Antibiotics

Question 1

Sulphonamides

Answer 1

• Sulfadiazine
• They competitively inhibit the enzyme dihydropteroate and interrupt folate production in the bacterial cell.
• This results in the interference of the cell’s ability to replicate and therefore reproduce and grow.
• Resistance via mutation of dihydropteroate enzyme gene

Question 2

Types of antibiotics

Answer 2

• Bactericidal- kills bacteria e.g penicillins
• Bactericidal reduce number of viable bacteria
• Bacteriostatic- prevents growth e.g. tetracyclines
• Static meds- full course is important to allow time for immune system to eliminate pathogens

Question 3

Broad vs narrow spectrum

Answer 3

• Each Abx will be effective against a range of microbes, the number will determine if broad or narrow
• BSA= ertapenem, mero, tazocin
• NSA= clindamycin, metro, fluclox
• Overuse of broad spec Abx will increase incidence of resistant + dormant microbes (C.diff) by eliminating microflora
• Narrow spectrum is useful once sensitivites are available. Reduce the risk of eliminating microflora and reduce incidence of anti-microbial resistance

Question 4

Trimethoprim

Answer 4

• Dihydrofolate reductase inhibitor- blocking this enzymes reduces bacterias ability to produce DNA/RNA + proteins
• Synergistic effective with sulphonamides hence broad spec cover of co-trimoxazole. Using both reduces incidence of resistance (have to have mutation for 2 genes)
• Trimethoprim resistance through mutation of dihydrofolate reductase enzyme gene.

Question 5

Quinolones

Answer 5

• Inhibit bacterial cell DNA gyrase (keeps DNA supercoilled)
• Bactericidal with broad G+ve and G-ve cover
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Question 6

Penicillin

Answer 6

• Beta lactam ring binds and prevents cross-linkage of peptidoglycan polymer that forms cell wall.
• Bacteria loses ability to maintain osomotic homeostasis and lysis occurs
• Resistance via beta-lactamase enzyme (metabolises penicillins and inactivates B-lactam ring).
• Example ESBL (mainly E.Coli + Klebseilla organisms)
• Pen V + G are narrow spectrum
• Mero is broad

Question 7

Bacterial cell wall

Answer 7

• G+VE: Thick peptidoglycogan wall (MOA for many ABx)
• G-ve: outer Phospholipid bilayer with thinner peptidoglycan cell wall
• Bacteria have porins- cross membrane proteins that can allow diffusion of meds

Question 9

Glycopeptides

Answer 9

• Vanc- works by preventing cross linking of peptidoglycan cell wall- ahain lysis occurs
• Only works of thick cell walls hence only covers G+VE

Question 10

Inhibitor of protein synthesis

Answer 10

• Macrolides- bind to 50s subunit of ribosomes
• Aminoglycosides- bind to 30s subunit of ribosome
• Tetracyclines- bind to 30s subunit of ribosome
• Macrolides and tetracyclines are bacteriostatic as inhibiting protein synthesis, cellular growth and development
• whilst aminoglycosides are cidal they inhibit protein synthesis like the others they also effect functionaility of cell membrane leading to death- only really functional against aerobic bacteria (O2 dependent transport to get across cell wall)
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Question 11

Oxazolidinones (e.g. linezolide)

Answer 11

• Prevents formation of 70s ribosome subunit hence protein synthesis
• Mainly effective against G+ve
• Resistance is through expulsion out of the cell

Question 12

Lipopeptide antibiotics (E.g. daptomycin)

Answer 12

• G+VE cover as hydrophobic tail binds irreversibly to the cell membrane, causes depolarisation and cellular dysfunction and death

Question 13

Key points when prescribing

Answer 13

• Indication- what is the diagnosis? Is there evidence of bacteria infection?
• Decide- are Abx needed or is this self-limiting
• Drug- pick the right Abx for most likely source of infection
• Dose- right dose, ?need dose adjustment
• Delivery- which formulation is most appropriate
• Duration- correct duration to treat infection
• Discuss- patient education on infection, importance of finishing course, escalation if not working
• Document- decisions and Mx plans