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PoD topics > Antimicrobial chemotherapy > Flashcards

Antimicrobial chemotherapy Flashcards

1
Q

What is a bactericidal?

A

An antimicrobial that KILLS bacteria (e.g. penicillins)

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2
Q

What is a bacteriostatic?

A

an antimicrobial that INHIBITS the growth of bacteria

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3
Q

What is a sensitive organism?

A

Organism which IS inhibited or killed by levels of the antimicrobial that are available at the site of infection

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4
Q

What is a resistant organism?

A

Organism which is NOT killed or inhibited by the levels of the antimicrobial that are available at the site of infection

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5
Q

What is MIC (minimal inhibitory concentration)?

A

minimum concentration of the antimicrobial needed to INHIBIT visible growth of a given organism

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6
Q

What is MBC (minimal bactericidal concentration)?

A

minimal concentration of the antimicrobial needed to KILL a given organism

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7
Q

What is a topical route of administration?

A

applied to a SURFACE, usually skin or to mucous membranes (e.g. conjunctiva)

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8
Q

What is a systemic route of administration?

A

taken INTERNALLY, either orally or parenterally (injection)

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9
Q

what is a parental route of administration?

A

administered either INTRA-VENOUSLY (IV) or INTRA-MUSCULARLY (IM), occasionally subcutaneously

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10
Q

What are the 2 possible actions that antibiotics can do?

A
  1. inhibit bacteria

2. kill bacteria

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11
Q

What are the 3 sites of antibiotic action?

A
  1. inhibition of cell wall synthesis
  2. inhibition of protein synthesis
  3. inhibition of nucleic acid synthesis
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12
Q

What are 2 examples of antibiotics which inhibit cell wall synthesis?

A

Penicillins and cephalosporins

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13
Q

What are 2 examples of antibiotics which inhibit protein synthesis?

A

Gentamicin and erythromycin

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14
Q

What are 2 examples of antibiotics which inhibit nucleic acid synthesis?

A

Trimethoprim and ciprofloxacin

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15
Q

What family of antibiotics are penicilin and cephalosporins?

A

Beta-lactam antibiotics (inhibit cell wall synthesis)

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16
Q

How does penicillin and cephalosporin inhibit the cell wall synthesis?

A

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

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17
Q

What is another name for the enzymes involved in the peptidoglycan synthesis?

A

Penicillin-binding proteins (PBPs)

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18
Q

What happens once the cell wall synthesis has been disrupted?

A

The organism is killed (by autolytic enzymes; self digestion by enzymes from the body)

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19
Q

What is the name of the original naturally occurring Beta lactam?

A

Benzyl penicillin (penicillin G)

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20
Q

Why have many semi-synthetic derivatives of Benzyl penicillin (penicillin G) have been produced?

A

they have an extended spectrum of action

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21
Q

What type of organisms are often resistant to benzyl penicillin? And why?

A

Gram negative bacteria: because of the impermeability of the gram negative cell wall

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22
Q

How do we categorise and describe cephalosporins?

A

“In generations”- more or less in the chronological order of first appearance

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23
Q

What are the 2 glycopeptide antibiotics which are common in clinical usage?

A
  • vancomycin

- teicoplanin

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24
Q

What do glycopeptide antibiotics (vancomycin and teicoplanin)

A

Act on cell wall synthesis at a stage prior to Beta-lactams, inhibiting assembly of peptidoglycan precursor (bind to amino acids within cell wall to prevent assembly of peptidoglycan/no units added)

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25
Q

What groups of organisms do glycopeptide antibiotics act on and why?

A

Only on GRAM POSITIVE; as they cannot penetrate gram negative cell wall

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26
Q

How are peptidoglycan antibiotics administered?

A

Given parenterally/intravenous (injection) except in special circumstances as they are not absorbed in GI tract

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27
Q

When are glycopeptide antibiotics used on patients? (3)

A
  • in severe cases/ critically ill patients
  • when patient is hypersensitive to Beta-lactams
  • patients infected with Beta-lactam resistant organisms
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28
Q

What is more toxic, vancomycin or teicoplanin?

A

Vancomycin

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29
Q

What are some side effects of vancomycin? (3)

A
  • ototoxicity
  • nephrotoxicity
  • skin rashes
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30
Q

Why do pre-dose levels of vancomycin need to be closely monitored?

A

To ensure serum concentration is high enough to be therapeutic but not so high that it becomes toxic

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31
Q

What is the main dosing advantage of teicoplanin?

A

It can have single daily dosing

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32
Q

The spectrum of activity of vancomycin and teicoplanin is the same, so what influences mainly which one is used?

A

the cost

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33
Q

What family of antibiotics does gentamicin belong to?

A

Aminoglycoside

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34
Q

What is the primary organism that aminoglycosides are used for?

A

Gram negative bacteria (especially serious coliform infections)

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35
Q

Which group of gram positive bacteria are sensitive to gentamicin?

A

Staphylococci (streptococci are not)

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36
Q

How are aminoglycosides administered?

A

Injectable/intravenously rather than orally

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37
Q

Is gentamicin a common and cheap aminoglycoside antibiotic?

A

yes

38
Q

What can toxicity of gentamicin lead to?

A

Renal and hearing problems

39
Q

What is a dosing administration for gentamicin?

A

Single daily dosing

40
Q

What does gentamicin require because of its toxicity? (2)

A
  • careful dosing regime

- careful monitoring levels

41
Q

What 4 antibiotic families inhibit protein synthesis in bacteria?

A
  • aminoglycosides
  • macrolides and tetracyclines
  • oxazolidinones
  • cyclic lipopeptide
42
Q

What are 2 common macrolides?

A

Erythromycin and clarythromycin

43
Q

What groups of bacteria do mactolides treat?

A

Gram positive bacteria

44
Q

What sort of patients are usually treated with mactolides?

A

Patients who are penicillin allergic

45
Q

What 3 gram positive bacteria species have a 10% rate of being resistant to mactolides?

A
  • staph. aureus
  • strep. pneumioniae
  • strep. pyogenes
46
Q

Clarithromycin provides a better cover for what gram negative bacteria because of good penetrating tissue properties?

A

Haemophilus Influenzae

47
Q

What is the main oxazolidinone antibiotic used?

A

Linezolid

48
Q

What is lizezolid (oxazolidinone) particularly good for treating?

A

Good activity against MRSA

49
Q

How is linezolid (ozaxolidinone) administered?

A

given orally

50
Q

What patients is linezolid (oxazolidinone) used for?

A

Patient with serious infection (severe infection), often with strains of bacteria which are resistant to other antibiotics

51
Q

What group of bacteria is linezolid used for treating?

A

Gram positive bacteria

52
Q

What is the main cyclic lipopeptide antibiotic? What is it used to treat?

A

Deptomycin; used to treat MRSA

53
Q

What 2 antibiotic families inhibit nucleic acid synthesis?

A
  1. trimethoprim and sulphamethoxazole

2. fluoroquinolones

54
Q

What do trimethoprim and sulphamethoxazole inhibit specifically in nucleic acid synthesis?

A

Inhibit purine synthesis (direct inhibition)

55
Q

What is the combined form of trimethoprim and sulphamethoxazole called? And what is it used for?

A

co-trimoxazole; used for chest infections such as bronchitis

56
Q

What is the main advantage of co-trimoxazole when it’s used for chest infections?

A

It’s less likely to cause C.difficile infections than broad spectrum antibiotics such as cephalosporin.

57
Q

Not including chest infections, what other condition is co-trimoxale used for?

A

Urinary tract infections (UTIs)

58
Q

What group of bacteria are trimethoprim and sulphamethoxazole used for?

A

Any UTI causing bacteria (positive or negative)

59
Q

What is the main fluoroquinolone antibiotic used?

A

Ciproflaxacin

60
Q

What does ciproflaxacin do?

A

Inhibits synthesis of nucleic acids more directly

61
Q

How can ciproflaxacin be administered?

A

Orally and parenterally

62
Q

What group of bacteria is ciproflaxacin used for?

A

Gram negative bacteria (including Pseudonomas)

63
Q

Why can’t ciproflaxacin (fluoroquinolone) be used in children?

A

Due to danger of interference with cartilage growth

64
Q

What is the name of the newer quinolone which is used?

A

Levoflaxacin

65
Q

What group of bacteria does levoflaxacin have a greater activity for?

A

Gram positive bacteria (e.g. pneumococcus)

66
Q

What are 2 types of resistance in bacteria?

A
  1. inherent or intrinsic resistance

2. acquired resistance

67
Q

What is inherent/ intrinsic resistance? What causes it?

A
  • ALL strains of a given bacteria species are naturally resistant to an antibiotic
  • the drug cannot penetrate the bacterial cell wall to exert its action
68
Q

what are 2 examples of inherent/intrinsic inheritance? (in terms of bacterial examples)

A
  • streptococci are always resistance to aminoglycosides

- gram negative bacteria are always resistant to vancomycin

69
Q

What is meant by acquired resistance?

A

Resistance may be present in some strains of species but not in others.

70
Q

What method is used to establish sensitivity of an individual and how resistant their strain of infection is to specific antibiotics?

A

Laboratory sensitivity testing

71
Q

What are the 2 ways in which resistance is ACQUIRED?

A
  1. Spontaneous mutation occurs which does not allow antibiotic to act on its target which has a changed structure and function
  2. Resistance can spread from organism to organism (or species to species), commonest mode of resistance, genes carried on plasmids and transposons (packets of DNA which insert themselves into chromosomes)
72
Q

Why is antibiotic resistance good? (if undesirable)

A

From biological perspective, it’s an evolutionary and selective advantage.
- it causes selective pressure and encourages new resistant organism to outgrow the sensitive strain

73
Q

What are 2 main mechanisms of Beta-lactam resistance?

A
  1. Beta-lactamase production

2. alteration of penicillin binding protein (PBP) target site

74
Q

What are Beta-lactamases and what do they do?

A

They are bacterial enzymes which cleave the Beta-lactam ring of the antibiotic and thus render it inactive

75
Q

Beta-lactamases have different patterns of activity on which two Beta lactam antibiotics?

A
  1. penicillin

2. cephalosporins (or both)

76
Q

What is the most popular bacteria which produced Beta-lactamase and are therefore resistant to benzylpenicillin?

A

Staphylococcus aureus

77
Q

In what bacteria groups are Beta-lactamases present in?

A

Both gram positive and gram negative bacteria

78
Q

What are the 2 ways to combat Beta-lactamase?

A
  1. introducing a second component to the antibiotic which is a Beta-lactamase inhibitor and protects antibiotic from enzymatic degradation
  2. Modifying the antibiotic side chains to produce an antibiotic which is resistant to the action of Beta-lactamase
79
Q

What is the best known Beta-lactamase inhibitor?

A

Co-amoxiclav

80
Q

What does co-amoxiclav consist of? (Beta-lactamase inhibitor)

A

consists of the antibiotic amoxicillin plus the Beta-lactamase inhibitor clavulanic acid

81
Q

What is the most common example of modifying an antibiotic side chain?

A

Flucloxacillin is a modified form of penicillin (flucloxacillin is resistant to Beta-lactamase and can be used to treat s.aureus)

82
Q

What are ESBLs? What group of bacteria produce them?

A

Extended Spectrum Beta-lactamases; produced by gram negative bacteria

83
Q

Why are ESBLs an increasing problem in hospitals?

A

They can break down third generation cephalosporins and penicillins making the organism resistant to ALL Beta-lactam antibiotics

84
Q

What are CPE/CRE bacteria resistant to?

A

Carbapenems (a very broad class of antibiotics)

85
Q

What group of bacteria are often CPE/CRE (carbapenemase producing/resistant enterobacteriaceae)?

A

Gram negative bacteria

86
Q

Why are CPE/CRE extremely problematic in hospitals?

A

Makes bacteria resistant to nearly all classes antibiotics sometimes leaving NO antimicrobial options for therapy.

87
Q

What are PBPs? (penicillin binding proteins)

A

Enzymes which are involved in in peptidoglycan synthesis and which are inhibited by binding of penicillins and cephalosporins.

88
Q

What do mutations in PBP genes cause?

A

Result in a modified target site to which B lactam antibiotics will no longer bind to ( penicllin and cephalosporins)

89
Q

What bacteria demonstrates the alteration of PBP target sites?

A

Methicillin resistant staph aureus (MRSA)

90
Q

What are VRE (vancomycin resistant enterococci)?

A

cause the peptidoglycan precursor (amino acids) to which vancomycin normally binds to, have an altered target site

91
Q

What is the biggest concern scientists have about VRE?

A

the resistance might be passed onto staph aureus producing staph. aureus which is resistant to vancomycin leading to major problems in public health

92
Q

What is another form of resistance mechanism that is not involving Beta-lactamase or alteration of PBPs? (2)

A

Blocking the transport of drug to the cell or actively transporting it out

PoD topics (34 decks)

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