Brainscape's Knowledge GenomeTM

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


See full index

DDT > DDT 16 - Antibiotics > Flashcards

DDT 16 - Antibiotics Flashcards

1
Q

New antibiotic

A

An antibiotic not used clinically before, but belonging to an existing class of antibiotics

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

novel antibiotics

A

An antibiotic with a mechanism of action that has never been used against bacteria before - less likeliness of resistance

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

name the 4 enzymes S. aureus normally produces

A

Penicillin Binding Proteins 1-4

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

how can antibiotics react to PBPs

A

PBP can be modified by B-lactam antibiotics and leads to inhibition and bacterial death

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

How does MRSA react to PBP inhibition from beta-lactam antibiotics

A

MRSA produces an altered PBP (PBP2a), which is not inhibited by b-lactam antibiotics and can perform the functions of the 4 PBPs of S. aureus.

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

last resort drug for MRSA

A

Vancomycin - resistance soon began

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

treatment of MRSA

A

linezolid
synercid
daptomycin

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

what class does linezolid belong in

A 
oxazolidinone class
novel antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

linezolid is effective against disease

A

MRSA and VRE infections

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

Mechanism in which linezolid is used to stop infection

A

inhibition of protein synthesis

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

synercid has what 2 variations

A

quinupristin

dalfopristin

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

what illness does synercid treat

A

intravenous treatment of VRE caused infections and skin infections of staphylococcus aureus and streptococcus pyogenes

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

how does synercid treat infection

A

inhibit protein synthesis by binding to 70S ribosome both agents bind at same place in ribosome

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

synercid bacteriostatic or bactericidal

A

Bacteriostatic when administrated individually, but act synergistically in combination (bactericidal).

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

daptomycin is used for what kind of infections

A

gram positive infections particularly in the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does daptomycin treat infection

A

Binds to cell membranes and causes their depolarisation

interrupts protein, DNA and RNA synthesis

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

why does daptomycin have slow emergence of resistance

A

is novel antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

enterococci

A

Antibiotic resistant opportunistic pathogens commonly found in patients hospitalized for prolonged periods and receiving multiple courses of antibiotics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what enterococci are most difficult to treat

A

Enterococcus faecium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

2 enterococci

A

Enterococcus faecalis and Enterococcus faecium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how many years were for emergence resistance against vancomycin to occur

A

32 years it took 5 genes

22
Q

how many years were for emergence resistance against penicillin to occur

A

2-3 years 1 gene

23
Q

what kind of antibiotic is vancomycin

A

glycopeptide antibiotic

24
Q

how does vancomycin treat infection

A

inhibit cell wall biosynthesis
blocks substrate
must interact with peptide chain with 5 hydrogen bonds

25
Q

how does bacteria for vancomycin occur?

A

Loss of a single hydrogen bond when vancomycin binds to substrate = 1,000-fold
drop in drug-binding affinity:
enough for the bacteria to become resistant

26
Q

clostridium difficile Associated Disease

A

Clostridium difficile is a Gram-positive, spore-forming, obligate anaerobic bacterium.

27
Q

what does clostridium difficile mainly cause

A

nosocomial diarrhoea

toxins A and B can cause extensive damage to colonic mucosa

28
Q

when does clostridium difficile Associated Disease occur

A

90 of CDAD occur after or during antibiotic treatment

29
Q

treatment of CDAD

A
  1. medical therapy - discontinuation of the inciting antibiotics
  2. specific antibiotic treatment
    metronidazole = first line antibiotic agent
    - vancomycin as alternate agent for second line therapy
    spores can still stay in colon of patient
30
Q

metronidazole is what kind of compound

A

prodrug

Nitroaryl compound

31
Q

how is metronidazole activated

A

Prodrug activated by anaerobic organisms by reduction of the nitro group to hydroxylamine group
During reduction, reactive derivative/species produced that can damage bacterial cell components such as DNA, proteins, membranes

32
Q

advantages of metronidazole as first line agent

A

Prevent selection of vancomycin-resistant enterococci

Reserve vancomycin use for the treatment of MRSA infections

33
Q

when is vancomycin prescribed instead of metronidazole

A

Failure to respond to metronidazole after 3-5 days of treatment
Pregnancy & lactation
Intolerance to metronidazole
Metronidazole-resistant infecting organism
Critically ill patients

34
Q

what percentage of gram negative bacteria are responsible for HAI

A

30%

35
Q

main HAIs caused by gram negative bacteria

A

pneumonia
bloodstream infection
urinary tract infection

36
Q

how does bloodstream infection occur

A

Most commonly caused by central vascular catheter.

Can be associated with an initial infection of the lung, genitourinary tract, or abdomen.

37
Q

how is UTI caused

A

Associated almost exclusively with urethral catheterization.

Risk of infection increases by 5 to 10% per day.

38
Q

bacterial resistant against penicillin

A

beta-lactamases

39
Q

reisstance against cephalosporins

A

Extended Spectrum

b-Lactamases (ESBLs)

40
Q

resistance against Carbapenems

A

Carbapenemases

41
Q

what does carbapenemases inactivate and what is it inhibited by?

A

Carbapenemases can inactivate all types of b-lactam antibiotics and are not inhibited by inhibitors of b-lactamases (clavulanic acid).
Represent one of the main clinical challenges.

42
Q

antibiotic treatment of HAI in response to resistance

A

Gram-negative pathogen expressing ESBLs:
Carbapenems (eg. meropenem Gram-negative pathogen expressing carbapenemases:
- Colistin or tigeclycine.

43
Q

what kind of antibiotic is meropenem

A

Carbapenem, b-lactam antibiotic

44
Q

describe how strcuture of meropenem is similar to penicillin

A

Structure similar to penicillins:

bicyclic structure, with 1 b-lactam ring and a 5-membered ring

45
Q

how does meropenem different to pencillin

A

however, sulfur atom not in the 5-membered ring, but attached on that ring as part of a functional side-chain

1 carbon-carbon double bond in the 5-membered ring

46
Q

what type of antibiotic is colistin

A

Polymyxin antibiotic.

Peptide antibiotic

47
Q

describe structure of colistin and from what process is it produced?

A

Mixture of 2 cyclic peptides (colistins A and B) produced by fermentation of Bacillus polymyxa.

48
Q

colistin is used as a last resort for what infection and why

A

‘last resort’ antibiotic against
MDR Gram-negative bacteria.
last resort because of nephrotoxicity

49
Q

how does colistin attack bacteria

A

Binds to phosphate groups in lipids on the cell cytoplasmic membrane. Disrupts its integrity

50
Q

describe type of tigecycline

A

Novel tetracycline class: glycylcyclines

Broad spectrum antibiotic.

51
Q

how is tigecycline characterised

A

Characterised by additional glycylamido substituent.

52
Q

how does tigecycline treat infection

A

Inhibitor of bacterial protein synthesis by binding to the 30S ribosomal subunit  blocks entry of amino-acyl tRNAs into the ribosome.

DDT (21 decks)

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