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module 102: T4 infection and immunity > antimicrobial chemotherapy > Flashcards

antimicrobial chemotherapy Flashcards

1
Q

What was the original penicillin?

A

benzylpenicillin (penicillin G)

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2
Q

How do penicillins work?

A

by binding bacterial transpeptidases, inhibiting cell wall formation

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3
Q

What is the functional unit in penicillin?

A

beta lactam ring

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4
Q

Which penicillin is naturally occuring?

A

benzylpenicillin (penicillin G)

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5
Q

Describe benzylpenicillin (penicillin G)

A
  • poor oral bioavailibility
  • rapid renal clearance, requires frequent dosing
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6
Q

Which penicillins are chemically modified penicillins?

A
  • phenoxymethulpenicillin (pen V)
  • amonipenicillins (e.g amoxicillin)
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7
Q

What is amoxicillin used against?

A
  • S. pyogenes infections (sore throat, skin infections)
  • pneumococcal infections (respiratory tract)
  • susceptible E.coli infections (UTIs)
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8
Q

What is amoxicillins mechanism of action?

A

inhibition of bacterial cell wall synthesis

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9
Q

What is the standard dose for amoxicillin?

A

250-1000mg 8 hourly

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10
Q

What are some adverse effects of amoxicillin?

A
  • allergy
  • damage to commensal microflora
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11
Q

How is amoxicillin excreted?

A

urine

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12
Q

What are the mechanisms of resistance against amoxicillin?

A
  • primarily enzymatic degradation
  • target modification (e.g MRSA strains)
  • efflux in some gram negatives
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13
Q

What is amoxicillins half life?

A

an hour

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14
Q

What are some interactions that amoxicillin can have?

A

can increase levels of other protein bound drugs

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15
Q

How is Staphylococcus aureus resistant to penicillin?

A

encode penicillinases which hydrolyse the beta-lactam ring

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16
Q

What were the first antibiotics developed to target the penicillin resistant strains of S. aureus?

A
  • methicillin (not used clinically, only as a lab test)
  • flucloxacillin (now the main one used)
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17
Q

What is co-amoxiclav?

A

amoxicillin plus clavulinic acid

18
Q

How are MRSA strains now resistant to all beta-lactam antibiotics?

A
  • target modification (modified transpeptidase enzyme)
  • encoded by mecA gene
19
Q

Why are mycoplasmas and chlamydias resistant to penicillin?

A

as they have no cell walls

20
Q

How are most gram negative bacteria resistant to penicillin?

A
  • most make beta lactamases
  • develop resistance through other mechanisms like antibiotic efflux pumps
21
Q

What are the 4 main ways bacteria become resistant to antibiotics?

A
  • enzymatic degradation of the drug
  • target modification
  • efflux of antibiotic from bacteria
  • reduced penetration through cell wall
22
Q

What are some antibiotic sites of action?

A
  • cell wall
  • protein synthesis
  • DNA replication
  • RNA synthesis
  • antimetabolites
23
Q

What is the most common pathogen causing cellulitis?

A

Streptococcus pyogenes

24
Q

What is clarythromycin?

A

a macrolide

25
Q

What is clarythromycin used for?

A

used in patients that have a penicillin allergy
- S. pyrogenes infection (sore throat, skin infections)
- pneumococcal infections (respiratory tract)
- gram -ve infections such as haemophilus influenzae (respiratory tract)

26
Q

What is clarythromycin’s mechanism of actions?

A

inhibition of protein synthesis in the bacterial ribosome (50S subunit)

27
Q

What is clarythromycin’s standard dose?

A

500mg 12 hourly

28
Q

What is clarythromycin’s half life?

A

1-6 hours

29
Q

How is clarythromycin excreted?

A

metabolites in bile

30
Q

What are the adverse effects on clarythromycin?

A
  • nausea and diarrhoea
  • may alter cardiac conduction, arrythmias
31
Q

Which interactions can clarythromycin have?

A

inhibits enzymes (cytochrome p450 enzymes) involved in he metabolism of other drugs

32
Q

What are the methods of resistance against clarythromycin?

A

primarily mutational target modification

33
Q

What is vancomycin?

A

a glycopeptide

34
Q

What is vancomycin active against?

A
  • gram +ve bacteria
  • many resistant strains including methicillin resistant S. aureus (MRSA)
35
Q

What is vancomycin’s method of action?

A

inhibits bacterial cell wall formation by a different target to beta lactams

36
Q

What is vancomycins method of resistance?

A
  • target modification
  • cell wall thickening, reduced penetration
37
Q

What is the standard dose for vancomycin?

A

500-1500mg 12 hourly
- narrow therapeutic window, levels needed to kill bacteria are close to levels that are toxic to patients

38
Q

What is vancomycin’s half life?

A

4-8 hours

39
Q

What is vancomycins oral bioavailability?

A

very low

40
Q

How is vancomycin excreted?

A

urine

41
Q

What are some adverse effects of vancomycin?

A
  • nephrotoxic
  • ototoxic
42
Q

What are some of the interactions that vancomycin has?

A

with any other nephrotoxic or ototoxic drugs

module 102: T4 infection and immunity (10 decks)

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