Walters Flashcards

1
Q

How do Bacteristatic antibiotics kill bacteria?

A

do not directly kill bacteria. Instead, they inhibit metabolic pathways thus weakening the organisms and then relying on the patient’s immune system to clear the infection.

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2
Q

How do Bactericidal antibiotics kill bacteria?

A

Mostly by causing lysis.

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3
Q

Name factors to consider when choosing an antibiotic.

A

Age, Hepatic function, Pregnancy, Disease condition, Genetics, Resistance, Route of administration, and Site of infection

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4
Q

Explain a) Acetylation.

A

Acetylation is one route of drug metabolism. Asians are fast acetylators.

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5
Q

Low levels of Glucose-6-phosphate dehydrogenase (G6PD) can cause pts to be at risk for what?

A

Sulfonamides, nitrofurantoin & chloramphenicol have a greater risk of causing hemolysis if low levels of G6PD.
(G6PD protects cells from free radicals.)

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6
Q

Sulfonamides are structurally similar to which drugs?

A

Sulfonamides are structurally similar to sulfonoureas, which stimulate the release of insulin and can cause hypoglycemia.

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7
Q

Tetracyclines

A
  • readily cross the placenta, secreted in breast milk.
  • They deposit in teeth and bone where they chelate with calcium phosphate causing a permanent brown discoloration of teeth
  • Can slow bone growth
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8
Q

Why are Fluoroquinolones not used in prepubertal kids?

A

Because they cause cartilage damage and arthropathy and are, therefore, not used in prepubertal kids.

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9
Q

T/F: In older patients, penicillins can cause neurotoxicity due to reduced renal function.

A

True.

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10
Q

What is kernicterus?

A

kernicterus is a form of jundice. In neonatas, Sulfamides can increase the amount of free bilirubin which readily crosses the blood brain barrier and deposits in neonatal basal ganglia and other areas causing generalized CNS depression —> kernicterus.

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11
Q

T/F : Aminoglycosides should not be given to pregnant women because they are nephrotoxic and ototoxic.

A

True

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12
Q

What is the rationale for multiple Rx therapy?

A
  • ↓ Risk selecting for resistant organisms
  • Multiple organism infections not covered by a single Rx
  • Synergism (two drugs producing an effect that is greater than the sum of either drug alone).
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13
Q

Describe the mechanisms of sulfonmides.

A

Sulfonoamides inhibit dihydropteropate synthase, the first step in the synthesis of folic acid. i.e. the joining of PABA with pteridine to form dihydropteroic acid, the immediate precursor of folic acid.

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14
Q

True or False. SULFAS are generally used with a DHFR INHIBITOR (DHFRI) for a synergistic effect

A

True

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15
Q

Name four DHFRIs (dihydrofolate reductase Inhibitors).

A

1- TRIMETHOPRIM– inhibits bacterial DHFR. Side effects: blood dyscrasias
2- PYRIMETHAMINE– antimalarial – inhibits protozoal DHFR
3- METHOTREXATE – inhibits mammalian, bacterial & protozoal DHFR. Used to treat psoriasis and various cancers.
4- PRALATREXATE – for T cell lymphomas

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16
Q

Name there oral ORAL SULFONAMIDES.

A

SULFISOXAZOLE, SULFAMETHOXAZOLE, DAPSONE

17
Q

Name 3 topical sulfonamides & their uses.

A
  1. SULFACETAMIDE : for Ulcerative blepharitis or bacterial conjuntivitis
  2. SILVER SULFADIAZINE :for burns to prevent sepsis
  3. MAFENIDE : for burns. Use limited – can cause metabolic acidosis by inhibiting carbonic anhydrase -> loss of HCO3- & thus loss of buffering capacity.
18
Q

Name 5 general side effects of sulfonamides.

A

Crystalluria, Kernicterus, Blood dyscrasias, Hyperkalemia, and Hypersensitivity.

19
Q

FLUOROQUINOLONES

A

Broad spectrum CIDAL agents used mostly for G- & some G

20
Q

Which enzymes do Fluroquinolones inhibit in G- and G+ bacteria?

A

Fluroquinolones inhibit DNA gyrase in G- and
topoisomerase V in G+.
*both pathways are active in both gram + and -. These inhibitions are the main forms.