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Antibacterials Flashcards

1
Q

What is the formula for the therapeutic index

A

Toxic concentration/effective concentration.

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2
Q

What does therapeutic index allow you to do

A

The therapeutic index of a drug allows you to find the optimal dosage which balances between efficacy without being unacceptably toxic to the patient.

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3
Q

What is the therapeutic window

A

The range of acceptable doses of a drug.

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4
Q

What is meant by “pharmacokinetics”

A

How the body handles a drug. It includes absorption, distribution, metabolism, excretion.

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5
Q

What is the formula for the volume of distribution

A

Vd = total amount of drug in the body/drug blood plasma concentration.

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6
Q

What is Cmax when applied to pharmacokinetics

A

The maximum serum concentration that a drug achieves in a specified compartment or test area of the body after the drug has been administered.

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7
Q

What is Tmax when applied to pharmacokinetics

A

The term used to describe the time at which the Cmax is observed.

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8
Q

What is meant by the half life of a drug

A

The period of time required for the concentration or amount of drug in the body to be reduced by half.

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9
Q

What is meant by the term “pharmacodynamics”

A

The interaction between the antibiotic and the bacteria. (How long does the drug take to have an effect, what dose is required for the effect etc)

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10
Q

What is meant by bacteriostatic

A

The antibiotic stops the replication of the bacteria but does not kill it.

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11
Q

What is meant by bacteriocidal

A

The antibiotic kills the bacteria.

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12
Q

What are the four possible target sites of antibiotics on bacteria

A
  • The cell wall
  • The cell membrane
  • Protein synthesis
  • Nucleic acid synthesis (RNA,DNA, folic acid synthesis)
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13
Q

Why do cell wall synthesis inhibitors work

A

They are selectively toxic to bacteria because mammalian cells do not have a cell wall. The target is peptidoglycan which is not present in humans.

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14
Q

Do cell wall synthesis inhibitors tend to be bacteriocidal and bacteriostatic

A

Removal of bacterial cell walls destroys the bacterial maintenance of osmotic pressure causing water to flood into the cell so cell wall synthesis inhibitors tend to be bacteriocidal.

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15
Q

What does parenteral administration of drugs involve

A

Administration by a route other than by the alimentary canal (from mouth to anus) for example IV, subcutaneous, intramuscular, or intrasternal.

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16
Q

What must a drug be able to survive in order to be given orally

A

The acidic conditions of the stomach.

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17
Q

How are oral drugs able to resist the acidic conditions of the stomach

A

Either by -

  • resistance to acid destruction
  • may have functional groups added to form esters which are then cleaved by acids to form functional antibiotics.
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18
Q

Are oral drugs typically direct or indirect

A

Oral drugs are typically indirect as they have to go round the body in the circulation to reach the site of infection.

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19
Q

What are the general side effects of antibiotics

A
  • Selective pressure and increased resistance
  • Alteration of normal flora which can lead to diarrhoea or fungal superinfections
  • May cause GI upset
  • Drug interactions
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20
Q

What are the benefits of combination therapy

A
  • Delay emergence of resistance

- Allow smaller doses of each agent (synergy)

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21
Q

What are the disadvantages of combination therapy

A
  • Worse side effects
  • Disturb normal gut flora
  • Superinfection by resistant bacteria
  • Additive toxicity.
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22
Q

Which two antibiotic combinations can cause QT prolongation and arrhythmias

A
  • Vancomycin and gentamicin

- Quinolones and macrolides.

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23
Q

What is the most important thing when dealing with infection

A

Source control - remove catheters/drain abscesses etc.

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24
Q

Which types of antibiotics are cell wall synthesis inhibitors

A
  • Beta lactams, for example penicillin

- Glycoproteins such as vancomycin

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25
Which types of bacteria do cell wall synthesis inhibitors such as beta lactams and glycoproteins tend to target
Gram positive bacteria.
26
What tends to cause antibiotic resistance
Rare spontaneous mutations, typically independent of antibiotic usage which ends in selection of resistant bacteria due to death of non-resistant bacteria.
27
What are the locations of gene resistance
- Plasmid - Chromosome - Integrin - Transposon
28
What is a plasmid
An extra chromosomal double stranded DNA that can self replicate and be transferred to other bacteria through conjugation through pilus.
29
What are transposons
"Jumping genes" - they can go between plasmids and chromosomes but cannot self replicate.
30
What is an integron
A genetic element within a transposon that takes resistant genes and inserts them into other DNA segments.
31
What are the four main mechanisms of resistance
- Target site alteration - Reduced access - Inactivation of the drug - Metabolic bypass
32
How does target site alteration work as a mechanism of antibiotic resistance
The bacterium modifies the target site so the affinity of the drug for the site is reduced and the antibiotic cannot bind.
33
How does reduced access work as a mechanism of antibiotic resistance
The antibiotic is removed from the bacterial cell or the drug is no longer able to permeate the bacteria.
34
How does inactivation of the drug work as a mechanism of antibiotic resistance
An example is that beta lactamases are enzymes which can be produced by targeted bacteria. These deactivate the beta-lactam ring of the beta lactam antibiotic drug.
35
What is clavulanic acid and when is it used
Clavulanic acid is a drug that can be used alongside beta lactam agents to allow them to work by inactivating the beta lactamase enzymes produced by the bacteria.
36
How does metabolic bypass work as a mechanism for antibiotic resistance
Metabolic bypass happens through the production of additional targets. This can be done by the production of a drug resistant enzyme to bypass the inhibited metabolic stage or by hyperproduction of the antibiotic target.
37
What are four resistant control strategies
1) conservation - reduced use, source control. 2) prudent use - discourage topical application, give a stopping date 3) surveillance 4) infection control - hand disinfectant.
38
What are the 4 broad spectrum antibiotics associated with C.diff infection (the 4 Cs)
- Co-amoxiclav - Clindamycin - Ciprofloxacin and other quinolones - Cephalosporins.
39
What are three examples of beta lactam drugs
Penicillin, Cephalosporin, Carbapenem.
40
What is penicillin used for
Group A strep, meingococci
41
What are cephalosporins used for
There are broader spectrum beta lactams but are not used to target enterococci.
42
What are carbapenems used for
These are broad spectrum antibiotics.
43
What is the mechanism of action of beta lactam antibiotics
Beta lactam antibiotics contain a beta lactam ring. Their target site is the bacterial peptidoglycan cell wall. Beta lactams bind to transpeptidases which are responsible for the polysaccharide cross link formation.
44
What do beta lactam antibiotics target and bind to
Beta lactam agents bind to transpeptidases on the peptidoglycan cell wall of gram positive bacteria.
45
What do beta lactam agents bring about in the cell wall of bacteria
They disrupt cross linking between polysaccharide chains in the peptidoglycan wall.
46
What are the side effects of beta lactam agents
- Hypersensitivity rash - Diarrhoea - Kidney excretion - Anaphylaxis - Allergy
47
Why must you reduce the beta lactam dose in people with kidney failure
Because beta lactam agents cause renal excretion.
48
Which beta lactam drug should be avoided for use in glandular fever (EBV)
Amoxicillin
49
What is an example of a glycopeptide
Vancomycin
50
What organisms are glycopeptides such as vancomycin used for
Gram positive bacteria. They are useful against MRSA.
51
What is the mechanism of action of glycopeptides such as vancomycin
It binds to terminal D-ala D-ala of the peptide chain and prevents the incorporation of new subunits into the cell wall.
52
What is the target on the bacteria of glycopeptide antibiotics
The bacterial cell wall - the D-ala-D-ala terminal chains of proteins.
53
What are the side effects of glycopeptides
Nephrotoxicity and ototoxicity (ear)
54
What is an example of an aminoglycoside
Gentamycin
55
What are the uses of aminoglycosides
Used against gram negative bacteria (such as E.coli, pseudomonas aeruginosa, mycobacteria) Also used against staphylococci
56
What are aminoglycosides not effective against
Anaerobes
57
What is the target of aminoglycoside antibiotics
Protein synthesis in bacteria
58
What is the mechanism of action of aminoglycosides
They inhibit the binding of the 30S subunit to mRNA, therefore inhibiting protein synthesis.
59
What are the side effects of amino glycosides
Ototoxicity and nephrotoxicity
60
What is an example of a tetracycline
Tetracycline
61
Are aminoglycosides bactericidal or bacteriostatic
Bactericidal
62
Are beta lactam agents bactericidal or bacteriostatic
Bactericidal
63
Are glycopeptides bacteriostatic or bactericidal
Bactericidal
64
Are tetracyclines bactericidal or bacteriostatic
Bacteriostatic
65
What are tetracyclines used for
They are broad spectrum but are used particularly to treat chlamydia
66
What is the target of tetracyclines
Protein synthesis
67
What is the mechanism of action of tetracyclines
They prevent the binding of tRNA
68
What are the side effects of tetracyclines
Teeth discolouration, nausea, diarrhoea
69
Which patients should not be given tetracyclines
Children and pregnant or lactating women.
70
What are two examples of macrolides
Erythromycin and clarithromycin
71
What are macrolides used for
They are narrow spectrum antibiotics. They are used to treat gram positive bacteria (S.aureus, group A strep), legionella, chlamydia and pneumonia
72
Are macrolides bacteriostatic or bactericidal
Mainly bacteriostatic.
73
What do macrolides target
Protein synthesis
74
What is the mechanism of action of macrolides
They prevent peptidyl transferase from adding the growing peptide attached to tRNA to the next amino acid, therefore inhibiting protein synthesis.
75
What are the side effects of macrolides
- GI upset | - Thrombophlebitis (when given IV)
76
What is an example of a lincosamide
Clindamycin
77
Are lincosamides bacteriostatic or bactericidal
Bacteriostatic
78
What are lincosamides used for
Gram positive bacteria (especially group A strep) and anaerobes
79
What do lincosamides target
Protein synthesis
80
What is the mechanism of action of lincosamides
They bind to the 50s subunit to inhibit protein synthesis.
81
What are the side effects of lincosamides
Colitis and diarrhoea
82
What are two examples of THFA (tetrahydrofolic acid) inhibitors
Sulphonamide and trimethoprim
83
Are sulphonamide and trimethoprim (THFA iinhibitors) bacteriostatic or bacteriocidal
Sulphonamide and trimethoprim are bacteriostatic when used individually but bactericidal when used together.
84
What is trimethoprim (THFA inhibitor) used for
Trimethoprim is mainly used in UTIs.
85
How are THFA inhibitors selectively toxic for bacteria
Because humans do not make folic acid.
86
Which group of patients should not be given trimethoprim
Those who are pregnant.
87
What is an example of an RNA synthesis inhibitor
Rifampicin
88
What are RNA synthesis inhibitors such as rifampicin used for
Rifampicin is used to treat TB in combination with three other drugs.
89
What is the mechanism of action of RNA synthesis inhibitors such as rifampicin
Rifampicin binds to DNA dependent RNA polymerase to inhibit the initiation of transcription. Nucleic acid synthesis is therefore inhibited.
90
What are the adverse effects of RNA synthesis inhibitors such as rifampicin
Drug interaction, inactivation of the oral contraceptive pill, hepatitis, nausea, body fluids go orange.
91
What is an example of a DNA synthesis inhibitor (fluoroquinolones)
Ciprofloxacin.
92
What are fluoroquinolones such as ciprofloxacin used for
They are broad spectrum antibiotics previously used for anthrax. Now used for meningococcal contact prophylaxis, UTIs and typhoid.
93
Are fluoroquinolones bacteriostatic or bactericidal
Bactericidal
94
What is the mechanism of action of quinolones such as ciprofloxacin
Quinolones bind to DNA gyrase and topoisomerase so that DNA coiling is inhibited. This inhibits the nucleic acid synthesis.
95
What are the adverse effects of quinolones such as ciprofloxacin
- Neurotoxicity - Confusion - Fits - Cartilage defects - Photosensitivity - Associated with C.diff infection.
96
What are the factors which promote the success of antibiotic resistance
1) Antibiotic usage - Too much antibiotic - Too little antibiotic 2) Effective genetic mobility 3) Efficient resistance mechanisms
97
What are the three things which can lead to effective genetic mobility
1) Plasmid carriage 2) Transposons 3) Integrons
98
What is the minimum inhibitory concentration (MIC)
The lowest concentration of a chemical that prevents visible growth of a bacterium - the concentration of an antibiotic at which it has bacteriostatic activity.
99
What is the minimum bactericidal concentration (MBC)
The lowest concentration of an antibacterial agent required to kill a particular bacterium - the concentration of an antibacterial agent at which it has bactericidal activity.
100
Why is flucloxacillin a good antibiotic to use
Flucloxacillin is a beta lactam antibiotic of the penicillin class. It is able toresistn degradation by penicillinases (a form of beta lactamase produced by the bacteria) so the beta lactam ring does not become cleaved and the antibiotic is effective.

The Respiratory System (20 decks)

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