Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Infectious Disease > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

What are anti-microbials?

A

Drugs which kills or inhibit growth of micro-organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are antibiotics classifications? Give examples the drugs in each classification?

A

Based on what they target:

Bacterial cell wall and membrane

  • penicillins
  • cephalosporins
  • carbapenems
  • monobactams
  • glycopeptides
  • polymxins

Nucleic acid synthesis

  • folate antagonists
  • DNA gyrase i.e. Quinolones
  • RNA polymerase i.e. Rifmycins
Protein synthesis 
-50s subunit:
Macrolides 
Linomycins (Clindamycin)
Oxozolidinones (linezolid)
Chroamphenicol 
-30s subunit:
Tetracyclines 
Aminoglycosides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the functional classification of antibiotics?

A

Bacteriostatic
-inhibit growth and replication = NON-LETHAL
E.g. Inhibitors of folate synthesis + quinolones

Bacteriacidal
-kill bacteria but can be bacteriostatic at lower doses
Eg penicillin + aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do beta-lactam antibiotics work and which antibiotics come under this class?

A

INHIBITION OF CELL WALL SYNTHESIS
Beta-lactam antibiotics have beta-lactam ring which acts a structural mimic of D-Ala-D-Ala of penicillin binding protein (PBP) Acts to prevent the cross-linking of DD transpeptide proteins which are important for the formation of peptidogylcan cell wall
I.e bacteria unable to survive osmotic pressures

penicillins
Cephalosporins
Carbapenems
Monobactams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 5 classes of penicillin? Give examples of types of penicillin.

A

Natural penicillins
Penicillinase-resistant penicillins (not really used clinically)
Aminopenicillins
Carboxypenicillins (not used clinically)
Acyl ureidopenicillins

Penicillin V
Amoxicillin
Flucloxacillin
Benzylpenicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical features of penicillins?

A

Narrow spectrum

Excellent absorption

Safe in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the clinical features of Cephalosporins? Give examples.

A

Broad spectrum

Safe in pregnancy

Cefuroxime
Ceftaxime
Ceftazidime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the clinical features of carbapenems? Give examples?

A

Broad spectrum

IV only

Safe in pregnancy

Meropenem
Ertapenem
Imipenem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the mechanism of action of glycopeptides?

A

Target gram +ve bacteria only, which are the bacteria without porins present in cell wall. Act to inhibit cell wall synthesis by binding to PBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the clinical features of glycopeptides? Give examples.

A

Narrow spectrum
IV admin only
Safe in pregnancy

Vancomycin
Teicoplanin
Dalbavancin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 3 types of antibiotics which causes inhibition of cell wall synthesis?

A

Beta-lactam antibiotics

Glycopeptides

Polymyxins (Colistin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which 2 antibiotics act by inhibiting folate synthesis? What is the mechanism of each?

A

Sulphonamides
-inhibits dihydropteroate sythetase (DPS) enzyme to inhibit conversion of PABA to folate

Trimethoprim
-inhibits dihydrofolate reductase to inhibit conversion of folate to tetrahydrofolate

THEREFORE both lead to inhibition of DNA production and are BACTERIOSTATIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are sulphonamides and trimethoprim used clinically?

A

Used in combination for synergistic effects

Broad spectrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why are sulphonamides and trimethoprim contraindicated in pregnancy?

A

Inhibition of folate means that foetus does not receive sufficient folate= leads to neural tube defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the mechanism of Quinolones? What are their clinical features and give examples of types?

A

Inhibit DNA gyrase= important bacterial enzyme for correct topological formation of DNA

Can be broad or narrow spectrum and have excellent bioavailability

Eg:
Ciprofloxacin 
Levofloxacin
Ofloxacin
Gatafloxacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechanism of Rifamycins? What are the important considerations when using this drug?
How could you identify a patient on these drugs?

A

RNA polymerase inhibitor

Acts as potent liver enzyme inducer (CYP3A) which can lead to increased liver metabolism of other medications and therefore decrease the plasma concentration

Has low genetic barrier meaning it is vulnerable to genetic resistance being developed = SHOULD NOT BE USED ALONE

Orange urine/tears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the mechanism of Macrolides? Give examples of antibiotics in this class.

A

Targets 50s subunit to dysregulate protein production leading to bacteriostatic affect

Erythromycin
Azithromycin
Clarithromycin

18
Q

What is the mechanism of Lincosamide (Clindamycin)? Which infections is it particularly effective against?

A

Targets 50s subunit and can have bacteriostatic or bacteriacidal effect depending on dose

Gram positive and anaerobic infections

19
Q

What is the mechanism of Oxazolidinones (linezolid)? Which infections are they affective against?

A

Targets 50s subunit to have bacteriostatic effect

Gram positive infections

20
Q

What is the mechanism for chloramphenicol? What infections is it useful in targeting?

A

Targets 50s subunit to have bacteriostatic effect

Topical infections such as ear or eye infections
CNS infections as is able to penetrate into CNS and cross BBB

21
Q

What are the 2 antibiotic classes which target 30s subunit? What are their clinical features and indications?

A 
Tetracyclines 
-broad spectrum bacteriostatic 
-contraindicated in preg, breast feeding and children 
-can cause teeth staining
Eg 
-doxycycline 
-tetracycline 
-minocycline
Aminoglycerides 
-narrow spectrum= gram -ve infections 
-given IV
Eg
-Gentamycin 
-Amikacin
-Tobramycin 
-Streptomycin
22
Q

Which antibiotics are safe for use in pregnancy?

A

Penicillins

Cephalosporins

Clindamycin

Glycopeptides

Metronidazole

23
Q

Which antibiotics are not safe for use in pregnancy and breasting feeding? Give a brief reason why

A

Carbapenams= Manufacturing warning

Macrolides=. Manufacturing warning

Quinolones= can affect skeletal development

Folate antagonist= neural tube defects

Tetracyclines= affect skeletal development

Aminoglycosides= auditory/vestibular nerve damage

24
Q

What are the 3 methods of assessing in vitro antibiotic effectiveness?

A

Minimum inhibitory concentration (MIC)
-minimum in vitro concentration which can inhibit growth of bacteria

Minimum bactericidal concentration (MBC)
-minimum in vitro concentration of antibiotic which can kill bacteria

Detection of resistance mutations by PCR
-due to effecting bacteriostatic and bactericidal activity of ab

25
Q

What does the “breaking point” refer to in terms of antibiotic effectiveness?

A

Point where certain concentration of antibiotic can no longer inhibit bacterial growth

26
Q

What in vivo factors can affect the effectiveness of an antibiotic? How might present in a clinical setting?

A

Pharmackinetics

Pharmacodynamics

Foreign material

Source control

Host immune response

Patient might not be responding to an antibiotic despite it being the appropriate antibiotic for the bacterial infection they have

27
Q

What does pharmacokinetics refer to in the context of antibiotics? What are the 4 components influencing pharmacokinetics?

A

Time course of antibiotics

  1. Absorption:
    - Route of administration important ensure Ab reaching the site of infection
    - bioavailability i.e. proportional drug absorbed into systemic circulation
  2. Distribution:
    - Volume of distribution i.e. serum [drug] relative to dose
  3. Metabolism:
    - CYP3A4 inducers (Rifampicin)
    - CYP3A4 inhibitors (Ketoconazole)
  4. Excretion:
    - half-life
    - renal excretion
    - non-renal excretion i.e. Ceftriaxone = biliary and Azithromycin = gut
28
Q

Which antibiotics have excellent bioavailability? What is the benefit of this?

A 
Amoxicillin
Linezolid
Clindamycin 
Levofloxacin 
Ciprofloxacin 
Rifampicin 
Metronidazole

Means that lower dose of drug is required to achieve the same therapeutic effect meaning body will not be exposured to high doses

29
Q

What is the significance of a small and large volume of distribution in context of antibiotics?

A

Small= drug is plasma bound i.e confined to circulation
-means lower dose required to reach certain plasma volume

Large= fat soluble i.e. drug more likely to be found on tissue
-means larger dose required to reach certain plasma volume

30
Q

Which antiobitics can affect liver metabolism and what is the significance of this?

A

Rifampicin= CYP3A4 inducer

Ketoconazole/Clarithromycin= CYP3A4 inhibitor

Can lead to fatal drug interactions if patient on other medication which is relying on these metabolic pathways

31
Q

How does pharmacokinetics lead to differences in how often different antibiotics need to be taken?

A

Some antibiotics able to stay w/i therpeutic range (above MIC) for longer meaning fewer doses required

32
Q

What are the 3 different forms of killing dependent on pharmacodynamics of antibiotics? Give examples of antibiotics associated with each.

A

Concentration dependent killing (Cmax/MIC ratio)
I.e. peak drug concentration
Eg Aminoglycosides/Fluoroquinolones

Time dependent killing (AUC/MIC ratio)
I.e. time drug needs to spend above MIC
Eg Vancomycin/Azithromycin/fluoroquinolones/aminoglycerides/linezolid

Exposure dependent killing (AUC24/ratio)
Eg beta-lactams/vancomycin/macrolides/Clindamycin

33
Q

What is the post-antibiotic effect? (PAE) What type of killing leads to greater PAE? Give an example of antibiotic with high PAE.

A

Time when bacterial growth is still inhibited when drug con < MIC

Concentration-dependent killing leads to greater PAE

GENTAMYCIN
-v high dose w/i 1 hour of taking which means only one dose needed a day because associated with very high PAE

34
Q

What is the pharmacodynamic advantage of combining Co-amoxiclav and Gentamycin?

A

Gentamycin causes very high concentration in short among of time and has high PAE to continue to kill bacteria after peak

Co-amoxiclav requires regular doses to achieve MIC but then maintains steady killing action

THEREFORE:
Combined use can lead to more optimal treatment of infection

35
Q

What are the 3 main AMR pathogens?

A

Methicillin-resistant staphylococcus aureus (MRSA)

Vancomycin resistance enterococci (VRE)

ESBL

36
Q

What are the 3 main mechanisms of AMR? Give examples of resistance to specific antibiotics.

A
  1. Production of enzymes:
    - beta-lactamase enzyme and beta-lactam molecule hydrolysis
    - carbapenamase enzymes
  2. Changes to target site/metabolic pathway:
    - b-lactams= mutation in PBPs
    - macrolides + lincosomides= methylation of rRNA
    - Quinolones= DNA gyrase mutations
    - Carbapenems= porin channel mutation
    - folate antagonist= use of exogenous thymidine or thymidine
  3. Efflux pumps
    - Tetracyclines= actively pumping enzymes out of cell
37
Q

What types of mutation are associated with AMR?

A

Natural resistance

Point mutations

Transformations by up taking DNA from other cells

Transduction= infection from bacteriophage

Conjugation= exchange of genetic material via plasmids or transposons

38
Q

What are the two types of allergic reaction most commonly associated with antibiotic allergic reaction? What are the signs associated with each?

A 
Type 1:
Immediate, IgE mediated reaction 
Signs:
-urticaria 
-angioedema= histamine mediated 
-anaphylaxis

Type 4:
Delayed hypersensitivity
Signs:
-multiple organs can be involved over number of weeks
-DRESS= drug rash with eosinophilia and systemic symptoms
-SJS= Steven-Johnson syndrome
-TEN= Toxic epidermal necrosis

39
Q

What are the main ways which AMR has been accelerated?

A

Drug prescribing

Drug access

Veterinary use

Global travel

Environment

40
Q

What are the 3 main mechanisms of action of antibiotics targetting aerobic bacteria? Give examples of the antibiotics in these classes.

A 
1. Inhibition of cell wall synthesis 
With beta-lactam ring
-penicillin
-carbapenems 
-cephalosporins 
Without beta-lactam ring
-vancomycin
-teicoplanin
  1. Inhibition of folic acid metabolism (due to bacteria reliant on one production of folic acid)
    - sulfamethoxazole= blocks PABA->DHFA
    - trimethoprim = blocks DHFA->THFA
    - co-trimoxazole= combo of 2 above
  2. Inhibition of protein synthesis by targetting ribosomes
    - macrolides I.e. erythromycin
    - clindamycin
    - tetracylines i.e. doxycyclines
    - gentamicin
    - chloramphenicol
41
Q

What antibiotic is used to target anaerobic cells?

A

Metronidazole

I.e. only reduced to active form in anaerobic cells

42
Q

What is a stepwise approach of treating someone with antibiotics and what is the reasoning for the additional antibiotics?

A

Amoxicillian
-covers streptococcus, listeria and enterococcus

Co-amoxiclav
-covers staphlococcus, haemophilus + ecoli

Tazocin
-covers pseudomonas

Meropenem
-covers ESBLs

Teicoplanin or vancomycin
-MRSA

Clarithromycin or doxycycline
-atypical bacteria

Infectious Disease (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions