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Respiratory Medicine Midterm > Sulfas, antifolates, Fluoros- Fitzpatrick > Flashcards

Sulfas, antifolates, Fluoros- Fitzpatrick Flashcards

1
Q

For trimethoprim/sulfamethoxazole (TMP-SMX)
A. what’s the clinical use
B. Pertinent PK
C. AE

A

A. uncomplicated UTI; opportunitic infections- toxoplasmosis; pneumocystis jiroveci

B. given PO or IV; renal clearance; half life 8-10 hrs

C. Rash (steven-johnson), fever, leukopenia, acute hemolysis in pts with G6Pd deficiency, hyperkalemia.

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2
Q

For sulfadoxine/pyrimethanmine indicate:
A. clinical use
B. pertinent PK
C. AE

A

A. Malaria tx and prevention
B. hepatic and renal. Sulfa can displace albumin bound warfarin, bilirubin; half life 4-8 days
C. same as other sulfa (Rash (steven-johnson), fever, leukopenia, acute hemolysis in pts with G6Pd deficiency, hyperkalemia. )

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3
Q

For sulfadiazine/pyrimethamine indicate:
A. use
B. PK
C. AE

A

A. toxoplasmosis (for those did not respond to sulfamethoxazole/trimetho; or pt wo HIV/AIDS
B. Sulfa about 10hrs half life. Pyrimethamine 4 days
C. Same as other sulfa (Rash (steven-johnson), fever, leukopenia, acute hemolysis in pts with G6Pd deficiency, hyperkalemia. )

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4
Q

Sulfasalozine (pro drug)
A. Use
B. PK
C. AE

A

A. ulcerative colitis, chron’s disease (anti inflammatory- NOT abx)
B. Metabolism: via colonic intestinal flora to sulfapyridine and (5-aminosalicylic acid (5-ASA). 5-ASA undergoes hepatic N-acetylation
C. same as other sulfa drugs (Rash (steven-johnson), fever, leukopenia, acute hemolysis in pts with G6Pd deficiency, hyperkalemia. )

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5
Q

Sulfacetamide:
A. Use
B. PK
C. AE

A

A. ocular infections; trachoma
B. Tpical eye drops, pointment
C. hypersensitivity; Steven-Johnson syndrome

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6
Q

Silver sulfadiazine
A. Use
B. PK
C. AE

A

A. dressing - prevent and treat infection 2nd and 3rd degree burns
B. topical cream
C. Hypersensitivity; Steven-Johnson syndrome

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7
Q

Sulfisoxazole/erythromycin
A. Use
B. PK
C. AE

A

A. otitis media
B. Powder for suspension (peds pt)
C. superinfection; a diff diarrhea/pseudomembranous colitis

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8
Q

For anthrax what is the drug of choice?

A

ciprofloxacin

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9
Q

for penumocystitis jirovecii pneumonia in an immunocompromised pt what is the drug of choice?

A

TMP-SMX

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10
Q

For Toxoplasmosis in an AIDS pts what is the drug of choice?

A

TMP-SMX

Also used as prophylaxis in pts with HIV treated with ART therapy.

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11
Q

what is the MOA of sulonamides?

A

Sulfonamides resembles para-amino benzoic acid (PABA) which is a substrate for bacterial folic acid synthesis. It is a competitive inhibitor of dihydropteroate synthase, an essential enzyme in folic acid (folate) biosynthesis pathway of many bacteria

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12
Q

Sulfa drugs today rarely are used alone in clinical setting. They are usually paired with an synergictic component. In sulfamethoxazole/trimethoprim explain how they are synergistic

A

Sulfa = inhibits dihydropteroate synthase which is one of the enzme in the pathway of bacterial folate production.

Trimethoprim inhibits dihydrofolate reductase which is a second enzyme further down in that same pathway.

Alone, they are bacteriostatic agents but when used in combo they are bactericidal.

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13
Q

what class of bacterias are sensitive to sulfa drugs?

A

gram (+) or gram (-) that fill their dihydrofolate pools by de novo biosynthesis of folic acid

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14
Q

sulfa drugs don’t really affect human folate because we get our folate from diet. However, in small number of cases, how does sulfa drug affect human folate?

A

Sulfa drugs can interfere with folate reuptake from diet.

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15
Q

what organisms/infections are sensitive to TMP-SMX

A
  1. Gram (-) rods: E.coli (cystitis, prostatitis); Proteus mirabilis (Cystitis, prostatitis); Salmonella typhi (diarrhea); shigella (diarrhea); some H. influenza (sinusitis)
  2. P.jiroveci (pneumonia); toxoplasmosis (encephalitis)
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16
Q

How is TMP/SMX resistance developed?

A

Sulfa resistance: mutation of dihydropteroate synthase; enhanced acquisition of PABA

TMP resistance: mutation of DHFR and overexpression of DHFR

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17
Q

what bacteria is folic acid auxotrophs and thus naturally is resistant to TMP-SMX?

A

E. faecalis

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18
Q

What AE are associated with sulfonamides?

A
  1. Hypersensitivity (steven-johnson)
  2. Kernicterus
  3. hemolytic anemia (in pts with X linked inherited G6Pd-deficiency)
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19
Q

severe manifestation of Steven johnson syndrome occur with which sulfa combo more than other sulfa drugs?

A

TMP-SMX

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20
Q

Explain how sulfa causes kernicterus

A

Sulfa binds to the same site on albumin as bilirubin. So with sulfa taking up space, bilirubin is free circulating in blood. Neonates with their immature liver cannot clear the bili and thus it builds up and this build up is esp dangerous in the neonatal brain giving rise to kernicterus (Extreme jaundice, Absent startle reflex, Poor feeding or sucking, lethargy and hypotonia)

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21
Q

A pt taking sulfa drugs with G6PD deficiency will develop weakness, hematuria, jaundice due to hemolytic anemia. Explain how the anemia is caused

A

Sulfa causes oxidative stress on erythrocytes. In G6PD deficiency, glycolysis cannot be used to turn NADP+ into NADPH, thus NADPH is deficiency and excess GSSG and H202 causing hemolytic anemia.

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22
Q

Trimethoprim is contraindicated in pregnant women. Why/

A
  • Birth defects due to folate deficiency
  • esp at months 2-3 (end of 1st trimester)
  • high folate need by fetus at that time. without it leads to CV defects and oral clefts.
23
Q

What can correct anti-folate toxicity of TMP-SMX without impairing its antimicrobial activity?

A

Folinic acid

24
Q

What is the MOA of fluoroquinolone?

A

Inhibits DNA gyrase (topoisomerase II) and Topoisomerase IV. Inhibition of DNA gyrase is more significant in gram (-) bacteria. and Topoisomerase IV is more significant in gram+ bacteria. Both has lasting post antibiotic effect

25
Q

_ enters gram (-) bacteria through porins and is bactericidal esp with serum concentration > 30fold MIC and thus making this class of drug a concentration-dependent killer

A

Fluoroquinolone

26
Q

How is fluroquinolone resistance developed?

A
  • mutation of DNA gyrase/topoisomerase
  • cellular membrane efflux mechanisms
  • Decreased number of porins - MDR
27
Q

Give an example of 1st gen Fluoroquinolone and what is it effective for?

A

Nalidixic acid, used for Gram (-) UTIs

28
Q

Example of 2nd gen fluoroquinolone

A

Ciprofloxacin

29
Q

Example of 3rd gen fluroquinolone

A

Levofloxacin

30
Q

Example of 4th gen fluoroquinolone

A

Moxifloxacin

31
Q

Gen 2,3,4 fluoroquinolone are effective against which gram stain bacterias?

A

Gram (-) such as enterobacteria, pseudomoas, h influenza, moraxella.

32
Q

Due to it’s ability to penetrate bone, fluoroquinolone is used for _

A

osteomyelitis. High penetration even with oral administration

33
Q

Fluroquinolones are active agaainst several atypical organism that cause pneumonia, organism includes _

A

mycoplasma, chlamydia, mycobacteria, legionella.

34
Q

While Ciprofloxacin acts on mycoplasma, chlamydia, mycobacteria and legionella, Levofloxacin and moxifloxacin does not work on which of those four listed?

A

Mycobacteria

35
Q

which fluoroquinolone works against gram + cocci, bacilli and anaerobes

A

Moxifloxacin. The other guys do not work on anaerobes.

36
Q

Which fluoroquinolone cannot be used for pseudomonas?

A

Moxifloxacin

37
Q

Which fluoroquinilone works against anthrax?

A

Ciprofloxacin

38
Q

Which fluoroquinilone along with atypical pneumonia, is also able to treat strep pneumoniae?

A

Leveofloxacin

39
Q

which fluoroquinilone is best for UTI?

A

Ciprofloxacin

40
Q

which fluroquinolone can be used for acute eacerbation of chronic bronchitis?

A

Levo, moxi, and gemifloxacin

41
Q

Which Fluroquinolone can be used for acute bacterial rhinosinusitis; skin and skin structure infections?

A

Cipro, levo and moxi

42
Q

Which fluoroquinolone can be used for nosocomial pneumonia?

A

Cipro and levo

43
Q

Which fluoroquinilone can be used for bacterial prostatitis and UTI?

A

Cipro and levo

44
Q

Which fluoroquinilone is best for complicated intra-abdominal infections?

A

Moxifloxacin

45
Q

Which fluoroquinilone is best for Osteomyelitis, febrile neutropenia, typhoid fever, abd infections with metronidazole

A

Ciprofloxacin

46
Q

Which foods/drugs cannot be taken together with fluoroquinilone?

A
  • antacid with mag or aluminum
  • dietary products with Ca++
  • vitamin mineral supplements with iron or zinc

They all impair oral absorption and lower bioavailability of all fluoroquinolones

47
Q

which Fluoroquinolone is mainly excreted via urine?

A

levofloxacin (85%).

48
Q

Which fluoroquinolone is cleared mainly by hepatic?

A

moxifloxacin

49
Q

In an UTI which fluoroquinolones are best based on excretion?

A

Levo and cipro cuz they have more urinary excretion = more action in GU system

50
Q

What are some contraindications of Fluoroquinolones?

A
  • Kids younger than 18. Can cause cartilage erosion, arthropy
  • adults >60 (accumulation in tendons –> rupture)
  • adults gymnasts or climbers
51
Q

what AE are associated with Fluoroquinolones?

A
  • bones/tendon/lung accumulation
  • phototoxicity
  • QT prolongation (inadevertent binding to K channels)
  • peripheral neuropathy associated with PO or IV administration
52
Q

Fluoroquinolone with most QT prolongation

A

moxifloxcin

53
Q

Fluorquinolones applied _ do not carry the AE

A

topically and thus infection of eye can be treated with eye drops (topical).

Cipro comes in eye drops and ear drops. Levo and moxi comes in eye drops

Respiratory Medicine Midterm (7 decks)

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