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Biomedical subjects

T R Hendrix

Publications and source records attributed to T R Hendrix.

At least 19 recordsLinked to original sources
PubMed1992

Breath hydrogen testing as a physiology laboratory exercise for medical students.

Breath hydrogen testing (BHT) is a simple and reliable method for identifying impaired carbohydrate absorption. We describe a laboratory exercise in physiology for medical students using BHT as the teaching tool. The students collect fasting samples of expired air from each other using a simple nasal prong technique. They then drink one of several different aqueous carbohydrate solutions. Additional samples of expired air are collected by the students at 90 and 120 min after substrate ingestion and are analyzed by gas chromatography. Between sampling periods, discussions of digestive physiology are provided by the faculty. Students tabulate their BHT results as well as recording any symptoms using a standard scoring system. A total of 460 students have participated. We found that the percentage of students who malabsorbed a given substrate was similar each year. The results obtained in these student exercises closely parallel those reported in the literature. We conclude that BHT is an excellent teaching tool for illustrating carbohydrate digestion and absorption, even when performed by minimally trained subjects.

Animals↗
PubMed1992

Frank P. Brooks.

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Gastroenterology↗
PubMed1989

Lymphocytic enterocolitis in patients with 'refractory sprue'.

We describe a patient with refractory sprue with malabsorption, a flat small-bowel biopsy specimen unresponsive to a gluten-free diet, and colonic biopsy specimens consistent with lymphocytic (microscopic) colitis. To investigate further the relation between celiac disease and lymphocytic or collagenous colitis (a similar and possibly related entity), we examined colorectal and small-bowel biopsy specimens in patients indexed histologically as having celiac disease who have been seen at The Johns Hopkins Hospital since 1958. Of 135 indexed patients, 21 had colorectal biopsies. Colorectal biopsy specimens were abnormal in 7 of the 21 patients. Four patients had biopsy specimens resembling lymphocytic colitis, 2 patients had acute colitis, and another patient had both lymphocytic and acute colitis. No patients had collagenous colitis. Three of the patients with lymphocytic colitis and celiac-like changes of the small bowel never responded to a gluten-free diet and may represent a distinctive panintestinal disease for which the term "lymphocytic enterocolitis" with malabsorption is proposed.

Adult↗
PubMed1988

Campylobacter gastritis and associated disorders.

Our review of evidence that Campylobacter pylori is an important factor in gastritis, peptic ulcer disease, and "nonulcer dyspepsia" suggests that C pylori is the most common cause of chronic active gastritis. The association between C pylori gastritis and duodenal ulcer, which approaches 100%, leads to the suggestion that this infection plays an important role in the pathogenesis of duodenal ulcer. Evidence supporting a central role in the pathogenesis of gastric ulcer and nonulcer dyspepsia is less compelling.

Campylobacter Infections↗
PubMed1987

Granular small bowel mucosa: a reflection of villous abnormality.

Diffuse mucosal granularity was reported recently in small bowel Crohn's disease. The radiographic appearance corresponded on histopathologic examination to villous hypertrophy, fusion, or epithelial bridge formation. We have observed similar granularity in Crohn's disease but also in several other conditions, including radiation enteritis, pancreatic glucagonoma, protein-losing enteropathy, and small bowel ischemia. Histopathologic examination demonstrated various alterations in villous morphology, such as edema, hyperplasia, clubbing, or fusion. In Crohn's disease, this appearance was sometimes an indication of early inflammatory disease but was also seen following extensive small bowel resection, possibly due to villous enlargement resulting from intestinal adaptation. These findings suggest that granular mucosa in the small bowel is a nonspecific finding reflecting an alteration in villous structure.

Adult↗
PubMed1979

Gastric aspiration in localization of gastrointestinal hemorrhage.

We compared the findings from gastric aspiration for blood with the site of gastrointestinal (GI) hemorrhage ultimately identified by endoscopy or angiography in 1,190 patients whose cases were analyzed retrospectively and prospectively during a six-year period. Gastric aspirates were positive for blood in 837 patients. An upper GI site proximal to Treitz' ligament was identified in 93%, and none had a lower GI site. A negative aspirate was found in 353 patients; a lower GI site was identified in 60%, and 1% (three patients) had an upper GI site. In these three patients, hemorrhage occurred in clinical settings suggesting ulcer disease, and bleeding duodenal ulcers were found in all three. All of the other 180 patients with a bleeding duodenal ulcer had a positive gastric aspirate.

Aged↗
PubMed1979

Selective nonoperative management of contained intrathoracic esophageal disruptions.

Eight patients with intrathoracic esophageal disruptions were managed nonoperatively and without pleural drainage. Criteria for nonoperative treatment included the following: disruption contained in the mediastinum or between the mediastinum and visceral lung pleura; drainage of the cavity back into the esophagus; minimal symptoms; and minimal signs of clinical sepsis. Cause of the esophageal perforation was pneumostatic dilatation (1 patient), vomiting (2), and a leak following esophageal operation (5). Antibiotics were administered intravenously to all patients; hyperalimentation was accomplished intravenously in 5, and nasogastric suction was used in only 1. The cavities contracted and the esophageal leaks sealed in all instances. Time before oral intake was resumed ranged from 7 to 38 days (average, 18 days). Days until discharge ranged from 15 to 52 days (average, 28 days).

Adult↗
PubMed1979

Boerhaave syndrome.

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Aortic Dissection↗
PubMed1978

Prevention and reversal of cholera enterotoxin effects in rabbit jejunum by nicotinic acid.

The cholera enterotoxin produces intestinal secretion associated with an elevation of tissue levels of cyclic adenosine 3',5'-monophosphate levels of cyclic adenosine 3',5'-monosphosphate (cAMP). The objectives of this study were to determine whether intestinal secretion and cAMP elevation induced by cholera toxin could be prevented, or once initiated, reversed by nicotinic acid, an agent known to lower tissue levels of cAMP. In rabbits, four jejunal loops were constructed as alternating control (3-ml isotonic electrolyte solution) and cholera toxin (same solution containing 50 mug purified cholera toxin) loops. Net intestinal secretion was determined by measuring fluid accumulation, after which intestinal biopsies were taken for cAMP assay. The animals were pretreated either subcutaneously with 50 mg/kg nicotinic acid in saline 3 h and 1 h before the introduction of cholera toxin, or intraluminally with 200 mg/kg nicotinic acid in Ringer's lactate solution 15 min before the instillation of cholera toxin. Under these conditions, nicotinic acid blocked the cholera toxin-induced secretion and the rise in cAMP measured 3 h after the loops were exposed to cholera toxin. The effect of the nicotinic acid administered within the lumen on net intestinal secretion was studied. Maximal inhibition of net intestinal secretion was achieved with an intraluminally administered dose of nicotinic acid of 100 mg/kg. This dose was chosen for testing the ability of nicotinic acid to reverse the effects of cholera toxin. When nicotinic acid was instilled into a fifth loop constructed distally to the four experimental loops 3 h after exposure of these loops to cholera toxin, both intestinal secretion and elevation of cAMP were reversed. These results suggest that nicotinic acid can prevent and reverse the secretory effects of cholera toxin and may have a role in the therapy of cholera and other cAMP-associated diarrheal diseases.

Animals↗
PubMed1978

Relation between volume swallowed and velocity of the bolus ejected from the pharynx into the esophagus.

The velocity of the front face of a liquid saline bolus ejected from the pharynx into the esophagus was measured by recording changes of luminal electrical impedance with three sets of electrodes in 9 subjects. At a site 26 cm from the incisors, the mean velocity of the front face of the bolus increased from 10 to 70 cm sec-1 as the volume swallowed was raised from 5 to 30 ml. The velocity of the front face of the bolus was greater 26 cm from the incisors than it was 32 cm from the incisors.

Deglutition↗
PubMed1977

The association of heartburn with gastritis.

Esophageal, fundal, antral, and duodenal mucosal biopsies from 10 patients with heartburn were compared with biopsies from 18 patients with dyspepsia but without heartburn or radiographic or endoscopic evidence of peptic ulcer disease, gastric retention, or esophageal stricture. There was a highly significnt correlation between heartburn and antral gastritis and duodentitis (P less than 0.01). It is suggested that histologic reflux changes are determined by the severity of reflux and reparative potential of the esophageal mucosa. Heartburn, on the other hand, is more related to the nature of the refluxed fluid. The fluid most likely to induce heartburn is one containing duodenal fluid, which is also believed to be an important cause of antral gastritis.

Biopsy↗
PubMed1977

Role of lower esophageal sphincter incompetence in recurrent pneumonia after repair of esophageal atresia.

The etiology of recurrent aspiration pneumonitis after the successful repair of esophageal atresia has not been defined. In order to explain this occurrence, we performed esophageal manometric examinations on eight patients who had undergone repair of EA and tracheoesophageal fistula. Two patients who had had recurrent pneumonia had subnormal pressure of the lower esophageal sphincter; they also had a history of severe regurgitation, and a barium esophagram demonstrated free gastroesophageal reflux. The LES incompetence in these patients was apparently corrected by administration of bethanechol.

Adolescent↗
PubMed1977

Esophageal reflux. Diagnosis and therapy.

Diagnosis of esophageal reflux often can be made on the basis of the characteristic symptoms of heartburn and regurgitation. When the picture is not so typical, acid reflux testing and esophageal biopsy appear to be the best indicators of esophageal reflux. Medical management is directed toward preventing reflux, neutralizing refluxed gastric contents, and enhancing clearance of refluxed material. Antacids are a mainstay of therapy, along with restrictions on diet and certain types of activity. If conservative therapy fails to control symptoms and stricture is likely to develop, surgery may be indicated.

Esophagogastric Junction↗