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

Tuesday, February 2, 2021

GASTRITIS

GASTRITIS

GASTRITIS

Gastritis is an inflammation of the mucosal lining of the stomach. It can occur suddenly (acute) or gradually (chronic). Gastritis can be caused by irritation or inflammation from excessive alcohol use or the use of certain medications such as aspirin or other anti inflammatory drugs. It may also be caused by H. pylori and other bacterial and viral infections, pernicious anemia, and bile reflux.

Sunday, January 10, 2021

DIVERTICULUM OF STOMACH; GASTRODUODENAL PROLAPSE

DIVERTICULUM OF STOMACH; GASTRODUODENAL PROLAPSE

DIVERTICULUM OF STOMACH; GASTRODUODENAL PROLAPSE

Gastric diverticulum is an outpouching of the gastric wall. Gastric diverticula are rare, and they are commonly detected incidentally during routine diagnostic testing, such as upper endoscopy and upper gastrointestinal radiologic study. These diverticula of the stomach are often of little practical significance, but they may be worth considering in a differential diagnosis. Most gastric diverticula are asymptomatic, but they may present with a vague sensation of fullness or discomfort in the upper abdomen. The presenting complaint might also be the result of a complication of a gastric diverticulum, such as acute upper gastrointestinal bleeding or perforation.

HYPERTROPHIC PYLORIC STENOSIS

HYPERTROPHIC PYLORIC STENOSIS

HYPERTROPHIC PYLORIC STENOSIS

Hypertrophic pyloric stenosis is predominately a neonatal disorder. Its exact cause and pathogenesis remain debated. It may be due to a lack of localized nitric oxide synthase, which normally allows for smooth muscle relaxation. It is unknown if the lack of nitric oxide synthase is a primary or secondary event, as it is not seen in all cases. In hypertrophic pyloric stenosis, the interstitial cells of Cajal, which are the pacemaker cells of the gastrointestinal tract, are only seen near the submucosa rather than throughout the entire pylorus. Epidermal growth factors (EGFs), their receptors, and heparin-binding EGF-like growth factors are also increased in smooth muscle cells in hypertrophic pyloric stenosis, but the trigger for these increased growth factors remains unknown.

PARAESOPHAGEAL HERNIA AND GASTRIC VOLVULUS

PARAESOPHAGEAL HERNIA AND GASTRIC VOLVULUS

PARAESOPHAGEAL HERNIA AND GASTRIC VOLVULUS

A paracardial or paraesophageal hernia is seen less frequently than is a sliding diaphragmatic hernia and is characterized by the protrusion of the gastric fundus into the intrathoracic space alongside the esophagus, which is of normal length and in the usual and fixed position. The cardia and its attachment by the gastrophrenic ligament remains intact while the fundus slips through a fibromuscular defect directly to the left or right of the gastroesophageal junction. The parietal peritoneum, which normally covers the abdominal surface of the diaphragm, has prolapses and serves as the outer wall of the hernia sac. These anatomic relations explain why, with a paraesophageal hernia, there is no insufficiency of the lower esophageal sphincter mechanism and, hence, no occurrence of peptic esophagitis.

HELICOBACTER PYLORI INFECTION

HELICOBACTER PYLORI INFECTION

HELICOBACTER PYLORI INFECTION

Helicobacter pylori is a gram-negative bacteria initially cultured from the human stomach in 1982 and considered the most common cause of gastric mucosal injury. It produces large amounts of urease that protects from acid injury, enabling it to penetrate gastric epithelial cells. The transmission mechanism of H. pylori remains unclear. Interpersonal transmission appears to be the main route; transmission by environmental substances, such as contaminated water, is another cause.

GASTRIC ANALYSIS

GASTRIC ANALYSIS

GASTRIC ANALYSIS

Gastric analysis is a technique for measuring acid production of the stomach. Gastric analysis may, in this context, be classified as qualitative or quantitative. A qualitative gastric analysis is undertaken to ascertain whether the gastric glands can secrete acid. A quantitative gastric analysis seeks to determine the amount of HCl secreted by the stomach and is carried out by determining the basal secretion level or the secretory response to insulin hypoglycemia.

DIAGNOSTIC AIDS IN GASTRIC DISORDERS: ELECTROGASTROGRAPHY

DIAGNOSTIC AIDS IN GASTRIC DISORDERS: ELECTROGASTROGRAPHY

DIAGNOSTIC AIDS IN GASTRIC DISORDERS: ELECTROGASTROGRAPHY

Electrogastrography (EGG) is the recording of gastric myoelectric activity. The technique usually uses superficial abdominal wall electrodes placed on the abdominal skin overlying the stomach. The recorded signal is called an electrogastrogram and usually consists of signals of 3 cycles per minute, reflecting gastric slow wave (pacemaker) activity, which set the frequency for subsequent gastric contractions. Meal ingestion increases the amplitude of the EGG signal by increasing gastric electrical activity and contractility or by distention of the stomach. EGG measures the frequency and regularity of gastric myoelectric activity, detects abnormal rhythms of gastric myoelectric activity, and assesses the amplitude or power increase after a meal.

Tuesday, November 3, 2020

DIAGNOSTIC AIDS IN GASTRIC DISORDERS: ANTRODUODENAL MANOMETRY

DIAGNOSTIC AIDS IN GASTRIC DISORDERS: ANTRODUODENAL MANOMETRY

DIAGNOSTIC AIDS IN GASTRIC DISORDERS: ANTRODUODENAL MANOMETRY

Antroduodenal manometry measures the pressures over time in the antrum and duodenum. The procedure uses a catheter placed either nasally or orally into the stomach and out the pylorus and into the small intestine. The catheter is placed either fluoroscopically or endoscopically. Recordings are obtained from 5 hours (stationary recording) to 24 hours (ambulatory recording), measuring pressures from the stomach and small intestine and the coordination of their contractions, both in the fasting condition and in response to meals. The three main indications for antroduodenal manometry are to evaluate (1) unexplained nausea and vomiting; (2) the cause of gastric or small bowel stasis (e.g., neuropathic or myopathic disorders); and (3) suspected chronic intestinal pseudoobstruction when the diagnosis is unclear.

DIAGNOSTIC AIDS IN GASTRIC DISORDERS: GASTRIC EMPTYING SCINTIGRAPHY

DIAGNOSTIC AIDS IN GASTRIC DISORDERS: GASTRIC EMPTYING SCINTIGRAPHY

DIAGNOSTIC AIDS IN GASTRIC DISORDERS: GASTRIC EMPTYING SCINTIGRAPHY

Gastric emptying can be assessed by several methods: scintigraphy, breath testing, and motility capsule testing. Gastric emptying scintigraphy has been the classic test for measuring gastric emptying of a radiolabeled meal. It is quantitative and physiologic. It is used to assess for gastric emptying disorders (either slow or rapid) in a symptomatic patient (in whom structural or mucosal disorders are often ruled out with upper endoscopic or upper gastrointestinal radiologic studies). It is primarily used to diagnose gastroparesis in a patient who has symptoms of this disorder, such as nausea, early satiety, and postprandial fullness. The test can also assess for rapid gastric emptying, which is seen in the dumping syndrome.

ENDOSCOPIC EVALUATION OF THE STOMACH: UPPER ENDOSCOPY

ENDOSCOPIC EVALUATION OF THE STOMACH: UPPER ENDOSCOPY

ENDOSCOPIC EVALUATION OF THE STOMACH: UPPER ENDOSCOPY

Gastroscopy, esophagogastroduodenoscopy, or upper endoscopy is a procedure performed by a gastroenterologist that allows for visualization of the esophagus, stomach, and duodenum. It is an essential procedure used for both the diagnosis and treatment of disorders of the upper gastrointestinal tract. The examination has evolved from using rigid and semirigid instruments with fiberoptics to currently flexible instruments and videoendoscopy. At the tip of the endoscope there is a color chip that gathers images that are electronically transmitted to a video processor and a monitor in the endoscopy examination room. A light at the tip of the endoscope allows for illumination. Images are taken during the examination and can be stored. Endoscopes, which are typically 8 to 10 mm wide, also have a channel for biopsy. At the control head there are buttons that allow for air insufflation and suctioning of fluid and air. There are a number of indications for upper endos- copy, including dysphagia, GERD, eosinophilic esophagitis, Barrett esophagus, gastric metaplasia, peptic ulcer disease, dyspepsia, H. pylori infection, celiac disease, and management of upper gastrointestinal malignant lesions. Upper endoscopy has several therapeutic uses, including hemostasis of bleeding ulcers, varices, Dieulafoy lesions, and arteriovenous malformations; removal of foreign objects; dilation of the esophagus; and stent placement.

AEROPHAGIA AND BELCHING

AEROPHAGIA AND BELCHING

AEROPHAGIA AND BELCHING

Aerophagia is described as objectively observed or measured air swallowing. Aerophagia usually leads to troublesome repetitive belching. These symptoms must occur at least 3 times a week for over 6 months to be considered a functional gastrointestinal disorder by the ROME criteria, a consensus gastrointestinal guideline. Aerophagia with belching is seen more commonly in developmentally disabled or anxious persons but can be seen in any population.

NAUSEA AND VOMITING

NAUSEA AND VOMITING

NAUSEA AND VOMITING

Having the symptom of nausea is a disagreeable experience that is difficult to define as well as distressing to experience. Nausea is often described as a sick feeling or a feeling of imminent vomiting. Nausea generally precedes vomiting; a notable exception to this is vomiting because brain tumors are present. Nausea may occur, continuously or in waves, without vomiting, especially if the stomach is empty. Salivation, pallor, tachycardia, faintness, weakness, and dizziness are frequent concomitants.

PYLORIC OBSTRUCTION; EFFECTS OF VOMITING

PYLORIC OBSTRUCTION; EFFECTS OF VOMITING

PYLORIC OBSTRUCTION; EFFECTS OF VOMITING

When the outlet of the stomach at the pylorus becomes narrowed to the point of interference with gastric emptying, the gastric musculature responds at first with increased peristalsis in an effort to build up sufficient pressure to overcome the resistance at the stomach’s pyloric end. At this stage, the patient experiences a sensation of “burning” in the epigastrium or left hypochondrium. With persisting obstruction and further stagnation of the stomach contents, both of ingested food and of gastric secretions, the stomach begins to dilate; the musculature becomes atonic, and very little peristaltic activity is present. The patient now complains of fullness, vomiting (in the late afternoon or evening or during the night) of undigested food eaten many hours earlier, and foul eructation. If the obstruction is unrelieved, vomiting becomes more frequent and more copious. With so little gastric contents now passing into the intestine because of the profound gastric atony and pyloric obstruction, the patient is not able to keep up with the fluid and electrolytes lost in the vomitus; dehydration, hypochloremia, hypokalemia, and alkalosis supervene. These, in turn, affect renal function, with the consequent development of oliguria, azotemia, and retention of other electrolytes. Clinically, the patient is weak, anorexic, and drowsy. Unless measures are instituted to correct the metabolic disorder and relieve the obstruction, the condition progresses to irreversible tissue damage and a fatal outcome.

FUNCTIONAL CHANGES IN GASTRIC MOTILITY AND SECRETION IN GASTRIC DISEASES

FUNCTIONAL CHANGES IN GASTRIC MOTILITY AND SECRETION IN GASTRIC DISEASES

FUNCTIONAL CHANGES IN GASTRIC MOTILITY AND SECRETION IN GASTRIC DISEASES

Gastric secretion and motility vary considerably from one individual to another and in the same individual from time to time. In the stomachs of subjects in whom no disease of the upper gastrointestinal tract can be demonstrated, the emptying time of a standard meal may vary over 100% from the average, and the concentration of HCl (acid) secreted in the basal state or in response to the standard stimuli ranges from 0 to 100 mEq/L or more.

HORMONAL FACTORS INFLUENCING GASTRIC ACTIVITY

HORMONAL FACTORS INFLUENCING GASTRIC ACTIVITY

HORMONAL FACTORS INFLUENCING GASTRIC ACTIVITY

The stomach has multiple functions, which include digestion, secretion of acid, storage of food, and absorption. It is also involved in the regulation of appetite and satiety. Gut peptides play a major role in each of these diverse functions by modifying secretion, motility, and appetite regulation. More than 100 bioactive peptides have been discovered and function in autocrine, paracrine, or neurocrine ways. Five peptides, gastrin, CCK, secretin, somatostatin, and motilin, directly influence gastric activity and are described here in more detail.

FACTORS INFLUENCING GASTRIC ACTIVITY

FACTORS INFLUENCING GASTRIC ACTIVITY

FACTORS INFLUENCING GASTRIC ACTIVITY

Motor and secretory activities of the stomach are modified, usually simultaneously and in the same direction, by a number of factors, both local (gastric) factors and external or systemic factors. Chief among them are the following:

NEUROREGULATION OF GASTRIC ACTIVITY

NEUROREGULATION OF GASTRIC ACTIVITY

NEUROREGULATION OF GASTRIC ACTIVITY

EFFERENT INNERVATION

The cortical areas that influence gastric motility and secretion are in the posterior orbital gyrus and the adjacent anterior cingulate gyrus. Connections are made, via the medial thalamic nuclei, with the hypothalamus, where fibers descend in the dorsal longitudinal fasciculus, at least as far as the dorsal nucleus of the vagus. Impulses from the anterior hypothalamic region act on the cranial parasympathetic nuclei in the brainstem, and the posterior hypothalamus makes connections with the neurons of the lateral horns of gray matter in the thoracolumbar segments of the spinal cord.

Tuesday, October 20, 2020

MECHANISM OF GASTRIC ACID SECRETION

MECHANISM OF GASTRIC ACID SECRETION

MECHANISM OF GASTRIC ACID SECRETION

The stomach has three anatomic regions, the fundus, body, and antrum. It is functionally divided into two glandular regions, the oxyntic and pyloric mucosae. The oxyntic gland mucosa contains parietal cells (that produce gastric acid (hydrogen chloride [HCl]) producing) and forms 80% of the fundus and body. The pyloric gland mucosa contains G cells and forms 20% of the antrum. Chief cells predominate at the base and secrete pepsinogen and leptin. The distinct neuroendocrine cell types and their physiologic functions are the (1) enterochromaffin cells, which contain atrial natriuretic peptide, somatostatin, serotonin, and adrenomedullin; (2) enterochromaffin-like cells, which contain histamine; (3) D cells, which contain somatostatin; and (4) cells that contain ghrelin and obestatin.

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