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Year 3 - Clinical Science and Professionalism > Antimicrobial Agents > Flashcards

Antimicrobial Agents Flashcards

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1
Q

What is a magic bullet

A
  • Selective toxicity compounds harm pathogen not host
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2
Q

define antimicrobial

A

Any substance active against microbes

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3
Q

define antibiotic

A

a naturally occurring product active against bacteria

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4
Q

define broad spectrum

A

kills most gram positive and negative or anaerobes

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5
Q

define narrow spectrum

A

kills narrow range of microbes

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6
Q

define bactericidal

A

actively kills bacteria

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7
Q

define bacteriostatic

A

prevents bacteria multiplying

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8
Q

what are the dependents on an antibiotic being bacteriostatic and bactericidal

A

Depends on:

  • Microorganisms (bacterial inoculum)
  • antibiotic concentration - higher concentration more likely to be bactericidal
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9
Q

what can reduce the efficacy of antibiotics and mean that an antibiotic is no longer bactericidal

A
  • immune system compromised
  • neutropenia
  • renal failure
  • diabetes
  • hard to penetrate
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10
Q

what sites are hard for antibiotics to penetrate

A
  • endocarditis
  • meningitis
  • osteomyelitis
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11
Q

name bacteriostatic examples

A
  • Chloramphenicol
  • Erythromycin
  • Clindamycin
  • Sulphonamides
  • Trimethoprime
  • Tetracyclines
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12
Q

Name bactericidal examples

A
  • Aminoglycosides
  • Beta lactams
  • Vancomycin
  • Quinolones
  • Rifampin
  • Metronidazole
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13
Q

What is antibiotic synergy

A
  • synergistic if their combined activity is greater than the sum of the individual activities – e.g B-lactam and aminoglycoside – endocartitis
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14
Q

what is antibiotic antagonism

A
  • antagonistic if the activity of one drug is compromised by the other – e.g Tetracycline or Chloramphenicol associated with B-lactam or aminoglycoside, or 2 B- lactams together
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15
Q

name an example of antibiotic synergy

A

e.g B-lactam and aminoglycoside – endocartitis

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16
Q

Name an example of antibiotic antagonism

A

– e.g Tetracycline or Chloramphenicol associated with B-lactam or aminoglycoside, or 2 B- lactams together

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17
Q

Define therapeutic index

A

A ratio that compares the blood concentration at which a drug becomes toxic and the concentration at which the drug is effective.

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18
Q

the larger the therapeutic index the

A

The larger the therapeutic index (TI), the safer the drug is.

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19
Q

The smaller the therapeutic index

A

If the TI is small (the difference between the two concentrations is very small), the drug must be dosed carefully and the person receiving the drug should be monitored closely for any signs of drug toxicity.

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20
Q

what is the ratio of the therapeutic index

A

toxic/therapeutic

T1 = TD50/ED50

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21
Q

name a type of drugs that have a high therapeutic index

A

Beta lactase

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22
Q

name a type of drug that has a low therapeutic index

A

Aminoglycosides

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23
Q

describe what a therapeutic index looks like

A

therapeutic range

  • above that is where the drug becomes toxic
  • below is where the drug is subtherpatuic
  • on the Y axis is the anti microbial concentration
  • on the X axis is time
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24
Q

list anti gram positive antimicrobials

A
  • pencillins – streptococci, staphylococci, enterococci, listeria
  • fusidic acid
  • macrolides – streptococci
  • clindamycin – streptococci and some staphylococci
  • glycopeptides - streptococci – staphylococci, enterococci
  • oxazolidinones- streptococci, staphylococci, enterococci
  • daptomycin – streptococci, staphylococci, enterococci
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25
Q

list anti gram negative antimicrobials

A 
•	Polymyxin (Colistin)
•	Trimethoprim
•	Aminoglycosides*
•	Monobactams (Aztreonam)
•	Temocillin
-	Also active against streptococci, staphylococci, and enterococci
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26
Q

name the sites of action of antimicrobials

A

Cell wall synthesis

  • B- lactase
  • Glycopepetides

DNA gyrase

  • DNA gyrase- Quinolones
  • DNA replication = Metronidazole

DNA- directed RNA polymerase
- rifampicin

Protein synthesis 50S inhibitors

  • chloramphenicol
  • macrolides
  • clindamycin

Protein synthesis 30S inhibitors

  • aminoglycosides
  • tetracyclines

Cell wall

Cytoplasmic membrane structure
- polymixins

Folic acid metabolism

  • DHF - dihydrofolate
  • THF - tetrahydrofolate
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27
Q

List broad spectrum antimicrobials

A

Beta lactams

  • Carbapenems
  • Amoxicillin/clavulanate
  • Piperacillin/tazobactam
  • cephalosporins
  • chloramphenicol (gram positives, negatives, atypical and anaerobes)
  • tetracycline (gram positives, negatives, atypical and anaerobes, spirochetes)
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28
Q

What is the difference between antimicrobials and antibiotics

A

An antibiotics is a natural antimicrobial substance produced by a microorganism that is effective against bacteria whereas an antimicrobial is any substance of natural, semi-synthetic (chemically modified natural substances) or synthetic origin that kills or inhibits the group of microorganisms

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29
Q

define selective toxicity

A

Selective toxicity refers to the ability of the drug to targets sites that are relative specific to the microorganism responsible for infection. and not human cells
- this can be done by targeting sites that humans cells do not have for example the cell wall

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30
Q

what are examples of narrow spectrum bacteria

A

Aerobes examples – gram positive and gram negative
- Glycopeptides, Bacitracin, Penicillin - gram positive
- Polymyxins- gram negative
- Aminoglycosides, Sulfonamides, Actinomycin – both gram positive and gram negative
anaerobes
- Nitroimidazoles – both gram positive and gram negative

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31
Q

what is the difference between bacteria and humans

A
  1. Biochemistry is different – for example bacteria synthesise essential vitamins
  2. Bacterial cell wall, animal cells do not have a bacteria cell wall
  3. Bacteria have a 70s ribosome whereas eukaryotes have an 80s ribosome
  4. Mitochondria have 70s ribosomes
  5. DNA directed RNA polymerases are different
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32
Q

How does bacterial cell wall synthesis happen

A
  • Lattice structure of sugar residues that are formed of chains alternating NAM and NAG residues
  • Each NAM contains 4-5 AA chains (Lalanine, D-glutamine, L-lysine (m-DAP), D-alanine,)
  • Pentaglycine cross linking requires D-alanine-D-alanine, but the cross link itself is formed between D-alanine and L-lysine (m-DAP) catalysed by transpeptidase
  • Terminal alanine is lost
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33
Q

what antibiotics target bacterial cell wall synthesis

A

Beta lactam agents

  • pencillins
  • cepsphosporins
  • carbapenems
  • aztreonam

glycopeptides

  • vancomycin
  • teicoplanin
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34
Q

what do beta-lactams target
what is the action of beta lactams
what type of bacteria does betalactams target
is it bactericidal or bacteriostatic

A
  • Target – transpeptidase (pencillin-biding protein) is inhibited
  • Action; competitive inhibitor of transpeptidase, covalently activates serine in the active site of the enzyme
  • What does it target – gram negative, gram positive
  • bactericidal
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35
Q

what does transpeptidase do

A
  1. Formation of crosslinks between D-amino acids
  2. Hydrolysis of peptide bonds
  3. Hydrolyses peptide bond in penicillin
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36
Q

Name some examples of beta lactams

A
  • Pencillins (Penicillin G, Amoxicillin, Ampicillin) – contains a peptide bond similar to transpeptidase dipeptide substrante
  • Cephalosporins
  • 1st Gen – Cephaphrin, Cephalexin
  • 2nd Gen – Cefuroxime, Cefamandole, Cefotetan
  • 3rd Gen – Ceftriaxone, Ceftazidime, Ceftizoxome
  • 4th Gen – Cefepime
  • Carbapenems (Imipenem)
  • Monobactams (Azotreonam)
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37
Q

name the classification of pencillins and carbapenems

A

beta lactamase
narrow spectrum penicillins
- penicillin V
- Penicillin G

resistant pencillin

  • flucloxacillin
  • nafcillin

susceptible borad spectum pencillins

  • ampicillin
  • amoxicillin

pencillins with beta lactase inhibitor

  • amoxicillin and clavulanic aid
  • piperacillin and tazobactam (anti-pseudomonal)

susceptible extended spectrum pencillins (anti pseudomonal activity)
- piperacillin and tazobactam (anti-pseudomonal)

carbapenems

  • meropenem and imipenem
  • ertapenem (not an anti pseudomonal)
  • doripenem
  • faropenem
  • as the generations increase = there is an increasing activity against various gram negative bacteria including the pseudomonas
  • gram positive activity remains static
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38
Q

What are the pencillins used at parts trust

A
  • Pencillin V (oral) G (IV)
  • Benzylpencillin (IV)
  • Flucloxacillin (oral and iv)
  • Amoxicillin +/– clavulanic acid (a beta-lactamase inhibitor) (oral and iv)
  • Piperacillin + tazobactam (a beta-lactamase inhibitor) (iv)
  • Temocillin (iv)
  • Pivmecillinam (oral)
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39
Q

Penicillin

  • mechanism of action
  • spectrum
  • route of administration
  • dosing regime
  • tissue penetrated
  • clinical use
  • interactions
A
  • Mechanisms of action – inhibits cell wall synthesis
  • Spectrum – gram positive
  • Rout of administration – oral and IV
  • Dosing regimen – four to six times a day
  • Penetration – penetrates most tissues including inflamed meninges
  • Clinical use – drug of choice streptococcal and meningococcal disease
  • Interactions – Allopurinol and methotrexate
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40
Q

What are the side effects of penicillin

A
  • rule out penicillin allergy immediate IgE mediated anaphylaxis,
  • safe in pregnancy,
  • Jarisch herxheimer reaction in syphilis treatment,
  • coombs positive
  • haemolytic anaemia,
  • interstitial nephritis,
  • serum sickness,
  • hepatitis
  • drug fever
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41
Q

what are the issues to do with penicillin

A

resistance beta lactamase and other mehcnaisms,

allergic rhinitis

cross-hypersenstivity

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42
Q

what is the mechanisms of antimicrobial resistance in penicillin

A
  • Resistance – larger than 80% of staphylococci resistance, S pneumoniae resistance in USA, S Europe; gonococcal resistance worldwide

production of B-lactamase and alteration of penicillin binding proteins

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43
Q

what drugs does penicillin interact with

A

Allopurinol (gout treatment) - experience a skin rash when mixed with pencillin

methotrexate - increases the risk of toxicity when given with penicillin

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44
Q

what is a Jarisch herxheimer reaction in penicillin treatment of syphilis

A

shaking chills
a rise in temperature
intensification of skin rashes

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45
Q

Flucloxacillin

  • mechanism of action
  • spectrum
  • route of administration
  • dosing regime
  • penetration of tissues
  • clinical uses
A
  • Mechanism of action: inhibit cell wall synthesis
  • Spectrum: Gram positive
  • Route of administration: oral and IV
  • Dosing regimen: Four times a day
  • Penetration: penetrates most tissues
  • Clinical uses: drug of choice for all S. aureus infections except MRSA
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46
Q

what are the side effects of flucloxacillin

A
  • rule out penicillin allergy;
  • safe in pregnancy and in children,
  • cholestasis,
  • hepatitis,
  • rash,
  • D and V,
  • leukopenia,
  • anaemia,
  • thrombocytopenia
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47
Q

What is the resistance of flucloxacillin

A

> 80% of staphylococci resistant; S. pneumoniae resistance in USA, Spain; gonococcal resistance worldwide
- therefore it would not be effective in the US due to resistance
• Mechanism of microbial resistance: alteration of penicillin binding proteins (PBPs)

48
Q

What is the resistance of flucloxacillin

A

> 80% of staphylococci resistant; S. pneumoniae resistance in USA, Spain; gonococcal resistance worldwide
- therefore it would not be effective in the US due to resistance

• Mechanism of microbial resistance: alteration of penicillin binding proteins (PBPs)

49
Q

Amoxicillin

  • Mechanisms of action
  • spectrum
  • route of administration
  • doing regime
  • penetration of tissues
  • drug interaction
  • clincial use
A
  • Mechanisms of action – inhibit cell wall synthesis
  • Spectrum – gram positive and gram negative
  • Route of administration – oral and IV
  • Dosing regimen – three times a day
  • Penetration – penetrates most tissues including inflamed meniges
  • Interactions - allopurinol(rash)
  • Clinical uses – drug choice for streptococcal disease expect when empirically for a sore throat, listeria
50
Q

what is the side effects of amoxicillin

A

– rules out penicillin allergy,

  • safe in pregnancy and in children,
  • Antibiotic associated diarrhoea
  • fever
  • neutropenia
  • eosinophilia
  • rash with monucleosis
  • increased PT
  • kounis syndrome – coronary syndrome
51
Q

What is the resistance of amoxicillin and the mechanism of action of resistance

A
  • Resistance – greater than 80% of staphylococci resistance, S penumoniae resistance, gonococcal resistance
  • Mechanism of microbial resistance – production of beta lactamase and alteration of Penicillin binding proteins (PBPs)
52
Q

what drug does amoxicillin interact with

A
  • allopurinol(rash)
53
Q

What is kounis syndrome

A

Kounis syndrome is defined as acute coronary syndrome (symptoms such as chest pain relating to reduced blood flow to the heart) caused by an allergic reaction or a strong immune reaction to a drug or other substance.
- seen in amoxicillin

54
Q

Co-amoxiclav (amoxicillin and clavulanic acid)

  • Mechanisms of action
  • spectrum
  • route of administration
  • doing regime
  • penetration of tissues
  • clinical use
A
  • Mechanism of action: inhibit cell wall synthesis + B-lactamase inhibitor
  • Spectrum: Gram positive and Gram negative & anti-anaerobic action
  • Route of administration: oral and IV
  • Dosing regimen: three times a day
  • Penetration: penetrates most tissues
  • Clinical uses: polymicrobial infections, B-lactamase producing Gram positive and negative infections
55
Q

What are the side effects of co-amoxiclav

A

same as Amoxicillin plus drug induced liver injury in 13-23% (mild)

positive blood test for 1,3 beta D-glucan with iv drug.

56
Q

What two drugs is co-amoxiclav made out of

A

amoxicillin and clavulanic acid

57
Q

What is the resistance of co-amoxiclav

A
  • Resistance: MRSA, hospital acquired Gram – orgs incl pseudomonas
  • Mechanism of microbial resistance: ESBLS, Impermeability, efflux, altered Penicillin binding proteins (PBPs)
58
Q

what drugs is pitazobacterium made out of

A

piperacillin and tazobactam

59
Q

Pitazobacerium (piperacillin and tazobactam)

  • Mechanisms of action
  • spectrum
  • route of administration
  • doing regime
  • penetration of tissues
  • drug interaction
  • clincial use
A
  • Mechanism of action: inhibit cell wall synthesis + B-lactamase
  • Spectrum: Gram + and Gram - & anti-anaerobic action; anti-pseudomonal
  • Route of administration: IV
  • Dosing regimen: three to four times a day
  • Penetration: penetrates most tissues
  • Interactions: Methotrexate – causes acute kidney injury
  • Clinical uses: polymicrobial infections, B-lactamase producing Gram + and – infections, pseudomonas
60
Q

what is the side effects of Pitazobacerium (piperacillin and tazobactam)

A

rule out pen allergy;

hypernatremia,

neutropenia

diarrhoea

61
Q

what is the resistance of Pitazobacerium (piperacillin and tazobactam)

A
  • Resistance: MRSA, Hospital acquired gram – organisms including pseudomonas
  • Mechanism of microbial resistance: ESBLs, Impermeability, efflux, altered penicillin binding proteins (PBPs)
62
Q

what is the drug that interacts with Pitazobacerium (piperacillin and tazobactam)

A

• Interactions: Methotrexate – causes acute kidney injury

63
Q

name the generations of cephalosporins

A

First generation – typically used in surgical prophylaxsis

  • Cephalexin (prototype of this generation)
  • Cephalothin, cefazolin, cefadroxil

Second generation – gynaecology

  • Cefuroxime (prototype of this generation)
  • Cefotetan
  • Cefomandole
  • Cefoxitin – cystic fibrosis can be used

3rd generation – in hospitals

  • Cefotaxime
  • Ceftriaxone
  • Ceftazidime – active against P. aeruginosa

Fourth generation
- Cefipime – anti pseudomonas aeruginosa

5th generation
- Cephalosporin with ceftaroline which has activity against G+ therefore changing this previous rule and ceftolazone which is active against gram negative

64
Q

describe what happens to gram positive and gram negative as the cephalosporins escalate

A
  • As the generations escalate there is increasing activity against various gram negative bacteria including pseudomonads;
  • gram positive activity remains static or decreases for ceftazidime
  • none are active against enterococci
65
Q

Are cephalosporins narrow or broad spectrum

A

Very broadspecturm so can create a lot of resistance

66
Q

Cefuroxime (2nd generation)

  • Mechanisms of action
  • spectrum
  • route of administration
  • doing regime
  • penetration of tissues
  • clinical use
A
  • Mechanism of action: inhibit cell wall synthesis
  • Spectrum: Gram + and Gram -; not active against Pseudomonas spp
  • Route of administration: IV
  • Dosing regimen: three times a day
  • Penetration: penetrates most tissues
  • Clinical uses: Pneumonia; serious intra abdominal (add metronidazole) and urinary tract infections
67
Q

describe the side effects of cefuroxime (2nd generation)

A
  • rule out penicillin allergy
  • cross reacts in 10%
  • safe in pregnancy and in children
  • diarrhoea
  • C.difficile
68
Q

describe the resistance of cefuroxime (2nd generation)

A
  • Resistance: MRSA, resistance in Gram negative organisms
  • Mechanism of microbial resistance: production of extended spectrum B -lactamase and impermeability, efflux, altered penicillin binding proteins (PBPs)
69
Q

Ceftriaxone (3rd generation)

  • Mechanisms of action
  • spectrum
  • route of administration
  • doing regime
  • penetration of tissues
  • clinical use
A
  • Mechanism of action: inhibit cell wall synthesis
  • Spectrum: Gram + and Gram -; not active against Pseudomonas spp
  • Route of administration: IV
  • Dosing regimen: once/twice a day
  • Penetration: penetrates most tissues including inflamed meninges
  • Clinical uses: meningitis and pneumonia
70
Q

Describe the side effects of Ceftriaxone (3rd generation)

A
  • rule out penicillin allergy (cross reacts in 10%)
  • C.difficile pseudocholelithiasis,
  • diarrhoea
71
Q

describe the resistance of Ceftriaxone (3rd generation)

A
  • Resistance: MRSA, resistance in gram negative organisms
  • Mechanism of microbial resistance: production of extended spectrum B -lactamase and impermeability, efflux, altered Penicillin binding proteins(PBPs)
72
Q

Ceftazidime (3rd generation)

  • Mechanisms of action
  • spectrum
  • route of administration
  • doing regime
  • penetration of tissues
  • clinical use
A
  • Mechanism of action: inhibit cell wall synthesis
  • Spectrum: Gram + and Gram -; including Pseudomonas spp
  • Route of administration:
  • Dosing regimen: three times a day
  • Penetration: penetrates most tissues including inflamed meninges
  • Clinical uses: mainly used in serious intra abdominal and urinary tract infections especially if pseudomonas is involved; do not use for Community acquired pneumonia as little activity against on S. pneumoniae
73
Q

what is the side effects of Ceftazidime (3rd generation)

A
  • rule out penicillin allergy (cross reacts in 10%)
  • photosensitive rash,
  • C.difficile
  • diarrhoea
74
Q

what is the resistance of Ceftazidime (3rd generation)

A
  • Resistance: MRSA, resistance in Gram – orgs
    • Mechanism of microbial resistance: production of extended spectrum B -lactamase and impermeability, efflux, altered PBPs
75
Q

name an example of carbapenems

A

Meropenem

76
Q

Carbapenems: Meropenem

  • Mechanisms of action
  • spectrum
  • route of administration
  • dosing regime
  • penetration of tissues
  • clinical use
A
  • Mechanism of action: inhibit cell wall synthesis + B-lactamase inhibitor, incl ESBLs
  • Spectrum: Gram positive and Gram negative & anti-anaerobic action; anti-pseudomonal
  • Route of administration: IV
  • Dosing regimen: Three times a day
  • Penetration: penetrates most tissues including inflamed meninges
  • Clinical uses: polymicrobial infections, ESBL producing Gram – infections, (ICU, haem-onc)
77
Q

what is the side effects of carbapenems: Meropenem

A
  • rule out penicillin/cephalosporin allergy
  • rash
  • seizures
78
Q

what is the resistance of carbapenems: Meropenem

A
  • Resistance: MRSA, resistance is rare in Gram negative organisms
  • Mechanism of microbial resistance: production of metallo-B-lactamase and impermeability, efflux, altered PBP
79
Q

name examples of glycopeptides

A

Vancomycin and teicoplanin

80
Q

Glycopeptides: Vancomycin and teicoplanin

  • Mechanisms of action
  • spectrum
  • route of administration
  • dosing regime
  • penetration of tissues
  • clinical use
A
  • Mechanism of action: Acts on cell wall
  • Spectrum: Gram positive only incl. anaerobe C.diffcile
  • Route of administration: IV
  • Dosing regimen: 1-2 times a day
  • Penetration: large molecule, poor penetration and none into the CSF
  • Clinical uses: Problem Gram positive infections
81
Q

what are the side effects of Glycopeptides: Vancomycin and teicoplanin

A
  • Vancomycin is nephrotoxic
  • ‘’Red man syndrome – if given too quickly therefore needs to be infused slowly when giving a loading dose - with vancomycin
82
Q

what is red man syndrome

A

Red man syndrome (RMS) is a reaction caused by the rapid infusion of the glycopeptide antibiotic Vancomycin.

effects

  • pruritic erythematous rash to the face, neck and upper torso
  • can involve extremities to a lesser degree
83
Q

what is there resistance to Glycopeptides: Vancomycin and teicoplanin

A
  • Resistance: Vancomycin resistance Enteroccoci

* Mechanism of microbial resistance: alteration of binding site

84
Q

Name the agents that inhibit protein synthesis

A

• Aminoglycosides
• Tetracyclines
• Chloramphenicol
• Macrolides e.g. erythromycin, clarithromycin
• Clindamycin
• Fusidic acid
- Of the above agents the only agent that are bactericidal are the aminoglycosides

85
Q

of the agents that inhibit protein synthesis which one is bactericidal

A

aminoglycosides

86
Q

name examples of ahminoglycosides

A

Gentamicin and Amikacin

87
Q

Aminoglycosides: Gentamicin and Amikacin

  • Mechanisms of action
  • spectrum
  • route of administration
  • dosing regime
  • penetration of tissues
  • clinical use
  • drug interactions
A

• Mechanism of action: Acts on 30S ribosome – bactericidal
• Spectrum: Gram positive (staph) and Gram negative; anti-pseudomonal;
• Route of administration: IV, IM, topical or nebuliser
• Dosing regimen: Once a day or TDS/BD
• Penetration: 100% water soluble, poor lung (sometimes it is nebulised) and CNS penetration
• Clinical uses: Adjunct to serious systemic sepsis including pseudomonas; true anti-microbial synergy with the B-lactams for IE, Group B
- Uses: Pneumonia, MRSA, bactermia, sepsis, UTIs, endocarditis
• Interactions: Increased nephrotoxicity with vancomycin, colistin and ambisome

88
Q

what are the side effects of Aminoglycosides: Gentamicin and Amikacin

A
  • Nephrotoxicity - toxic to the nephrons in the kidney (reversible)
  • ototoxicity (reverse vestibular and irreversible auditory) - toxic to the ear
  • NMJ blockage at high dose
  • Pregnancy cat C (8th nerve)
89
Q

What drug interactions does Aminoglycosides: Gentamicin and Amikacin

A

Increased nephrotoxicity with vancomycin, colistin and ambisome

90
Q

what is the resistance to Aminoglycosides: Gentamicin and Amikacin

A
  • Resistance: acquired resistance in gram negative organisms
  • Mechanism of microbial resistance: impermeability, efflux
91
Q

Name some examples of macrolides

A

erythromycin,
clarithromycin
azithromycin

92
Q

Macrolides – erythromycin, clarithromycin, azithromycin

  • Mechanisms of action
  • spectrum
  • route of administration
  • dosing regime
  • penetration of tissues
  • clinical use
A
  • Mechanism of action: Acts on 50S ribosome which blocks translocation in protein synthesis: bacteriostatic
  • Spectrum: Gram + (H. influenzae)
  • Route of administration: oral and IV (thromboplebitis)
  • Dosing regimen: once or twice a day
  • Penetration: Azithromycin excellent intracellular penetration
  • Clinical uses: drug of choice atypical agents; in pen- allergy, STIs
93
Q

what is the side effects of Macrolides – erythromycin, clarithromycin, azithromycin

A
  • safe in children,
  • erythromycin inhibits P450
  • QT prolongation
  • nausea vomiting
  • diarrhea
  • abdominal pain
  • liver toxicity
  • drug interactions
  • increase QTC
94
Q

what is the resistance of Macrolides – erythromycin, clarithromycin, azithromycin

A
  • Resistance: Is known in staphs and streps

* Mechanism of microbial resistance: Mutation of the binding site

95
Q

What drugs affect nucleic acid synthesis and metabolism

A

Nucleotide synthesis and polymerisation is similar in bacterial and mammals therefore selective toxicity is often poor but there are exceptions including

  • Quinolones such as Ciprofloxacin, moxifloxacin, leveofloxacin
  • Rifampicin
  • Metronidazole (active against most anaerobes)
96
Q

What is the downside to inhibiting nuclear acid synthesis and polymerisation

A

Nucleotide synthesis and polymerisation is similar in bacterial and mammals therefore selective toxicity is often poor

97
Q

list examples of quinolone

A

Ciprofloxacin
moxifloxacin
leveofloxacin

98
Q

Quinolones: cipro/levo/moxifloxacin

  • Mechanisms of action
  • spectrum
  • route of administration
  • dosing regime
  • penetration of tissues
  • clinical use
A
  • Mechanism of action = Inhibits DNA gyrase
  • Spectrum: Gram positive (staph not streps) and Gram negative including anti pseduomonal
  • Route of administration: oral and IV
  • Dosing regimen: Twice a day
  • Penetration: penetrates most tissues including meninges
  • Clinical uses: serious intra abdominal and urinary tract infections especially if pseudomonas is involved; do not use for pneumonia as no action on S. pneumoniae;
99
Q

What are the side effects of Quinolones: cipro/levo/moxifloxacin

A
  • Not licensed in pregnancy,
  • AAD
  • lowers seizure threshold
  • tendon rupture.
  • Recently available for children.
100
Q

What is the resistance of Quinolones: cipro/levo/moxifloxacin

A
  • Resistance: high rates of resistance

* Mechanism of microbial resistance: impermeability, efflux

101
Q

What are the clinical uses of fluoroquinolone

A
  • Opthalamic infections
  • Respiratory infections and inhaled anthrax myobacterai
  • GI and abdominal infections
  • Prostatsis
  • UTIs
  • STDs
  • Infections of bone, joints and soft tissues
102
Q

what is the adverse side effects of fluoroquinolone

A
  • Tendon rupture
  • Children less than 18 (cartilage)
  • Seizures, prolong QT
  • Dizziness, confusion
  • Photosensitivity
103
Q

What is the mechanism of action of fluoroquinolone

A
  • Inhibits DNA gyrase and topoisomerase IV

- Bactericidal

104
Q

name the final steps in folate synthesis

A

pteridine pyrophosphate and P-aminobenzoate is converted to dyhydropteroate by dihydropteroate syntheses

  • dihydropterroate is converted to dihydrofolate
  • dihydrofolate is then converted to tetrahydrofolate by dihydrofolate reductase
105
Q

What is the difference between folic acid synthesis in bacteria and higher organisms

A
  • Human cells do not synthesise folic acid and lack dihydropteroate synthase
  • human cells only contain dihydrofolate reductase
106
Q

Name two examples of antifolates

A
  • Sulphonamides

- Trimethoprim

107
Q

What do sulphonamides inhibit

A

inhibits dihydropteroate synthease

108
Q

What does trimethoprim inhibit

A

inhibits dihydrofolate reductase, 50,000x more active on the bacteria enzyme

109
Q

why are membrane disorganising agents have poor selective toxicity

A
  • Show poor selective toxicity due to similarity of bacterial and mammalian membranes
110
Q

name examples of membrane disorganising agents

A
  • Examples include – amphotericin (antifungal agent), colistin (a polymyxin), daptomycin
111
Q

on the antimicrobial spectrum

A
  • fewer antimicrobials cover gram negative organisms
112
Q

How has antimicrobial resistance risen

A
  • Antibiotics were and are widely prescribed often for medicial conditions that did not require them
  • Started to be used in agriculture, dosing cattle with antibitoics increased yield and give a greater product, also reduce loss of livestock
113
Q

What are the main antimicrobial resistance problems

A
  • UTI
  • Respriaotry tract infections
  • Neisseria gonorrhoea
  • M tuberculosis
  • Diarrhoeal disease
  • Beta lactamase producing
  • Resistance pneumonococci and H influenzae
  • Penicillin resistance
  • Multi drug resistant
  • Resistant salmonella and shigella spp
114
Q

what antimicrobial resistant infections are growing

A

– Methicillin resistant S.aureus and coagulase negative staphylococci
– Multi-resistant enterococci
– Muti-resistant Gram-negative rods including Pseudomonas spp., Kebsiella spp. Enterobacter spp. and Acinetobacter spp.

115
Q

what should you consider when prescribing antibiotics

A
  • Timing of the antibiotic
  • Choice of antibiotics
  • Certain combinations can be detrimental
  • Loading doses

Year 3 - Clinical Science and Professionalism (32 decks)

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