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Pharmacology > Sulfonamides, Trimethoprim and Quinolones > Flashcards

Sulfonamides, Trimethoprim and Quinolones Flashcards

1
Q

Sulfonamides tend to be much more soluble at what pH?

A

Alkaline

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2
Q

What enzyme is inhibited by sulfonamide?

A

Dihyrdopteroate synthase

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3
Q

What mechanism is used by sulfonamide for its action against susceptible microorganisms?

A

Competitive inhibition

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4
Q

What drug inhibits dihydrofolate reductase?

A

Trimethoprim or pyrimethamine

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5
Q

Combination or sulfonamide and trimethoprim provides what kind of activity against microorganisms?

A

Synergistic activity

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6
Q

How do you classify sulfonamides?

A
  1. oral, absorbable
  2. oral, non-absorbable
  3. Topical
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7
Q

How do you classify oral, absorbable sulfonamides?

A
  1. short-acting
  2. intermediate-acting
  3. long-acting
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8
Q

What is the drug of choice for Pneumocystiis Jiroveci pneumonia?

A

Trimethoprim-sulfamethoxazole

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9
Q

Sulfisoxazole and sulfamethoxazole is used almost exclusively to treat what?

A

UTI

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10
Q

What is the first line therapy for the treatment of acute toxoplasmosis?

A

Sulfadiazine in combination with pyrimethamine

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11
Q

When giving sulfadiazine with pyrimethamine, you should also administer Folinic acid. Why is that?

A

To minimize bone marrow suppression

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12
Q

What drug is used for ulcerative colitis, enteritis and other inflammatory disease?

A

Sulfasalazine

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13
Q

Mafenide acetate, a sulfonamide used topically for burn sites causes metabolilc acidosis, how?

A

Inhibition of Carbonic Anhydrase

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14
Q

What is the uncommon yet serious adverse reaction of Sulfonamides?

A

Stevens-Johnson syndrome

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15
Q

Sulfadiazine when given in large doses and when fluid intakes is poor can cause crystalluria. How do you treat crystalluria?

A

Administration of sodium bicarbonate to alkalinize the urine and fluids to increase urine flow

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16
Q

What is the mechanism of action of trimethoprim?

A

Inhibition of bacterial dihydrofolate reductase

17
Q

Is sulfonamide alone bacteriostatic or bactericidal?

A

Bacteriostatic

18
Q

Is trimethoprim-sulfonamide bacteriostatic or bactericidal?

A

Bactericidal

19
Q

What causes resistance to trimethoprim?

A
  1. Reduced cell permiability
  2. Overproduction of dihydrofolate reductase
  3. Production of an altered reductase with reduced drug binding
20
Q

Which is more lipid soluble, therefore larger volume of distribution between sulfamethoxazole and trimethoprim?

A

Trimethoprim

21
Q

Trimethoprim has more antimicrobial activity in prostatic and vaginal fluids than many other antimicrobial drugs, why?

A

Trimethorpim is a weak base and concentrates in prostatic and vaginal fluid

22
Q

What are the adverse effects of trimethoprim?

A

Megaloblastic anemia, leukopenia and granulocytopenia

23
Q

What is the mechanism of action of quinolones?

A

Inhibition of bacterial topoisomerase I (DNA gyrase) and topoisomerase IV

24
Q

Fluoroquinolones have excellent activity against what organisms?

A

Gram-negative aerobic

25
Q

Sulfonamides are not given to patiens with G6PD deficiency, why?

A

Results in acute hemolysis

26
Q

What are the drugs that interact with sulfonamides?

A

Warfarin and Methotrexate

27
Q

What generation of fluoroquinolone has the highest gram, negative coverage?

A

2nd generation

28
Q

When do you take fluoroquinolone?

A

2 before or 4 hours after taking products that contain divalent and trivalent cations

29
Q

What is the drug of choice for prophylaxis and treatment of anthrax?

A

Ciprofloxacin

30
Q

What is the serious adverse reaction of fluoroquinolones?

A

Tendonitis and tendon rupture

31
Q

What are the drug interactions of fluoroquinolones?

A

Theophylline and other methylxanthines

32
Q

What drug has the most activity against microorganisms associated with community-acquired pneumonia?

A

Levofloxacin

33
Q

What quinolone drugs has the widest specturm of activity?

A

Gemifloxacin and Moxifloxacin

34
Q

Which drug exhibits postantibiotic effects?

A

Fluoroquinolones

35
Q

What is postantibiotic effect?

A

Bacterial growth continues to be inhibited even after the plasma concentration of the drug has fallen below the mean inhibitory concentrations

36
Q

What is the gene in gonococci that causes resistance to quinolones?

A

gyrA gene

Pharmacology (12 decks)

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