Antibiotics Flashcards

1
Q

MoA of antibiotics that acting on cell wall synthesis

A

Inhibition of cell wall synthesis -> bacteria dies

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2
Q

2 examples of classes of the antibiotics that act on cell wall synthesis

A
  • Beta-lactams: Penicillins, Cephalosporins
  • Glycopeptides: Bacitracin
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3
Q

MoA of antibiotics disturb cell membrane

A

Antibiotic binds to the cell membrane ->altering its structure -> cell membrane becomes more permeable -> disruption of osmotic balance -> leakage of cellular molecules -> increase water uptake -> cell death

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4
Q

(2) examples of classes of antimicrobials that ac by disruption of a cell membrane

A

Polymyxins and Polyenes (anti-fungal)

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5
Q

(2) examples of antibiotics that act by preventing DNA from being synthesised

A

Examples: Quinolines, nalidixic acid

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6
Q

Example of antibiotic that act by preventing of RNA being synthesised

A

Rifamycin

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7
Q

Examples of antibiotics that disturb protein synthesis by targeting 50s unit of ribosome

A

50s subunit: Erythromycin, Chloramphenicol

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8
Q

Examples of antibiotics that target protein synthesis at 30s unit of ribosome (2)

A

30s subunit: Tetracycline, Streptomycin

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9
Q

General mechanism of action of protein synthesis inhibitors

A

Subunit targeted by an antibiotic -> disruption of

ribosomes -> bacteria unable to make proteins

-> bacteria can stay alive but is unable to do

anything

(Therefore these antibiotics are bacteriostatic -

prevent bacterial growth)

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10
Q

Mechanism of action of inhibitors of folic acid metabolism

A
  • bacteria metabolise PABA (precursor) -> foliate (folic acid)
  • folic acid is essential for the synthesis of: thymine and adenine (2 out of 4 nucleic acids that make up DNA)

Antibiotics:

PABA cannot convert into folic acid -> prevent

DNA synthesis

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11
Q

(2) examples of antibiotics that act as folic acid inhibitors

A

Sulphonamides, Trimethoprim

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12
Q

Mechanism of action of beta-lactams

A

Beta-lactams = Penicillins

Mechanism of action: inhibit cell wall synthesis = bactericidal

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13
Q

Mechanism of resistance to beta-lactams

A

Mechanism of resistance: production of beta - lactamases -> hydrolysis of beta - lactam -> antibiotic structure is broken -> drug inactivation

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14
Q

What drugs can overcome resistance from beta-lactamases?

A

Co-amoxiclav and Tazocin

Can inhibit beta-lactamase so can overcome resistance -> however have little antimicrobial effect -> given in combination with amoxicillin and Pipercillin

  • mixed spectrum: gram positive and gram negative
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15
Q

MoA of cephalosporins

A

Cephalosporins = beta-lactams

MoA:inhibit cell wall synthesis = bactericidal

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16
Q

MoA of Carbapenems

A

Carbopenems= beta-lactams

Mechanism of action: inhibit cell wall synthesis = bactericidal (like all beta-lactams)

Binding to penicillin-binding proteins -> inhibition of cell wall synthesis

17
Q

Use of carbapenems

A
  • most stable beta-lactam -> broader spectrum of activity than penicillins and cephalosporins
  • broad spectrum (action against gram positive and gram negative organisms)
  • used against multi-drug resistant bacteria:
  • does not work against: MRSA, Enterococci and Pseudomonas)
  • last line of defence
  • used in hospitalised patients
18
Q

Example of antibiotics (2) that belong to glycopeptides class

A

Vancomycin (used for MRSA) and Teicoplanin

19
Q

Use of glycopeptides antibiotics

A
  • used only for gram positive bacteria
  • very toxic -> used as last line of defence (for patients critically ill or those with beta-lactam allergies)
  • narrow spectrum of action
  • bacterocidal only against enterococci
  • do not penetrate to CSF
  • usually given by IV
20
Q

MoA of glycopeptides antibiotic

A

Glycopeptides e.g. Vancomycin, Teicoplanin

Mechanism: bind to amino-acid within the cell wall* -> preventing the addition of new peptidoglycan units

-> inhibition of peptidoglycan synthesis -> inhibition of cell wall synthesis

21
Q

Side effects (3) of Vancomycin use

A
  • Red Man Syndrome - appears within 4 - 10 mins after administration of IV or after completion of infusion. Flushing, erythematous rash affecting face, neck and upper torso (as vancomycin mediate Ig- independent mast cell degranulation); Rx with antihistamines; symptoms less likely to occur with slow infusion (over at least 60 minutes)
  • Ototoxicity (rare)
  • Nephrotoxicity
22
Q

MoA of Aminoglycosides

A

Mechanism: act on 30s ribosomal unit -> block the initiation of translation -> misreading of mRNA

Examples: Gentamicin, Amikacin, Neomycin, Tobramycin

23
Q

Examples (4) of aminoglycosides

A

Examples: Gentamicin, Amikacin, Neomycin, Tobramycin

24
Q

Aminoglycosides

  • use
  • side effects
A

Examples: Gentamicin, Amikacin, Neomycin, Tobramycin

  • Effective against: gram -ve (except Streptococci and enterococci) and gram +ve
  • Side effects: Nephrotoxicity, Othotoxicity
25
Q

MoA of Tetracyclines

A

act on 30s ribosomal subunit -> block the attachment of tRNA to the ribosome

26
Q
  • Use of Tetracyclines
  • side effects
A
  • Effective against: many gram +ve and -ve, some parasites
  • Side effects: photosensitive rash, nausea, yellow teeth
27
Q

MoA of Macrolides

A

Mechanism: act on 50s subunit of a ribosome; prevent continuation of protein synthesis - bacteriostatic

Examples: Clarithromycin, Erythromycin

28
Q

Use of macrolides

A

Effective against: gram positive cocci, intracellular and anaerobes