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PT 1 > L27 Protein Synthesis Inhibitors > Flashcards

L27 Protein Synthesis Inhibitors Flashcards

1
Q

What is the mechanism of action of Clindamycin?

A

Protein synthesis inhibition via exclusive binding to the 50S ribosomal subunit

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2
Q

Clindamycin is ___ (static/cidal).

A

Bacteriostatic

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3
Q

What are the mechanisms of resistance to Clindamycin?

A
  1. Altered target sites (altered 50S, encoded by erm gene)
  2. Efflux pump (encoded by mef gene)
  3. Drug inactivation
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4
Q

Discuss the spectrum of activity of Clindamycin broadly.

A
  1. Gram-positive aerobes
  2. Anaerobes
  3. Other bacteria
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5
Q

What is the most important Gram positive bacteria Clindamycin has activity against?

A

MSSA, MRSA

Also: PSSP, group/viridans strep

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6
Q

What is the most important anaerobic bacteria Clindamycin has activity against?

A

Bacteroides species

Also: Peptostreptococcus, Actinomyces, Propionibacterium, Prevotella, Fusobacterium, Clostridium (not C. diff)

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7
Q

What other bacteria does Clindamcyin have activity against?

A

Pneumocystis carinii, Toxoplasmosis gondii, Malaria

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8
Q

Discuss the absorption, distribution, and elimination of Clindamycin.

A
  1. Rapid and complete absorption (IV and PO)
  2. Distribution: good, includes bone, minimal CSF
  3. Elimination: hepatic, not removed during dialysis
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9
Q

What are the clinical uses for Clindamycin?

A
  1. Anaerobic infections (NOT CNS)
  2. SSTI (penicillin allergic patients, MRSA)
  3. Alternative for C. perfringens, PCP, Toxo, malaria, bacterial vaginosis
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10
Q

What are the most important adverse effects of Clindamcyin?

A

C. difficile colitis

Also: GI, rare hepatotoxicity, rare allergy, rare neutropenia and thrombocytopenia

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11
Q

What are the three macrolides?

A
  1. Erythromycin
  2. Clarithromycin
  3. Azithromycin
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12
Q

What is the mechanism of action of macrolides?

A

Protein synthesis inhibition via exclusive binding to the 50S ribosomal subunit (same as Clindamycin)

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13
Q

Macrolides are ___-dependent and ___ (cidal/static).

A

Time (E/C); Concentration (A); static, but can be cidal at higher concetrations against susceptible organisms

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14
Q

What are the mechanisms of resistance to Macrolides?

A
  1. Altered target sites (altered 50S, encoded by erm gene)

2. Efflux pump (encoded by mef gene)

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15
Q

Discuss the spectrum of activity of Macrolides broadly.

A
  1. Gram-positive aerobes (C>E>A)
  2. Gram-negative aerobes (A>C>E)
  3. Anaerobes
  4. Atypical bacteria
  5. Other bacteria
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16
Q

What are the most important Gram positive bacteria Macrolides have activity against?

A

MSSA

Other: PSSP, group/viridans strep, Bacillus, Corynebacterium

17
Q

What are the most important Gram negative bacteria Macrolides have activity against? What does it NOT have activity against?

A

H. influenzae (not E), M. catarrhalis, Neisseria (none highlighted)

NO Enterobacteriaceae activity

18
Q

What are the most important anaerobic bacteria Macrolides have activity against?

A

ADAs

19
Q

What are the most important atypical bacteria Macrolides have activity against?

A

Legionella pneumophila

Also: Chlamydophila/Chlamydia, Mycoplasma

20
Q

What are the most important other bacteria Macrolides have activity against?

A

MAC (A/C), M. chelonae, H. pylori, Bordetella, Brucella, Pasteurella (none highlighted)

21
Q

Discuss the absorption, distribution, and elimination of Macrlodies.

A

Absorption: variable - food may decrease (E), acid stable (C, A)
Distribution: extensive (C, A better), minimal CSF
Elimination: bile (E), kidney (C)

22
Q

What are the clinical uses for Macrolides?

A
  1. Respiratory tract infections
  2. Uncomplicated skin infections
  3. STDS (A)*
  4. MAC (A/C)*
  5. Alternative for PCN allergic patients (GAS, bacterial endocarditis prophylaxis, syphilis/gonorrhea, RF prophylaxis)
23
Q

What are the most important adverse effects of Macrolides?

A

Prolonged QTC

Also: GI, cholestatic hepatitis, thrombophlebitis, tinnitus/deafness

24
Q

What are the important drug interactions with Macrolides?

A

E and C are inhibitors CYP450 (increase concentrations of drugs metabolized by these)

25
Q

Why were the Streptogramins developed and what is good about them?

A

Improved activity against resistant gram-positive bacteria (VRE)

26
Q

What is the major streptogramin?

A

Quinupristin-Dalfopristin (Synercid)

27
Q

What is the MOA of Synercid?

A

Protein synthesis inhibition via exclusive binding to the 50S ribosomal subunit

28
Q

Synercid is ___-dependent and ___ (cidal/static).

A

Concentration; cidal

29
Q

What are the mechanisms of resistance to Synercid?

A
  1. Altered target sites (altered 50S, encoded by erm gene)
  2. Efflux pump (encoded by mef gene)
  3. Enzymatic inactivation
30
Q

Discuss the spectrum of activity of Synercid broadly.

A
  1. Gram-positive

2. Atypical bacteria

31
Q

What are the most important Gram positive bacteria Synercid has activity against?

A

Coagulase negative staph, PRSP, VRE

Also: MSSA, MRSA, group/viridans strep, Corynebacterium, Bacillus, Listeria, Actinomyces, Clostridium (not C. diff), Peptococcus, Peptostreptococcus

32
Q

What are the most important atypical bacteria Synercid has activity against?

A

Mycoplasma, Legionella

33
Q

Discuss the absorption, distribution, and elimination of Synercid.

A

Absorption: parenteral
Distribution: extravascular tissue, lung, skin/soft tissue, minimal CSF
Elimination: hepatic and biliary

34
Q

What are the clinical uses for Synercid?

A
  1. VRE bacteremia

2. Complicated SSTIs due to MSSA and S. pyogenes

35
Q

What are the important drug interactions with Synercid?

A

Synercid inhibits CYP450 3A4

36
Q

What are the major adverse effects of Synercid?

A

Venous irritation

Also: GI, myalgias, arthralgias, rash

PT 1 (34 decks)

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