ddt 16 Flashcards

1
Q

an antibiotic that hasn’t been used in clinics beadier but belonging to class of antibiotics

A

new antibiotics

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

an antibiotics w mechanism of action never used against bacteria

A

novel antibiotics

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

infections are mostly associated w

A

invasive medical devices and surgical procedures

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

S.aureus produces

A

4 enzymes ( peniclin binding proteins PBP ) for cell wall biosynthesis

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

PBP 1-4 can be modified by

A

b-lactam antibiotics leading to their inhibition and bacterial death

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

MRSA produced —- which is not inhibited by— and can produce all functions of —-

A
  • altered PBP. (PBP2a)
  • b- lactam
  • all 4 PBP of S aueures.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

the production of altered PBP is considered to be

A

recent resistance mechanism in gram +ve compared to the b-lactamase is ancient evolutionary

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

Treatment of infection caused by MRSA

A
  • antibiotics other than penicillin/ b- lactam
    ( almost 50% of mrsa strains r resistant to all but few antibiotics )
  • vancomycin destroys mrsa and resistant bacteria
    ( first case was VRSA and there are 52 VRSA strains )
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

novel antibiotics for mrsa treatments

A
  • linezoid ( oxazolidinone )
  • synercid ( combination of streptograms, quinupristin, dalfopristin )
  • daptomycin ( lipopeptide )
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

linezolid is a

A

oxazolidinone class of antibiotics

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

linezoilds works for —- by inhibiting —- in only gram — bacteria

A

mrsa and VRE , inhibition of protein synthesis , gram +ve only

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

intravenous treatment caused by VRE, staph. aureus, and strep. pyogen

A

Synercid by inhibiting protein synthesis both agents at same place in the ribosome

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

—– when administered individually and —- when in combination

A

bacteriostatic, synerically and becomes bactericidal

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

intravenous treatment of gram +ve infections by binding to cell membrane and causes depolarisation

A

daptomycin ( cubcin )
- it interrupts protein, dna and rna sythesis
- slow emerges of resistance in clinic

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

patient being hostiblized for prolonged period of times and receiving multible course of antibiotics results in

A

antibiotic resistance

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

enterococcus faecalis and enterococcus fascium are

A

more difficult to treat and higher incidence of resistance against vancomycin ( 15-20% of isolates )

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

32 before emerges requires — genes mutation for resistance against vancomycin but 2-3 years against penicillin requires — mutation

A

5 genes , 1 gene

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

vancomycin works by

A

inhibiting the cell wall beiosystheis and block the substrate while peciline blocks the enzyme

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

is a glycopeptide antibiotic

A

vancomycin

20
Q

bacteria becomes resistant when

A
  • loss of a single hydrogen bond = 1,000 folds drop in drug binding affinity ( from D-Ala to D- Lac )
21
Q

Clostridium difficile associated diseases ( CDAD)

A
  • gram +ve
  • requires anaerobic bacterium
  • spores forming
  • toxigenic strains: toxins A + B causes extensive damage to colonic mucosa
22
Q

—- causes major nosocomial diarrhoea

A

CDAD

23
Q

more than — produced — and — antibiotic treatment

A

90% after and during

24
Q

treatments of CDAD includes

A

1- medical therapy includes discontinuation of inciting antibiotic if possible
2- specific antibiotic treatment if persisent diarrhoea:
- metrazodiale at first line antibtioc agent
- vancomycin as alternate agent for 2nd line therapy
- both are taken orally

25
Q

20-25% of the patients will get — of the symptoms once ——

A

recurrence, vancomycin. metronidazole withdrawal

26
Q

metronidazole is a

A

nitroaryl compound and exact mechanism is unknwon,

27
Q

how is the prodrug metronidazole is activated

A

activated by anaerobic organisms by reduction of nitro group to hydroxylamine group. During reduction it can damage bacterial cell components dna protein and mebrance

28
Q

the advantages of metronidazole as a first line therapy

A
  • reserves vancomycin for MRSA
  • prevent selection if VRE
29
Q

when is vancomycin is used instead of metronidazole

A
  • failure to reposed to metronidazole after 3-5 days
  • pregnancy , lactation
  • intolerance to metronidazole
  • critically ill patients
  • metronidazole- resistant infecting organisms
30
Q

gram — is responsible for — of HAI

A

gram -ve , 30%

31
Q

gram — is responsible for — ICU ( intensive care unit)

A

gram -ve , 70%

32
Q

the main HAI caused by gram -ve

A
  • pneuminia: associated w mechanical ventilations
  • bloodstream infections: associated mostly from central vascular catheter and initial infections in the lungs, abdomen, and genitourinary tract
  • Urianry tract infections (UTI): associated mostly from urtheral cathetrization increased risk from 5-10%
    best management is to remove the catheter instead of antibiotic treatment
33
Q

many strains of gram -ve bacteria causing HAI are

A

-multi-drug resistant ( MDR , resist at least 3 different antibiotic classes )
- can have more than 1 resistance mechanism
- requires the use of older antibiotic not used before bc toxicity issues lead to polymyxin

34
Q

some organisms resist all currently available antibiotic called

A

XDR : extreme drug resistance , including polymyxin ( acintobacter baemanni )

35
Q

the antibiotic carbapenems resistance is

A

carbapanese

36
Q

—- can inactivate all type of b lactam antibiotics and are not inhibited by inhibitors of b- lactamasse aka clavulenic acid which is a clinical challenge

A

carbapebenases

37
Q

treatment of HAI caused by gram -ve drug resistant

A
  • gram -ve expressing ESBLS ( extended spectrum b- lactamase) : carbapene as meropenum
  • gram -ve expressibg carbapenemse : colistrin , trigcylin
38
Q

is a carbapenum b lactam antibiotic

A

meropenum

39
Q

meropenum structure similar to —-

A

penicillin
- bicyclic structure , 1 b lactam ring , 5 membered ring
- sulphur is not part of the 5-membered ring , its attached to a ring of functional side chain
- carbon- carbon double bond in the 5-membered ring

40
Q

colistin ( polymyxin E)

A
  • peptide antibiotic
    -polymyxin antibiotic
  • mixture of 2 cyclic peptide ( colistin A and b) produced by the fermentation of bacillus polymyxa
  • clinical use is perviously limited bc of nephrotoxity
  • reserved as last resort antibiotic of MDR gram -ve bacteria
  • binds to phosphate group in lipid on the cell cytoplasmic membrane and disturbs its integrity
41
Q

reserved as last resort antibiotic of MDR gram -ve bacteria

A

colistin

42
Q

tigecycline is

A

novel tetracycline class: glycylclines

43
Q

characterised by additioal glyclyamido substients

A

tigecyclin and it inhitbis bacteria protein sythesis and is broad spectrum antibiotic

44
Q

all novel antibiotics are effective against gram +ve but not -ve bc

A

gram -ve outer membrane is the main barrier

45
Q

number of novel classes of antibiotics for gram -ve bacteria under development

A

NONE LOL