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Infection&immunity > Julie Letch S1 > Flashcards

Julie Letch S1 Flashcards

1
Q

Name 4 sites of action of antimicrobials

A

Cell wall
Protein synthesis
Cell membrane
Nucleic acid synthesis

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2
Q

Do gram negative have a Thinner or thicker layer of peptidoglycan

A

Thinner

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3
Q

What part of the cell do B-Lactams target?

A

Cell wall synthesis

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4
Q

How do B-lactam antibiotics exert their effects?

A

Bind to penicillin binding proteins to prevent X-linking
Mimic D-Ala D-Ala residues on side chain
Indirect effect they stimulate autolysins that break down cell wall

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5
Q

Name two types of antibiotics that exert their effects by acting on cell wall synthesis

A

B-lactams and glycopeptides

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6
Q

Give two examples of a glycopeptide

A

Vancomycin

Teicoplanin

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7
Q

How do glycopeptides exert their effects on cell wall synthesis

A

Binds terminal D-Ala D-Ala on peptide side chain to prevent transglycosylase enzyme from adding PG monomer onto glycan chain, prevents X-linking

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8
Q

Name a class of antibiotics that act on the cell membrane

A

Polymyxins

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9
Q

Give two examples of Polymyxins

A 
Polymyxin B
Polymyxin E (colistin)
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10
Q

How do Polymyxins work

A

Work on cell membrane: cationic binds to lipid A component of gram -ve to distort and increase permeability of outer membrane resulting in leakage

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11
Q

Do Polymyxins work on gram +ve?

A

NO peptidoglycan too thick

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12
Q

Name two antibiotics that are metabolic inhibitors of NUcleic acid synthesis

A

Sulphonamides

Trimethoprim

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13
Q

Name an antibiotic that affects DNA replication

A

Fluroquinolones

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14
Q

Name an antibiotic that affects RNA polymerase

A

Rifamycins

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15
Q

Do nitroimidazoles affect DNA

A

YES

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16
Q

Name two examples of fluoroquinolones that inhibit DNA replication

A

Ciprofloxacin

Levofloxacin

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17
Q

What’s the role of DNA gyrase

A

Removes DNA supercoils ahead of replication fork

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18
Q

What’s the role of topoisomerase IV?

A

Separating DNA after replication

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19
Q

How do the fluoroquinolones inhibit DNA replications

A

They decrease type 2 DNA gyrase and/or type IV topoisomerase

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20
Q

Name two aminoglycosides/oxazolidinones that work by inhibiting protein synthesis

A

Gentamicin

Linezolid

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21
Q

How do most aminoglycosides work?

A

Inhibit protein synthesis by binding to 30S subunit

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22
Q

Do some aminoglycosides and oxazolidinones work by binding to the 50S subunit

A

Yes only some

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23
Q

How do tetracyclines work and give two examples

A

Inhibit protein synthesis by binding to 30S subunit e.g doxycycline and minocycline

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24
Q

How does chloramphenicol work

A

Inhibits protein synthesis by binding 50S subunit and reduces peptide bond formation

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25
Q

How do macrolides work

A

Inhibit protein synthesis by binding 50S subunit decreasing translocation a and tRNA release

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26
Q

Give two examples of macrolides

A

Clarithromycin

Erythromycin

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27
Q

How does fusidic acid work

A

Inhibits protein synthesis by binding to EF-G ribosome complex and preventing translocation of tRNA from A to P site

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28
Q

How do cycloserine and bacitracin work?

A

They work by affecting cell wall synthesis

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29
Q

Where does daptomtcin (cubicin) exert its effects as an antimicrobial

A

Cell membrane

30
Q

Lincosamides and streptogramins act where?

A

Protein synthesis

31
Q

Sulphonamides, trimethoprim and rifamycin all effect what?

A

NUcleic acid

32
Q

Define antimicrobial

A

Chemicals which kill or inhibit microbial growth

33
Q

What’s intrinsic antimicrobial resistance and give an example

A

Innate properties of bacterial cell E.g cell wall

34
Q

Give three mechanisms by which microbial resistance can occur

A

Inactivate/modify drug
Alter drug target site
Alter drug uptake/exit

35
Q

Where are the beta lactamases in gram negative bacteria?

A

In the periplasmic space (still excreted out but accumulates)

36
Q

In gram positive bacteria where are beta lactamases

A

They’re released out into medium (need dense bacterial population)

37
Q

Name two limited spectrum beta lactamases in E.coli and which one is most common

A

TEM-1 (most common)

TEM-2

38
Q

Name two extended spectrum beta lactamases

A

CTX-M (e.coli & S.thyphimurium)

NDM-1 (e.coli) resistant to all beta lactam drugs

39
Q

Name three beta lactamase inhibitors

A

Clavulanic acid
Sulbactam
Tazobactam

40
Q

Methicillin resistance in S.aureus is because of what?

A

Altered target site:

PBP2 –> PBP2a

41
Q

What is resistance in haemophilus influenzae due to?

A

Altered target site:

PBP3–> PBP3a and 3b

42
Q

What is resistance in streptococcus pneumoniae due to?

A

Altered target site:
PBP1–> PBP1a & b
PBP2–> PBP2a

43
Q

Altered uptake can also be a cause of resistance to beta lactam drugs .. But in what type of bacteria and how?

A

GRAM -ve YO

reduced no./size of porins

44
Q

How does bacteria become resistant to vancomycin

A

Changes in terminal amino acids of peptide chain:

D-Ala-D-Ala—> D-Ala-D-lactate (vancomycin can’t bind/binds weakly)

45
Q

How can you get resistance to aminoglycosides?

A

Inactivating enzymes
Acetylase
Adenylylase
Phosphorylase

46
Q

What antibiotics are effected by efflux pumps?

A

Tetracyclines

Quinolones

47
Q

What does the R group of penicillins determine

A 
Selectivity
Solubility 
Stability 
Bioavailability 
B-lactamase resistance
48
Q

What are the 4 classifications of penicillins

A

1) b-lactamase sensitive
2) b-lactamase resistant
3) broad spectrum
4) anti-pseudomonal

49
Q

Give three examples of bacteria that cause meningitis

A

Neisseria meningitidis
Strept pneumoniae
Haemophilus influenzae

50
Q

Name two first generation cephalosporins

A

Cefazolin

Cefradine

51
Q

Name two second generation cephalosporins

A

Cefuroxime

Cefaclor

52
Q

Name two third generation cephalosporins

A

Cefotaxime

Ceftriaxone

53
Q

Name two fourth generation cephalosporins

A

Cefepime

Cefpirome

54
Q

Carbapenems inhibit what

A

Cell wall synthesis

55
Q

Give three examples of carbapenems

A

Imipenem
Meropenem
Doriopenem

56
Q

What’s the only monobactam used clinically

A

Aztreonam

57
Q

Name four classes of beta-lactams

A

Penicillins
Cephalosporins
Carbapenems
Monobactam

58
Q

Name the Bacteria that causes tuberculosis

A

Mycobacterium tuberculosis

59
Q

Why type and shape of bacteria causes tuberculosis

A

Slowing growing rod bacillus- acid fast bacteria

60
Q

What does acid fast bacteria mean?

A

Doesn’t show in gram stain due to rich lipid layer of fatty acids

61
Q

Describe the four stages of TB

A

1) phagocytose by macrophages but they don’t destroy
2) TB multiplies in macrophage for 7-21 days and bursts, incoming macrophages phagocytose released TB, release cytokines
3) cell mediated response initiated tubercules formed
4) bacteria multiply inside macrophage uncontrolled lysis, enzymes destroy local tissue

62
Q

Name two ways you can diagnose active TB

A

Chest X-Ray

Sputum test

63
Q

Name two ways you can diagnose latent TB

A

Tuberculin skin test

Molecular assays

64
Q

When do you need to be screened for TB

A

If travelling to UK from country where TB is common if wishing to stay in UK for >6 months

65
Q

Name four first line anti-TB drugs

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

66
Q

The anti TB drugs isoniazid and ethambutol exert their effects where?

A

Cell wall synthesis

67
Q

Where does the anti-TB drug pyrazinamide exert its effects

A

Disrupts plasma membrane, increased permeability

68
Q

In TB where does the anti TB drug rifampicin exert its effects?

A

Inhibits RNA synthesis

69
Q

Streptomycin is the only aminoglycoside that can do what?

A

Get inside cells (second line for TB)

70
Q

Name 5 second line anti TB drugs

A 
Streptomycin 
Capreomycin 
Cycloserine
Ciprofloxacin 
Azithromycin

Infection&immunity (9 decks)

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