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Principles of Disease > Antimicrobial Chemotherapy > Flashcards

Antimicrobial Chemotherapy Flashcards

1
Q

What are antibiotics effective against?

A

Bacteria?

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2
Q

What does bactericidal mean?

A

Antimicrobial that kills bacteria.

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3
Q

What does bacteriostatic mean?

A

Antimicrobial that inhibits the growth of bacteria.

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4
Q

What is the MBC?

A

Minimum bactericidal concentration- minimum concentration required to kill the bacteria.

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5
Q

What is the MIC?

A

Minimum inhibitory concentration- minimum concentration required to inhibit the growth of the bacteria.

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6
Q

What are the routes of antimicrobial administration?

A

Topical
Systemic
Parenteral

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7
Q

How are topical antimicrobials administered?

A

Applied to a surface (skin/mucous membranes)

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8
Q

How are systemic antimicrobials administered?

A

Taken internally (oral/parenteral)

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9
Q

How are parenteral antimicrobials administered?

A

Intravenously.

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10
Q

What are the 3 areas of metabolic activity that antimicrobials use to kill/inhibit bacteria?

A

Inhibition of the cell wall synthesis
Inhibition of protein synthesis
Inhibition of nucleic acid synthesis

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11
Q

What drugs inhibit cell wall synthesis?

A

Beta-lactams (Penicillin and Cephalosporins)

Glycopeptides

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12
Q

What are beta-lactams and what are they effective against?

A

Bactericidal

Effective against gram positive bacteria

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13
Q

How do beta-lactams work?

A

They disrupt peptidoglycan synthesis by inhibiting the enzymes (PBPs) which are responsible for cross-linking the carbohydrate chains.

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14
Q

Why are many gram-negative bacteria resistant to beta-lactams?

A

Inability to penetrate the gram-negative cell wall.

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15
Q

What are glycopeptides and what are they effective against?

A

Bactericidal

Effective against gram-positive bacteria

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16
Q

How do glycopeptides work?

A

They act on cell wall synthesis at a prior cell to B-lactams; inhibiting the assembly of a peptidoglycan precursor.

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17
Q

How are glycopeptides administered and why?

A

Parenterally- not absorbed in the GI tract.

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18
Q

Give an example of a toxic glycopeptide.

A

Vancomycin

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19
Q

What drugs inhibit protein synthesis?

A 
Aminoglycosides 
Macrolides
Tetracyclines
Oxazilidinones 
Cyclic lipopeptide
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20
Q

What are aminoglycosides used for?

A

Bactericidal (concentration-dependent)

Treat gram-negative infections

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21
Q

What is the most common aminoglycoside?

A

Gentamycin- toxic.

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22
Q

What are macrolides used for?

A

Bactericidal / bacteriostatic

Treat gram-positive infection

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23
Q

What category of patients are macrolides particularly useful in?

A

Patients who are allergic to penicillin.

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24
Q

What are tetracyclines used for?

A

Bacteriostatic

Treat gram-positive infection

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25
Q

What is a disadvantage of macrolides and tetracyclines?

A

Increasing antibiotic resistance (S.aureus/S.pyogenes/Strep)

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26
Q

What are oxazolidinones used for?

A

Bacteriostatic/bactericidal

Gram-positive infection

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27
Q

Give an example of an oxalidinone.

A

Linezolid- reserved for serious infection (MRSA).

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28
Q

What are cyclic lipopeptides used for?

A

Bactericidal (strong)

Gram-positive infection

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29
Q

Give an example of a cyclic lipopeptide .

A

Daptomycin

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30
Q

What drugs inhibit nucleic acid synthesis?

A

Purine synthesis inhibition drugs

Fluoroquinolones

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31
Q

How do drugs work in purine synthesis inhibition?

A

Bacteriostatic but can kill when combined.

Combined form is co-trimoxazole.

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32
Q

How do fluoroquinolones work?

A

Bactericidal

Gram-negative including pseudomonas.

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33
Q

Why can fluoroquinolones not be used in children?

A

Adverse effect on cartilage development.

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34
Q

Give an example of a fluoroquinolone.

A

Ciprofloxacin / levofloxacin.

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35
Q

What is the clinical definition of antibiotic resistance?

A

An antibiotic is considered to be resistant when it is unable to respond to attainable levels of that drug in tissues.

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36
Q

How is antibiotic resistance measured for clinical practice?

A

Sensitivity is measured in laboratory.

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37
Q

What are the two types of antibiotic resistance?

A

Inherent (due to mutation/changes etc)

Intrinsic (natural resistance through binding etc)

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38
Q

How does the widespread use of antibiotics lead to resistance?

A

Creates a selective pressure and encourages new resistant organisms to outgrow sensitive strains.

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39
Q

What are B-lactamases?

A

B-lactamases are bacterial enzymes which cleave the B-lactam ring of the antibiotic and thus render it ineffective.

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40
Q

What bacteria produce B-lactamases?

A

Most strains of staphylococcus aureus

Many gram-negative bacteria

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41
Q

How is B-lactamase combatted?

A

Modification of the antibiotic side chain, producing a new antibiotic resistant to the effects of B-lactamse
(Co-trimoxaclav- Amoxycillin + Clavulanic acid).

To produce a second component (B-lactamase inhibitor) to the antibiotic- preventing enzyme degradation.
(Flucloaxcillin- modified form of penicillin).

42
Q

What drugs are resistant to B-lactamases?

A

Co-trimoxaclav

Flucloaxicillin

43
Q

What are ESBL’s?

A

Extended spectrum B-lactamases:
Problem in hospitals with some gram-negative organisms- ESBL carrying patients have selective infection control measures in addition to usual regulations.

44
Q

What are carbapenems?

A

Very strong antibiotic agents which are used for the treatment of moderate/high-risk infections.

45
Q

What are carbapenems reserved for?

A

Multi-drug resistant (MDR) bacterial infection.

46
Q

What class of antibiotics are carbapenems in?

A

B-lactam.

47
Q

What are CPE/CRE?

A

Carbapenemase producing enterobacteriae

Carbopenem resistant enterobacteriae

48
Q

What are the major issues with CPE/CRE?

A

Carbopenem resistance is mainly an issue in gram-negative organisms and is becoming a huge problem in terms of clinical infection control and the fact that there are often no antimicrobial therapies available for it.

49
Q

How does alteration of PBP target sites allow resistance?

A

Altering the target sites for penicillin binding proteins can allow resistance as the structure changes and penicillin is thus unable to bind.

50
Q

How do alterations in the PBP target sites develop?

A

Mutations in the PBP gene conferring structural change.

51
Q

What is the best known example of PBP target site alterations causing antibiotic resistance?

A

MRSA.

52
Q

What is MRSA?

A

MRSA refers to any staphylacoccus aureus which has, through horizontal gene transfer/mutations, developed multiple drug resistance to B-lactams.

53
Q

How are bacteria resistant to B-lactams treated?

A

Flucoaxicillin not MRSA
Vancomycin
Linezolid

54
Q

Is glycopeptide resistance common?

A

Gram-positive resistance to vancomycin has been uncommon but is now developing.

55
Q

What are glycopeptide resistant bacteria called?

A

VRE (Vancomycin resistant enterococci)

56
Q

How does resistance to glycopeptides work?

A

Vancomycin acts by inhibiting the production of a peptidoglycan precursor in cell wall formation. In VRE, the peptidoglycan precursor to which vancomycin usually binds has an altered structure.

57
Q

Why is VRE a problem?

A

Could potentially spread into S.aureus.

58
Q

What is benzyl penicillin used to treat?

A

Gram-positive infection
Intravenous administration
Best choice of IV for serious streptococcus pneumonia.

59
Q

What is amoxycillin used to treat?

A

Gram-negative infection
Better oral absorption
20-30% coliforms resistant.

60
Q

What is ampicillin used to treat?

A

Gram-negative infection

Better oral

61
Q

What is co-amaxiclav used to treat?

A

Gram-negative

Combines amoxycillin with clauvanic acid to inhibit B-lactamase.

62
Q

What is flucoaxicillin used to treat?

A

Staphylococci

Modified form of penicillin resistant to B-lactamase

63
Q

What is piperacillin used to treat?

A

Broad spectrum, extensive gram-negative cover, pseudomonas

64
Q

What is imipenem used to treat?

A

Most bacterium including anaerobes. (widest range)

65
Q

What is meropenem used to treat?

A

Carbopenem- wide range of most bacterium including anaerobes.

66
Q

What do cephalosporins treat?

A

Gram positive/negative infection

Described in generations.

67
Q

How does cephalosporin activity relate with generations?

A

Gram negative activity increase from first to subsequent generations.
Activity against gram positive activity decreases from first to subsequent generations.

68
Q

What are the glycopeptides called and how are they administered?

A

Gram positive only
Vancomycin
Teicoplanin

69
Q

Describe an example of an aminoglycoside.

A

Gentamycin- toxic

Parenteral administration

70
Q

How do tetracyclines act?

A

Broad spectrum

Useful in chlamydia/resp. tract infections

71
Q

Give examples of macrolides and their use.

A

Allergy to penicillin:
Erythromycin
Clarithromycin
Azithromycin (chlamydia)

72
Q

Give an example of an oxazolidinone and its use.

A

Linezolid- MRSA use

73
Q

Give an example of a cyclic lipopeptide and its use.

A

Daptomycin- Gram positive and MRSA use

74
Q

What agents are used only in the treatment of UTIs?

A

Nalidixic acid

Nitrofurantoin

75
Q

What are quinolones used to treat?

A

Gram-negative, pseudomonas

76
Q

What are the Fluoroquinolones?

A

Ciprofloxacin / Levofloxacin

77
Q

Why are Fluoroquinolones not used in paediatrics?

A

Disruption to cartilage development.

78
Q

What is the incidence of ADR’s dependent on?

A

Dosage and drug.

79
Q

What happens in immediate hypersensitivity to an antibiotic?

A

Anaphylactic shock (parenteral administration of the antibiotic)- IgE mediated response occurs within minutes of administration. Can include itching, nausea, urticaria, vomiting, wheezing and shock. Laryngeal oedema can prove fatal unless the airway is cleared.

80
Q

What happens in delayed hypersensitivity to an antibiotic?

A

Takes hours or days to develop, immune complex or cell-mediated mechanism. Can include rashes, fever, serum sickness.

81
Q

What are the gastrointestinal side effects of antibiotics?

A

Vomiting / nausea / diarrhoea

82
Q

Why is thrush a common side effect?

A

Suppression of normal flora, resulting in growth of resistant organisms.

83
Q

What body systems often experience side effects?

A

Liver and renal (nephrotoxicity of excretion)

84
Q

How can antibiotics affect haematology?

A

There can be a toxic effect on the bone marrow resulting in the selective depression of one cell line or unselective depression of all bone marrow elements.

85
Q

When should antibiotics be prescribed?

A

When absolutely necessary.

86
Q

When is antimicrobial prophylaxis used?

A

Patients in close contact with contagious others.

Following surgery with high post-op infection rates.

87
Q

What is the simplest type of therapy?

A

Monotherapy

88
Q

What are the 3 outcomes of antimicrobials being used in combination?

A

Additive
Antagonistic- combined effect less than individual
Synergistic- combined effect greater than individual

89
Q

What antibiotics should be monitored even more closely?

A

Those with a low therapeutic index.

90
Q

Why would the laboratory monitor the serum levels of antibiotic?

A
  1. To ensure that the therapeutic levels have been achieved

2. To ensure that the levels are not high enough to reach toxicity

91
Q

Do antibiotics affect fungal infection?

A

No.

92
Q

What are the 4 types of fungal drug?

A

Polyenes
Azoles
Allylamines
Echinocandins

93
Q

What do polyenes do?

A

Active against yeast and moulds

94
Q

What do azoles do?

A

Inhibit ergosterol synthesis.

95
Q

What do allylamines do?

A

Suppress ergosterol synthesis at various points

Terbinafine

96
Q

What do echinocandins do?

A

Inhibit synthesis of gluten polysaccharide.

97
Q

Do antibiotics affect viruses?

A

No.

98
Q

What is aciclovar used to treat?

A

Herpes

99
Q

What therapy is usually given for HIV?

A

Combination triple-drug therapy.

100
Q

What are Interferon-A and ribavirin used for?

A

Chronic hepatitis B/C.

101
Q

What are ribavirin and zanamivir used for?

A

Viral respiratory infection.

102
Q

What must still be monitored in viral therapy?

A

Balance of therapeutic index/toxicity and links to resistance.

Principles of Disease (22 decks)

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