciillin.

Answer 2

Think of am**o**xicillin (**PO**) and amp**i**cillin (**IV)** as **AMP**ed up peni**cillins**. ## Footnote Imagine amp (stereo amp) in GI tract - this is to help you remember that ampicillin is also good for enterococcus faecalis (Group D strep, which normally colonizes GI, but also causes UTIs, many nosocomial infections (esp. after cephalosporins), etc). Enterococcus needs ampIcillin (IV), b/c it is opportunistic and needs strong stuff. BUT AMOXICILLINS CANNOT RESIST BETA LACTAMASES, so need some extra stuff, like gentamicyn for added oumph. **Amoxicillin/ampicillin HELPSS kill enterococci AND enterobacter. ** **H. I**nfluenza, **E.C**oli, **L**isteria, **P**roteus **M**irabilis, **S**almonella, **S**higella. **GENTAMYCIN helps kill ENTEROBACTER**, so amoxicillin and getnamycin often used together = AMP-GENT combo, since serious infections, say UTIs could be either enterococcus (faecalis) or enterobacter (like E.coli).

Answer 3

* less than 10% of penicillin allergy people have true IgE mediated allergic reation (hives, anaphylaxis, etc) * anaphylaxis risk with PO penicilin = 0.01-0.02% * mortality 0.0015-0.02% * anaphylaxis NOT genetic * 50% of patients loose sensitivity to penicillin in 5 years * 80% of patients loose sensitivity to penicillin in 8 years * if distant reaction (\> 10 yrs) could have a graded penicillin challenge * ampicillin and cephalexin have similar side chains so try not to give * 1% risk with cephalosporins with reported penicillin allergy, 2.5% risk with confirmed pecicillin allergy (less likely to have allergy if 3rd or 4th generation cephalosporin, like ceftriaxone (IV), cefixime (PO), or cefepime (IV-4th) *

Answer 4

**Vancomycin is of glycopeptide class PO or IV** It works by i**nhibiting cell wall synthesis** by a mechanism different from penicillins (beta lactams) - it gets involved in an earlier phase. glycopeptides attach to the end of peptidoglycan precursor units **(short D-alanyl-D-alanine = d-ala-d-ala termini)** - this step is called transglycosylation. precursor is then not released from the carrier and peptidoglycan synthesis stops. Vancomycin resistant enterococci become resistant by not allowing the drug to bind to D-ala-D-ala. **MRSA: good coverage** **give Vancomycin PO for C.difficile infections** **give Vanco for enterococci, pecicillin-resistant Strep, coagulase -ve staph. ** **gram +ves: good coverage** Think D-ala-D-ala = singing in Vancouver Side effects: **Flushin**g: when vancomycin is administered quickly, the **blood pressure can fall because of histamine release. Therefore vancomycin must be administered slowly (usually over 1 hour).** The flushing caused by histamine release has been called red man syndrome and is not an allergy but a predictable response to rapidly administered vanco. **Ototoxicity**: very rare, unless vancomycin is administered with another ototoxic agent, such as aminoglycosides (gentamicin) **Nephrotoxicity**: is rare (6-7%), unless administered with another nephrotoxic agent such as aminoglycoside (gentamicin) Neutropenia: low WBC count possible. If resistant to Vancomycin, can treat with daptomycin - similar mechanism of action (good for VRE).

Answer 5

**gentamicin is of aminoglycosides** class. also tobramycin, streptomycin. they are antibiotics derived from bacteria and inhibit protein synthesis by **irreversibly binding to small ribosomal subunit (30 S ).** **Gentamicin is really good against gram -ve bacteria, and is bacteriostatic. ** **Poorly absorbed in the GI** and so not administered orally, but do c**ollect around proximal tubule in the kidney and cause nephrotoxicity of the drug!** Excreted by kidney, so have to watch for renal dysfunction and change dosage accordingly: monitor GFR. Side effects: **ototoxicity (10%)** thought to damage hair cells in inner ear. **nephrotoicity (up to 10%**) - watch creatinine, if rises stop! usually nephrotoxicity is mild and can be reversed. **REMEMBER AMP -GENT** **Gentamicin was great for gram -ves, like those causing UTIs, pseudomonas, etc so often administered in synergy with ampicillin to get gram + and gram -ves out. ** 10 vacteria: enterococcus faecalis = amp+gent, also used for E.coli.

Answer 6

a**ntibiotic that iinhibit the 23S bacterial ribosome. blocking tthe transfer of the new amino acid onto the growing chain. because of its action on protein synthesis, has thought to be good in toxin-producing infections - ex. GAStrep, like in necrotizing fasciitis. ** ## Footnote **Good for strep** **S. aureus** **MRSA** **anaerobes** **not good for gram negative organism** **predisposes to C.diff - the worst drug to predispose to C.diff**

Infectious Diseases - Meds Flashcards

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