miscellaneous beta lactams and other inhibitors of cell wall synthesis Flashcards

1
Q

what is a monobactam active against G- aerobes?

A

aztreonam

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2
Q

which drug’s mechanism is binding to penicillin-binding-protein-3 (PBP-3) of G- bacteria?

A

aztreonam

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3
Q

aztreonam is given via ____ and is excreted _____ in urine

A

IV, unchanged

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4
Q

which drug is given as IV for MRSA or MSSA if allergic to beta-lactams?

A

vancomycin

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5
Q

when given orally, which drug that’s not normally absorbed orally is used for local action for pseudomembranous colitis from C. diff?

A

vancomycin

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6
Q

which drug’s mechanism is via binding to D-ala-D-ala terminus to prevent the removal of terminal D-ala of the pentapeptide chain attached to N-acetylmuramic acid residues of peptidoglycan?

A

vancomycin

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7
Q

ototoxicity, nephrotoxicity, and red man syndrome are side effects of which drug that inhibits cell wall synthesis?

A

vancomycin

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8
Q

what is red man syndrome’s mechanism and outcome?

A

histamine is released, causing vasodilation and a decrease in BP (hypotension) which leads to reflexive tachycardia to compensate and sometimes ends in shock. flushing of upper body and face also occurs

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9
Q

is vancomycin static or cidal?

A

static for G+ cocci and cidal for gram + rods

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10
Q

what is a cidal lipoglycopeptide for G+ skin infections that

  1. binds to D-ala-D-ala to inhibit cross linking
  2. disrupts bacterial membrane potential and increases membrane potential to cause cell lysis?
A

telavancin

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11
Q

what are the side effects of telavancin?

A

NVD, taste disturbance, foamy urine, could be teratogenic in pregnant woman

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12
Q

what lipoglycopeptide is used for ABSSSI’s from G+ organisms including MRSA that

  1. inhibits polymerization
  2. inhibibing crosslinking
  3. disrupting membrane integrity to increase permeability and cause cell lysis?
A

oritavancin

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13
Q

side effects of oritavancin?

A

NVD, headache, limb and SQ abscesses, C. diff and induced colitis

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14
Q

which drug is contraindicated with IV unfractionated heparin (coagulant) for 48 hours after administration due to aPTT test remaining falsely elevated?

A

oritavancin

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15
Q

what is a cidal semisynthetic lipoglycopeptide for ABSSI that has same mechanism as vancomycin?

A

Dalbavancin

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16
Q

side effects for dalbavancin?

A

nausea, diarrhea, headache

17
Q

what drug is cidal vs various G+ cocci and bacilli rods that works by preventing dephosphorylation of bactoprenol carrier (which when dephosphorylated, attaches NAG/NAM to growing peptidoglycan chain), thus inhibiting cell wall synthesis?

A

bacitracin

18
Q

what drug inhibits enolpyruvate transferase, blocking the addition of phosphoenolpyruvate to UDP-N-acetylglucosamine, the second step in synthesis of park nucleotide leading to inhibition of cell wall synthesis?

A

fosfomycin

19
Q

what class of drugs are two amino sugars attached in glycosidic links to an aminocyclitol ring?

A

aminoglycosides

20
Q

what class of drugs are cidal, very polar polycations usually given IV, or sometimes given orally to clean out the bowel?

A

aminoglycosides

21
Q

what class of drugs works by flowing down their concentration gradient to enter G- bacteria through porin channels to

a) inhibit initiation of protein synthesis
b) cause misreading of mRNA, creating faulty proteins
c) cause premature termination of protein synthesis

A

aminoglycosides

22
Q

are aminoglycosides effective against anaerobes and why?

A

no b/c anaerobes don’t have an electron transport chain for aminoglycosides to pass through to disrupt the cell

23
Q

which class of drugs can cause post-antibiotic effects in G-rods and how?

A

aminoglycosides- by breaking up polysomes into non-functional monosomes that can continue to suppress bacterial growth and cause cell death long after drug falls below minimal inhibitor concentration

24
Q

what class of drug mostly for G- organisms can be used with B-lactams for synergism and G+ coverage? what’s the mechanism for synergism?

A

aminoglycosides, B-lactams inhibit cell wall synthesis and thus facilitate penetration of aminoglycosides

25
Q

aminoglycosides attain their highest levels in?

A

renal cortex causing reversible nephrotoxicity and endolymph of inner ear causing irreversible ototoxicity

26
Q

ototoxicity can result in what two things?

A

Auditory Sx and vestibular Sx

27
Q

which rx’s can accumulate in fetal plasma leading to neonatal ototoxicity?

A

aminoglycosides

28
Q

what are the GI drugs for G- coverage?

A

neomycin (used for bowel surgery) and paromomycin and they are both aminoglycosides

29
Q

what two drugs are interchangeable and used for burns, wounds, and ophthalmic for G- coverage?

A

gentamicin and tobramycin-both aminoglycosides

30
Q

what is used for nosocomial infections that are resistant to gentamicin and tobranycin?

A

amikacin

31
Q

what drug is gender specific for uncomplicated UTI’s in women?

A

fosfomycin

32
Q

aminoglycosides are generally given ____x a day and why?

A

1, b/c of significant post-antibiotic effect

33
Q

what does the cockcroft-gault formula give you and what do you need to find it?

A

clearance (how much blood volume of creatinine is cleared per minute) and you need to know the pt’s age, lean wt, and serum creatinine levels

34
Q

true or false: the peak and trough levels for Gent/tobra and amikacin are similar.

A

false! they are significantly different

35
Q

what drug class should not be used in conjunction with a neuromuscular blocker during anesthesia and why?

A

aminoglycosides b/c it can cause neuromuscular block leading to respiratory paralysis

36
Q

what is the mechanism for neuromuscular block?

A

aminoglycosides block calcium uptake, thus decreasing ACh released, and it also blocks ACh receptors

37
Q

what are alternatives when taking neuromuscular blockers?

A

giving IV calcium to increase the uptake of ca or giving neostigmine instead of aminoglycosides (neostigmine is a AChase inhibitor that increases ACh levels which stimulates respiratory muscles

38
Q

what should you avoid giving to pts with myasthenia gravis and why?

A

aminoglycosides b/c myasthenia gravis is an autoimmune disease with an antibody against nicotinic receptors at the neuromuscular junction, creating extreme muscle weakness. aminoglycosides can also block the receptor exacerbating the condition