Antimicrobials Flashcards

1
Q

Generally, discuss how bacteria differ from human cells

A

Bacteria have no nucleus

Ribosomes are the only internal organelles

Rapidly reproduce –> binary fission, recombination

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2
Q

Explain Obligate aerobes

A

Only aerobic growth, req O2

Only grow in areas where large [O2] have fused into medium

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3
Q

Explain facultative anaerobes

A

Both aerobic and anaerobic growth

Grow best when O2 is present but can grow in absence

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4
Q

Explain obligate anaerobes

A

Obligate anaerobes can only grow in the absence of O2

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5
Q

Explain Aerotolerant anaerobes

A

Only anaerobic growth but continues in the presence of oxygen

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6
Q

Where would you find aerobic bacteria on the body?

A

Skin

Some parts of the respiratory system

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7
Q

Where would you commonly find anaerobic bacteria?

A

Found in mucosal membranes and soils

Skin, brain, blood, intrabdominal, pelvic, skin and soft tissue

They’re unable to deal with the O2 radicals such as peroxides

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8
Q

Discuss the difference between Gram +ve and Gram -ve bacteria

A

Gram +ve (STaph, STrep) have a thick peptidoglycan layer whilst Gram -ve bacteria dont have a thick peptidoglycan layer on the surface of the cell

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9
Q

Which antibiotic mechanism would work better on Gram +ve bacteria compared to Gram -ve? Why?

A

Gram +ve bacteria are prone to cell wall disruption due to thick peptidoglycan layers in comparison to Gram -ve bacteria

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10
Q

Name some Gram+ve Cocci aerobic bacteria

A

staphylococci
streptococci
Enterococci

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11
Q

Name some Gram+ve rod-shaped anaerobic bacteria

A

Acintomyces
Clostridium

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12
Q

Name some Gram-ve Cocci aerobic facultative anaerobic bacteria

A

Neisseria

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13
Q

List the mechanistic targets of antibacterials (generally)

A

Nucleic acid synthesis (DNA gyrase)

RNA polymerase

Folate synthesis

Protein synthesis (50s and 30s subunits)

Cell wall synthesis

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14
Q

What factors influence the pharmacokinetics of antibiotics?

A

Bioavailability, clearance, vol of dist, ability to reach infection site and have desired concentration in target tissue

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15
Q

Which antibiotics target nucleic acid synthesis?

A

Quinolones

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16
Q

Which antibiotics target RNA polymerase?

A

Rifamyxins

17
Q

Which antibiotics target folate synthesis?

A

Sulfonamides

trimethoprim

18
Q

Which antibiotics target cell wall synthesis?

A

Penicillins
Cephalosporins
Carbapenems
Monobactams
Glycopeptides

19
Q

Which antibiotics target Protein synthesis?

A

50s = macrolides, chloramphenicol
30s = aminoglycosides, tetracyclines

20
Q

What do bactericidal antibiotics do?

A

Kill the bacteria, is bacteriocidal at low doses

e.g. penicillin, cephalosporins, monobactams, carbapenems, glycopeptides

21
Q

What do bacteriostatic antibacterials do

A

Prevent the replication/duplication of bacteria

e.g.Tetracycline, spectinomycin, macrolides, trimethoprim, chrloamphenicol

22
Q

Outline the principles of the antimicrobial creed

(Hint: MIND ME)

A

M = microbiology guides therapy wherever possible
I = indication should be evidence-based
N = narrowest spectrum therapy required
D = dosage individualised to patient and site/type of infection

M = minimise therapy duration
E = ensure oral therapy used where clinically possible

23
Q

Describe prophylactic antibiotic use

A

Aims to prevent infection when significant risk of developing infection is present, basing antimicrobial choice on likely pathogen

Restrict only to indications for which there is evidence of efficacy/consequences of infection are sig

24
Q

Discuss empirical antibiotic therapy

A

Treats an established infection when causative organism has not been identified, treatment guided by clinical presentation (most likely cause)

Restricted to clear indication and clinical benefit, using narrowest therapy possible , review after 28-72 hrs

25
Q

Under which circumstances is empirical antibiotic therapy warranted?

A

When treatment must be started before culture sus results available

When clinical situation not serious enough to warrant taking culture

Sample culture cannot be obtained

26
Q

Discuss directed antibiotic therapy

A

Treats established infection where the pathogen has been identified

Ensure culture is critically evaluated, accounting: antimicrobial susceptibility, direct therapy in accordance w/ guidelines, use most effective/least toxic, narrowest spectrum drug available

Duration of therapy as short as possible, do not exceed 7 days

27
Q

When is combination antibiotic therapy used? How does it work?

A

Used for = polymicrobial infections, minimise the development of resistance

Works through synergy = e.g. one antibiotic breaks cells wall whilst the other (that can’t break wall) enters bacteria and works

28
Q

What are some direct ADRs of antibiotics?

A

hypersensitivity, toxicity (in preg, breastfeeding), drug interaction

29
Q

What are some indirect ADRs of antibiotics?

A

Effect on commensal flora (w/ clostridium infections) = candidiasis, inc risk of colonisation and/or infection w/ drug-resistant pathogens

Effect on environmental flora = inc risk of C. difficile or drug-resistant pathogens spreading to env/other people

30
Q

Discuss penicillin hypersensitivity

A

Caused not by the beta-lactam ring but by R-group side chains

Patients hypersensitive to penicillins may be allergic to structurally similar drugs, mainly limited to carbapenems (1%) and cephalosporins (2.5%)

Can use desensitisation = up-titrating dose over 15 mins

31
Q

Briefly discuss the use of antibiotics in pregnancy

A

Plasma [drug] dec in preg women –> less effective

Many antibiotics appear in breast milk of nursing mothers, may cause ADRs in infant

Sulfonamides may lead to toxic bilirubin accumulation in new-born’s brain

32
Q

Briefly discuss the use of antibiotics in pregnancy

A

Plasma [drug] dec in preg women –> less effective

Many antibiotics appear in breast milk of nursing mothers, may cause ADRs in infant

Sulfonamides may lead to toxic bilirubin accumulation in new-born’s br

33
Q

When is parental antibiotic administration required?

A

Oral admin not tolerated/not possible

GI absorption sig red

oral antimicrobial is not available

higher doses than can be easily administered oraaly are required for site of infection

urgent treatment is required

34
Q

What are the mechanism of antimicrobial resistance?

A

Inactivation = add a phosphate grp on antibiotic –> dec ability to bind to bact ribosomes

Pumping out = inc active efflux of the drug

Modification = modified the drug’s target

impermeability = modify cell wall protein