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Pharm > Sulfonamides and Quinolones > Flashcards

Sulfonamides and Quinolones Flashcards

1
Q

what is prontosil?

A

prodrug of the active sulfonamide, p-aminobenzenesulfonamide

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2
Q

sulfamonide MOA

A

competitively inhibit dihydropteroate synthase, preventing incorporation of PABA into folic acid nucleus
(bioisosteres of PABA)

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3
Q

why do sulfonamides not affect human cells?

A

mammal cells use preformed folates in diet, while some bacteria make their own folic acid

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4
Q

alternate sulfonamide MOA

A

antimetabolite: some strains use drug as a substrate, but then the product is not capable of the next rxn

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5
Q

can sulfonamide action be reversed?

A

yes- increase [PABA]

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6
Q

describe PABA vs. sulfanilamide activity at physio pH

  • why is this a problem?
  • how it is overcome?
A

PABA pKa 6.5 -> anion at physio pH
sulfanilamide pKa 10.4 -> weak acid a physio pH

fix by attaching an e- withdrawing heteroaromatic ring to acidify the sulfonamide N and increase potency (due to electronegativity of R + resonance stabilization of anion)

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7
Q

what side effect does the increase in acidity of sulfonamides with a more EN R group mediate?

A

increased acidity causes decreased incidence of crystalluria

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8
Q

specific names of 9 sulfonamide drugs

A 
sulfisoxazole 
sulfacetamide 
sulfabenzamide 
sulfamethizole 
sulfamethoxazole 
sulfathiazole 
sulfadiazine 
acetyl sulfisoxazole

sulfasalizine (different MOA)

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9
Q

general uses of sulfonamides

A 
G(+) and G(-) 
Nocardia 
Chlamydia 
some protozoa/fungi 
E. coli 
Klebsiella 
Salmonella 
Shigella 
Enterobacter
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10
Q

how are sulfonamides normally given? what is one example and what is it used for

A

combinations: Bactrim (TMP-SMX)

- used for AIDS pneumocystis

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11
Q

MOA of TMP (trimethoprim)

A

inhibits DHFR, a sequential step in the THF synthesis pathway past where sulfamethoxazole works on DHPS

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12
Q

most popular sulfonamide and use?

A

sulfisoxazole - UTIs

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13
Q

sulfamethoxazole use

A

UTIs

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14
Q

what is the triple sulfas combination and what does it treat?

A

1: 1:1 sulfabenzamide, sulfacetamide, sulfathiazole

- used for Gardnerella vaginalis

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15
Q

what are the triple sulfas also combined with? what does this treat?

A

triple sulfas + phenylpropanolamine-pheniramine p.o.
-sinus/throat infections

pheniramine = antihistamine to decrease inflammation

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16
Q

what sulfonamide is different than the rest? why and what does it treat?

A

prodrug is not well-absorbed by GI: bacteria metabolize it to 5-aminosalicylic acid (anti-inflammatory)

  • used for ulcerative colitis and Crohn’s disease
  • SE: irritates gastric mucosa, but not as badly as other salicylates
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17
Q

sulfadoxine use

A

long-acting: prevents/treats malaria (inhibits falciparum DHFR)

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18
Q

what is sulfadoxine often combined with and what is this combo called?

A

sulfadoxine + pyrimethamine = Fansidar

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19
Q

sulfadiazine use

A

first line chemo for acute toxoplasmosis

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20
Q

AE of sulfonamides: general mechanisms

A
  • cross allergenic
  • these drugs used for more than abx activity:
    • CAIs (acetazolamide)
    • thiazides (ydrochlorothiazide)
    • furosemide
    • sulfonyurea hypoglycemic agents (tolbutamide)
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21
Q

most common AE of sulfonamides

A

allergies: rash, photosensitivity, drug fever

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22
Q

rare AE of sulfonamides

A 
Stevens-Johnson syndrome 
crystalluria and hematopoietic disturbances 
anorexia 
nausea 
vomit
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23
Q

three mechanisms of sulfonamide resistance

A
  1. overproduction of PABA
  2. decrease affinity of DHPS for drug
  3. decrease cell permeability to drug
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24
Q

how common is sulfonamide resistance? implications?

A

common- no longer used as single-use dudes

25
Q

mechanism of resistance to TMP

A

plasmid borne version of DHFR

26
Q

TMP PK:

  • absorption?
  • distribution?
  • half life?
  • clearance?
A
  • absorbed 85-90%
  • distributed more rapidly than sulfas
  • T1/2 = 10-12h
  • drug + inactive metabolites cleared in urine
27
Q

SMX PK:

  • distribution
  • elimination rate
  • half life
A
  • widely distributed, including CSF (but not as distributed as TMP b/c differences in lipophilicity)
  • rapidly eliminated
  • T1/2 = 10-12h
28
Q

sulfonamide metabolism

A

metabolized by N-4 N-acetylation, sometimes N-1 glucuronidation -> inactive
-hydroxylamine + nitroso metaoblites toxic

29
Q

division of humans in terms of sulfonamide metabolism

A

fast and slow acetylators-> affects metabolism

30
Q

what are the four core structures of quinolones?

A

quinolone
cinnolone
1,8-naphthyridone
pyridopyrimidone

31
Q

first gen quinolones:

  • activity?
  • uses?
  • examples?
A

activity: G(-), limited G(+)
- don’t get systemic [drug] that are useful

uses: lower UTIs
ex: oxolinic acid, nalidixic acid

32
Q

second gen quinolones:

  • how are they different from first gen?
  • activity?
  • examples?
A

diff: F at C6, heterocyclic ring (piperazine) at C7
activity: broader, more potent - more G(-) and G(+)
ex: norfloxacin, ciprofloxacin, levofloxcin

33
Q

what is the most potent fluoroquinolone?

A

cipro!

34
Q

3rd/4th gen quinolones:

  • differences?
  • activity?
  • examples?
A

diff: multiple F atoms
activity: improved G(+), especially S. pneumo + still good G(-) (but none as good for G(-) as cipro)
ex: moxifloxacin (4), sparfloxacin (3)

35
Q

which of the quinolones is a drug of last resort? why?

A

moxifloxacin: severe SE
- irreversible peripheral neuropathy
- tendon rupture
- acute liver failure
- Steven-Johnson syndrome

36
Q

quinolone MOA

A

inhibits action of Topoisomerase II -> stabilization of cleavage complex, which blocks DNA religation

37
Q

most common use for quinolones + which ones?

A

UTIs

  • norfloxacin
  • cipro
  • ofloxacin
  • nalidixic acid
38
Q

other uses for quinolones?

A
  • prostatitis
  • STDs (gonorrhea, chlamydia, H. ducreyi)
  • GI bugs (travelers, shigella, cholera)
  • resp tract (S. pneumo, CF exacerbations)
  • bone/joint/soft tissue
  • intracell dudes (chlamydia, mycoplasma, legionella, brucella, TB)
39
Q

specific quinolones for gonorrhea

A

cipro (but resistance)

-now first line is ceftriaxone

40
Q

specific quinolones for chlamydia

A

ofloxacin

sparfloxacin

41
Q

specific quinolones for H. ducreyi

A

cipro

42
Q

specific quinolones for prostatitis

A

norfloxacin
cipro
ofloxacin

43
Q

specific quinolones for shigella

A

norfloxacin
cipro
ofloxacin

44
Q

specific quinolones for cholera

A

decreases duration -norfloxacin

45
Q

specific quinolones for S. pneumo

A

moxifloxacin

46
Q

specific quinolones for CF exacerbations

A

fluoroquinolones

47
Q

specific quinolones for bone/joint/soft tissue

A

fluoroquinolones except norfloxacin

48
Q

specific quinolones for diabetic foot infections

A

Cipro!

49
Q

specific quinolones for intracellular dudes

A

norfloxacin

cipro

50
Q

5 mechanisms of resistance to quinolones

A
  1. point mutations in A subunit of DNA gyrase (lower affinity)
  2. mutations of B subunit of DNA gyrase (lower level resistance)
  3. additive effects of A + B subunit mutations
  4. efflux pumps
  5. point mutations -> cross resistance
51
Q

describe PK of quinolones

A
  • good p.o. bioavaliability and absorption
  • widely distributed (including CNS)
  • renal + hepatic clearance (except oxafloxacin 95% renal)
52
Q

quinolones: drug concentrations in different places after different times

A

after 2h: ISF [drug] are 50-100% of serum [drug]
4-24h: ISF [drug] > serum [drug]

CSF [drug] are 40-90% of serum [drug]

53
Q

chemical reactions with quinolones?

A

form insoluble chelates with heavy metals

54
Q

metabolism of quinolones

A

major inactive metabolite = glucuronide at 3C=O

-excreted in urine

55
Q

AE of quinolones

A
  • generally well tolerated
  • nausea, vomit, diarrhea (most common)
  • headache, dizzy (CNS)
  • hallucinations, delirium, seizures, skin rash, liver fxn abnormal, tendonitis (rare)
  • peripheral neuropathy w/ quins
56
Q

contraindications of fluoroquinolones

A

-f’quins damage growing cartilage, cause reversible arthropathy

therefore, don’t give to patients less than 18 y/o, unless for CF patients w/ pseudomonas

57
Q

specific AE of lomefloxacin

A

photosensitivity

58
Q

specific AE of gatifloxacin

A

hyperglycemia or hypoglycemia in diabetics

Pharm (19 decks)

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