18B10: Exam Report
Compare and contrast the pharmacology of vancomycin and flucloxacillin.
49% of candidates passed this question.
Most candidates structured their answers well. Expected information included: the class of antibiotic of each agent, their respective pharmaceutics, pharmacodynamics, pharmacokinetics, indications and adverse effects. Better answers provided pharmacodynamic and pharmacokinetic information relevant to each drug rather than generic statements. Good answers also included the common resistance mechanisms for both agents.
16A22: Exam Report
Compare and contrast the mechanism of action (25% of marks), antimicrobial profile (25% of marks), pharmacokinetics (25% of marks) and adverse effects (25% of marks) of Flucloxacillin and Vancomycin.
83% of candidates passed this question.
The structure required to score well was provide by the questions asked. Marks were lost by not mentioning that flucloxacillin is a beta lactam that it does not cover MRSA and that vancomycin covers enterococcus. Better answers could identify that vancomycin is slower at killing sensitive staph than flucloxacillin. Adverse effects were specifically asked for in the question so omitting facts such as associated nausea/vomiting/diarrhoea/anaphylaxis etc. cost some candidates marks. If 25% of marks are allocated to side effects then it is expected more than one adverse effect would be mentioned. Some candidates had incorrect facts – Enterococcus is not a gram negative organism.
T2i / 18B10 / 16A22: Compare and contrast the pharmacology of vancomycin and flucloxacillin
30mg/kg (load) + 1.5mg bd (normal renal fn)
Cell Wall Inhibitor
Cell Wall Inhibitor
Binds D-Ala-D-Ala sequence on bacterial cell wall
Interrupts peptidoglycan synthesis → Bactericidal
- B lactam ring mimics shape of D-Ala-D-Ala sequence that is the substrate for cell wall transpeptidases
This is the final step in bac cell wall synthesis that allows cross linking
By pretending to be D-Ala-D-Ala, it binds transpeptidases -> inhibits enzyme activity → bac without cell wall → die
- Exerts bacterial autolytic effect
Inhibits certain penicillin binding proteins (PBP) related to the activation of autolysis →promotes bac lysis & cell death
Time v Concentration
Time: time spent above minimal inhibitory dose is what determined efficacy
Time Dependent -> time spent above minimal inhibitory concentration determines efficacy
Post Dose Effect
Ability to continue bactericidal effects post dose is small
Short 2hrs – bactericidal
Skin and soft tissue infections
Respiratory tract infections
Poor. Only po for C diff
PPB 50%. Vd 2L/kg
Renally excreted unchaged. ∴needs dose adjustment in renal failure
Minimally metabolized by liver
Red man syndrome: mass histamine release
Ototoxicity: related to peak dose
Bacteria mutate to D-Ala-D-lactate
∴no binding site for Vanc
b-lactamase producing bacteria
Monitor trough level & renal fn
LFTs Renal fn