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Case 2 > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What is the difference between Gram + and Gram - bacteria?

A

Gram + = purple
1 inner lipid membrane + thick peptidoglycan layer

Gram - = pink
2 lipid membranes + thin peptidoglycan layer

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2
Q

What do antibiotics target?

A
  1. Cell wall synthesis
  2. Protein synthesis
  3. Nucleic acid synthesis
  4. Folate metabolism
  5. Cell membrane
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3
Q

What is the therapeutic index?

A

Difference between effectiveness + toxicity

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4
Q

What is the therapeutic spectrum?

A

Bacteria antibiotic effective against - narrow + extended

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5
Q

What’s the difference between pharmacokinetics and pharmacodynamics?

A 
Pharmacokinetics = movement of drugs in body
Pharmacodynamics = what drug does to body
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6
Q

What are the cell wall synthesis inhibitors?

A
  • Penicillins
  • Co-amoxiclav
  • Cephalosporins e.g Cefotaxime
  • Vancomycin (MRSA)
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7
Q

What are the protein synthesis inhibitors?

A
  • Clarithromycin (Chlamydia)
  • Gentamicin
  • Oxytetracycline
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8
Q

What are the DNA/RNA synthesis inhibitors?

A
  • Ciprofloxacin
  • Nitrofurantoin (UTI)
  • Metronidazole
  • Rifampicin
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9
Q

Name a folate antagonist

A

Trimethoprim

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10
Q

Which group are the beta lactam antibiotics?

A

Penicillins + Cephalosporins

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11
Q

How do beta lactam antibiotics work?

A
  • Binds to PBP via beta lactam ring, inhibiting transpeptidase + preventing cross linking of peptidoglycan layer
  • Penicillin binding protein (PBP) = normally causes cross linking of peptidoglycans in cell wall
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12
Q

How do protein synthesis inhibitors work?

A
  • Target ribosomes structurally different enough from human ribosomes
    = Selective toxicity
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13
Q

How do DNA & RNA synthesis inhibitors work?

A
  • Selective toxicity for bacterial enzymes involved in replication
  • Narrower therapeutic index than cell wall synthesis inhibitors
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14
Q

How do folate synthesis inhibitors work?

A
  • Humans take up folate through food, bacteria have to make it themselves
  • Trimethoprim = enzyme inhibitor of this folate synthesis metabolic pathway
  • Combined with sulphonamides to act synergistically to reduce folate synthesis
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15
Q

When are folate synthesis inhibitors not effective?

A

Presence of pus as it contains dead bacteria +. neutrophils that the bacteria can take their building blocks from

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16
Q

Why are there so many different antibiotics?

A
  • antibiotic may not be able to reach target
  • may cause side effects
  • bacteria resistance
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17
Q

What are the routes of administration for antibiotics ?

A
  • oral
  • topical
  • IV
  • intramuscular
  • intrathecal
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18
Q

What chemical properties affect the distribution of drugs?

A
  • Lipid soluble - well absorbed + widely distributes, can lead to accumulation
  • Polar - extracellular, low vol of distribution, pKa/pH dependent
  • Protein binding - limits distribution, displaces other drugs
19
Q

What are difficult targets for drugs to reach?

A
  • BBB
  • Prostrate
  • Eye
  • Intracellular bacteria
20
Q

What are easy targets for drugs to reach?

A
  • Inflammation - due to increased vasodilation + vasc permeability
  • Pregnancy + breastfeeding
21
Q

Why is it hard for dugs to cross the BBB?

A
  • Tight junctions + active pumping mechanisms
22
Q

Which antibiotic can penetrate the BBB?

A

Chloramphenicol

23
Q

What affect do inflamed meninges have on antibiotic penetration?

A

More permeable to penicillin = rapid penetration of drug into CSF

24
Q

Which antibiotics are used for intracellular bacteria?

A
  • Macrolides - Azithromypcin + Clarithromycin

- Fluroquinolones - Ciproflaxcin

25
Q

Are Neisseria Gonorrhoea intracellular bacteria?

A

No

Chlamydia IS

26
Q

How is Gonorrhoea treated?

A

Azithromycin often used in combination with Cephalosporins as…

  • co-infection with Chlamydia
  • prevention of development of resistance to Cephalosporins
27
Q

How are antibiotics eliminated?

A
  • Liver + Kidneys
  • UTI = renal impairment = accumulation toxicity
  • Elderly patients = reduced kidney function
28
Q

What are the types of ADR’s in patients?

A 
Type A:
- predictable 
- dose-related
- gentamycin - contra indicated in renal dysfunction + elderly 
Type B: 
- unpredictable 
- immune mediated 
- penicillin allergy (IgE antibody against penicillin) - rash - anaphylactic shock
29
Q

What are the ADR’s of Tetracycline?

A

Ca binding: in children affect bone + teeth growth

30
Q

What are the ADRs of Chloramphenicol?

A
  • Lipophilic so can easily penetrate mitochondria

= interferes with mitochondrial protein synthesis = Grey baby syndrome = under developed hepatic function

31
Q

Describe the antibiotic spectrum

A
  • Narrow: only few bacteria respond
  • Extended: wider range
  • Broad: v. wide range - risk of damage to commensal flora = superinfection
32
Q

What is a superinfection an d what causes it?

A

= after killing of commensal flora

  • Tetracycline e.g. candida
  • Clindamycin or Penicillins = C.diff infection = pseudomembranous colitis
33
Q

What is polypharmacy?

A

Interference with breakdown of other drugs via competition/inhibition/activation

e.g. Warfarin, Oral contraceptives, Prednisone

34
Q

What is the effect of competition of drugs on liver function?

A
  • competition for same metabolic pathway
  • shortage of enzymes
  • slower metabolism
  • longer half life
35
Q

What is antibiotics inhibit metabolism?

A

Fluorquinolones + Macrolides

Longer half life e.g. warfarin = bleeding

36
Q

What antibiotics enhance metabolism?

A

Rifampicin - reduces half life of oral contraceptives by increasing metabolic activity of Liver

37
Q

What factors should you consider when prescribing antibiotics?

A

Status of patient:

  • Neonates - under developed haptic function
  • Children - bone + teeth (tetracyclines) + cartilage growth (fluoroquinolones)
  • Preg + breast feeding - drugs cross placenta
  • Elderly - renal function + polypharmacy
  • Allergies - Beta lactam antibiotics
  • Poor perfusion - diabetes
38
Q

Which people are more susceptible to infections?

A
  • immune deficiencies
  • immunosuppressive drugs
  • anti-cancer drugs
  • age
  • diabetes
  • alcoholism
  • malnutrition
  • immune-privileged sites (brain, placenta, testis, eyes)
39
Q

What is the difference between bacteriostatic and bactericidal antibiotics?

A
  • Bacteriostatic: stops growth
  • Bactericidal: kills

For patients more susceptible to infection - increase the dose/duration or use bactericidal

Proper functioning IS - bacteriostatic enough but bacteria would start to grow again in immune-compromised

40
Q

Why are combination of antibiotics used?

A
  • prevents resistance
  • in serious infection
  • infection with 1+ microorganism
  • unknown microorganism
  • enhances efficacy: synergism
41
Q

What is synergism?

A

Most favourable combination of antibiotics
e.g. cell wall synthesis inhibits weaken ell wall + facilitate entry of ahminoglycosides + fluoroquinolone which can’t penetrate cell wall

42
Q

How does antibiotic resistance work?

A

Penicillin resistance:
- Bacteria have B-lactamases which cleaves beta-lactam ring of some penicillins + cephalosporins = inactivation

Quinolone resistance:
Bacteria have mutated tropoisomerases that antibiotic can’t bind to and/or Qnr plasmids

43
Q

How do B-lactamase inhibitors work?

A

e. g. clavulanic acid
- Block action of B-lactamase by acting as substrate
- No antibacterial activity itself

Case 2 (7 decks)

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