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?

Study These Flashcards
A
  • complex polymer peptidoglycan forms straight chains cross-linked together
  • made of N-acetylglucosamine and N-Acetylmuramic acid
25
Absorption of penicillin
- vary when given orally - delayed release preparations available (procaine and benzanthine)
26
Distribution of penicillin
- widely distributed in body - although concentrations in tissues and body fluids vary - don't normally enter CSF (except with meninges inflammation)
27
Metabolism of penicillin
short half life (30-80 minutes)
28
Excretion of penicillin
- 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
Adverse reactions to penicillins
- 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
Give chain of folate biosynthesis
- pABA with dihydropteroate forms folate - folate with dihydrofolate forms tetrahydrofolate - goes to synthesis of thymidylate etc to form DNA
31
How does sulphonamide work?
- 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
Is sulphonamide selective?
- bacteriostatic in nature - stops folic acid entering the bacterial cell
33
Absorption of sulphonamide
- 80-100% of drug given orally is absorbed from stomach and intestines
34
Distribution of sulphonamide
- widely distributed including CNS
35
Metabolism of sulphonamide
occurs in liver by n-acetylation
36
Excretion of sulphonamides
- in urine after around 30 minutes
37
Adverse reactions to sulphonamide
- photosensitivity - Stevens-Johnson syndrome (less than 1% frequency) - hemopoietic disturbances
38
Explain fluoroquinolones
- broad spectrum - effective against Gram pos and neg - discovered during search for antimalarial drugs - targets DNA replication via type II topoisomerases
39
What do quinolones typically inhibit?
- DNA-gyrase in Gram negatives - topisomerase in Gram-positives
40
What does DNA-gyrase do?
- regulates amount of supercoiling - facilitates movement of transcription and replication complexes through DNA helix - removes knots and helps fold DNA
41
What does DNA topoisomerase IV?
- homologue of gyrase - unlinks daughter DNA replicons
42
Absorption of quinolones
oral admin more effective
43
Distribution of quinolones
- very well absorbed in upper GIT
44
Metabolism of quinolones
potent inhibitor of CYP1A2
45
Excretion of quinolones
mainly excreted in tubular secretion
46
Adverse reactions to quinolones
- hypersensitivity - GIT disturbance
47
Explain prokaryotic ribosomes
- 70S size - 50S comprises 2 subunits of 23S and 5S - 50S is the main site of protein synthesis
48
Action of macrolides
- block translocation of newly forming peptide - binds to site near RNA exit tunnel - causes peptidyl-transferase RNA drop off
49
Absorption of macrolides
- oral admin requires protected tablets - to avoid inactivation by gastric juice
50
Distribution of macrolides
- diffuses readily into most tissues - doesn't cross blood brain barrier - does cross placenta
51
Metabolism of macrolide
- metabolised by demethylation (CYP3A4) - can potentiate effects of other drugs
52
Macrolides are excreted in ...
bile
53
Adverse reactions to macrolides
- cholestatic hepatitis can occur after prolonged use of erythromycin estolate - GIT disturbances at large dose - transitory auditory impairment - hypersensitivity
54
How do tetracyclines work?
- interrupts elongation phase of synthesis - several binding sites on 30S RNA subunit - sterically inhibits transfer RNA binding - unbinds, rebinds, futile loop
55
Absorption of tetracyclines
- greater in fasting state - inhibited in concurrent ingestion of dairy products, metal ions, certain antacids
56
Distribution of tetracyclines
widely - enters most tissues
57
Metabolism of of tetracyclines
- relatively long half lifes (6-18 hrs) due to enterohepatic recirculation
58
Excretion of tetracyclines
via both bile and kidneys via glomerular filtration
59
List types of antibiotics
- penicillin - sulphonamides - fluoroquinolones - macrolides - tetracyclines
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