Miscellaneous ABX Flashcards

1
Q

What is the antimetabolite ABX?

A

TMP-SMX

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2
Q

Sulfa MOA

A

Inhibit dihydrofolic acid synthesis (structural analogue of PABA) -> interferes with bacterial folate synthesis

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3
Q

Trimethoprim MOA

A

Inhibits dihydrofolic acid reduction to tetrahydrofolate

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4
Q

TMP-SMX MOR

A
  • Altered enzyme targets
  • ↓ sulfa accumulation
  • ↑ production of PABA
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5
Q

TMP & SMX are substrates of and moderate inhibitors of CYP___

A

CYP2C9

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6
Q

Drug interactions for TMP-SMX

A

Drugs that cause hyperkalemia (ACEI/ARB/spironolactone)

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7
Q

TMP-SMX pharmacology

A
  • Renal excretion

- Bacteriostatic

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8
Q

TMP-SMX ADRs

A
  • Hypersensitivity, esp. reversible myelosupression (w/ larger dose)
  • Hemolytic anemia in G6PD pts. (AA male)
  • hyperkalemia
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9
Q

Microbial coverage of TMP-SMX

A
  • P. jiroveci

- Most E. coli, Klebsiella, Proteus, MRSA

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10
Q

Clinical indications for TMP-SMX

A
  • Lower UTIs (2nd line)
  • PCP/PJP
  • MRSA treatment/suppression (not serious infections)
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11
Q

Nitrofurantoin MOA

A

Inhibits bacterial enzyme systems, including acetyl CoA, interfering with metabolism & possibly cell wall synthesis

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12
Q

Nitrofurantoin pharmacology

A

Renal excretion (does NOT penetrate renal tissue)

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13
Q

Nitrofurantoin contraindication

A

CrCl <60

- BUT new data suggests short term use is safe & effective if CrCl >30

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14
Q

Nitrofurantoin ADRs

A

Acute -> chronic pulmonary toxicity/fibrosis

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15
Q

Microbial coverage of nitrofurantoin

A

GNB & enterococci

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16
Q

Microbial resistance to nitrofurantoin

A
  • E. coli <2%

- Klebsiella 1/3

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17
Q

Clinical indications for nitrofurantoin

A
  • Lower UTI (cystitis)

- Prophylaxis of recurrent UTI

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18
Q

Fosfomycin MOA

A

Irreversibly binds pyuvyl transferase (enzyme in early step of bacterial cell wall synthesis)

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19
Q

Fosfomycin pharmacology

A
  • Excreted unchanged in the urine
  • Bacteriocidal
  • May ↓ bacterial adhesion to urothelial cells
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20
Q

Microbial coverage of fosfomycin

A

GNB & enterococci / staph

- Includes MDR/EBSL CRE (GNBs) & VRE/MRSA; +/- for pseudomonas

21
Q

Most E. coli is resistant OR susceptible to fosfomycin

A

Susceptible!

22
Q

Clinical indications for fosfomycin

A

Uncomplicated cystitis (3g powder dissolved in water)

23
Q

Two ABX derived from rifampin

A
  • Rifaximin

- Rifamycin

24
Q

Route of rifaximin, rifamycin

A

PO (non-absorbed)

25
Q

Rifaximin, rifamycin MOA

A

Inhibit bacterial RNA synthesis

26
Q

Clinical indications for rifaximin, rifamycin

A
  • Noninvasive E. coli causing traveler’s diarrhea (NOT effective if bloody stool or fever)
  • Prevention of hepatic encephalopathy in pts. w/ CLD
  • IBS-D
27
Q

Microbial coverage of chloramphenicol

A
  • H. flu
  • S. pneumo
  • N. meningitides
  • Some anaerobes
28
Q

Chloramphenicol pearl

A

Reaches therapeutic levels in the CNS (used as last resort in CNS infections)

29
Q

Why is chloramphenicol rarely used?

A

Toxicities: bone marrow suppression and possibly fatal aplastic anemia

30
Q

1st gen anti-mycobacterial agents

A
  • Rifampin (RIF)
  • Isoniazid (INH)
  • Pyrazinamide (PZA)
  • Ethambutol (ETH)
31
Q

2nd gen anti-mycobacterial agents

A
  • Streptomycin
  • Kanamycin
  • Amikacin
  • Levofloxacin
  • Moxifloxacin
  • Capreomycin
  • Cycloserine
  • Ethionamide
  • Aminosalicyclic acid
32
Q

Rifampin MOA

A

Inhibits RNA polymerase (protein synthesis)

33
Q

Rifampin is an INDUCER of

A

MOST CYP enzymes (remember: 2C9, 3A4)

34
Q

Clinical indications of rifampin

A
  • Active Tb
  • Latent Tb (alternative option)
  • Meningococcal meningitis prophylaxis
35
Q

Rifampin ADRs

A
  • Red lobster syndrome
  • Hepatitis
  • Flu-like illness
36
Q

Isoniazid MOA

A

Inhibits synthesis of mycolic acids

37
Q

Isoniazid is an INHIBITOR of

A

MOST CYP enzymes (remember: 2D6, 3A4)

38
Q

Acetylation determines blood concentration of isoniazid and is controlled by

A

Genetics

39
Q

Rapid acetylators of isoniazid are more likely to get…

A

Hepatitis (↑ w/ ETOH)

40
Q

Slow acetylators of isoniazid are more likely to get…

A

Peripheral neuropathy (↓ risk w/ vitamin B6)

41
Q

Clinical indications of isoniazid

A
  • Latent Tb (drug of choice)

- Component of active Tb tx

42
Q

Clinical indication of pyrazinamide

A

Component of active Tb tx

43
Q

Pyrazinamide ADRs

A
  • Non-gouty polyarthralgias (tx w/ NSAIDs)
  • Asymptomatic hyperuricemia
  • Dose-related hepatitis
44
Q

Ethambutol MOA

A

Inhibits cell wall synthesis

45
Q

Clinical indications of ethambutol

A

Component of active Tb tx

46
Q

Ethambutol ADR

A

Dose-related optic neuritis

47
Q

Pathogenesis of ethambutol-induced optic neuritis

A

ETH is a metal chelator

  • Chelation of copper or zinc though to play a role
  • Supplementation does not help
48
Q

Sx of ethambutol-induced optic neuritis

A
  • ↓ visual acuity/color discrimination (red, green)
  • Constricted fields
  • Scotoma
  • can lead to irreversible blindness
49
Q

Management of pt. on ethambutol

A

Monthly f/u with ophthal for monthly visual acuity & color perception checks