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Microbiology for Dentists > 39. Antibiotics > Flashcards

39. Antibiotics Flashcards

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1
Q

Why with developing antimicrobial resistance do we not make new antibiotics?

A
  • number of antibioitcs reaching market has dropped hugely over past 10 years
  • resistance reduces effective life of a product
  • too little profit, government restrictions, lack of new biological targets
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2
Q

3 antibiotic modes of action

A
  • bactericidal
  • bacteriostatic
  • bacteriolytic
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3
Q

Explain bacteriostatic antibiotics

A
  • hold everything in steady growth state
  • total cells stays the same over time and so does viable cells
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4
Q

Explain bacteriocidal antibiotics

A
  • after addition of it, number of viable cells rapidly decreases
  • total number of cells stays the same
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5
Q

Explain bacteriolytic antibiotics

A
  • both total and viable cells decrease drastically in numbers
  • kills bad and normal cells
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6
Q

Common bacterial targets for antibiotics are …

A
  • cell membrane
  • cell wall
  • protein synthesis
  • RNA polymerase
  • DNA synthesis
  • folate metabolism
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7
Q

Penicillins target what?

A

cell wall

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8
Q

Sulphonamides target what?

A

folate metabolism

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9
Q

Fluroquinolones target what?

A

DNA synthesis

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10
Q

Macrolides target what?

A

protein synthesis

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11
Q

Tetracycline target what?

A

protein synthesis

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12
Q

Why do antibiotics target what they do?

A
  • unique components to invading organism
  • non toxic to host (relatively)
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13
Q

Structure of penicillins

A
  • beta lactam ring
  • a lactam is a cyclic amide
  • a beta-lactam is a lactam with a heteroatomic ring structure, consisting of 3 carbon atoms and 1 nitrogen atom
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14
Q

List types of penicillins

A
  • benzylpenicillin
  • beta-lactamase-resistant forms e.g flucloxacillin
  • broad-spectrum penicillins e.g amoxicillin
  • extended-spectrum penicillins
  • reversed-spectrum penicillins
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15
Q

Benzylpenicillin are the … form and not very active against …

A
  • original
  • gram negatives
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16
Q

Explain early penicillins

A
  • acid labile
  • given orally (not very well absorbed) or parenteral route (slow IV, preverable IM, high availability)
  • narrow spectrum of activity - gram positives but only a few gram negs
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17
Q

Main difference between benzylpenicillin and broad-spectrum penicillins

A
  • broad spec more effective against gram negative bacteria
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18
Q

Penicllin development

A
  • needed derivatives of penicillin which could treat a wider range of infections
  • offered a broader spectrum of activity than original penicillins e.g ampicillin
  • amino group facilitates penetration of outer membrane of gram neg bacteria
  • further development led to amoxicillin with improved duration of action
  • much better absorption profile
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19
Q

Beta-lactamase-resistant forms are important against …

A

beta-lactamase producing bacteria

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20
Q

Extended spectrum penicillins are important against …

A

pseudomonads

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21
Q

Reversed spectrum penicillins have greater activity against …

A

gram neg than gram pos

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22
Q

Why is beta lactamase bad for penicillin?

A
  • defence mechanism from bacteria
  • breaks down lactam ring so antibiotic can’t act
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23
Q

How does a penicillin target the cell wall?

A
  • penicillins - beta-lactam antibiotics
  • inhibit the enzyme (transpeptidases) which are responsible for reaction to establish cross links in peptidoglycan cell wall
  • bacteria swell and rupture
  • only effective against multiplying organisms
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24
Q

How are bacterial cell walls strong?

A
  • complex polymer peptidoglycan forms straight chains cross-linked together
  • made of N-acetylglucosamine and N-Acetylmuramic acid
25
Q

Absorption of penicillin

A
  • vary when given orally
  • delayed release preparations available (procaine and benzanthine)
26
Q

Distribution of penicillin

A
  • widely distributed in body
  • although concentrations in tissues and body fluids vary
  • don’t normally enter CSF (except with meninges inflammation)
27
Q

Metabolism of penicillin

A

short half life (30-80 minutes)

28
Q

Excretion of penicillin

A
  • mainly through kidney with 90% excreted by tubular secretion
  • clearance reduced in neonates
  • reduce excretion rate by use of probenecid, which inhibits tubular secretion
29
Q

Adverse reactions to penicillins

A
  • hypersensitivity (seen with all penicillins, rash, fever, anaphylactic shock, serum sickness, 10-15% will show repeat reaction)
  • GIT disturbance (altered gut flora)
  • haemostatic effects - blood clotting
30
Q

Give chain of folate biosynthesis

A
  • pABA with dihydropteroate forms folate
  • folate with dihydrofolate forms tetrahydrofolate
  • goes to synthesis of thymidylate etc to form DNA
31
Q

How does sulphonamide work?

A
  • not used in clinical practice
  • target metabolism
  • PABA precursor to folic acid - sulphonamides are a derivative of PABA, look similar sturcturally
  • can bind to same enxymes in synthetic pathway and stop it from working
  • work specifically on dihydropteroate whereas trimethoprim (a type of sul) works on dihydrofolate reductase
32
Q

Is sulphonamide selective?

A
  • bacteriostatic in nature
  • stops folic acid entering the bacterial cell
33
Q

Absorption of sulphonamide

A
  • 80-100% of drug given orally is absorbed from stomach and intestines
34
Q

Distribution of sulphonamide

A
  • widely distributed including CNS
35
Q

Metabolism of sulphonamide

A

occurs in liver by n-acetylation

36
Q

Excretion of sulphonamides

A
  • in urine after around 30 minutes
37
Q

Adverse reactions to sulphonamide

A
  • photosensitivity
  • Stevens-Johnson syndrome (less than 1% frequency)
  • hemopoietic disturbances
38
Q

Explain fluoroquinolones

A
  • broad spectrum
  • effective against Gram pos and neg
  • discovered during search for antimalarial drugs
  • targets DNA replication via type II topoisomerases
39
Q

What do quinolones typically inhibit?

A
  • DNA-gyrase in Gram negatives
  • topisomerase in Gram-positives
40
Q

What does DNA-gyrase do?

A
  • regulates amount of supercoiling
  • facilitates movement of transcription and replication complexes through DNA helix
  • removes knots and helps fold DNA
41
Q

What does DNA topoisomerase IV?

A
  • homologue of gyrase
  • unlinks daughter DNA replicons
42
Q

Absorption of quinolones

A

oral admin more effective

43
Q

Distribution of quinolones

A
  • very well absorbed in upper GIT
44
Q

Metabolism of quinolones

A

potent inhibitor of CYP1A2

45
Q

Excretion of quinolones

A

mainly excreted in tubular secretion

46
Q

Adverse reactions to quinolones

A
  • hypersensitivity
  • GIT disturbance
47
Q

Explain prokaryotic ribosomes

A
  • 70S size
  • 50S comprises 2 subunits of 23S and 5S
  • 50S is the main site of protein synthesis
48
Q

Action of macrolides

A
  • block translocation of newly forming peptide
  • binds to site near RNA exit tunnel
  • causes peptidyl-transferase RNA drop off
49
Q

Absorption of macrolides

A
  • oral admin requires protected tablets
  • to avoid inactivation by gastric juice
50
Q

Distribution of macrolides

A
  • diffuses readily into most tissues
  • doesn’t cross blood brain barrier
  • does cross placenta
51
Q

Metabolism of macrolide

A
  • metabolised by demethylation (CYP3A4)
  • can potentiate effects of other drugs
52
Q

Macrolides are excreted in …

A

bile

53
Q

Adverse reactions to macrolides

A
  • cholestatic hepatitis can occur after prolonged use of erythromycin estolate
  • GIT disturbances at large dose
  • transitory auditory impairment
  • hypersensitivity
54
Q

How do tetracyclines work?

A
  • interrupts elongation phase of synthesis
  • several binding sites on 30S RNA subunit
  • sterically inhibits transfer RNA binding - unbinds, rebinds, futile loop
55
Q

Absorption of tetracyclines

A
  • greater in fasting state
  • inhibited in concurrent ingestion of dairy products, metal ions, certain antacids
56
Q

Distribution of tetracyclines

A

widely
- enters most tissues

57
Q

Metabolism of of tetracyclines

A
  • relatively long half lifes (6-18 hrs) due to enterohepatic recirculation
58
Q

Excretion of tetracyclines

A

via both bile and kidneys via glomerular filtration

59
Q

List types of antibiotics

A
  • penicillin
  • sulphonamides
  • fluoroquinolones
  • macrolides
  • tetracyclines

Microbiology for Dentists (37 decks)

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