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Pharm - Final exam > PCN lecture > Flashcards

PCN lecture Flashcards

1
Q

What is the main diff bw bacterial and mammalian cells

A

rigid cell wall of peptidoglycan that protects bacterial cells from osmotic rupture

G+ have thick layer, stain purple
G- have thin layer, stain pink, have outer membrane

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2
Q

What is peptidoglycan composed of

A

a back bone of NAG-NAM, a chain of 4 aa linked to NAM and a peptide bridge that cross links tetrapeptide chain D-gln to D-ala

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3
Q

Process of peptidoglycan formation

A
  1. addition of subunits (sugar and 5 aa) assembled in cytoplasm
  2. transport to cell surface
  3. cross linking by cleaving terminal stem-peptide aa; performed by transpeptidases or PBP
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4
Q

Where can antibiotics target to ICWS

A
  1. transglycosylation (NAG-NAM)
    • vancomycin (a glycopeptide), B-lactams
  2. Transpeptidation (cross link peptides)
    • B-lactam (PCN, ceph, Carbapenems, mononbactams)
  3. NAG –> NAM reduction
    • fosfomycin??
  4. Transport across inner membrane
    • Bacitracin
  5. AA mimicry (pentapeptide chain)
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5
Q

What are the natural PCNs?

A

*PCN G -IV, IM, oral?
Benzathine PCN - IM
Procaine PCN G -IM
PCN V - oral

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6
Q

What are the extended spectrum PCNs?

A

*Ampicillin -
Amoxicillin (Amoxil)
Bacampicillin (Spectrobid)

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7
Q

What are the PCNase resistant PCNs aka antistaphylococcal PCNs

A

*Nafcillin (Unipen), IM/IV
Oxacillin (Prostaphlin), oral
Dicloxacillin (cloxapen), oral
Methicillin (testing only!)

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8
Q

Name all the anti-pseudomonal PCNs

A

*Piperacillin (Pipracil)
Mezlocillin (Mezlin)
Ticarcillin (Ticar)
Carbenicillin (Geocillin)

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9
Q

How are ICWS bactericidal?

A

cause cell death due to osmotic lysis
- autolysins cleave peptidoglycan bonds in normal course of cell growth. This combined with agents that inhibit cell wall growth –> no repair –> weakness and lysis

*note: protein synthesis inhibitors (chloramphenical) PREVENT action of ICWS

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10
Q

List the properties of ICWS

A

G+ activity, spectrum (G-,anaerobic etc), P aeruginosa activity, PCNase resistance, acid resistance, CNS penetration, unique adverse effects, route of admin

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11
Q

list the B lactams

A
  1. PCN
  2. Cephalosporins
  3. Carbapenems
  4. Monobactams
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12
Q

list ICWS that are not B lactams

A
  1. Vancomycin
  2. Phosphomycin
  3. Bacitracin
  4. Cycloserine
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13
Q

Where do B-lactamases reside?

A

periplasmic space

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14
Q

where are PCN binding proteins (PBP) located

A

cytoplasmic membrane

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15
Q

Describe the activity of Natural PCN (remember, PCN G, Benzathine PCN, Procaine PCN G, PCN V)

A
  • highest activity again G+, including anaerobic
  • some G-
  • inactivated by PCNase/B-lactamase
  • not effective against s. aureus
  • no antipseudomonal
  • renal/kidney elim
  • poor CNS penetration
  • PCN V is relatively acid resistant
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16
Q

Procaine PCN V - IM is used for..

A

only syphilis and rheumatic fever
*note: PCN is leading drug for syphylis (spirochete), lost sensitivity for N gonorrhea (now ceftriaxone is DOC for gonorrhea - 3rd gen ceph)

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17
Q

What is PCN G good against

A

Many things!

  • G+ cocci: s pneumo, S. pyogenes (causes of pneumococcal pneumonia)
  • Syphilis (spirochetes)
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18
Q

List and describe the activity of PCNase resistant PCNs aka antistaphyloccocal PCNs?

A
  • Nafcillin, Oxacillin, Dicloxacillin, Methicillin (testing only bc toxic)
  • lower G+ activity than natural PCN
  • PCNase resistant
  • some G-
  • some acid stable and pro bound (PCN V)
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19
Q

What is the metab and excretion for PCNase resistant PCNs

A

hepatic metabolism, renal excretion

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20
Q

What is the DOC for PCNase producing s. aureus (MSSA)

A

PCNase resistant PCNs

*note: more than 20% s. aureus isolates are resistant (MRSA)

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21
Q

What are the PCNase resistant PCNs that can be taken orally

A

Oxacillin (Prostaphlin)

Dicloxacillin (cloxapen)

22
Q

How is methicillin resistant s. aureus (MRSA) resistant, meaning what is it’s MOR?

A

produces alternate PBP that decreases affinity of B lactam antibiotics to PBPs…. thus NO b-lactam can treat MRSA, except CETAROLINE FOSAMIL (unnamed gen of cephalosporins)

23
Q

identify the extended spectrum PCNs and their activity

A
  • Ampicillin (Omnimen), Amoxicillin (amoxil)
  • lower G+ than natural PCN, but extended G-
  • no antipseudomonal
  • resistance freq develops
  • B lactamase susceptible
  • acid resistant
24
Q

How are extended spectrum PCNs excreted

A

urinary excretion

25
Q

What is the DOC for listeria infections

A

extended spectrum PCNs ie ampicillin (+/- aminoglycoside)

26
Q

What should happen if an ampicillin rash occurs

A

nothing.. do not stop drug bc ampicillin rash is not a hypersensitivity rxn

27
Q

What is the activity of antipseudomonal PCNs (*Piperacillin (pipracil), Mezlocillin (Mezlin), Ticarcillin (Ticar), Carbenicillin (Geocillin))

A

*same coverage as extended spectrum PCNs (lower G+, extended G-, no antipseudomonal, freq resistance, B-lactamase susceptible, acid resistant) PLUS additional coverage of enteric G- bacilli

  • major use: p aeruginosa, acinetobacter but never use alone; combo with aminoglycosides to prevent resistance
  • B lactamase susceptible, acid sensitive
28
Q

How are antipseudomonal PCNs excreted

A

renal

29
Q

What are the B lactamase inhibitors and what are they added to

A

B lactamase inhibitor: clavulanic acid, sulbactam, tazobactam

added to: ampicillin, amoxicillin, ticarcillin or piperacillin

30
Q

Though adding a b lactamase inhibitor to ampicillin, amoxicillin, piperacillin, or ticarcillin may extend the spectrum of these agents, what is the catch?

A
  • not all B lactamases are inhibited

- bacteria may dev resistance independent of b-lactamase production (ex: MRSA is altered PBP prod)

31
Q

Ampicillin is combined with what B lactamase inhibitor?

A

ampicillin; sulbactam (unasyn) - IV,IM

*remember, not active against MRSA

32
Q

amoxicillin is combined with what B lactamase inhibitor

A

amoxicillin; clavulanic acid (augmentin) - oral

*remember, not active against MRSA

33
Q

Piperacillin is combined with what B lactamase inhibitor

A

Piperacillin; taxobactam (zosyn) - IV

  • remember, not active against MRSA
34
Q

Ticarcillin is combined with what B lactamase inhibitor

A

Ticarcillin; clavulanic acid (Timentin) - IV

35
Q

What are the reasons for bacterial resistance against PCNs?

A
  • inactivation by PCNase (inducible enzyme)
  • decreased permeability of bacterial cell to PCN
  • alt in PBP (MRSA)
  • autolytic enzymes not being activated –> tolerant organisms (listeria, staphylococci)
  • lack cell wall (mycoplasma L forms, chlamydia (no peptidoglycan wall))
36
Q

Describe potential toxicities that can develop from PCN use?

A

allergy (all forms) but note that ampicillin rash is NOT an allergy
electrolyte imbalances
GI disturbances
Superinfections

37
Q

overall pharmacokinetics of PCN?

A

good tissue penetration but poor CNS
mostly renal elimination
filtration and tubular excretion
probenecid inhibits renal elimination

38
Q

DOC H pylori (note: H pylori is precursor for stomach cancer) (G- rod aerobe)

A

bismuth +metronidazole+tetracycline OR

amoxicillin

39
Q

DOC P aeruginosa (G- rod aerobe)

A

antipseudomonal PCN +aminoglycosides

40
Q

DOC s. pneumo G+ cocci

A

PCN

*note: if G+, think PCN… PCN G is Gold! and Good for many

41
Q

DOC s pyogenes (group A) (G+ cocci)

A

PCN, clindamycin

42
Q

DOC S agalactiae (group B) (G+ cocci)

A

PCN (+aminoglycoside)

43
Q

DOC viridans streptococci (G+ cocci)

A

PCN

44
Q

DOC S aureus Beta lactamase neg (G+ cocci)

A

PCN

45
Q

DOC S auerus Beta lactamase positive (G+ cocci)

A

PCNase resistant PCN

46
Q

MRSA (G+ cocci) DOC

A

Vancomycin

47
Q

DOC Enterococcus species (G+cocci)

A

PCN + aminoglycoside

48
Q

DOC Listeria species (G+ rod)

A

ampicillin (+/- aminoglycoside)

49
Q

DOC B burgdorferi (spirochetes)

A

amoxicillin

50
Q

DOC leptospira species (spirochetes)

A

PCN

51
Q

DOC Treponema species (spirochetes)

A

PCN

52
Q

what is most potent against G+

A

PCN G (natural PCN)

Pharm - Final exam (3 decks)

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