Antibiotics Flashcards
What does selective toxicity mean
Drugs which target invaders not host cells
Explain the structure of penecillin
Beta lactam ring with 3C and 3N
What do b lactam penecillin target
Peptidoglycan wall
They inhibit transpeptidase enzyme from forming peptide cross links
Why are gram -ve harder to kill with penecillin (first class of penecillin)
Thin peptidoglycan and can’t penetrate through the outer membrane
What is the name of the original penecillin and what is its problems
Benzyl penecillin
It works only on gram +ve
It is acid labile (degraded in stomach)
Poor absorption orally
Why other than the large om are gram -ve harder to kill
Larger amounts of b lactamase
Which penecillins can now work also on gram -ve unlike benzyl penecillin
Broad spectrum
What makes broad spectrum penecillins able to penetrate gram -ve outer membrane
Addition of amino group
Why are broad spectrum penecillins easier absorbed/last longer than benzyl
Addition of hydroxyl OH
Name the other 3 penecillins other than the benzyl and broad spectrum
B lactamase resistant forms
Extended spectrum
Reverse spectrum
What do extended spectrum penecillins kill
Pseudomonads
What do reverse spectrum penecillins mean
Kill more gram -ve than +ve
Where is penecillin not distributed unless meningitis inflammation
Csf
Why are penecillin taken regularly
Short half life (30-80mins) - excreted 90% via tubular secretion
What are the 3 major adverse effects of penecillin
Hypersensitive (rash etc)
Blood clotting
GI changes in gut flora
What do sulphonamides and trimethoprim do
They are inhibitors of enzymes (because same shape as paba) which convert paba to tetrahydrofolate then to nucleotides
(Stop dna synthesis)
Why don’t sulphonamides/ trimethoprim stop dna synthesis of host
We don’t produce folate ourselves we get it from diet
What is good kinetically about sulphonamides
80-100% absorbed easily orally
What is diff about distribution of sulphonamides to penecillin
Penecillin can’t cross csf
Sulphonamides do go to cns
Where are sulphonamides metabolised
Liver
Which antibiotics target type II isomerases and type IV to stop dna rep
Fluroquinolones
Which topoisomerase is targeted in gram -ve by fluroquinolone and which gram +ve
- = dna gyrase
+ = IV
What is an issue with fluroquinolones in ADME
They are inhibitors of CYP 1a2 (stop metabolism of other drugs)
Which drugs target ribosomes/protein synthesis
Macrolides and tetracycline
What do macrolides do
Bind to the 50s subunit and prevent the translocation of the AA on the trna from the A site to the peptide site = no peptide bond
Where on the 50s do macrolides bind
Exit site (PAE)
Why do macrolides have to be coated for absorption
Destroyed in the stomach
Where can’t macrolides distribute
Cns can’t cross BBB like penecillins
How are macrolides metabolised
Cyp3a4
How are macrolides excreted
Bile
Name some adverse effects of macrolides
GI disturbance like penecillin
Hypersensitive reactions
Damage to ear drum
How does tetracycline work
Binds to 30s and stops the binding of new trna
Stops ELONGATION
When is absorbance of tetracycline highest
In fasting state
Which drugs have large half life
Tetracycline (18hra)
How is tetracycline excreted
Bile and kidney filtration
