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Year 2 intro to clinical sciences > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What is an antibiotic?

A

Antibiotics are molecules that work by binding a target site on a bacteria

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2
Q

what class of antibiotic is penicillin

A

B lactam

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3
Q

List some B lactam antibiotics

A

penicillin derivatives

cephalosporins and cephamycins

monobactams

carbapenems and carbacephems

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4
Q

what does the antibiotic polymyxin work on

A

Cell Membrane

Treats gram negative infections, last line of antibiotics, narrow spec

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5
Q

What are the classes of antibiotics that work on 30s

A

Tetracyclines
Aminoglycosides

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6
Q

What are the classes of antibiotics that work on 50s

A

Macrolides
Clindamycin
Linezolid
Chloramphenacol
Streptogramins

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7
Q

what are the classes of antibiotics that work on RNA polymerase

A

Rifampin

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8
Q

What are the classes of antibiotics that work on DNA gyrase

A

Quinolones

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9
Q

What are the classes of antibiotics that work on folalte synthesis

A

Sulfonamides
Trimethoprin

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10
Q

What type of antibiotics are Vancomycin +
Teicoplanin

A

Glycopeptides

Treat beta lactam resistant gram +ve bacteria

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11
Q

Describe how Beta lactam antibiotics
work

A
  • disrupt peptidoglycan production
  • bind covalently and irreversibly to Penicillin Binding Proteins (PBP’s)
  • To bind to the PBPs, the β-lactam antibiotic must first diffuse through bacterial cell wall
  • Gram -ve have an LPS layer that decreases antibiotic penetration
  • cell wall is disrupted and lysis occurs
  • results in a hypo-osmotic or iso-osmotic
  • Active only against rapidly multiplying organisms
  • Differences in broad vs narrow spectrum are due to affinity for PBPs

gram +ve more susceptible to β-lactams than gram-negative bacteria

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12
Q

Briefly describe what a bactericidal antibiotic is

A
  • Kills 99.99% bacteria
  • Inhibits cells wall synthesis

-usually beta lactams
-good for needing to get rid of bacteria quickly (meningitis)

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13
Q

Briefly describe what a bacteriostatic antibiotic is

A

*inhibit growth
*Inhibit protein synthesis, DNA replication or metabolism

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14
Q

How do bacteria become resistant to Penicillins and cephalosproins

A

Both types of antibiotic contain a beta lactam ring

Beta-lactamase hydrolysis this ring and the antibiotic and now unable to bing to the PBP’s

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15
Q

Why do bacteria develop resistance?

A

*Intrinsic - Naturally resistant

*Extrinsic - Naturally acquired through spontaneous gene mutation or horizontal gene transfer (conjunction, transduction, transformation)

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16
Q

what are the two major determinants of anti bacterial effects

A

concentration and the time

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17
Q

Describe intrinsic bacterial resistance.

A

D

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18
Q

Briefly describe Horizontal gene transfer: Transduction with and example.

A

*Insertion of DNA by bacteriophages
*mecA genes for MRSA

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19
Q

Briefly describe horizontal gene transfer: Conjugation and and example.

A

*Sharing of extra chromosomal DNA plasmids
*New Delhi metallo-B-lactamase

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20
Q

Briefly describe horizontal gene transfer: Transformation and example

A

*foreign DNA from S. mitis to S. pneumoniae, conferring penicillin resistance

21
Q

What does MRSA stand for

A

Methicillin resistant Staphylococcus aureus

22
Q

What is MRSA resistant to

A

resistance to all β-lactam antibiotics in addition to methicillin

23
Q

what does VRE stand for

A

vancomycin-resistant enterococci

24
Q

How did MRSA become resistant to antibiotics

A
  • transduction - Bacteriophage mediated acquisition of Staphylococcal cassette chromosome mec (SCCmec)
    containing resistance gene mecA

*encodes penicillin-binding protein 2a (PBP2a)

25
Q

How did VRE become resistant to antibiotics

A

*Plasmid-mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding

*Promoted by cephalosporin use

26
Q

What gram is MRSA

A

+VE

27
Q

What gram is VRE

A

+ve

28
Q

What gram is ESBL

A

-VE

29
Q

What does ESBL stand for

A

extended spectrum beta lactamase (ESBL)

30
Q

what gram bacteria do Vancomycin and Teicoplanin treat

A

+ve only

31
Q

whe should you use vancomycin and teicoplanin?

A

*Gram-positive bacteria resistant to beta-lactams
*when the patient is allergic to penicillin

32
Q

which classes of antibiotics work on cell wall synthesis

A

B lactams
Vancomycin
Bacitracin

33
Q

Which classes of antibiotics work on nucleic acid synthesis

A

*Rifampin working on RNA pol

*Quinolones working on DNA gry

*Sulfonamides Trimethoprin working onFolate synthesis

34
Q

what cells can beta-lactams not enter?

A

*Eukaryotic cell

Beta lactams arent so useful for bacteria that can enter euk cells

35
Q

which antibiotics work on protein synthesis

A

*Tetracyclines and aminoglycosides working on 30s
*macrolides clindamycin etc working on 50s

36
Q

what are some consequences (bodily) of antibiotics

A

Direct- destroy phagocytes cells which bacteria replicate

Indirect - inflammation

Diarrhoea

Toxins- exotoxin (protein product) and endotoxin ( gr -ve)

37
Q

The amount of antibiotic needed is called …..

A

minimum inhibitor conc (MIC)

38
Q

what is used to treat staph aurious

A

Flucloxacillin

39
Q

why cannot vancomyocin treat gram negative

A

Cannoy penetrate the cell membrane.

40
Q

what are some things to consider when prescribing antibiotics

A

*Drug interactions

*risk of c diff

*pregnancy

*Allergies

*age

*Renal and liver function

41
Q

gram +ve and catalyse +ve =

A

Staph coccus

42
Q

gram +ve and Catalase -ve =

A

Strep coccus

43
Q

Streptococcus when undergoing haemolysis on blood agar if beta will be …..

A

Group A C G

44
Q

Streptococcus when undergoing haemolysis on blood agar if alpha will be …..

A

tested with optochin and if sensitive will be Streptococcus pneumoniae

45
Q

What are A C G groups of s. aurius

A

Flucloxacillin

46
Q

Why cant you treat a CNS infection with vancomycin

A

Vancomycin does not effectively cross the blood-brain barrier.

47
Q

what could you use to treat necrotizing facsch

A

Clindamycin

48
Q

which gram negative use lactose as a food source

A

Klebs, e.coli

49
Q
A

Year 2 intro to clinical sciences (46 decks)

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