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Year 1 SBA revision > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What can’t give macrolides alongside?

A

Statins - can increase risk of statin induced myopathy

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2
Q

How does Metronidazole work?

A

Damages DNA by forming reactive intermediates to inhibit DNA synthesis

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3
Q

Examples of glycopeptides

A

Vancomycin, Teicoplanin

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4
Q

When treating staphylococcus - what do you need to consider in terms of resistance?

A

90% of staphylococcus produces B-lactamase

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5
Q

What are plasmids?

A

Extrachromosomal genetic elements that exist in the cytoplasm and can replicate independently. Not known how they develop but can contain genes for antibiotic resistance. Can transfer between bacteria.

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6
Q

Problems with targeting Class I biochemical reactions?

A

Similar to human cells and pathogens can use alternative energy sources.

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7
Q

How does Rifampicin work?

A

Inhibits RNA polymerase to prevent mRNA transcription.

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8
Q

Key elimination routes for drugs

A

Usually liver metabolism and renal excretion but can be just renal.Other route - lungs, breast milk, sweat, tears, faeces.

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9
Q

How do tetracyclines work?

A

Bind 30S subunit. Competitive inhibition of tRNA.

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10
Q

How should time-dependent drugs be prescribed?

A

Need to maintain minimum inhibitory concentration for as long as possible. Give multiple doses throughout the day.

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11
Q

What is membrane permeability?

A

How well a drug can cross membranes to reach the site of action.

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12
Q

What is a B-lactam ring

A

Part of structure of penicillin that patients can develop an allergy to. Can then develop further allergies to other antibiotics that have the same structure.

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13
Q

How to remember quinolones

A

Ends floxacin

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14
Q

Examples of quinolones

A

CiprofloxacinLevofloxacin

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15
Q

Blood brain barrier and drug permeability

A

Drugs normally cannot cross. In meningitis the blood-brain barrier swells so there are larger gaps between the cells. Allows drugs through

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16
Q

What are Gram positive bacteria?

A

Bacteria can be classified on the basis of their cell wall.Gram positive bacteria have a cell wall made of multiple peptidoglycan layers.

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17
Q

What does Tazocin contain?

A

Piperacillin and TazobactimAntibiotic + B-lactamase inhibitor

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18
Q

How to B-lactamase inhibitors work and why are they used?

A

Irreversibly binds to B-lactamases. Broadens spectrum of antibiotics that contain B-lactam rings.

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19
Q

What is empiric antibiotic choice?

A

Choose antibiotic based on available information rather than the actual organism present. Allows to start treating right away instead of waiting for microbiology.

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20
Q

What is a steady state of drugs

A

When [drug] in plasma remains constant. Same amount entering as leaving.

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21
Q

How does chloramphenicol work

A

Inhibits transpeptidation (transfer of growing peptide chain to the amino acid attached to tRNA_

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22
Q

How do sulphonamides target antimetabolite activity

A

Targets enzyme required for folate synthesis

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23
Q

What is selective toxicity and what does it rely on?

A

Chemotherapy should be toxic to pathogens but leave host unharmed. Relies on exploiting biochemical differences between host and pathogen.

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24
Q

3 general classes of biochemical reactions that can be targeted.What is class III?

A

Pathways converting small molecules into macromolecules.

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25
Q

4 mechanisms of action in antibiotics

A
  • Disruption of cell wall* Inhibition of nucleic acid synthesis* Inhibition of protein synthesis* Antimetabolite activity
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26
Q

What are transposons?Why are they important?

A

Stretches of DNA that can be easily transferred from plasmid to chromosome as transfer can occur outside of mitosis. Can inset even if host is unable to replicate. Likely cause of widespread distribution of antibiotic resistance between unrelated bacteria.

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27
Q

How do bacteriostatic antibiotics work?

A

Stops further growth of bacteria but won’t kill bacteria already present.

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28
Q

What does co-amoxiclav contain?

A

Amoxycillin and clavulanic acidAntibiotic + B-lactamase inhibitor

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29
Q

Adverse affects of glycopeptides

A

Red man syndrome. Generalised erythema and poss hypotension/bronchospasmNephrotoxicity

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30
Q

How should concentration dependent drugs be prescribed

A

Higher concentrations of these drugs are most effective.. Give a high dose to reach a large peak which is allowed to drop before the next dose is given. Once a day dosage.

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31
Q

3 general classes of biochemical reactions that can be targeted.What is class I?

A

Reactions to produce ATP

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32
Q

What are the 3 key differences between bacteria and human cells?

A

Bacterial cell wall - no counterpart in eukaryotes.No nucleus in bacteria - have a single chromosome in the cytoplasm.No mitochondria in bacteria - generate energy by enzyme systems in plasma membrane.

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33
Q

What is an antibiotic?

A

A drug used to treat infections caused by bacteria. Most commonly prescribed drug in primary care.

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34
Q

How can antibiotics target formation of the peptidoglycan cell wall?

A

Peptidoglycan are formed inside the bacterial cell, transported outside by a lipid carrier and cross-linked to form a strong lattice with other amino acids. Target either release of peptidoglycan or cross-linking.

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35
Q

How do spontaneous mutations cause antibiotic resistance?

A

Spontaneous mutations - low rate for a given gene but as so many cells with short generation time, rate of mutation is reasonably high.

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36
Q

Side Effect of rifampicin

A

Stains body secretions orange

37
Q

How do aminoglycosides work

A

Bind to 30S subunit and cause misreading of mRNA - production of non-functional proteins.

38
Q

How do antibiotics target antimetabolite activity?

A

Folate is essential for DNA synthesis. Bacteria need to synthesise folate while humans get it from their diet. Either inhibit mechanism of synthesis or inhibit folate usage.

39
Q

How do antibiotics target nucleic acid synthesis

A

Inhibit the enzymes involved in various stages of nucleic acid synthesis.

40
Q

Use of vancomycin

A

Last resort drug for MRSA

41
Q

When choosing empiric antibiotics need to consider:

A
  • Active against likely organisms* Reaches site of infection - appropriate route?* Low toxicity - not taken if poorly tolerated* Suitable for patient
42
Q

Resistance in staphylococci

A

Many strains now resistant to almost all antibiotics. One of commonest causes of hospital acquired infections.

43
Q

How does trimethoprim target antimetabolite activity

A

Targets enzyme required to metabolise folate into useful metabolites

44
Q

How to remember aminoglycides

A

Ends in cin (not thromycin)

45
Q

Adverse effects with tetracyclies

A

Concentrates in tissues undergoing calcification. Can stain teeth. Not used in children/pregnancy.Also causes phototoxicity - like sunburn.

46
Q

How to remember Cephalosporins

A

Starts Cef

47
Q

What are patients with penicillin allergies often also allergic to?

A

Cephalosporin - 2.5% of those with penicillin allergies are also allergic to this.

48
Q

Lipophilic drugs - what needs to be considered when prescribing?

A

Accumulate in adipose tissue.

49
Q

Use of Trimethoprim

A

First line treatment for uncomplicated UTIs

50
Q

3 general classes of biochemical reactions that can be targeted.What is class II?

A

Pathways using energy and class I compounds to produce small molecules.

51
Q

What are macrolides useful alternatives to

A

Penicillins

52
Q

When to avoid quinolines

A

Epileptics - reduces seizure threshold

53
Q

How do glycopeptides work?

A

Disrupt cell membrane - Inhibit release of building block for peptidoglycan layer from the lipid carrier.

54
Q

What is a pro drug

A

Drug given in inactive form and converted to active form in body

55
Q

What is chemotherapy?

A

Use of drugs selectively toxic to pathogens with minimal effects on the host.

56
Q

2 key methods of transfer of resistance genes:

A

Conjugation - Cell-cell contact. Main method.Transduction - Plasmid DNA enclosed in bacteriophage.

57
Q

Examples of Beta lactams

A

Penicillins, Cephalosporins, Carbapenems.

58
Q

How to remember tetracyclines

A

Ends cyclone

59
Q

Patient experienced diarrhoea when taking antibiotic previously - how to consider for future prescriptions

A

Intolerance not a side effect. Doesn’t stop giving antibiotics if needed.

60
Q

How could gene amplification cause antibiotic resistance?

A

Theory that antibiotic use can increase the number of copies of preexisting resistance genes.

61
Q

Example Cephalosporins

A

Cefadrine, Cefaclor, Cefotaximine

62
Q

How to extend spectrum of penicillins

A

Mix with clavulnic acid

63
Q

What are Gram negative bacteria?

A

Bacteria can be classified on basis of cell wall.Gram negative bacteria have a single peptidoglycan layer in their cell wall.

64
Q

Example aminoglycosides

A

Gentamicin, Amikacin

65
Q

Example tetracyclines

A

TetracyclineDoxycycline

66
Q

How do Beta lactams work?

A

Disrupt cell membrane - Inhibit cross linking of bacterial peptidoglycan wall by forming covalent bonds with penicillin-binding proteins.

67
Q

Examples of macrolides

A

ClarithromycinErythromycin

68
Q

What are the most important class of biochemical reactions for drug targets?

A

Class III. Act to inhibit nucleic acid synthesis, protein synthesis or peptidoglycan synthesis.

69
Q

What does B-lactamase do?

A

Bacterial enzyme that breaks the B-lactam ring and inactivates the antibiotic.

70
Q

Recent changes to vancomycin resistance

A

Resistance seems to have developed spontaneously. Potential for major clinical implications.

71
Q

How to remember penicillins

A

End cillin

72
Q

How to remember macrolides

A

Ends thromycin

73
Q

Examples of B-lactamase inhibitors

A

Clavulanic acidTazobactam

74
Q

What bacteria doesn’t penicillin work on

A

Mycoplasma as no cell walls. No use for pseudomonas.

75
Q

How are Class II biochemical reactions targeted?

A

Bacteria have to synthesise folate but humans get it through diet. Target folate synthesis/usage to stop DNA synthesis.

76
Q

What drug to use for anaerobic bacteria?

A

Metronidazole

77
Q

How do quinolones work

A

Inhibit DNA gyrase enzyme to prevent DNA supercoiling

78
Q

How to Cephalosporins work

A

B-Lactam antibiotics - target cell wall

79
Q

Advantages and side effects of flucoxacillin

A

Good penetration of soft tissueSide effects include liver damage esp if taken on long term basis.

80
Q

How do antibiotics inhibit protein synthesis

A

Protein synthesis occurs in ribosomes. Bacterial ribosomes are 30S/50S compared to 40S/60S in humans so can specifically target the bacterial ribosome.

81
Q

What is the minimum inhibitory concentration of an antibiotic

A

The lowest concentration of antibiotic that will inhibit visible growth of a microorganism.

82
Q

What is drug clearance

A

Volume of blood cleared of drug per unit time

83
Q

Side effects of metronidazole

A

Metallic taste (awful)Vomiting and rashesInstant, severe hangover if mixed with alcohol

84
Q

3 ways of spread of antibiotic resistance

A

Transfer of resistant bacteria between peoplePlasmidsTransposons

85
Q

How do macrolides work?

A

Binds to 50S subunit and inhibits translocation.

86
Q

Why should care be taken when prescribing antibiotics?

A

Multi-drug resistance increasing
Loss of antibiotics would be devastating - would make routine operations impossible.
Gaining resistance may make bacteria stronger.

87
Q

4 common conditions where antibiotics should not be used routinely?

A

Upper respiratory tract infection
Acute sinusitis
Acute conjunctivitis
Acute otitis media

88
Q

What to consider before prescribing antibiotics?

A 
Patients life in danger?
Infection could cause permanent damage?
Will infection resolve fully?
Will antibiotics shorten illness?
Will antibiotics reduce symptoms
Patient's ICE - managing
89
Q

What is a self-limiting illness

A

Resolves without treatment. Minimal change in course of illness if antibiotics take. May reduce symptoms and shorten course of illness.

Year 1 SBA revision (37 decks)

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