13 - Antimicrobials

Question 1

What are the 5 main ways that antibiotics work and give some examples of each?

Answer 1

Question 2

What is the difference between bactericidal and bacteriostatic antibiotics?

Answer 2

• Cannot use two together as bacteriocidal work best on bacteria that are replicating and bacterostatic stop division

- Bacteriostatic: macrolides, tetracycline

- Bactericidal: penicllin, ceflasporins

Question 3

What are some ways that bacteria develop resistance to antibiotics?

Answer 3

• Usually beta lacatamases
• Plasmid DNA can be passed from cell to cell

Question 4

When do we need to drug monitor antibiotics?

Answer 4

Vancomycin monitored every 4th dose

Question 5

What does it mean when an antibiotic has time dependent or concentration dependent killing?

Answer 5

The major killing effect against an organism is produced by either the time or the concentration of the drug at the binding site

Time dependent: drugs spend a long time at binding sites as have long half life so this is what kills them e.g penicillins and macrolides

Concentration Dependent: need a certain concentration at binding sites e.g aminoglycosides

Question 6

Why do we use antibiotics in general?

Answer 6

• Post infective treatment
• Prophylaxis before high risk surgery or for those who have conditions like asplenic to prevent infections

Question 7

What is co-amoxiclav and why is it prescribed as a combination?

Answer 7

Question 8

Which groups of people are at increase risk of infection?

Answer 8

Question 9

Which factors helps one determine which antibiotic is the best choice?

Answer 9

- Allergies and reactions e.g metronidazole and drinking

- Hepatic/Renal Impairment or Pregnancy

• What is the likely infectious agent?
• Is the patient in a high risk group? If so use 2nd line antibiotics as likely to be carrying resistant bacteria

Question 10

What are the adverse events of antibiotics?

Answer 10

• Toxicities
• Allergic reactions
• Idiosyncratic reactions (Type B)
• Ecological effects – C.difficile, selection of resistance
• Drug interactions

Question 11

What are some antimicrobial stewardship practices in place in UHL?

Answer 11

• Restricted antibiotics need authorisation from microbiology department
• Start broad and then narrow to appropriate antibiotics when get swabs and cultures back
• Questioning if patient actually needs antibiotics, thinking of resistance and side effects, e.g C.Diff

Question 12

What is the A to F approach of identifying infection in the I5 model?

Answer 12

Question 13

When can aciclovir be usedin the treatment of herpes simplex virus?

Answer 13

Same for genital, dose depends if immunocompromised or relapsing

Can also be used in varicella zoster and herepes zoster!

Slows the growth of the virus so speeds up the healing process by about half but doesn’t eradicate the virus!

Question 14

What is the MOA of cephalexin, what are the DDIs and ADRs?

Answer 14

- Cephalosporin - Inhibits cell wall synthesis

• Used for prophylaxis of recurrent UTI, hospital acquired pneumonia, acute pyelonephritis

- DDIs: can increase blood metformin levels

• ADRs: diarrhoea, ab pain, headache, vomiting, thrush, eosinophillia

Question 15

What is the MOA of azithromycin and clarithromycin, what are the DDIs and ADRs?

Answer 15

Macrolides: stop protein synthesis

Used for: resp infections, ear infections and skin/soft tissue infections in those that are allergic to penicillin

DDIs: Clarithromycin with CCBs can cause AKIs, clarithromycin is CYP3A4 inhibitor

ADRs: Hepatotoxicity, Nausea, Diarrhoea, QT prolongation so arrhythmias, anaphylaxis, Steven Johnson syndrome, C.Diff, can aggravate Myasthenia Gravis

Question 16

What is the MOA of amoxicillin, flucloxacillin, co-amoxiclav and penicillin V, what are the DDIs and ADRs?

Answer 16

Penicillins so inhibit cell wall synthesis, co-amoxiclav being used for severe respiratory infections

ADRs: hepatotoxic so can cause jaundice, allergies diarrhoea, nausea, thrombocytopenia

Question 17

What is the MOA of ciprofloxacin, what are the DDIs and ADRs?

Answer 17

Quinolone: inhibits DNA synthesis by inhibiting DNA gyrase

Used for eye and ear infections

ADRs: headache, N+V, rash

DDIs: Inhibits CYP1A2 and 3A4 so can interact with warfarin, theophylline and phenytoin and etc

Question 18

What is the MOA of doxycycline, what are the DDIs and ADRs?

Answer 18

Tetracycline: Inhibits protein synthesis

Used for: H Pylori, Chlamydia, Acne

ADRs: photosensitivity, discolouring of teeth, angiooedema, pericarditis, thrush, rash, diarrhoea

DDIs: Can worsen myasthenia gravis and SLE, inhibits CYP3A4 so bleeding risk with warfarin and other drugs metabolised by this

Question 19

What is the MOA of trimethoprim, what are the DDIs and ADRs?

Answer 19

Binds to dihydrofolate reductase and inhibits the reduction of dihydrofolic acid (DHF) to tetrahydrofolic acid (THF)

Used for: UTIs and acne

ADRs: diarrhoea, electrolyte imbalance, headache, nausea, rash

DDIs: Don’t use with spironolactone as risk of hyperkalaemia, can inhibit CYP2C8 so can potentiate warfarin and phenytoin

Question 20

What is the MOA of metronidazole, what are the DDIs and ADRs?

Answer 20

Inhibits DNA synthesis

Used for BV, PID and endocarditis

ADRs: metallic taste in mouth, loss of appetite, thrush, headache, vomiting

DDIs: don’t drink as will vomit, see image

Question 21

What is the MOA of nitrofurantoin, what are the DDIs and ADRs?

Answer 21

Stop DNA synthesis, used for UTIs and prophylaxis of UTIs

ADRs: see image

DDIs: minimal but may decrease activity of quinolones, can use with warfarin, bad if renally impaired

Question 22

What are the ADRs and DDIs with aciclovir?

Answer 22

ADRs: nausea, photosensitivity reactions, thrombocytopenia, rash

DDIs: may interact with other antibiotics like tobramycin and amphotericin B

Question 23

Which heparin has a lower risk of osteoporosis?

Answer 23

LMWH