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Antibiotic Therapy Flashcards

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1
Q

what is an antibiotic?

A

a drug used to treat or prevent an infection caused by micro-organisms (molecules that at small levels can inhibit or kill bacteria by reducing pathogenicity of bacteria/prokaryotes)

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2
Q

what is bacteriostatic?

A

inhibition of the growth of bacteria

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3
Q

what is bacteriocidal?

A

killing of bacteria (remeber as “cidal” like sui”cidal”)

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4
Q

what is a narrow spectrum antibiotic?

A

one that kills only one group e.g. gram negative

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5
Q

what is a broad spectrum antibiotic?

A

killing of lots of different group like gram - and gram + etc

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6
Q

what is penicillin spectrum?

A

narrow spectrum = active against gram + bacteria

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7
Q

what is tetracyline spectrum?

A

broad spectrum = active against many gram - and gram +

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8
Q

what are ideal antibiotic components?

A
  1. selective toxicity/minimal toxicity
  2. cidal (kills bacteria
  3. long half life (low binding to plasma proteins)
  4. appropriate tissue distrubution
  5. no adverse drug interaction/side-effects
  6. oral & pareneteral preparations
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9
Q

what is price of taking antibiotic?

A

effect on host natural microbiome, bacteria that gives host some protection

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10
Q

what does it mean by selective toxicity/minimal toxicity to host in antibiotics?

A

idea that antibiotic molecule inhibits something in micro-organism that isn’t present in host e.g. peptidoglycan wall is unique so could target that

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11
Q

what are antibiotic targets?

A
  • cell wall structures e.g. petidoglycan synthesis
  • ribosomes (protein synthesis)
    -DNA replication (nucleic acid synthesis)
    -DNA gyrases
    -metabolic pathways (as different nutrients required, diffferent enzymes involved)
    -cell membrane functions

=extra enzymes involved in these areas/functions could be targeted by antibiotic

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12
Q

what does pharmodynamic mean?

A

how much of antibiotic you have, what activity etc

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13
Q

what does pharmokinetic mean?

A

about delivery of antibiotic, how body deals with it & secretion is important

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14
Q

what factors are involved in pharmodynamics?

A

MIC/MBC = minimum inhibitory/bacteriocidal concentration (in vitro)

time dependant action (in vitro/in vivo blood concentration)

spectrum (broad to narrow range) in vitro e.g. gram +, gram -, anaerobic bacteria

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15
Q

what factors are involved in pharmokinetics?

A

absorption (peritoneal Vs IV, acid sensitivity)

distrubution (plasma binding proteins, GI/urinary tract, environment permissive for activity)

elimination (liver or kidney)

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16
Q

what are cell wall antibiotics?

A
  • penicillins (beta lactam)
    -cephalosporins (beta lactam)
    -glycopeptides (not beta lactam)
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17
Q

what is beta-lactam?

A

structural element within molecules that look like component (terminal peptide amino acid) of bacterial cell wall
= flexible side chain & structure that can be altered to change spectrum & resistance

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18
Q

what is lysis?

A

breakdown of cell wall as no new material is syntheisised so gap

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19
Q

what is molecular mechanims of beta-lactam antibiotics?

A

beta lactam looks like terminal peptide amino acid so enzyme binds to beta lactam instead, but beta lactam doesn’t go anywhere and remains bound - when found it had radioactive penicillin bound to them so called it PBP (penicillin binding protein) - result of this is lysis going ahead without synthesis, weakening & bursting cell wall. as beta-lactam has bound and stuck so corss link side chain not holding cell wall together (irreversibly binds)

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20
Q

what are target of beta lactam antibiotics?

A

penicillin-binding protein

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21
Q

what would normal molecular mechanism be if no beta lactam for synthesis of cell wall?

A

terminal amino acid usually binds to enzyme, enzyme breaks it open and transfers energy and through series of chemical reactions forms chemical bridge an makes rigid cell wall

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22
Q

what are positives of penicillin?

A
  • Safe, very few side effects
  • Variety, very flexible molecule with side groups & chains able to alter multiple
    features
  • Range from narrow spectrum to broad spectrum i.e. empiric prescribing & can act on a wide range of bacteria, usually both Gram negative
    & Gram positive organisms, but also some can be quite specific
  • Excreted (rapidly) via kidney
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23
Q

what are the limitations of penicillin?

A
  • resistance causes major issue, resistance was observed almost immediately
  • certain group of patients tended to have hypersensitivty (allergy)
    -rapid secretion by kidneys so requires frequent dosage
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24
Q

what are the 3 principle compound of penicillin?

A

Benzylpenicillin = Penicillin G, Intravenous IV

Phenoxymethyl penicillin = Penicillin V, oral delivery too

Benzathine penicillin = long-acting, Intramuscular

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25
Q

what was discovered to help resistance?

A

that you can combine certain antibiotics with a second compound that inhibits the enzyme that would degrade them

e.g. beta lactamase inhibitor to inhibit beta lactamase so it doesn’t degrade beta lactam

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26
Q

what are properties of co-amixclav?

A

amoxicillin & clavulanic acid

contains:
-b-lactam & b-lactamase inhibitor
* Clavulanic acid

  • Inhibits the action of b-lactamase
  • Microbial resistance enzyme
  • Does NOT have antibiotic properties of its own

Combination extends range of bacteria that can be treated, similar for Piperacillin & tazobactam

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27
Q

what are some properties of flucloxacillin?

A

narrow spectrum antibiotic
* Useful for Staphylococci and Streptococci ONLY
* Replaced methicillin or meticillin (better tissue distrubution)
* MRSA is resistant to Flucloxacillin
* Reporting labs use oxacillin to report resistance
* Commonly prescribed antibiotic
* i.e. very common Staph and Strep skin infections
* Skin and soft tissue infection
* Wound infection
* Cellulitis (infection of the soft tissues under the skin)

  • modify side chains allow beta lactam to resist degredation
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28
Q

what are the key clincical penicillins?
a) gram +?
b) gram -?
c) gram + and gram -?

A

a) flucloxacillin (IV, oral) & penicillin V
b) temocillin (IV only)
c) amoxicillin (IV, oral), co-amoxiclav (IV, oral)

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29
Q

what are beta lactams examples?

A
  1. penicillins
  2. cephalosporins
  3. carbapenems
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30
Q

how frequently used is cephalosporins?

A

very restricted use in tayside as they kill off normal gut bacteria and allow overgrowth of c.difficiles so many hospitals try to avoid using them. each successive generation increases broad spectrum over next which means it just wipes out again and again which in this case isn’t a good thing as it leaves nothing left (even good)

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31
Q

how is cephalosporins excreted?

A

via kidneys and urine

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32
Q

what makes B lactams the most successful group of antibiotics?

A
  • pharmokinetics

-development of formulations with extended spectrum (pharmodynamics altered, can extend spectrum)

-development of less resistant forms insensitive to beta lactamases (carbapenems)

-development of beta lactamases inhibitors

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33
Q

describe some properties of carbapenems?

A
  1. Broad spectrum Gm+ ve & Gm-ve
    Resistant to b-lactamase
    Abiot of last resort for some Gm-ve
    e.g. Meropenem usually IV admina

(good for when you don’t know whats wrong with them as kills broad range. bad as wipes out everything including good bacteria)

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34
Q

what are penicillin binding proteins?

A

PBP = proteins that make cell wall structure rigid by cross linking side chains (they bind to D-alanine D-alanine)
-> it’s what beta lactam antibiotics target

*PBP is a subgroup of transpeptidase

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35
Q

what are the side effects of cephalosporin antibiotics?

A

very few side effects (reduced allergy side effects)
- therefore safe in prgenancy

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36
Q

what is a negative of cephalosporins antibiotics?

A

generally they’re more resistant to beta lactamases but gram - still has developed resisitance

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37
Q

How do cephalosporin act as antibiotic?

A

it’s a beta lactam antibiotic that inhibits cell wall synthesis and bactericidal (cell wall targeting)

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38
Q

what are the side effects of penicillin?

A

safe - very few side effects
apart from allergy - certain groups of patients have hypersensitivity (allergy)

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39
Q

what is general penicillins spectrum?

A

range from narrow to broad - can act on wide range of bacteria
= you can subtly alter them to extend spectrum

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40
Q

how are penicillins excreted?

A

rapidly through urine - means has to be taken in frequent dosage

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41
Q

what are negatives of penicillin?

A

resistance is major issue, bacteria showed resistance very early on
(need lots of penicilllin in frequent doses as excreted quickly)

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42
Q

what is penicillin V spectrum?

A

narrow spectrum - mostly gram positive

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43
Q

how is penicillin V get into system?

A

absorbed through intestine

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44
Q

what is negative to penicillin V?

A

sensitive to stomach acid so have to co-ordinate doses with eating times which can be awkward and annoying
-it also takes longer for drug to get into blood system (30-60 mins)and doesn’t stay there for very long (3–60 mins)

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45
Q

what does it mean by % of plasma binding for types of antibiotics?

A

the degree to which medications attach to blood proteins within the blood plasma. A drug’s efficacy may be affected by the degree to which it binds. The less bound a drug is, the more efficiently it can traverse or diffuse through cell membranes

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46
Q

is lots of plasma protein binding good or bad?

A

bad as high binding means that the antibiotics don’t diffuse into cells easily and are secreted quicker

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47
Q

what is plasma binding level for penicillin V?

A

75-90% binds to plasma proteins (not very good)

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48
Q

what types of bacteria do penicillin V tackle?

A

streptococci, straphylococci, clostridia, neisseria, treponema, listeria, bacillus

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49
Q

what are negatives of amoxicillin?

A

-effectiveness challenged by beta-lactamases
-disrupts gut flora as broad spectrum & absorbed through intestine

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50
Q

what are side effects of amoxicillin?

A

safe & well tolerated

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51
Q

what is plasma binding like in amoxicillin?

A

20% (low) plasma binding so good distrubution to tissues

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52
Q

why is amoxicillin good?

A

good absorption when given orally
-stable in presence of stomach acid so not inconvenient for eating times

53
Q

what is amoxicillin spectrum?

A

extends to gram +ve and gram -ve

54
Q

what is half life of antibiotics?

A

the time it may take for the strength or concentration of the medication to decrease by half of its original strength so you want a high half life for good effectiveness

55
Q

what is half life of amoxicillin?

A

plasma half life = 60 minutes

56
Q

what is half life like in cephalosporins?

A

longer half life (which is good)

57
Q

what is co-amoxiclav?

A

a combination drug of amoxicillin & clavulanic acid

also contains: beta lactam & beta lactamase inhibitor

58
Q

why did they want combination drug? e.g. co-amoxiclav

A

extends range of bacteria that can be treated (also includes beta lactamase to try and reduce resistance)

59
Q

what is beta lactamase?

A

enzyme produced (by bacteria) to degrade beta lactam (from antibiotic) which is what gives resistance (when antibiotics don’t work on bacteria due to resistance)

60
Q

what is flucloxacillin spectrum?

A

narrow spectrum - straphylococci & streptococci ONLY

61
Q

what is negative of flucloxacillin?

A

narrow spectrum & MRSA is resistant to it

62
Q

when and how often if flucloxacillin prescribed?

A

commonly prescribed. for straph & strep infections
e.g. Skin and soft tissue infection
* Wound infection
* Cellulitis (infection of the soft tissues under the skin)

63
Q

how does flucloxacillin try to resist beta lactam degredation?

A

by modifying side chains so beta lactamase can’t bind/fit and degrade it

64
Q

why did flucloxacillin replace methicillin?

A

better tissue distrubution

65
Q

why is temocillin good?

A

beta lactamase resistant as targets beta lactamase producers

66
Q

what is temocillin spectrum?

A
  • largely restricted to coliforms (gram -) like GI tract and e.coli
    -Active against ESBL-producing organisms
  • Extended spectrum to b-lactamases producers
  • Also resistant to ampC b-lactamases
67
Q

what is problem with temocillin?

A

only given IV not orally

68
Q

what is carbapenems spectrum?

A

broad spectrum = gram +ve and gram -ve

69
Q

why is carbapenem good?

A

resistant to beta lactamase and can be a bit of a lost resort - if you don’t know whats wrong with patient then kills broad range

70
Q

what are 2 types of glycopeptide?

A

vancomycin
teicoplanin
(both IV)

71
Q

what is action of glycopeptide?

A

it’s not beta lactam antibiotic but still targets cell wall

=binds to end of peptide chain (D-alanine D-alanine) & prevent its incorporation into the cell wall.
= this block PBP from binding to cell so reduced cross linking so lysis and weakening of cell wall

(Also interferes with membrane & PG precursor carrier molecule (Lipid II))

72
Q

how is glycopetide excreted?

A

via kidneys & urine

73
Q

how can glycopeptide help cause kidney damage?

A

-toxic levels of vancomycin in blood can build up in patients who have kidney failure causing further kidney damage

74
Q

what is glycopeptide spectrum?

A

Restricted activity means limited to bacteria with a Gram-positive cell wall
* Oral Vancomycin can target Gram+Ve GI microbes as builds up in intestine
* NO activity against Gram negative organisms
* Excluded by outer membrane

75
Q

what is function of protein synthesis inhibitors?

A

they block different steps in protein synthesis with transient & permanent binding

76
Q

what are protein synthesis inhibitors?

A

antibiotics that inhibit protein synthesis by attaching to bacterial ribosomes (which are STRUCTURALLY DIFFERENT from mammalian ribosomes)

77
Q

what does it mean by bacteriostatic antibiotic & what are some examples?

A

bacteriostatic - when protein synthesis resumes after antibiotic antibiotic removed

examples = macrolides & tetracyclines

78
Q

what does it mean by bacteriocidal antibiotics & what are some examples?

A

bacteriocidal = when binding of antibiotics is lethal and protein synthesis doesn’t ever continue

example = aminoglycosides (gentamicin)

79
Q

what are 3 key examples of protein synthesis inhibitors (the specific antibiotic & the group of antibiotics they’re in)

A
  1. gentamicin (in aminoglycosides group)
  2. deoxycyline/minocycline (tetracycline group)
  3. erythromycin (macrolide group)
80
Q

how is gentamicin given?

A

IV only - not absorbed in the gut
(occasionally intramuscular)

81
Q

how does gentamicin inhibit protein synthesis?

A

binds to ribosome 30S inhibiting protein sythesis
- it’s irreversible binding & bacteriocidal (kills bacteria)

82
Q

what is gentamicin active against?

A

mainly gram -ve aerobic organisms e.g. coliforms & pseudonomas aeruginosa
-> for people who are seriously ill (in hospital)

83
Q

what is negative of gentamicin?

A

toxicity = causes damage to kidneys and VIIth carnial nerve (deafness & dizzyness) so blood levels need to be monitored of aminoglycosides complicating therapy

84
Q

how is gentamicin excreted?

A

by urine

85
Q

what is mode of action of tetracyline?

A

actively transported into cell
= binds to 30S subunit on ribosome & prevents attachment of tRNA to acceptor sites (stops chain elongation)

86
Q

what is spectrum of tetracycline?

A

broad spectrum
= useful against intracellular bacteria & atypical bacteria e.g. chlamidyia

87
Q

is there resistance against tetracyclins?

A

more resistance after each use

88
Q

what are negatives of tetracyclins?

A

destruction of normal intestinal flora resulting in increased secondary infections
- staining & impairment of the structure of bone & teeth
- restricted use in infants, children & pregnancy

89
Q

what tetracylins have more efficient absorption?

A

deoxcyclin & minocycline
(lower concentration in gut so less disturbance & higher concentration in serum)

90
Q

are the following bacteriocidal or bacteriostatic?
a) aminoglycides (gentamicin)
b) tetracyclins
c) macrolides

A

a) bacteriocidal
b) bacteriostatic
c) bacteriostatic

91
Q

when are macrolides commonly prescribed?

A

for penicillin allergy & intracellular pathogens

92
Q

what is mode of action for macrolides?

A

bind to 50S subunit on ribosome and block translocation = no release of peptide

93
Q

what are examples of macrolides?

A
  • erythromicin
  • clarythromicin (gram -ve)
  • azithromycin (gram +ve)
94
Q

how are macrolides excreted?

A

by the liver - biliary tract and into gut
(NOT URINE)

95
Q

is erythromycin safe in pregnancy?

A

yes

96
Q

what type of infections are macrolides useful for?

A

treating certain infections where intracellular bacteria “hide” from the host’s immune system

97
Q

what are examples of antibiotics that target nucleic acid?

A
  1. fluoroquinoles (gram - & +)
  2. metranidazole (anaerobes & protozoa)
  3. Trimethroprim = +/- sulphonamides (urinary tract infections)
98
Q

what is main example of quinolones?

A

ciprofloxacin

99
Q

what is mode of action of quinolones?

A

bind to the A subunit of DNA gyrases (topoisomerase) and prvent supercoiling of DNA
= indirectly inhibits DNA synthesis

100
Q

are quinolones bacteriocidal or bacteriostatic?

A

bacteriocidal

101
Q

what does DNA gyrase do?

A

catalase the supercoiling of DNA
- belong to group of enzymes called topoisomers

102
Q

how is ciprofloxacin given?

A

IV or orally

103
Q

what activity does ciprofloxacin target?

A

gram -ve activity e.g. e.coli, H.influenza, pseudonoma etc

104
Q

what is spectrum of quinolones?

A

broad spectrum therefore use now severely restricted to reduce risk of c.difficile GI infection (especially in elderly)

105
Q

what do you prescribe quinolones for?

A
  • bones
  • UTI’s
  • community acquired ammonia

-> severely restricted due to broad spectrum = risk for c.diff

106
Q

what antibiotic group does metronidazole belong to?

A

nitroimadazoles

107
Q

how can metronidazole be given?

A

IV or orally

108
Q

what is metronidazole active against?

A

anaerobes (important to know)& parasites/protozoa

109
Q

what is mode of action of metronidazole?

A
  • drug activated by reduction process
  • intracellular low Eh leads to reduction (found in anaerobes)
  • forms toxic intermediate that induces DNA strand breakage
110
Q

what is resistance for metronidazole like?

A

very rare

111
Q

what are negatives for metronidazole?

A

adverse reactions are limited as long as alcohol is avoided
- complaints of metallic taste
- furred tongue

112
Q

why would you want drugs to inhibit folic acid synthesis?

A

because then a key intermediate metabolism is blocked
- it’s a pathway we don’t use in eukaryotic cells
- folic acid vitamin is required for synthesis of key cellular components

113
Q

what are 2 types of folic acid synthesis inhibitors?

A
  1. sulphonamides
  2. Trimethroprim
114
Q

how is trimethroprim excreted?

A

in urine

115
Q

when is trimethroprim commonly prescribed?

A

for acute UTI’s e.g. e.coli

116
Q

how can trimethroprim be given (hint = on it’s own & in combination)?

A

on it’s own = orally
in combination with a sulphonamide (sulphamethoxazole) (called co-trimoxazole) = orally or IV

117
Q

what is trimethrprim spectrum?

A

some gram -ve and some gram +ve

118
Q

why isn’t trimethroprim used more often?

A

it’s not used sytstemicly, beta lactam drug preferred over it

119
Q

what is presumptive prescribing?

A

also called empiric prescribing
= without laboratory identification based on likely pathogens for infection under treatment

120
Q

what is targeted prescribing?

A

-nature & extent
= Laboratory investigation (identification & sensitivity of pathogen)

121
Q

what are considerations for when picking what antibiotic to prescribe?

A

-drug choice
- nature of infection
-dose route & frequency
- allergy
-interactions
-compliance

= prescribing should be limited but still prescribe as saves lives

122
Q

what are COMMON side effects of antibiotics?

A

nausea, vomiting, diarrhoea

= all antibiotics interrupt gut bacterial flora
= may affect absorption of oral contraceptives

123
Q

what is gentamicin main problems?

A

renal & VII nerve damage

124
Q

what is ciprofloxacin main problems?

A

tendonitis - avoid use in pregnancy & breast feeding women

125
Q

what is main problem with metronidazole?

A

interacts with alcohol

126
Q

what are the 4C’s?

A

high risk - restricted antibiotics

  1. Cephalosporins
  2. Co-amoxiclav
  3. Ciprofloxacin
  4. Clindamycin

= they kill a broad range of bacteria but means high c.diff risk

127
Q

why are antibiotics sometimes given in combination? (reasons for)

A
  1. To cover a broad range of possible infecting organisms, e.g. for the treatment of pneumonia
  2. To prevent the development of resistance, e.g in the treatment of tuberculosis (TB)
  3. For the synergistic (co-operation) effect of combination (1+1 = 3), e.g in the treatment of some cases of endocarditis (means they work together to get good outcome)
128
Q

what should you never combine?

A

bacteriostatic & bacteriocidal e.g. protein synthesis inhibition with cell wall antibiotics - cell wall synthesis has stopped

Microbiology (6 decks)

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