Exam 2: Inhibitor Of Cell Wall Synthesis 2 Flashcards

1
Q

What type of drug are cephalosporins and what is their mechanism?

A

They are B-lactams and they inhibit cell wall synthesis

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2
Q

What is the mechanism of action for monobactams?

A

Inhibitors of cell wall synthesis

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3
Q

What type of drug is Azetreonam?

A

Monobactam

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4
Q

What type of drugs are imipenem, meropenem, and ertapenem?

A

Carbapenems

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5
Q

What are the two first generation cephalosporins and how are they administered?

A

Cefazolin (ancef)- IM or IV

Cephalexin (Keflex)- Oral

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6
Q

What are the three second generation cephalosporins and how are they administered?

A

Cefaclor (ceclor) -Oral

Cefuroxime (Zinacef) - IM or IV

Cefprozil (cefzil) - Oral

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7
Q

What are the four third generation cephalosporins and how are they administered?

A

Ceftriaxone (rocephin)- IM or IV

Cefixime (Suprax) - Oral

Cefotaxime sodium (claforan) -IM or IV

Ceftazidime (Fortaz) -IM or IV

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8
Q

What is the fourth generation Cephalosporin and how is it administered?

A

Cefepime (maxipime) - IV

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9
Q

What is the fifth generation cephalosporin and how is it administered?

A

Ceftaroline (Teflaro)-IV

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10
Q

What is the advantage that cephalosporins have over penicillins?

A

They have 7 methyl groups with increases their resistance to B-lactamases

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11
Q

What is the DOC for surgical prophylaxis?

A

Cefazolin (first generation cephalosporin)

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12
Q

What are first generation cephalosporins effective against?

A

They have good activity against G+ bacteria and relatively moderate activity against G- organisms

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13
Q

How are first generation cephalosporins eliminated?

A

Renal excretion

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14
Q

Are E. Coli, klebsiella, and proteus G- or G+?

A

G-

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15
Q

What are second generation cephalosporins effective against?

A

When compared to first generation cephalosporins, the have lower activity against G+, but increased activity against G-.

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16
Q

What are the two generations of cephalosporins that are broad spectrum?

A

third and fourth generation

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17
Q

How are second generation cephalosporins eliminated?

A

Renal excretion

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18
Q

What cephalosporins have good CNS penetration and what generation are they in?

A

Ceftriaxone (rocephin) and cefotaxime sodium (Clarforan)

Third generation cephalosporins

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19
Q

What is the DOC used to treat Neisseria Gonorrhoeae?

A

Ceftriaxone (Rocephin)

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20
Q

What are the third generation cephalosporins effective against?

A

They are less active against G+, but much more active against Enterobacteriaceae (penicillinase producing strains)

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21
Q

What is the contraindication for third generation cephalosporins and why?

A

-Neonates

Ceftriaxone and bilirubin are very highly protein bound. Ceftriaxone can displace bilirubin and cause jaundice

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22
Q

What cephalosporin is used to treat pseudomonas aeruginosa?

A

Ceftazidime combined with aminoglycosides.

Both however are renal toxic, so this is not the first choice.

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23
Q

What generation of cephalosporins have the broadest coverage?

A

4th generation

Cefepime (Maxipime)

24
Q

Which cephalosporins is the best choice for empiric treatment?

A

Cefepime (maxipime)

It has the broadest coverage

25
Q

What are the 5th generation cephalosporins effective against?

A

They have no antipseudomonal activity, but has both G- and G+ activity.

Can be used for MRSA and VRSA coverage- The only B-lactam active against MRSA

26
Q

How do 5th generation cephalosporins (ceftaroline Fosamil) work?

A

Ceftaroline can bind to PBP2A with very high affinity (this is the mutated PBP that other B-lactamase cannot bind to)

27
Q

What is the DOC for moraxella catarrhalis infections?

A

Second or third generation cephalosporins

28
Q

What is the DOC for E. Coli, Klebsiella, and proteus infections?

A

First or second generation cephalosporins

29
Q

What is the DOC for salmonella?

A

Third generation cephalosporins

30
Q

What is the DOC for penicillin resistance streptococcus pneumoniae?

A

Ceftriaxone

31
Q

What is the DOC for late disease Borrelia Burgdorferi infections?

A

Ceftriaxone

32
Q

What kind of reaction can happen if a patient drinks alcohol while also taking a cephalosporin?

A

Disulfiram-like reaction

Only happens with patient noncompliance

33
Q

What type of drug do cephalosporins have cross sensitivity with?

A

Penicillins (10% cross sensitivity)

34
Q

What are monobactrams effective against?

A

Only active against aerobic G- rods including pseudomonas, Serratia, klebsiella, and proteus.

No activity against G+ or anaerobes

35
Q

Why are monobactrams a good choice for patients allergic to penicillin?

A

It has no cross sensitivity with other B-lactams

36
Q

What must imipenem be give with and why?

A

Imipenem is rapidly inactivated by renal tubule dihydropeptidases and much be give Cilastatin, a dihydropeptidase inhibitor

37
Q

What are imipenem and meropenem effective against?

A

They have broad spectrum activity including anaerobes, G+, and G- activity (good for mixed infections)

38
Q

Can Imipenem and meropenem be broke down by B-lactamases?

A

No

39
Q

What does imipenem commonly cause and with who should you have caution prescribing this to?

A

Imipenem can cause seizures and should be used cautiously in patients with renal failure, brain lesions, head trauma, or a history of CNS disorders

40
Q

What is the DOC for B-lactamase producing Enterobacter infections?

A

Imipenem (superior activity) or meropenem

41
Q

What is ertapenem effective against?

A

Activity against a wide variety of G+, G-, and anaerobic microorganisms particularly enterobacteriaceae.

It is less active against pseudomonas and should not be used.

42
Q

What are the cell wall inhibitors that are not B-lactams?

A

Vancomycin, bacitracin, fosfomycin, and daptomycin

43
Q

What can develop rapid resistance against imipenem and meropenem and how do you prevent this?

A

Pseudomonas may develop rapid resistance, so aminoglycoside use is also recommended.

** imipenem and meropenem are not commonly used for pseudomonas

44
Q

How does vancomycin work?

A

It is bactericidal and prevents transpeptidation of the peptidoglycan chain (binds to the D-ala-D-ala)

45
Q

How does resistance again vancomycin occur?

A

There is a mutation of the terminal D-ala site and vancomycin can no longer bind

46
Q

What is vancomycin effective against?

A

Effective only against G+. Very useful against penicillinase and MRSA infections and for treating G+ infections in penicillin allergic patients.

47
Q

What is the DOC for C. Diff and a staphylococcus superinfection?

A

Oral vancomycin

48
Q

Why is vancomycin a drug of last resort?

A

It can cause the emergence of vancomycin resistant enterococci.

49
Q

What are the adverse effects of vancomycin?

A
  • Ototoxic
  • nephrotoxic
  • Red man syndrome (not a hypersensitivity reaction and will go away when pt is taken off drug)
50
Q

How does fosfomycin work?

A

It inhibits cell wall synthesis at one of the first steps in the synthesis of peptidoglycan. It is an analog of PEP (prevents NAG to NAM reduction) and is structurally unrelated to other drugs

51
Q

What is fosfomycin effective against?

A

Both G+ and G-

52
Q

What is fosfomycin commonly used for?

A

Uncomplicated UTIs in women

53
Q

What drugs have synergistic effects with fosfomycin?

A

The combination of fosfomycin and a B-lactam, aminoglycoside, or fluoroquinolone is synergistic

54
Q

How does bacitracin work?

A

It interferes with the final dephosphorylation step in the phospholipid carrier cycle. NAG and NAM cant be transported across the membrane

55
Q

What is bacitracin effective against?

A

G+ bacteria

56
Q

What is bacitracin commonly used in combination with?

A

Neomycin and polymixins (gives it G- coverage as well)

57
Q

What is bacitracin most commonly used to treat?

A

Used topically to prevent superficial skin and eye infections following minor injuries