RX of LUT infections and STIs (Waller DSA) - SRS Flashcards

1
Q

What are the penicillin drugs highlighted for tx of LUT and STI?

A
  1. Penicillin G (IV, IM)
  2. Ampicillin (PO, IV, IM)
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2
Q

Which cephalosporin was highlighted for tx of LUT and STI?

A

Ceftriaxone

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3
Q

What beta-lactamase inhibitors were highlighted for LUT and STI?

A
  1. Ampicillin-sulbactam [Unasyn] (IV)
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4
Q

Which fluoroquinolone was highlighted for the treatment of LUT and STI?

A

Cipro

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5
Q

What macrolide/ketolide was highlighted for tx of LUT/STI?

A
  1. Azithromycin [Zithromax, Z-pak] (PO, IV, topical)
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6
Q

Flagyl was in red on our drug list, what do we also know this drug as?

A

Metronidazole

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7
Q

What sulfonamides/trimethoprim was in red on the drug list?

A
  1. Sulfamethoxazole/trimethoprim [Bactrim] (PO, IV)
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8
Q

What are the two urinary tract antiseptics?

A
  1. Methenamine (PO)
  2. Nitrofurantoin (PO)
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9
Q

Fosfomycin is on our drug list, what is the only route of administration listed for it?

A

PO (just not sure what else to ask at this point)

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10
Q

What azole antifungal is in red on our drug list?

A

Fluconazole (PO, IV)

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11
Q

What is the MOA of Trimethoprim/sulfamethoxazole (TMP/SMX)?

A

sulfonamides are bacteriostatic, competitive inhibitors of dihydropteroate synthase; while synergistic trimethoprim inhibits dihydrofolate reductase.

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12
Q

What are the ADRs of TMP/SMX?

A
  1. Allegic skin rashes
  2. nausea
  3. vomiting
  4. CNS- headache and depression
  5. photosensitivity
  6. renal dysfunction
  7. Stevens-Johnson Syndrome
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13
Q

What is a key DDI for TMP/SMX?

A

CYP inhibitor, so it potentiates the effects of warfarin.

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14
Q

If paired with ACEi, ARBs and spironolactone, what is a possible negative consequence you may see from TMP/SMX?

A

Enhanced hyperkalemic effects

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15
Q
  1. Nitrofurantoin MOA?
  2. Explain the selectivity of this drug
A
  1. MOA: drug reduced forming highly reactive intermediates which damage DNA, bacteria reduce drug more rapidly than mammalian cells, thought to account for selective activity.
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16
Q

ADRs of nitrofuranatoin

A

N/V

Diarrhea

17
Q

In what patients is nitrofurantoin CI?

A

Pregnant women

Children under 1 month

those with impaired renal function

18
Q

While not a primary ITI drug Methenamine has value as a chronic suppressive therapy. What is the MOA Methenamine?

A
  1. MOA: decomposes in water to formaldehyde, acidification of urine promotes formaldehyde formation, slow process (requires 3 hours to complete).
19
Q

What are the ADRs of methenamine?

A
  1. GI distress,
  2. painful/frequent micturition,
  3. hematuria,
  4. rash,
  5. low systemic toxicity at usual doses.
20
Q

What is the MOA of fosfomycin?

A
  1. MOA: bactericidal, inhibits very early stage of bacterial cell wall synthesis. Inactivates pyruvyl transferase which leads to reduced formation of N-acetylmuramic acid, which is only found in bacterial cell walls.
21
Q

What ADRs for fosfomycin?

A

Diarrhea

Nausea

ab pain

headache

22
Q

MOA ciprofloxacin?

A
  1. MOA: concentration-dependent killing, targets bacterial DNA gyrase and topoisomerase IV.
23
Q

MOA Beta lactam drugs?

A
  1. MOA: inhibits the transpeptidation reaction, the last step in peptidoglycan synthesis. Peptidoglycan composed of two alternating sugars (N-acetylglucosamine and N-acetylmuramic acid). Five-amino-acid peptide linked to final N-acetylmuramic acid which terminates in D-alanyl-D-alanine. Penicillin binding proteins (PBPs) remove the terminal D-alanine in the process of forming the cross-link. B-lactams are structural analogs of D-Ala-D-Ala. B-lactams covalently bind PBPs preventing cross-linking ultimately leading to cell autolysis.
24
Q

ADRs of fluoroquinolones?

A
  1. GI 3-17% most common (mild nausea, vomiting, abdominal discomfort),
  2. CNS 0.9-11% (mild headache, dizziness, delirium, rare hallucinations)
  3. , rash,
  4. photosensitivity
  5. , Achilles tendon rupture.
25
Q

What is the DOC for susceptible enterococci?

A

Ampicillin (IV)

26
Q

What are some ADRs of Penicillin G?

A
  1. allergic reactions (0.7-10%),
  2. anaphylaxis (0.004-0.04%)
  3. interstitial nephritis (rare),
  4. pseudomembranous colitis,
  5. Jarisch-Herxheimer reaction.
27
Q

MOA azithromycin?

A
  1. MOA: bacteriostatic, binds reversibly to 50S ribosomal subunit, inhibits translocation of newly synthesized peptidyl tRNA molecule from acceptor site on ribosome to peptidyl donor site.
28
Q

ADRs azithromycin?

A
  1. ADRs: GI (epigastric distress), hepatotoxicity, arrhythmia, QT prolongation.
29
Q

What does azithromycin do to CYP?

A

Inhibits CYP3A4

30
Q

What is the MOA of metronidazole?

A
  1. MOA: prodrug, requires reductive activation of nitro groups. Single electron transfer in anaerobic bacteria forms highly reactive nitro radical anions, kills organisms by radically mediated mechanisms that target DNA. Increasing 02 inhibits metronidazole as 02 competes for electrons.
31
Q

What are some ADRs of metronidazole?

A

headache, nausea, dry mouth, metallic taste. Vomiting, diarrhea, abdominal distress occasionally. Neurotoxic: dizziness, vertigo, very rarely encephalopathy. Well-reported disulfiram effect à abdominal distress, vomiting, flushing, headache, if alcohol consumed during/within 3 days of drug.

32
Q

What are some DDIs of metronidazole?

A

induced metabolism of phenobarbital, prednisone, and rifampin. Prolongs prothrombin time in those receiving warfarin.

33
Q

MOA of azole antifungals?

Explain the selectivity

A
  1. MOA: inhibits fungal cytochrome P450, reducing production of ergosterol.
    1. Selective toxicity due to greater affinity for fungal rather than human cytochrome P450 enzymes.
34
Q

What are some ADRs from azoles?

A

minor GI upset, abnormalities in liver enzymes.

35
Q

Describe the impact of the azoles on the CYPs

A
  1. DDIs: MANY!! Inhibits CYP1A2 (weak), CYP2C19 (strong), CYP2C9 (moderate), CYP3A4 (moderate).
36
Q
A