antibiotic pharmacology Flashcards
process of resistance of antibiotics
selection pressure from repeated exposure to antibiotics has greatly increased resistance
- emergence of resistance almost inevitably follows was releasing new antibodies
- now cannot do that because of fear of losing the drug to resistance
affected by the antibiotic prescribing rates in the country/ area
antibiotic stewardship
reduce antibiotic consumption
restrict worst offender agents
promote logical antibiotic choices
limit co-lateral damage
- prevent damage to patients
C. diff
part of a normal gut microbiome
good spore forming
when we are exposed to antibiotics, it can mess with the gut flora and C. diff can take over
- leads to illness that can lead to death (esp. in elderly people)
correlation between overprescribing and c. diff infection
resistance mechanisms
3 principle mechanisms of resistance
- mutation/ modification of target size
- inactivating enzymes
- limit access (reduced permeability; increased efflux)
- genes mediating resistance be easily transferred
guided therapy
depends on identifying cause of infection and selecting agent based on sensitivity testing
mild infections that can wait a few days to be treated (e.g. cystitis, mild wound infections)
rationalising therapy in patients already on treatment (after empirical)
empirical therapy
beset (educated) guess therapy based on clinical/ epidemiologic acumen
used when therapy cannot wait for the culture e.g. meningitis/ sepsis
delay in therapy would result in worsening of condition
need to cover all likely causes
prophylactic therapy
preventing infection before it begins
healthy people exposed to: surgery, injury, infected material (e.g. bite)
immunocompromised individuals: HIV, transplantation, splenectomy
ideal characteristics - target effects
highly toxic to bacteria causing infection
penetrate the body area affected by infection
limit release of toxins from bacteria
convenient admin
ideal characteristics - co-lateral damage
non-toxic to patient
limited effect on colonising bacteria which reduces
- mucosal candida
- clostridium difficile infection
- selection of resistance bacteria
low potential for bacteria to escape treatment through developing resistance
compromising ideal characteristics
GUIDED THERAPY
use antibiotic which had limited action to the bacteria causing infection
if possible, limit penetration to site of infection
achieve clinical cure with as little impact on colonisation and resistance as possible
narrow spectrum
EMPIRICAL THERAPY
antibiotic which has extensive action against any bacteria that might be causing infection
need to penetrate broadly throughout the body
accept that impact on colonisation and resistance may be greater
broad spectrum
antibiotic action - bactericidal
achieve sterilisation of infected site by directly killing
- e.g. penicillin
- lysis of bacteria can lead to release of toxins and inflammatory material (patient often given steroids to help combat this)
antibiotic action - bacteriostatic
prevents growth
- e.g. clarithromycin - protein synthesis inhibitor
- requires additional factors to clear bacteria - immune mediated killing
areas antibiotics target
target cell wall peptidoglycan - human cells don’t have cell walls, so effective in targeting only bacteria
target metabolism
target ribosome function
target DNA replication + repair
antibiotic classes
cell wall agents
penicillins
glycopeptides
cell wall agents
vancomycin
large molecule - cannot penetrate Gram negative cell wall
useful against penicillin resistant bacteria such as MRSA
