pediagenosis: Digestive
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Showing posts with label Digestive. Show all posts
Showing posts with label Digestive. Show all posts

Friday, June 11, 2021

The “Acute Abdomen”

The “Acute Abdomen”

The “Acute Abdomen”

CAUSES OF ACUTE ABDOMEN
CAUSES OF ACUTE ABDOMEN


An acute abdominal condition should be described as acute abdomen when a patient complains of abdominal pain that persists for more than a few hours and is associated with tenderness or other evidence of an inflammatory reaction or a visceral dysfunction. The diagnosis of the cause of acute abdominal conditions remains one of the most challenging problems in medicine. Many pathologic processes, both intraabdominal and extra-abdominal, may result in an acute abdomen. An accurate history, thorough physical examination, and proper laboratory examinations help to make the broad differential diagnosis of causes.

Overview of Digestive Tract Obstructions

Overview of Digestive Tract Obstructions

Overview of Digestive Tract Obstructions

Overview of Digestive Tract Obstructions


Any organic or functional condition that primarily or indirectly impedes the normal propulsion of luminal contents from the esophagus to the anus could be considered a partial or complete obstruction. In the newborn, a variety of congenital anomalies (esophageal, intestinal, anal atresias, colonic malrotation, volvulus of the midgut, meconium ileus, aganglionic megacolon) resulting in obstruction are illustrated here. Other causes of mechanical interference of intestinal function in early infancy include incarceration in an internal or external (inguinal) hernia, congenital peritoneal bands, intestinal duplications, volvulus due to mesenteric cysts, and annular pancreas, though the latter may not become clinically manifested until the patient is an adult or an aged adult.

Laparoscopic Peritoneoscopy

Laparoscopic Peritoneoscopy

Laparoscopic Peritoneoscopy

Laparoscopic Peritoneoscopy


Laparoscopic peritoneoscopy is the direct inspection of the peritoneal cavity and its contents by means of an endoscopic instrument introduced through the abdominal wall. Laparoscopic surgery has revolutionized the field of surgery and has gradually been replacing many conventional surgical procedures. The procedure is used in gastroenterologic, general surgical, and gynecologic disorders in which a positive diagnosis cannot be established by simpler methods. Its value lies in the fact that it can frequently supply information that otherwise would be obtained only by exploratory laparotomy. In addition to being a surgical method, it is particularly valuable as a diagnostic tool for visualizing and obtaining biopsies from peritoneal surfaces, the liver, the omentum, and the small bowel, as well as the pelvic organs. Intraabdominal adhesions, peritoneal carcinomatosis or tuberculosis, ascites, or hemorrhage can readily be recognized and sampled via a laparo- scope. In malignant disease, laparoscopy is useful for staging.

Overview of Gastrointestinal Hemorrhage

Overview of Gastrointestinal Hemorrhage

Overview of Gastrointestinal Hemorrhage

CAUSES OF GASTROINTESTINAL HEMORRHAGE
CAUSES OF GASTROINTESTINAL HEMORRHAGE


Many gastrointestinal disorders manifest themselves by bleeding. Intestinal bleeding may present as bright-red blood, suggesting gross lower bleeding (hematochezia), passage of black stool (melena), or other findings of bleeding but no change in stool color (occult bleeding). When no cause of bleeding can be detected with the usual examinations, obscure gastrointestinal bleeding is occurring.

Secretory, Digestive, and Absorptive Functions of Small and Large Intestines

Secretory, Digestive, and Absorptive Functions of Small and Large Intestines

Secretory, Digestive, and Absorptive Functions of Small and Large Intestines

DIGESTION OF PROTEIN
DIGESTION OF PROTEIN


The purpose of the complex enzymatic reactions to which foodstuffs are exposed within the intestinal lumen is to prepare nutrients for transfer into and assimilation within the organism. The lumen of the digestive system, which is the space encompassed by the wall of the digestive tube, belongs, fundamentally speaking, to the outside world, and the processes by which the products of digestion enter and pass through the intestinal wall into the circulation are called secretion and absorption, respectively. The mucosa of the small intestine throughout its length is lined by cells involved with both secretion and absorption: mucus-secreting cells, neuroendocrine cells, and immune active cells. The incredible efficiency of intestinal function is emphasized by the fact that of the approximately 8 L of fluid that enters the small intestine, only 100 to 200 mL is excreted from the rectum, for an efficiency rate in excess of 98%. In disease states, the large and small intestines absorb even more fluid, sometimes exceeding 25 L per day. Alternatively, in secretory dis- orders and infection, the volume of diarrhea lost may rapidly pose a life-threatening risk of dehydration, with the loss of many liters of fluids and their accompanying electrolytes.

Sunday, March 7, 2021

BARIATRIC SURGERY

BARIATRIC SURGERY

BARIATRIC SURGERY

Obesity is associated with a decrease in the quality of life as well as the life expectancy. Although both medical therapy and caloric reduction remain the first-line therapies for obesity, bariatric surgery is the most effective therapy for sustained weight loss. Bariatric surgery is considered for people with a body mass index greater than 40 kg/m2, or for those with a body mass index less than 40 kg/m2 and obesity-related diseases. Bariatric surgery involves surgical manipulation of the gastrointestinal tract to alter normal anatomy and physiology to accomplish weight loss. Weight loss has been described through two mechanisms: restriction of food intake and malabsorption of ingested food. Additionally, the neurohormonal effects of bariatric surgery are now recognized as an important mechanism for both weight loss and improvement in comorbid conditions. Along with weight loss, bariatric surgery can improve comorbidities, including diabetes mellitus, hypertension, hyperlipidemia, obstructive sleep apnea, and GERD. Relative contraindications include poorly managed psychiatric disease, a history of eating disorders, poor compliance with dietary modifications, or high concern about the patient’s ability to comply with medical follow-up.

PRINCIPLES OF OPERATIVE PROCEDURES

PRINCIPLES OF OPERATIVE PROCEDURES

PRINCIPLES OF OPERATIVE PROCEDURES

Treatment of a peptic, gastric, or duodenal ulcer begins with medical management (diet, antacid therapy, anti-secretory drugs). No rule of thumb can be given or used to fix the period of time during which medical treatment should be continued in the hope of improvement in symptoms. A great variety of individual factors must be considered before concluding that further medical efforts to regulate diet, habits, and gastric secretion will not be helpful. In general, however, the physician and patient should avail themselves of the benefit of consultation with the surgeon if the symptoms do not abate after several months of adhering strictly to sound medical therapy. Failure of response with a well-planned regimen, repeated recurrences of severe symptoms, intractable ulcer pain, lack of endoscopic evidence that the ulcer has not completely healed after a few months (even though marked subjective improvement is noted), persistence of blood in the stool, and any other signs of a threatening complication are fairly universally accepted as indications for surgical intervention.

CARCINOMA OF STOMACH

CARCINOMA OF STOMACH

CARCINOMA OF STOMACH

Gastric cancer affects more than 22,000 Americans yearly. Cancer of the stomach is seen more than twice as often in men as in women. It is essentially a disease of middle and old age, about 85% of cases arising after the age of 40. Gastric cancer was previously the most common malignant neoplasm causing death in the male population, but today its incidence has slowly decreased, to between 16% and 25%. The increased incidences of lung carcinoma and esophageal cancer, primarily esophageal adenocarcinoma, have now caused these cancers to become the leading malignant causes of death in men. In women, cancers of the uterus and of the breast are more frequent than of the stomach.

HEALING OF GASTRIC ULCER

HEALING OF GASTRIC ULCER

HEALING OF GASTRIC ULCER

In most cases, gastric ulcers heal without complications. Inflammation and edema of the ulcer wall subside. As a result, the wall tends to become flattened. The fibrinopurulent exudate on the floor of the ulcer separates off, is discarded, and is replaced by healthy granulation tissue and, subsequently, fibrous tissue. The size and depth of the ulcer are reduced, chiefly by cicatrization (a process of wound healing that produces scar tissue) and the contraction of the fibroblasts on the floor and in the wall of the lesion. In addition, the epithelium grows inward from each margin to cover the area of ulceration. From this epithelial layer, projections down-ward eventually develop, forming simple glands. Finally, the entire area is covered by epithelium. As the contraction of the fibrous tissue progresses, a permanent scar and, in some cases, radiation of the mucosal folds develop. During the healing process the ends of the muscular coat may fuse with the muscularis mucosae. But, although severed ends of the muscular layer approximate one another as a result of the cicatrizing process, restitution of a muscular breach is never complete. This remains as permanent evidence of the original lesion. Puckering and radiating streaks on the serosal surface are further evidence of the scar produced in the healing process of the chronic gastric ulcer. This can be seen endoscopically, as medical practice suggests following these ulcers until healing occurs. The healing of a chronic gastric ulcer sometimes is complete, but not infrequently such ulcers are prone to recur, particularly if the newly formed mucous membrane is thin and its vascular supply deficient. In other cases the recurrence of ulcer symptoms is due to an entirely new ulcer, the scar of the original lesion remaining permanent.

COMPLICATIONS OF GASTRIC AND DUODENAL ULCERS

COMPLICATIONS OF GASTRIC AND DUODENAL ULCERS

COMPLICATIONS OF GASTRIC AND DUODENAL ULCERS

GASTRIC PERFORATION

The two most serious complications of gastric or duodenal peptic ulcers are perforation and hemorrhage. The frequency of acute perforations in patients hospitalized for peptic ulcer varies from 2% to 25%. Perforation occurs with far greater frequency in men than in women. It is also recognized that peptic ulcer tends to perforate more often in individuals between the ages of 25 and 50 years than in younger or older persons. Fortunately, these two complications appear to have decreased over the last several decades with the wide-spread use of flexible upper endoscopy for diagnosis of ulcer disease and the advent of improved medical treatments with proton pump inhibitors and for H. pylori infection.

Tuesday, February 16, 2021

PEPTIC ULCER: DUODENAL ULCERS DISTAL TO DUODENAL BULB; MULTIPLE ULCERS

PEPTIC ULCER: DUODENAL ULCERS DISTAL TO DUODENAL BULB; MULTIPLE ULCERS

PEPTIC ULCER: DUODENAL ULCERS DISTAL TO DUODENAL BULB; MULTIPLE ULCERS

Peptic ulcers in a region distal to the duodenal bulb are rare, and their frequency, altogether probably less than 5% of all duodenal ulcers, decreases with their distance from the pylorus. Ulcers in the second portion of the duodenum give rise to the same symptoms and are beset with the same dangers and complications as are ulcers of the bulb. The acute clinical picture and later significance, however, may be far more complex because of the functional and anatomic implications for the adjoining structures. By the edema of its margin and surroundings, by penetration or by shrinkage, such an ulcer may cause obstruction and eventually stenosis of any one of several structures (the papilla of Vater, the lower part of the common bile duct, and one or both of the pancreatic ducts), so that chronic pancreatitis and/or biliary obstruction with jaundice may result. Deep penetration may give rise to a choledochoduodenal fistula. The presence of duodenal ulcers distal to the duodenal bulb should raise concern for the presence of Zollinger-Ellison syndrome, or gastrinoma, in which excessive gastrin is secreted, leading to excessive secretion of gastric acid.

PEPTIC ULCER: DUODENITIS AND ULCER OF DUODENAL BULB

PEPTIC ULCER: DUODENITIS AND ULCER OF DUODENAL BULB

PEPTIC ULCER: DUODENITIS AND ULCER OF DUODENAL BULB

Duodenitis refers to an inflammation of the mucosa in the duodenal bulbar region. Duodenitis is usually diagnosed endoscopically, often when it is performed for abdominal pain or evidence of acute or chronic gastrointestinal bleeding. The diagnosis may be supported in radiologic contrast studies when the mucosa of the most proximal part of the duodenum appears somewhat mottled and when, fluoroscopically, spasms and an increased motility of the duodenal cap can be observed. The inflamed duodenal mucosa has a relatively strong tendency to bleed, even in the absence of an actual ulcerative process. At times, however, duodenitis may be associated with multiple superficial erosions. On the other hand, diffuse duodenitis may also be present in association with a characteristic chronic peptic ulcer. Duodenitis is usually confined to the most proximal parts of the duodenum, but, occasionally, the antral mucosa as well may participate in the inflammatory reaction. Medical treatment for duodenitis is the same as that for peptic ulcer. Massive hemorrhages from duodenitis with erosion may, in rare cases, make exploration necessary, although, as a matter of general principle, surgical intervention is not recommended unless the source of the bleeding has been determined.

FUNCTIONAL DYSPEPSIA

FUNCTIONAL DYSPEPSIA

FUNCTIONAL DYSPEPSIA

Dyspepsia refers to symptoms originating in the upper gastrointestinal tract; the term is used to describe upper abdominal pain or discomfort, early satiety, and postprandial abdominal bloating or distention. Some examples of structural or biochemical disorders causing dyspepsia include gastroduodenal ulcer, gastritis, GERD, and gastric cancers; medication side effects may also be a cause. In many patients, the cause of dyspepsia is idiopathic and not obvious after an evaluation including the history, a physical examination, blood work, and upper endoscopy; this is termed functional dyspepsia. ROME criteria for functional dyspepsia developed to help describe these particular patients include the following requirements: (1) the presence of one or more of the following: bothersome postprandial fullness, early satiation, epigastric pain, or epigastric burning; and (2) no evidence of structural disease (including at upper endoscopy) that is likely to explain the symptoms. Functional dyspepsia in the ROME classification is divided into (1) postprandial distress syndrome characterized primarily by early satiation and postprandial fullness; and (2) epigastric pain syndrome characterized primarily by epigastric pain and burning. Several mechanisms have been proposed for the pathogenesis of functional dyspepsia. The gastric acid or inflammation hypothesis suggests that gastric acid or inflammation from gastric acid, bile, GERD, or H. pylori infection is responsible for symptoms. The motor disorder hypothesis suggests that gastric motility disorders, such as gastroparesis, impaired fundic accommodation, antral distention, or gastric dysrhythmias, are important. The visceral hypersensitivity hypothesis proposes exaggerated symptoms in response to physicochemical stimuli, such as distention, contraction, acid, and bile. The psychological hypothesis suggests that some of the symptoms are related to or enhanced with depression, anxiety, or a somatization disorder.

GASTRIC ELECTRICAL STIMULATION FOR GASTROPARESIS

GASTRIC ELECTRICAL STIMULATION FOR GASTROPARESIS

GASTRIC ELECTRICAL STIMULATION FOR GASTROPARESIS

Gastric electrical stimulation is an emerging treatment for refractory gastroparesis. There are several techniques for stimulating the stomach. First, in gastric electrical pacing the goal is to entrain and pace the gastric slow waves with low-frequency, high-energy, long-duration pulses. Pacing at 10% higher than the basal rate is used to try to accelerate gastric emptying and to improve dyspeptic symptoms. Second, stimulation with high-frequency, low-energy, short-duration pulses has been shown to decrease symptoms but has less effect on gastric emptying; it may affect proximal stomach function and activate sensory afferent nerves to reduce symptoms. Third, sequential gastric neurostimulation of the stomach has been used to entrain gastric slow waves.

GASTROPARESIS

GASTROPARESIS

GASTROPARESIS

Gastroparesis is a chronic symptomatic disorder of the stomach characterized by delayed emptying without evidence of mechanical obstruction. The delay in gastric emptying can have a number of causes, including antral hypomotility, pylorospasm, gastric dysthymias, and lack of interstitial cells of Cajal. Symptoms from gastroparesis include nausea, vomiting, early satiety, postprandial fullness, and, in some patients, upper abdominal pain. This classic motility disorder of the stomach can lead to marked dysfunction in patients, with a poor quality of life. Gastroparesis is identified by recognizing the clinical symptoms and documenting delayed gastric emptying. The three main causes are diabetic, postsurgical, and idiopathic.

Monday, February 15, 2021

GIANT GASTRIC ULCER

GIANT GASTRIC ULCER

GIANT GASTRIC ULCER

Giant gastric ulcers are rare in the overall group of gastric ulcers, especially since upper endoscopy evaluation has become available and ulcer treatments with proton pump inhibitors and for H. pylori have also become available. The site of origin is usually on the posterior wall of the gastric body and may progressively involve the lesser curvature by extension. The ulcers may penetrate the gastrohepatic ligament and even involve the liver and pancreas. They are particularly deceptive because the flattened floor of the ulcer is extensive, so that it resembles an atrophic area of gastric mucosa. A very similar pathologic picture can be produced acutely by the corrosive action of acids or alkalis. When caustic agents are involved, however, the contrast material puddles in the prepyloric region and on the posterior wall of the stomach if the patient assumes a supine position immediately after the accident of ingestion.

Tuesday, February 2, 2021

CAMERON LESIONS AND DISORDERS OF THE CARDIA

CAMERON LESIONS AND DISORDERS OF THE CARDIA

CAMERON LESIONS AND DISORDERS OF THE CARDIA

Cameron lesions are either gastric erosions or linear ulcerations that occur at the level of the diaphragm in patients with a hiatal hernia sac. Cameron lesions were first described in 1986 by Cameron and Higgins, who discovered them in a series of patients. They occur in approximately 5% of patients who undergo upper endoscopy and are found to have a hiatal hernia. They are more common in elderly patients and in those with large sliding hiatal hernias. The cause of these lesions is either mechanical trauma or ischemia secondary to sliding of the hiatal hernia. Medication effects from NSAIDs as well as acid peptic disease also play a part in their formation. Most patients with Cameron lesions present with iron deficiency anemia, although overt upper gastrointestinal bleeding can be seen. Treatment of a Cameron ulcer varies; the use anti secretory agents should be the first line of therapy. In addition, stopping any caustic medications should be advised. For those patients with persistent symptoms or findings, a surgical procedure should be recommended which mainly focuses on reducing the hiatal hernia and preventing its recurrence.

CHRONIC GASTRIC ULCER

CHRONIC GASTRIC ULCER

CHRONIC GASTRIC ULCER

The chronic gastric ulcer is almost invariably single, although scars of previous ulcers that have healed can be found in association with the sole active chronic lesion. Not infrequently, a duodenal ulcer develops simultaneously with a chronic gastric ulcer.

SUBACUTE ULCER OF STOMACH

SUBACUTE ULCER OF STOMACH

SUBACUTE ULCER OF STOMACH

An ulcer in the transitional stage between acute and chronic has been termed subacute ulcer. Morphologically, it differs in degree from an acute ulcer insofar as it is more rounded and has a greater depth. Its walls are thicker and higher, and its shape is occasionally funnel-like, with irregular contours. The subacute phase of a peptic ulcer has involved both the mucosa and submucosa, but at times it may reach the muscular coat. In any event, the subacute ulcer may have the same potential danger for perforation or profuse bleeding as does an acute or a chronic ulcer. At the floor of the ulcer, one finds purulent, grayish-yellow, necrotic material. The grayish-white color on the floor or edges may be due also to proliferating fibroblasts, as a token of a healing tendency and the beginning of scar formation.

ACUTE GASTRIC ULCER

ACUTE GASTRIC ULCER

ACUTE GASTRIC ULCER

The cause of gastric or duodenal ulcers was a matter of debate during several decades; there are now known to be two main causes. H. pylori infection is a factor in many peptic ulcers, both gastric and duodenal; its causative role appears to be decreasing, however. Aspirin and other NSAIDs are also a known cause of gastric ulcers. A significant minority of these ulcers have causes other than H. pylori infection or NSAID use.

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