الخميس، 14 مارس 2013

MCQs In Pediatric Pharmacotherpy

Q1:


Q 1:

A 12-year-old girl who has a history of juvenile idiopathic arthritis is brought to the emergency department with severe epigastric abdominal pain. She has been taking ibuprofen to control her joint pains. Physical examination demonstrates a well-developed, well-nourished girl in moderate distress from pain. The remainder of the general physical examination shows direct tenderness in the epigastrium without rebound. The rectal examination shows normal sphincter tone and a scant amount of dark brown, hemoccult-positive stool in the rectal vault. Initial laboratory data include the following:

White blood cell count, 10,500/µL (10.5 × 109/L)
Hemoglobin, 11.7 g/dL (117 g/L)
Erythrocyte sedimentation rate, 32 mm/h
Serum electrolytes, normal
Blood urea nitrogen, normal
Creatinine, normal
Of the following, the MOST likely mechanism responsible for her symptoms is

A.  decreased pepsinogen production
B.  duodenal stress ulceration
C.  gastritis induced by peptidoglycans
D.  hypersecretion of gastric acid
E.  inhibition of prostaglandin synthesis

Answer :

E


The girl described in the vignette presents with abdominal pain, hemoccult-positive stools, and anemia. These findings indicate chronic gastrointestinal blood loss, and the presence of epigastric tenderness strongly suggests a lesion in the upper gastrointestinal tract (ie, proximal to the ligament of Treitz). Although the differential diagnosis of chronic upper gastrointestinal bleeding is broad and includes erosive esophagitis, Helicobacter pylori infection, and Crohn Disease, the most likely diagnosis is gastritis or peptic ulcer disease caused by her use of ibuprofen. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, inhibit prostaglandin synthesis. Prostaglandin E stimulates gastric mucus production and helps maintain the protective mucin glycoprotein-bicaA rbonate layer, without which gastric mucosa is exposed to the deleterious effects of gastric acid as well as to the proteolytic effects of chief cell-produced pepsin, which can result in gastritis or peptic ulcers.

NSAIDs are highly effective anti-inflammatory agents that act via inhibition of the enzymes cyclooxygenase-1 (COX-1) or cyclooxygenase-2 (COX-2) or both. The NSAIDS that inhibit both COX-1 and COX-2 are termed nonselective cyclooxygenase inhibitors and include aspirin, ibuprofen, and naproxen. These agents are associated with a significantly higher risk for both gastrointestinal and renal toxicity when compared with selective COX-2 inhibitors (eg, celecoxib). However, the COX-2 inhibitors have been associated with an increased incidence of deleterious cardiovascular effects in adults.

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Q 2:


You are talking to a group of medical students about the antibiotic vancomycin and its
associated adverse effects. One of the students asks you to explain “red man syndrome.”
Of the following, the MOST appropriate response is that “red man syndrome” is

A. a manifestation of a life-threatening anaphylactic reaction
B. a manifestation of the development of ototoxicity
C. related to cytokine release from cells
D. related to endotoxin release from cells
E. related to histamine release from cells

Answer

E



A reaction that is peculiar to vancomycin and occurs in 3.4% to 11.2% of infusions is referred to
as “red man” or “red neck” syndrome. It consists of pruritus; an erythematous rash that
involves the face, neck, and upper torso; and occasionally hypotension. The manifestations of
the reaction are due to the nonimmunologically mediated release of histamine from basophils and
mast cells. This complication can be avoided by slowing the infusion rate, decreasing the dose,
and administering antihistamines prior to the infusion. Red man syndrome is not a manifestation
of a life-threatening anaphylactic reaction or the development of ototoxicity.

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