Antimicrobials: Antimetabolites Flashcards

1
Q

T-F–antifolate antibiotics act in a single step to block bacterial folic acid synthesis? Does it inhibit, DNA, RNA, or protein synthesis?

A
  1. False-sequential steps

2. All three, reduce thymidine, purine, and methionine

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

What is a major synergistic combination of antifolate antibiotics? Are they cidal or static?

A
  1. sulfonamide+ trimethoprim

2. together they are bactericidal. Static alone.

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

What step do sulfonamides block?

A

1.competitively blocks DHPS (binding to PABA) which takes pteridine+PABA to dihydropteroic acid.

[first step to becoming methionine, thymidine, purine]

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

High levels of what block sulfa activity?

A

PABA pus

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

Does DHPS enzyme function in humans?

A
  1. No, bacteria must synthesize folic acid, but we obtain it from our diet.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is sulfonamides administrated? Is it distributes to CNS and CSF? Metabolism? Excretion? Broad or narrow spectrum?

A
  1. orally but can be IV
  2. Yes
  3. Liver
  4. Kidney
  5. Broad (can target parasites)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is sulfonamides not used for?

A

Rickettsia

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

What are the 3 mechanisms of antibacterial resistance in sulfonamides that is Common in Staph, Strep, Enterobacteriaceae, Neisseria?

A

1) Overproduction of PABA
2) Encode mutant DHPS enzyme with decreased affinity for
sulfas (often plasmid mediated)
3) Upregulation of efflux pumps

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

When is hemolytic anemia seen with sulfonamide use?

A

G6PD

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

What is kernicterus?

A

in infants, sulfa competes for
bilirubin binding sites on albumin and increases
levels of unconjugated bilirubin = CNS toxicity

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

What is stevens-johnsons syndrome?

A

Hypersensitivity

with mucosal sloughing, skin eruptions

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

When might sulfonamides be used alone because they usually aren’t because they are typically combined with trimethoprim in bacteria?

A
  1. malaria

2. CNS toxoplasmosis

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

What does trimethoprim block?

A

DHFR- which takes dihydrofolic acid to tetrahydrofolic acid–inhibits bacterial DHFR 100,000 times for than human DHFR

[STATIC ALONE!!]

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

How are Tmp-sulfa excreted? oral?

A
  1. in the urine

2. yes

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

Tmp-sulfa is a broad spectrum antibiotic used for multiple G+ and G-. What is it typically not used for in regards to bacteria/

A
  1. pseudomonas
  2. anaerobes
  3. atypical bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 2 major resistance pathways for trimethoprim? Is resistance dependent on location?

A

1) Overexpression of DHFR
2) Expression of mutant DHFR that is resistant to Tmp
(often plasmid-mediated)

YES

17
Q

What is one of the most common seen severe side effects of TMP-sulfa?

A

bone marrow suppression with neutropenia

-can cause anti-folate effect.

18
Q

Can TMP-sulfa be used for MRSA? what bacteria is efficacy decreasing in?

A
  1. Yes [also UTI, Pneumocytis, sinusitis and otitis media]

2. E. coli

19
Q

Are quinolines bacteriostatic? Do they inhibit RNA synthesis? What proteins does it inhibit? reversible damage?

A
  1. Bactericidal
  2. No- DNA
  3. gyrase and topoisomerase [unwinding]
  4. No-irreversible
20
Q

T-F–quinolones adhere to concentration dependent killing concepts?

A

True

21
Q

How man more times is the AUC/MIC for the immunocompromised patient from the immunocompetent patient?

A

4 times

[100 vs. 25]

22
Q

Do fluoroquinolones have great GI absorption? Do they get in CSF? what reduces its absorption? what type of elimination?

A
  1. YEs- same serum levels as IV
  2. CSF low
  3. Forms chelates with cations
  4. Hepatic or renal
23
Q

What is the order of quinolones based on efficacy for G- and pseudomonas?

A

cipro > levo > moxi

24
Q

What is the order of quinolones for G+ and strep in regards to efficacy?

A

moxi > levo > cipro

25
Q

What are 3 methods of resistance for quinolines? What bacteria specifically?

A
  1. decreased permeability,
  2. Efflux pump
  3. mutation of the enzymes
    [all MRSA, N. gonorrhea, Salmonella, Campylobacter]
26
Q

T-F–fluoroquinolones majority of use considered inappropriate?

A

True