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Pharmacology- Test 4 Material > Cell Wall Synthesis Inhibitors > Flashcards

Cell Wall Synthesis Inhibitors Flashcards

1
Q

allergenicity

A

-the ability of a substance to cause an allergy

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2
Q

beta-lactam

A
  • family of ATBs that inhibit transpeptidases (PBPs), activate autolytic enzymes in cell wall, are bactericidal and have time dependent action
  • wide distribution, except CNS
  • renal excretion, not metabolized (except nafcillin, imipenem)
  • mostly effects gram+ aerobes
  • resistance results mostly from B-lactamases/penicillinases
  • adverse effects mainly allergy
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3
Q

beta-lactamase (penicillinase)

A
  • enzymes that breakdown B-lactam ATBs (except cephalosporins) inactivating them
  • common mechanism of resistance against B-lactam ATBs
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4
Q

beta-lactamase inhibitor

A
  • prevent breakdown of B-lactam ATBs by B-lactamases

- have little ATB effect on there own but extend the range of B-lactam ATBs

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5
Q

broad spectrum

A

-target many types of microbes both gram+ and gram- as well as other microorganisms (Rickettsia)

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6
Q

cephalosporinase

A

-enzyme that inactivates cephalosporins and is a common mechanism of resistance against cephalosporins

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7
Q

extended spectrum

A

-affects a variety of gram+ and gram- bacteria

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8
Q

Gram Negative

A

-thin peptidoglycan layer sandwiched between an inner and outer cell membrane thus they are less dependent on peptidoglycan layer for survival and are generally harder to eradicate with ATBs

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9
Q

Gram Positive

A
  • have a thick peptidoglycan layer that forms cell wall outside of plasma membrane
  • more dependent on this cell wall for survival and without it bacteria will lyse
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10
Q

low-affinity penicillin-binding protein

A

-PBPs with a decrease binding affinity for ATBs and is a common mechanism of resistance to ATB therapy

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11
Q

narrow specturm

A
  • targets one specific type of bacteria, usually either gram positive or negative microbes
  • optimal against specific organisms
  • lower risk of superinfections
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12
Q

penicillin binding protein

A
  • enzyme responsible for synthesis of peptidoglycan which is important component of bacterial cell walls
  • inhibition of PBPs leads to destruction of bacterial cell wall and lysis
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13
Q

peptidoglycan layer

A
  • major component of bacterial cell walls produced by PBPs

- inhibition of its synthesis (mechanism of many ATBs) leads to destruction of cell walls and bacterial cell lysis

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14
Q

porin

A

-channel in bacterial cell membrane that functions as a channel that is permeable to select substances

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15
Q

transpeptidase

A

-bacterial enzyme that cross-links the peptidoglycan chains to form rigid cell walls

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16
Q

fosfomycin

A

Cell Wall Synthesis Inhibitor- non-B-Lactam

  • Mechanism: structural analog of phosphoenol pyruvate (PEP), blocks step-1 PDG synthesis
  • Pharmacokinetics: well absorbed and distributed, excreted unchanged in urine
  • Broad spectrum with few adverse effects
  • rapid resistance emerges from mult. dosing
  • Uses: single dose oral treatment of uncomplicated UTIs
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17
Q

D-cycloserine

A

Cell Wall Synthesis Inhibitor- non-B-Lactam

  • Mechanism: structural analog of D-alanine, blocks step-2 in PDG synthesis
  • Pharmacokinetics: oral, good CNS penetration, active form in urine
  • broad spectrum, dose related CNS effects but reversible
  • Uses: restricted second-line M. TB drug
18
Q

bacitracin

A

Cell Wall Synthesis Inhibitor- Non-B-Lactam

  • Mechanism: depletes lipid carrier for PDG synthesis preventing its recycling
  • TOPICAL application only
  • narrow spectrum (gram+)
  • severe nephrotoxicity
  • Uses: skin and ophthalmologic infections; good in combo w/ polymyxin B (membrane inhibitor)
19
Q

vancomycin

A

Cell Wall Synthesis Inhibitor- Non-B-Lactam

  • glycopeptide structure
  • Mechanism: binds D-Ala-D-Ala terminus of pentapeptide; blocks PDG synthesis (step 4: transglycosylase and step 5: transpeptidation) by binding substrate; rapidly bactericidal for dividing bacterial cultures (except enterococci)
  • Mostly IV administration (rarely oral, IM for intestinal)
  • distribution through out body (CNS if meninges inflammed)
  • narrow spectrum against Gram+ microbes and MRSA
  • Resistance: VRE due to bacteria with diff. cell wall units with dec. binding affinity to vanco; VRSA, bacteria overexpresses D-Ala-D-Ala which binds up drug
  • can cause Red Man Syndrome, ototoxicity and nephrotoxicity
  • Reserved for serious Gram+ infections resistant to other less toxic drugs and MRSA
20
Q

daptomycin

A

Cell Membrane Agent

  • Mechanism: novel cyclic lipopeptide which causes membrane depolarization (creates open pores in membrane in presence of Ca ??)
  • bactericidal, IV admin with renal clearance
  • Uses: narrow spectrum (gram+) used to treat VRE and MRSA
  • Can cause myopathy
21
Q

cephalexin

A

Cell Wall Synthesis Inhibitor

  • 1st generation cephalosporin
  • acid stability
  • broadest spectrum against gram+ cocci, effective against gram- bacilli
  • better against gram +/S. aureus
  • adverse effects: cutaneous allergy– NOT for patients with anaphylaxis to penicillin
22
Q

cefuroxime

A

Cell Wall Synthesis Inhibitor

  • 2nd generation cephalosporin
  • only group with significant activity against anaerobes
  • adverse effects: cutaneous allergy (NOT for patients with anaphylaxis to penicillin), disulfiram-like reaction and bleeding disorder
23
Q

ceftriaxone

A

Cell Wall Synthesis Inhibitor

  • 3rd generation cephalosporin
  • resistance to beta-lactamases
  • CNS penetration
  • anti-pseduomonal and -pneumococcal, gram- infections (meningitis, pneumonia, gonorrhea)
  • adverse effects: cutaneous allergy (NOT for patients with anaphylaxis to penicillin), disulfiram-like reaction, bleeding disorder, pseudomembranous colitis (CDAC)
24
Q

cefepime

A

Cell Wall Synthesis Inhibitor

  • 4th generation cephalosporin
  • resistance to beta-lactamases– usual for treating enterobacter & penicillin-resistant streptococci
  • CNS penetration
  • anti-pseudomonal
  • adverse effects: cutaneous allergy (NOT for patients with anaphylaxis to penicillin), pseudomembranous colitis (CDAC)
25
Q

imipenem

A

Cell Wall Synthesis Inhibitor
-carbapenem
-bind more efficiently with PBPs
-penetrate outer membrane of gram- bacteria
-BROADEST activity of all beta-lactam drugs
-resistant to degradation by most beta-lactamases, but induce those that inactivate pens/cephs
-active against extended-spectrum beta-lactamase producing organisms
-drug resistance d/t alteration of PBP– carbapenemases (CRE)
-renal metabolism and inactivation
administer with cilastatin
-adverse effects: cross allergy to penicillin? rare effects– GI, superinfections, neurotoxicity
-clinical use: 2nd line therapy for serious nosocomial infections

26
Q

meropenem

A

Cell Wall Synthesis Inhibitor

  • carbapenem
  • bind more efficiently with PBP
  • penetrate outer membrane of gram- bacteria
  • BROADEST activity of all beta-lactam drugs
  • resistant to degradation by most beta-lactmases, but induce those that inactivate pens/cephs
  • active against extended-spectrum beta-lactamase producing organisms
  • drug resistance d/t alteration of PBP
  • adverse effects: cross allergy with penicillin? rare effects– GI, superinfections, neurotoxicity
  • clinical use: 2nd line therapy for serious nosocomial infections
27
Q

cilastatin

A 
inhibits dehydropeptidases (inactivates imipenem)
administer with imipenem
28
Q

aztreonam

A

monobactam

  • binds to PBPs
  • relatively resistant to beta-lactamases
  • IM or IV, drug penetrates inflamed CNS
  • NO significant cross reaction with penicillin
  • narrow spectrum: limited to gram- aerobes, including pseudomonas
  • uses: gram- UTIs, lower RTIs, systemic infections
29
Q

primaxin

A

imipenem + cilastatin

30
Q

Penicillin G

A

PCN ATB

  • beta lactame ATB
  • t1/2
31
Q

Penicillin V

A

PCN ATB

  • beta lactame ATB
  • t1/2
32
Q

dicloxacillin

A

beta lactamase resistant PCN’s

  • most acid stable (can give PO but food affects absorption).
  • Use: penicillinase-producing staphylococcus and streptococci
  • resistance occurs 2/2 PBP with lower affinity for drugs.
  • S/E: less than that with PCN’s
33
Q

oxacillin

A

beta lactamase resistant PCN’s

  • most acid stable (can give PO but food affects absorption).
  • Use: penicillinase-producing staphylococcus and streptococci
  • resistance occurs 2/2 PBP with lower affinity for drugs.
  • S/E: less than that with PCN’s
34
Q

amoxicillin

A 
Extended spectrum PCN's
-used with beta lactamase inhibitors (destroyed by beta lactamases).
-acid stable (can give PO).
   \+absorption better than ampicillin.
   \+absorption NOT affected by food
-t1/2 1.5' (dose BID-TID)
35
Q

ampicillin

A 
Extended spectrum PCN's
-used with beta lactamase inhibitors (destroyed by beta lactamases).
-acid stable (can give PO).
   \+absorption better than ampicillin.
   \+absorption NOT affected by food
-t1/2 1.5' (dose BID-TID)
36
Q

ticarcillin (Timentin with clavulanate)

A

Carboxypenicillin ATB

  • IV
  • Used for pseudomonal infections
  • rarely used alone
37
Q

piperacillin

A

Ureidopenicillin ATB

  • IV
  • Used for pseudomonal infections and severe systemic infections caused by Klebsiella
  • often combined with aminoglycosides to prevent resistance.
38
Q

clavulanic acid

A

beta lactamase inhibitor

  • irreversible inhibition of beta lactamase (“suicide substrates).
  • Used in combinations because they are weak ATB’s when given alone.
  • Augmentin= clavulanic acid + amoxicillin
  • Timentin= clavulanic acid + ticarcillin
39
Q

sulbactam

A

beta lactamase inhibitor

  • irreversible inhibition of beta lactamase (“suicide substrates).
  • Used in combinations because they are weak ATB’s when given alone.
  • Augmentin= clavulanic acid + amoxicillin
  • Timentin= clavulanic acid + ticarcillin
40
Q

tazobactam

A

beta lactamase inhibitor

  • irreversible inhibition of beta lactamase (“suicide substrates)
  • Used in combinations because they are weak ATB’s when given alone.
  • Augmentin= clavulanic acid + amoxicillin
  • Timentin= clavulanic acid + ticarcillin

Pharmacology- Test 4 Material (12 decks)

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