Duodenum duodenitis

Peptic ulcers Ulcer of the digestive tract, caused by digestion of the mucosa by acid and pepsin. May occur in, for example, the duodenum (duodenal ulcer) or the stomach (gastric ulcer)... 

Decubitus ulcer (e.g. bed sores, pressure sores) Diabetic ulcers Varicose ulcers Rodent ulcers Peptic ulcers Ulcer due to continuous pressure exerted on a particular area of skin often associated with bed-ridden patients Ulcers (e.g. diabetic leg ) caused by complications of diabetes Due to defective circulation, sometimes associated with varicose veins An ulcerous cancer (basal cell carcinoma), usually affecting the face Ulcer of the digestive tract, caused by digestion of the mucosa by acid and pepsin may occur in e.g. the duodenum (duodenal ulcer), or the stomach (gastric ulcer)... 

H2 Antagonists and the Treatment of Peptic Ulcers. Treatment of peptic ulcers is a complicated and multilevel therapy in which Hj antagonists are very successful and widely used (and abused). Peptic ulcers may affect either the stomach (gastric ulcers, less common overall but more common in people with iatrogenic [i.e., physician-induced] ulcers from the use of nonsteroidal anti-inflammatory drugs [NSAIDs]) or the duodenum (duodenal ulcers). The lining of the stomach or duodenum is attacked by the digestive juices to such an extent that the protective mucous layer on the surface has... 

A common duct from the pancreas and gall bladder enters the duodenum. Duodenal pH is 6 to 6.5 due to the presence of bicarbonate that neutralizes the acidic ch5une emptied from the stomach. The pH is optimum for enzymatic digestion of protein and peptide food. Pancreatic juice containing enzymes is secreted into the duodenum from the bile duct. Trypsin, ch5unotrypsin, and carboxypeptidase are involved in the hydrolysis of proteins into amino acids. Amylase is involved in the digestion of carbohydrates. Pancreatic lipase secretion hydrolyzes fats into fatty acids... 

Most peptic ulcers occur in the presence of acid and pepsin when HP, NSAIDs, or other factors (see Table 33-2) disrupt normal mucosal defense and healing mechanisms. Hypersecretion of acid is the primary pathogenic mechanism in hypersecretory states such as ZES. Ulcer location is related to a number of etiologic factors. Benign gastric ulcers can occur anywhere in the stomach, although most are located on the lesser curvature, just distal to the junction of the antral and acid-secreting mucosa (see Fig. 33-1). Most duodenal ulcers occur in the first part of the duodenum (duodenal bulb). 

In general, ulcers related to HP infection more commonly affect the duodenum whereas ulcers related to NSAIDs more frequently affect the stomach. However, ulcers maybe found in either location from either cause. Gastric ulcers (GUs) tend to occur much later in life than duodenal ulcers (DUs), with the peak incidence of GU occurring in patients over 60 years of age. Malignancy is more commonly found with GU than DU. 

The location of the tip of the feeding tube is important when considering medication administration down a feeding tube. This is particularly true if the medication acts locally in the GI tract itself. For example, sucralfate and antacids act locally in the stomach. Therefore, administration of these medications through a duodenal or jejunal tube is not logical. Likewise, for medications such as itraconazole that require acid for best absorption, administration directly into the duodenum or jejunum would be expected to result in suboptimal absorption. Absorption of drugs when administered directly into the small bowel, especially the jejunum, rather than into the stomach is another area where more research would be useful. 

As the volume of the chyme in the duodenum increases, it causes distension of the duodenal wall and stimulation of mechanoreceptors. This receptor stimulation elicits reflex inhibition of gastric motility mediated through the intrinsic and vagus nerves. Distension also causes release of gastric inhibitory peptide from the duodenum, which contributes to inhibition of gastric contractions. 

Pancreatic juice neutralizes the acidic chyme entering the duodenum from the stomach. Neutralization not only prevents damage to the duodenal mucosa, but also creates a neutral or slightly alkaline environment optimal for the function of pancreatic enzymes. The pancreas also secretes several enzymes involved in the digestion of carbohydrates, proteins, and lipids. 

Sucralphate Should not be given in a duodenal tube since the effect is directly on a damaged mucosa in the stomach and pylorus. Change drug if the tube ends in the duodenum. 

Sinko et al. [92] established an Intestinal and Vascular Access Port (IVAP) model where dogs were fitted with three intestinal catheters for site-specific administration to various section of the intestine (i.e. duodenum, ileum, and colon), one vascular catheter for access to the portal vein, and a peripheral vein (e.g. branchial) for IV access. The animals were allowed to recover for 2 weeks prior to initiation of studies. The extent of intestinal versus hepatic first-pass metabolism was determined by comparing blood levels following intra-duodenal (AUQ.d.) versus portal (AUVi.p.v.) versus intravenous (AUQ.V.) administration. The model also lends itself to a comparison of the impact of site-specific preferential absorption, and hence a determination of the optimal site for intestinal delivery. 

Duodenal Ulcer An ulcer in the lining of the first part of the small intestine (duodenum). 

The effect of. S divinorum on duodenal smooth muscle is not clear, although the extract appears to decrease the frequency of phasic contractions while increasing their duration. Typically, contractions occurred approximately once every two seconds when the muscle was bathed in pure Tyrode s solution. However, when bathed in 100% S. divinorum extract, contractions appeared to stop completely. When flushed with Tyrode s solution, the muscle recovered almost completely. Wlien the duodenum was bathed in 50%. S divinorum extract, the muscle would contract for approximately 15 seconds, relax for about 2 seconds, and then contract again. By comparison, when the muscle was bathed in extract of L. nobilis, the muscle would stop contracting and would not recover when flushed with Tyrode s solution. Figure 3 shows the tracings produced from a single strip of duodenal smooth muscle treated with. S divinorum. 

Increases tone and amplitude of gastric contractions, relaxes the pyloric sphincter and the duodenal bulb, and increases peristalsis of the duodenum and jejunum, possibly by sensitizing tissues to the action of acetylcholine, resulting in accelerated gastric emptying and intestinal transit... 

At the duodenal pH of 7.0, 96.9% of the phenytoin is in the nonionized form, which favors its absorption. The absorption of phenytoin is greatest in the duodenum and decreases in the lower parts of the small intestine. The absorption from the cecum and the large intestine is several-fold lower than that in the duodenum. 

In rats, papaverine had a choleretic effect (271). It caused relaxation of the duodenum, of the sphincter of Oddi, and of the muscles of the bile duct (272-277). It paralyzed the spasmogenic effect of morphine on these structures. Papaverine (0.36 g) in combination with 100 ml of 60% sorbitol, administered to man by means of a duodenal probe, showed a higher choleretic and a lower cholecystokinetic effect than a 30% solution of magnesium sulfate (277). 

In 1972 we found that injections of propionitrile (Figure 1) consistently produced solitary, often perforating duodenal ulcers in the rat (5.). These lesions occurred 3-5 mm from the pylorus of the stomach, mostly - as in humans - on the anterior wall of the duodenum. The ulcers developed 24-48 h after the initial administration of propionitrile and frequently penetrated into the liver or pancreas ( ). 

The lesion in the duodenum developed even more rapidly (e.g., perforation in 24 h after a single dose) and more predictably than with propionitrile. Acetanilide was the first aryl chemical noted to cause duodenal ulcer ( 18). Subsequently, 3,4-toluenediamine ( ) and 3,4-toluenedithiol (20) were also shown to induce duodenal ulcers and occasionally adrenal necrosis in rats. 

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