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Year 2 Clinical Pathology > Antibacterial Agents 1 > Flashcards

Antibacterial Agents 1 Flashcards

1
Q

What is meant by the term antibiotic?

A

Chemical products of microbes which kill or inhibit other organisms

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2
Q

What is meant by antimicrobial agents?

A

Overarching term including, antibacterial, antifungal, antiviral compounds.
It also includes antibiotics, synthetic compounds and semi synthetic compounds

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3
Q

What is meant by semi-synthetic compounds?

A

Modified antibiotics - to give them different antimicrobial activity/spectrum, pharmacological properties or toxicity

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4
Q

What is meant by the term bacteristatic?

A

Inhibit bacterial growth eg. protein synthesis inhibitors

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5
Q

What is meant by bactericidal?

A

Kill bacteria eg. cell wall-active agents

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6
Q

What is meant by MIC?

A

Minimum inhibitory concentration

The minimum conc of an Abx at which visible growth is inhibited

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7
Q

Would a more potent antimicrobial agent have a high or a low MIC?

A

Low

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8
Q

How can mode of bacterial killing change with concentration of an Abx?

A

Some Abx are bacteristatic at low concentrations and bactericidal at high concentrations

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9
Q

What is meant by synergism?

A

Activity of 2 antimicrobials together is greater than the sum of their activity seperately

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10
Q

What is meant by antagonism?

A

One antimicrobial agent diminishes the activity of another

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11
Q

What is meant by indifference?

A

Activity of an antimicrobial agent is unaffected by the addition of another

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12
Q

Give an example of synergism in clinical use?

A

beta-lactam and aminoglycaside combination therapy therapy of streptococcal endocarditis

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13
Q

What is meant by antibacterial targets?

A

The things or processes targeted or inhibited in a bacterial cell by an antibacterial agent, the most common are enzymes, molecules or structures (things bigger than molecules)

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14
Q

What is meant by selective toxicity of antibacterial agents?

A

They affect bacteria but not humans

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15
Q

Give 2 common ways in which selective toxicity of antibacterial agents is achieved?

A

1) Antibacterial target is not present in human host

2) Antibacterial target is significantly different in human host

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16
Q

Give 5 common antibiotic targets?

A

1) Cell wall
2) Protein synthesis
3) DNA synthesis
4) RNA synthesis
5) Plasma membrane

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17
Q

What is the major component of bacterial cell wall?

A

Peptidoglycan

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18
Q

Is peptidoglycan found in gram positive or gram negative bacteria?

A

Both

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19
Q

What is peptidoglycan made up of?

A

Polymer of glucose derivatives and amino acids N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG) which form cross links to form a network providing the bacteria with structural rigidity

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20
Q

Why does a cell wall as an antibacterial target provide ideal potential for selective toxicity?

A

No cell wall found in humans

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21
Q

Give 2 examples of Abx which are cell wall synthesis inhibitors?

A

1) Beta-lactams

2) Glycopeptides

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22
Q

What is the rough structure of beta-lactam Abx?

A

All contain the beta-lactam ring which is a 4-membered ring structure (C-C-C-N)

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23
Q

How do beta-lactam Abx prevent cell wall synthesis?

A

The beta-lactam ring they contain is a structural analogue of D-alanyl-D-alanine (one of the components of peptidoglycan) so beta-lactam Abx can interfere with ‘penicillin binding proteins’ which are transpeptidase enzymes involved in peptidoglycan cross linking and thus synthesis and maintenance of peptidoglycan - a major component of bacterial cell walls

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24
Q

Which was the first true Abx in clinical practise and what type was it?

A

Benzylpenicillin - a beta-lactam Abx

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25
Name the 4 types of beta-lactam Abx?
1) Penicillins 2) Cephalosporins 3) Carbapenems 4) Monobactams
26
What is the spectrum of penicillins?
Relatively narrow spectrum
27
What is the spectrum of cephalosporins?
Broad spectrum
28
What is the spectrum of carbapenems?
Extremely broad spectrum
29
What is the spectrum of monobactams?
Gram negative only
30
Name 3 common penicillins?
1) Benzylpenicillin 2) Amoxicillin 3) Flucloxacillin
31
Name 2 common cephalosporins?
1) Cefuroxime | 2) Ceftazidime
32
Name 2 common carbapenems?
1) Meropenem | 2) Imipenem
33
Name a common monobactam?
Aztreonam
34
Which type of bacteria do glycopeptides work against and why?
Only gram-positive bacteria as they are unable to penetrate gram-negative outer membrane porins
35
Name 2 common glycopeptides Abx?
1) Vancomycin | 2) Teicoplanin
36
What is the structure of glycopeptide Abx and how do they work?
Large molecules, bind directly to terminal D-Alanyl-D-Alanine on NAM pentapeptides. This inhibits binding of transpeptidases and thus peptidoglycan cross linking
37
How does protein synthesis occur in bacteria?
1) Translation of RNA into a protein takes place on a ribosome 2) Ribonucleoprotein complexes (2/3 RNA, 1/3 protein) 3) 50s and 30s subunits come together to form 70s initiation complex
38
Aminoglycosides kill bacteria how?
Protein synthesis inhibitors Bind to the 30s ribosomal subunit Mechanism of action not fully understood
39
In terms of Abx what does MLS stand for?
Macrolides, Lincosamides, Streptogramins
40
Give an example of 2 macrolides?
Erythromycin, Clarithromycin
41
Give an example of a lincosamide?
Clindamycin
42
How do the MLS category of Abx kill bacteria?
Protein synthesis inhibitors
43
How do lincosamides kill bacteria?
Protein synthesis inhibitors Bind to 50s ribosomal subunit - blockage of exit tunnel for newly synthesised protein Inhibit protein elongation
44
Name 2 tetracycline Abx?
1) Tetracycline | 2) Doxytetracycline
45
How do tetracylcines kill bacteria?
Protein synthesis inhibitors Bind to 30s ribosomal subunit Inhibit RNA translation - interfere with tRNA binding to rRNA
46
Give an example of an oxazolidnone?
Linezolid
47
How does the oxazolidinone linezolid kill bacteria?
``` Protein synthesis inhibitor Inhibits initiation of protein synthesis Binds to 50s ribosomal subunit Inhibits assembly of initiation complex May also bind to 70s subunit ```
48
Name 6 types of Abx which act by inhibiting protein synthesis in various ways?
1) Aminoglycosides 2) MLS (macrolides, Lincosamides, Streptogramins) 3) Tetracyclines 4) Oxazolidinones 5) Mupirocin 6) Fusidic acid
49
How do Trimethoprim and Sulfonamides kill bacteria?
Inhibit DNA Synthesis Inhibit folate synthesis which is a purine synthesis precursor Trimethoprim inhibits Dihydrofolate reductase Sulfonamides inhibit Dihydropteroate synthetase
50
Which enzyme is inhibited by trimethoprim?
Dihydrofolate reductase
51
Which enzyme is inhibited by sulfonamides?
Dihydropteroate synthetase
52
What is co-trimoxazole?
Trimethoprim and Sulfonamides combined
53
How do quinolones and fluoroquinolones kill bacteria?
Inhibit DNA synthesis Inhibit one or more of two related enzymes, DNA gyrase and topoisomerase IV, involved in remodelling of DNA during DNA replication
54
Give 3 examples of quinolones or fluoroquinolones?
1) Nalidixic acid 2) Ciprofloxacin 3) Levofloxacin
55
How does Rifampicin kill bacteria?
RNA synthesis inhibitor RNA polymerase inhibitor Prevents synthesis of mRNA
56
Give an Abx which targets the cell membranes of gram-negative bacteria?
Colistin
57
Give an abx which targets the cell membranes of gram positive bacteria?
Daptomycin
58
Dpatomycin has what kind of structure?
Cyclic lipopeptide which destroy plasma membranes
59
What are the 4 main possible adverse effects of use of Abx?
1) Adverse effects of all drugs 2) Generation of Abx resistance 3) Fungal infection 4) C.Diff infection
60
What are the possible adverse effects of all drugs? 3
1) General - nausea, vomiting, headache, skin rashes etc. 2) Infusion reactions (when drugs given IV) 3) Allergic reactions
61
What are the 2 main mechanisms of generation of Abx resistance through Abx treatment?
1) Selection of resistant strains in patients (resistant bacteria colonies no longer reduced by the presence of other bacteria as that is destroyed by abx) 2) Preferential colonisation on exposure to resistant strains (if pt on abx touches another pt, the resistant strains are most likely and able to colonise)
62
What is a common fungal infection caused by the use of Abx?
Superficial and invasive candidiasis (vaginal and oral thrush)
63
What are the specific adverse effects of aminoglycosides? 2
1) Reversible renal impairment on accumulation 2) Irreversible ototoxicity (toxic to the ear) (therapeutic drug monitoring indicated)
64
What are the specific adverse effects of beta-lactams?
Main problem is allergic reactions Generalised rash in 1-10% Anaphylaxis in approx. 0.01%
65
What is the specific adverse effect of linezolid?
Bone marrow depression
66
What symptoms would indicate an intolerance rather than an allergy to beta-lactams?
Nausea, diarrhoea, headaches etc
67
What symptoms would indicate a minor allergy to beta-lactams?
Non-severe skin rash
68
What symptoms would indicate a severe allergy to beta-lactams?
Anaphylaxis, Urticaria, angio-oedema, bronchospasm, severe skin reaction (Steven-johnsons syndrome)
69
What type of beta-lactam abx are safe to use in patients with a non severe penicillin allergy? 2
1) Cephalosporins | 2) Carbapenems
70
Which beta-lactam Abx is safe to use in patients with a severe penicillin allergy?
Aztreonam
71
What is the most commonly diagnosed cause of Abx associated diarrhoea?
C.Difficile infection
72
How does C.Diff cause infection due to Abx use?
Occasional constituent of the normal intestinal flora (in 20% of elderly people) Produces toxins A&B Assumed cause by abolition of colonisation resistance Combination of enterotoxin and spore production accounts for clinical features and transmissibility
73
What is significant about the hypervirulent C.Diff strain 027?
Causes more severe disease
74
What are the 4 common precipitating abx for C.Diff infection (the 4 C's)?
1) Co-amoxiclav 2) Cephalosporins 3) Ciprofloxacin 4) Clindamycin
75
What are the 4 less common precipitating abx for c.diff infection?
1) Benzylpenicillin 2) Aminoglycasides 3) Glycopeptides 4) Piperacillin-Tazobactam
76
What is the strategy for abx use?
Following a history taking and examination a clinical diagnosis is made, following this: 1) Empiric therapy - based on predicted susceptibility of likely pathogens and local antimicrobial policies Following a lab investigation you get a microbiological diagnosis, following this: 2) Targeted therapy - Based on predicted susceptibility of infecting organism and local antimicrobial policies Following antimicrobial sensitivity results: 3) Susceptibility-guided therapy - based on susceptibility testing results
77
What happens to the level of knowledge of infecting organism and antimicrobial spectrum of the agent used as you move along the abx prescribing strategy?
The level of knowledge of infecting organism increases | The spectrum of the antimicrobial agent used narrows
78
What is the policy for Abx prescribing from the Dept of Health?
Start Smart then Focus (at 48 hours)
79
What is meant by 'start smart' in the dept of health policy for abx prescribing?
1) Only start using abx if there is clinical evidence of infection 2) Use local guidelines 3) Document indication, duration or review date 4) Obtain cultures first 5) Use single dose abx for surgical prophylaxis
80
What is meant by 'Focus' in the dept of health policy for abx prescribing?
1) Stop abx if their is no evidence of infection 2) Switch abx from IV to oral 3) Change abx - ideally to a narrower spectrum - or broader if required 4) Continue and review again at 72 hours 5) Outpatient parenteral abx therapy (OPAT)
81
Which key abx is used to treat staph aureus (not MRSA)?
Flucloxacillin
82
Which key abx is used to treat streptococcus pyogenes?
Benzylpenicillin
83
Which key abx is used to treat gram negative bacilli?
Cephalosporins (avoid in the elderly)
84
Which key abx is used to treat anaerobes?
Metronizadole
85
Which key abx is used to treat gram positives (including MRSA)?
Vancomycin
86
Which key abx is used to treat most clinically relevant bacteria?
Meropenem
87
Which key abx is the last option for multi-resistant gram negatives?
Colistin
88
An important determinant of in vivo efficacy is concentration at site of action, which abx has good and which has poor availability in CSF?
Good availability in CSF in presence of inflammation = beta-lactams Poor availability in CSF = Aminoglycosides and vancomycin
89
An important determinant of in vivo efficacy is concentration at site of action which abx has good and which has poor availability in urine?
Good availability in urine = trimethoprim and beta-lactams | Poor availability in urine = MLS abx
90
Combination therapy should only be carried out with good reason, what are the 3 reasons for combining abx?
1) To increase efficacy - synergistic combination may improve outcome 2) To provide adequately broad spectrum - single agent may not cover all organisms eg. polymicrobial infection, emperic treatment of sepsis 3) To reduce resistance - Organism would need to develop resistance to multiple agents simultaneously eg. antituberculous chemotherapy
91
When considering pharmacodynamics what is meant by conc. dependent abx?
Main determinant of bacterial killing is the factor by which concentration exceeds MIC
92
How would a conc dependent abx be administered differently to a time dependent abx?
1) Conc dependent - administered intermittently at high conc to achieve high peaks 2) Time dependent - administered frequently to maintain a high level
93
Give an example of a conc dependent and a time dependent abx?
``` Conc = Aminoglycosides Time = Beta-lactams ```
94
When considering pharmacodynamics what is meant by time dependent abx?
Main determinant of killing is the amount of time for which the abx conc exceeds MIC

Year 2 Clinical Pathology (64 decks)

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