Session 5 - Antibiotics Flashcards Preview

Semester 5 - Farmocology > Session 5 - Antibiotics > Flashcards

Flashcards in Session 5 - Antibiotics Deck (39)
1

How do antibiotics damage bacteria but not host cells?

By exploiting the differences that exist between the structure and physiology of the prokaryotic bacterial cells and the host eurkaryotic cells

2

What are two different overall mechanisms by which antibiotics effect bacteria

Bacteriostatic (inhibit bacterial growth)
Bacteriacidal (kill bacteria)

3

Give four sites on bacteria targeted by antibiotics

Peptidoglycan cell wall
Nucleic acids
Protein synthesis
Cytoplasmic membrane

4

Why can bacterial cell walls be targeted, and by which three main classes of AB?

Peptidoglycan cell wall only present in prokaryotic cell.

Penicillins
Cephalosporins
Glycopeptides

5

Why can nucleic acids be targeted, and by which three classes of AB?

Bacterial genome is a single, circular strand of DNA unenclosed by a nuclear envelope, in contrast to eukaryotic chromosomal arrangement within the nucleus Antifolates
Quinolones
Rifampicin

6

How can protein synthesis be targeted, and name three ABs which do thus

Bacterial ribosome (50s+30s subunits) is different to the mammalian ribosome (60s+40s subunits) Aminoglycosides
Tetraclyclines
Macrolides
Chloramphenicol
Fusidic acid

7

How can the cell membrane of bacteria be targeted, and give 1 AB that does thus

Bacterial plasma membrane does not contain any sterols, unlike mammalian. Polymyxins

8

Give four primary reasons for prophylaxis of bacterial infections

o Peri-operative (Prevention of surgical site infections)
o Short term
 Meningitis contacts
o Long term
 Asplenia (encapsulated bacteria)
 Immunodeficiency

9

Give two ways ABs can be used to treat significant bacterial iunfections

o Treatment of cultured, proven infection
o Empirical treatment of suspected infection

10

What is the ideal antibiotic? (2)

o Clean killing of infecting bacteria
 Minimal impact on non-target commensal organisms
 No resistance in any surviving pathogens
o No adverse effects on patient

11

Give 8 factors which help determine the likely infectious agent in an infection

o Anatomical Site
o Duration of illness
o Past medical history
o Occupational history
o Travel history
o Time of year
o Age
o Personal background

12

Give four factors which determine which antibiotics are likely to be effective

o Community or healthcare onset?
o Severity of infection
o Baseline rate of resistance
o Immune status of patient
 Immunocompromised patients will need IV Antibiotics immediately

13

What three factors do you need to consider when choosing best antibiotic?

o Efficacy
o Cost
o Administration Route

14

Give some common antibiotic adverse drug reactions

Pharmcological (toxicities, drug interactions)
Allergic reactions
Impact on normal flora (c.diff)

15

What is therapeutic drug monitoring?

Therapeutic drug monitoring is used to ensure and adequate, non-toxic dose.

16

Give two antibiotics which require therapeutic monitoring

Gentomicin
Vancomycin

17

What class of AB is gentomicin>

Aminoglycoside

18

What are the effects of gentomicin?

 Dose related ototoxicity and nephrotoxicity at high plasma levels

19

What type of AB is vancomycin?

Glycopeptide

20

Give five side effects of vancomycin

 Dose related ototoxicity and nephrotoxicity at high plasma levels
 Fever, rashes
 Local phlebitis at site of infection

21

Give two overarching methods via which bacteria develop AB resistance

Chromosomal gene mutation
Horizontal Gene transfer

22

What is chromosomal gene mutation and how does it pre-dispose to development of AB resistant pop of bacteria?

o Chromosomal gene mutates in one bacteria in a population, conferring a resistance to antibiotic
o Antibiotic kills all other bacteria, acting as a selection pressure, giving resistant bacteria an advantage
o Population of antibiotic resistant bacteria daughter cells

23

Give three types of horizontal gene transfer

Transformation
Transduction
Conjugation

24

What is transformation?

o Bacteria with antibiotic resistance gene releases DNA
o Uptake of DNA by recipient cell, conferring antibiotic resistance

25

What is transduction?

o Phage infected, antibiotic resistant Bacterial donor cell
o Phage passes the DNA conferring resistance to recipient cell

26

What is conjugation?

o Connection is made between antibiotic resistant donor cell, and recipient cell
o Plasmid containing resistance gene is replicated and passes from donor cell to recipient cell
o Plasmid may even become incorporated into recipient cell DNA

27

Give four methods of antibiotic resistance

- Antibiotic Inactivation
- Alteration of Drug Binding Site
- Alteration of Metabolic Pathways
- Reduced Intracellular Antibiotic Concentration

28

What is antibiotic inactivation?

o Production of enzyme that inactivate the drug
 E.g. β-lactamase which inactivates Penicillins

29

What is alteration of drug binding site?

o Modified binding sites so drugs no longer have affinity for them
 E.g. Bacterial ribosome alteration, meaning Aminoglycosides and Erythromycin cannot bind

30

What is alteration of metabolic pathways?

o Development of altered metabolic pathways
 E.g. bacteria can become resistant to Trimethoprim due to acquired changes in their Dihydrofolate Redctase enzyme, which gives it very little affinity for the drug

31

What is reduced intracellular antibiotic concentration?

o Active Efflux Mechanisms
 E.g. Active transport mechanisms used (e.g. p-glycoprotein) to pump a drug out of the bacterial cell because it accumulates to an effective level
o Decreased permeability
 E.g. Some bacteria become resistant to Tetracycline because they alter their cell membrane to make it impermeable to the drug

32

Give three stages of the emergence of antibiotic resistnace

1. Local selection (e.g. in a hospital)
2. Clonal dissemination (e.g. around the country)
3. Global spread

33

Give five main antibiotic resistant bacteria

o Methicillin Resistant Staphylococcus Aureus (MRSA)
o Glycopeptide Intermediate susceptibility Staphylococcus Aureus (GISA)
o Glycopeptide Resistant Enterococci (GRE)
o Extended Spectrum Beta Lactamase enterobacteriaceae (ESBLs)
o Extensively Drug Resistant Klebsiella Pneumoniae (XDR-KP)

- MDRTB

34

Give four parts of anti-microbial stewardship

o Right antibiotic
o Right time
o Right dose, frequency and duration (Pharmacokinetics – ADME)
o Right route

35

Give two stages of infection control

Prevent the spread of recognised resistant bacteria
Prevent bactrerial exposure to antiotics

36

How can we prevent the spread of recognised resistant bacteria?

 Isolation or cohorting
 Hand hygiene
 Decolonisation of patients

37

How can we prevent bacterial exposure to antibiotics?

 Minimise risk of infection
 Monitor and control antibiotic prescribing

38

What are two different types of AB killing?

Time dependent killing
o Prolonged antibiotic presence at the site of infection, but not high concentration
Concentration dependent killing
o High antibiotic concentration at the site of infection, but short duration

39

What is MIC?

Minimum Inhibitory Concentration – MIC
The MIC is the lowest concentration of an antibiotic that will inhibit the visible growth of a microorganism after overnight incubation.
A MIC is generally regarded as the most basic laboratory measurement of the activity of a microbial agent against an organism.