ISB 1 Intro Flashcards
Penicillin G is used to treat
Admin via
For STIs such syphilis
Via injection
Was the first antibiotic made
Why can concentration of antibacterials be high?
Don’t generally have mammalian targets
Why is pen G not delivered orally
V reactive square right cleaved by acids and bases
Oral alternative to pen g?
Pen v
- more stable we don’t know why, still not 100% BA though
If it’s resistant to this it’s resistant to everything…
Why?
Methicillin
It’s bulky and doesn’t fit into the active site that cleaves the ring
Contrast four generations of ceplasporins
2 more selective
3 injection only, fantastic gram neg killers
4 attempt to get oral BA but not as good
Having a bacterial cell wall makes things more or less resistant?
More - traps beta lactamases
Beta lactams have a ……. membered lactam ring
Four
Beta lactams fit beautifully where..
Into enzymes building the cell wall
It’s about distance and angle
Why are humans not affected by beta lactams
They cannot produce D Ala anyway. And these mimic D
Ala
Penicillin binding proteins are actually
Enzymes - what a silly name
What happens if cross linking of the cell wall does not occur in time?
Wall imports water and nutrients, swells and explodes
What produces delicious diarrhoea with penicillins?
Exploding bacterial cells
Why are penicillins more effective?
It’s the last step to make the cell wall so loads of energy has been expended and wasted
Basically structural unit of the cell wall
Muropeptides
A repeating disaccharide liked through a lactyl ether to a tetra peptide.
Peptides are cross linked by a …. chain
Pentaglycine
Penicillins are more effective against gram positive of negative
Positive
( wall is covered with outer membrane
Where as the negative cell wall is lipopolysaccarides)
What is the reactive inhibited by beta lactams?
During cross linking the terminal fifth alanine needs to be split off by enzyme
How does beta lactam penetrate the membrane of gram neg bacteria?
Through porin channels
some bacteria may be existent due to smaller ones
Four main resistance mechanisms?
Pump it out
Don’t allow it in
Metabolise it
Mutate/change target site
What is the difference between Dala and DLac ( when beta lactam mimics DAla?)
OH instead of NH2
No H bond is formed
How do porins work to be resistant
Reduce drug access or accumulation(by decreasing permiability)
How do pumps work to make resistance? (3)
Increasing active efflux if drugs by Pgp (known as MDR1)
Or
ATP binding cassette sub family B member 1 (ABCB1)
Or
Cluster differentiation 243
Three metabolic modes of resistance
1 deactivation of ceph/pen with ß-lactamases
2 hydrolysis of amides to break down anti-folate in folic acid mimetic antibiotics
3 oxidative demethylation with CYP
