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PYLORIC STENOSIS (GASTRIC OUTLET OBSTRUCTION)

Pyloric stenosis is rarely due to stenosis at the pylorus. More commonly, the obstruction is on one side of the pylorus, either in the first part of the duodenum due to chronic scarring from a duodenal ulcer or in the antrum due to a carcinoma. True pyloric stenosis can arise from a pyloric channel ulcer or very rarely from a congenital web or adult hypertrophic pyloric stenosis. Some instances of gastric stenosis are caused by inflammatory oedema surrounding an active ulcer and these often resolve with conservative treatment. The common causes of gastric outlet obstruction are:

•         chronic duodenal ulceration/fibrosis;

•         antral gastric carcinoma;

•         carcinoma of the head of the pancreas.

Barium meal showing gastric outlet obstruction caused by fibrosis following healing of chronic duodenal ulcer.

Barium meal showing hour-glass deformity caused by a lesser curve ulcer in the middle third of the stomach. The deformity resolved with medical treatment. However, some of these deformities are fibrotic in nature (contractures) when obstructive symptoms persist depite ulcer healing. These require dilatation or surgical treatment.

Rare causes include a variety of benign tumours, lymphomas, Crohn's disease, duodenal haematoma, adult pyloric hypertrophy, annular pancreas and mucosal diaphragm. Benign pyloric stenosis usually occurs in a patient with long-standing symptoms of ulceration. Vomiting and anorexia supervene. The typical vomiting of pyloric stenosis is projectile and the vomitus is characterized by an absence of bile and the presence of partially digested food eaten hours or even days previously. With repeated vomiting and failure to eat, the patient often becomes constipated, although in some cases diarrhoea may develop. Examination usually shows an underweight patient, dehydration and often a degree of iron-deficiency anaemia. A succussion splash may be present and visible contractions passing across the upper abdomen from left to right may be observed on inspection. Prolonged vomiting of gastric contents results in characteristic electrolyte disturbances. Initially, the major loss is fluid rich in hydrogen and chloride ions so that dehydration is accompanied by hypochloraemic alkalosis. At this stage the serum sodium is usually normal and hypokalaemia may not be obvious. More marked metabolic changes supervene as a result of continued losses and secondary changes in renal function. Initially, the urine is characterized by a low chloride content and is appropriately alkaline because of enhancedbicarbonate excretion compensating for the metabolic alkalosis but at the expense of sodium. If gastric losses continue, the patient becomes progressively hypovolaemic and hyponatraemic. In an attempt to conserve circulating volume, sodium is retained by the kidneys and exchanged for hydrogen ions and potassium. At this late stage, the patient has a metabolic alkalosis and, paradoxically, an acid urine. As a secondary effect of the alkalosis, the concentration of plasma ionized calcium may fall so that disturbances of consciousness and tetany may be apparent. The priority in management of the advanced case of pyloric stenosis is correction of the fluid and electrolyte

CT showing pyloric obstruction by an antral carcinoma.

disturbances. Rehydration is achieved by saline infusions with potassium supplements as indicated by electrolyte determinations. Gastric lavage is performed with a widebore tube using isotonic saline daily until the returning

fluid becomes clear. The surgical treatment of pyloric stenosis caused by duodenal ulceration/fibrosis is truncal vagotomy and posterior gastroenterostomy. In western countries the majority of cases of gastric outlet obstruction are caused by distal gastric cancer.

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PEPTIC ULCER DISEASE

Worldwide, duodenal ulcers are more common than gastric ulcers and there is a significantly higher incidence of duodenal ulceration in males of all age groups. Dietary factors, drug ingestion (NSAIDs) and smoking are important in the aetiology. The most common causes are environmental ulcerogens (chemical or infective) acting in consort with factors that impair gastric mucosal resistance to injury and healing of mucosal lesions thereby leading to chronicity. The most important infective agent responsible for peptic ulceration (duodenal and gastric) is H. pylori. Not all patients who are infected with this organism develop ulcers. The risk of peptic ulceration is determined by the severity of the H. pylori-associated gastritis. The organism impairs the mucus-bicarbonate protective layer and is responsible for the chronicity and the tendency to relapse, as evidenced by the permanent healing when infection is eradicated by appropriate antibiotic therapy. Strains of H. pylori with vacA signal-sequence type S1A are associated with severe gastritis and duodenal ulcers, whereas vacA S2 strains cause mild gastric mucosal inflammation without ulceration. The most important group of chemical ulcerogens is constituted by aspirin and other NSAIDs. These are the most common cause of peptic ulceration in H. pylorinegative individuals. However, these drugs are not specific gastroduodenal ulcerogens as they also induce damage and ulceration of the small and large intestine. There are a number of differences between ulcers caused by H. pylori and those caused by NSAIDs.

•      NSAID-associated ulcers are more likely to cause gastrointestinal haemorrhage. Thus, overall 75% of patients with upper gastrointestinal bleeding from peptic ulcers are on NSAID medication.

•      Gastric ulcers caused by H. pylori are rarely encountered on the greater curve (5%), being most commonly situated on the lesser curve (85%). In contrast, NSAIDassociated ulcers (in the absence of H. pylori infection) occur along the lesser and greater curvatures in 35 and 45% respectively.

Infection with H. pylori and use of NSAIDs is encountered in 20% of patients. Eradication of the infection does not influence the healing and recurrence of gastric and duodenal ulcers associated with chronic NSAID medication.

Although some 30-40% of duodenal ulcer patients exhibit acid hypersecretion, the overlap between the acid secretory status of these patients and controls is considerable. Gastric acid is an important factor in the chronicity of the disease and suppression of acid secretion by medical or surgical treatment undoubtedly permits healing in the majority of patients. The secretory characteristics of the usual duodenal ulcer patient include increased acid secretory capacity, increased gastrin response to food and insulin, increased sensitivity to gastrin and defective inhibition of acid secretion. There is an increased concentration of pepsins in the gastric juice of patients with duodenal ulceration, especially pepsin I (the most mucolytic). The disruption of the mucus-bicarbonate layer by pepsin I exposes the underlying mucosa to injury by ulcerogens and impairs healing by removal of the protective mucus cap (blister effect). Stress induces gastric hypersecretion and can lead to acute (stress) ulceration in seriously ill patients.

Upper gastrointestinal endoscopy showing duodenal ulcer.

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UPPER GASTROINTESTINAL BLEEDING

Bleeding from the gastrointestinal tract may be caused by lesions located in the foregut (oesophagus, stomach and duodenum), midgut (small bowel up to mid transverse colon) and hindgut (distal colon and rectum). The bleeding  may be acute when the patient presents with hypovolaemia, or chronic when the clinical picture is that of symptomatic anaemia. The common causes of acute upper gastrointestinal haemorrhage are:

• •         chronic peptic ulceration;
• •         NSAID-induced bleeding;
• •         oesophagogastric varices.

Irrespective of the cause, the vomited blood (haematemesis) may be fresh (in severe active bleeding as from ruptured oesophageal varices) or chemically altered (because acid digestion simulates 'coffee grounds'). Extensive gastrointestinal bleeding also gives rise to the passage of black  foul-smelling liquid faeces known as melaena. Patients taking NSAIDs have a threefold risk of gastrointestinal haemorrhage, surgery and death compared with non-users. The risk from bleeding is greatest in:

• •         first few months of treatment;
• •         the elderly (> 65 years);
• •         patients with concomitant steroid use;
• •         patients with a previous history of gastrointestinal events.

Of all the NSAIDs known to cause bleeding or perforation, aspirin produces the most damage. There is some evidence that the newer NSAIDs (e.g. nabumetone) that selectively inhibit cyclooxygenase-2 are less damaging to the gastroduodenal mucosa and hence significantly less ulcerogenic but they appear to be less effective clinically in relieving pain. The other problem with NSAIDs is the development of non-specific ulceration of the upper small intestinal mucosa, which can bleed and perforate. Gastrointestinal haemorrhage may be caused by both benign and malignant tumours. However, acute haemorrhage is more commonly associated with benign  lesions such as neurofibromatosis and mesenchymal (smooth muscle) tumours. Malignant tumours (carcinoma and lymphomas) more usually cause chronic blood loss with the development of iron-deficiency anaemia, although massive bleeding may be precipitated by combination chemotherapy (see later). Life-threatening bleeding or perforation from necrosis of the tumour may complicate chemotherapy for gastrointestinal tumours,  especially lymphomas. Stress ulceration is usually encountered in critically ill patients nursed in the intensive care unit, although its incidence has declined.

Other causes of acute upper gastrointestinal bleeding include Dieulafoy's lesion, portal hypertensive gastropathy and watermelon stomach.

•         Dieulafoy's lesion (exulceration simplex) consists of a nodule containing a visible vessel covered with normal mucosa. Treatment is by endoscopic electrocoagulation or sclerotherapy.

•         Portal hypertensive gastropathy develops in some patients with cirrhosis and portal hypertension with progressive liver damage and affects predominantly the fundus but may be generalized.

•         Diffuse vascular ectasia (watermelon stomach) consists of ectatic mucosal sacculated vessels in the lamina propria traversing the antrum and sometimes the duodenum. The endoscopic appearance bears some resemblance to the stripes of a watermelon. The bleeding is often recurrent requiring multiple transfusions. Portal hypertensive gastropathy and diffuse gastric vascular ectasia are probably related.

The treatment of acute upper gastrointestinal haemorrhage is based on the following principles.

•         Resuscitation: volume replacement with crystalloids, colloids and blood.

•         Early endoscopy: for diagnosis and endoscopic control of bleeding.

•         Combined management by gastroenterologists and surgeons with early recourse to surgery if bleeding continues or recurs.

Sometimes there is clear evidence of upper gastrointestinal bleeding without apparent cause. In these patients, mesenteric angiography and small-bowel enteroscopy often locate the source of the bleeding.

Chronic gastrointestinal bleeding is unnoticed by the patient and for this reason is referred to as occult. The constant drain results in depletion of iron stores and thus the development of iron-deficiency (hypochromic microcytic) anaemia. When discovered this must always be investigated as follows:

•         faecal occult blood;

•         upper gastrointestinal endoscopy;

flexible sigmoidoscopy and barium enema or colonoscopyif upper gastrointestinal endoscopy is negative. Carcinoma of the caecum and ascending colon most commonly presents as iron-deficiency anaemia as does carcinoma of the stomach.

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DYSPEPSIA

Gastroduodenal disease produces varied symptoms described by the term 'dyspepsia'. Dyspeptic symptoms are extremely common in the general population. An agreed international definition is 'episodic or persistent abdominal symptoms, often related to the intake of food, which patients or physicians believe to be due to disorders of the proximal portion of the digestive tract'. The symptoms included in this generic definition of dyspepsia are:

•         pain or discomfort in the upper abdomen;

•         nausea and vomiting;

•         early satiety;

•         epigastric fullness and regurgitation.

There are two categories of dyspepsia: organic and nonorganic (no demonstrable focal lesion). The prevalence of organic dyspepsia increases above the age of 40-45 years. There are four subgroups of dyspeptic patients based on the predominant symptoms:

•          ulcer-like;
•          reflux-like;
•          dysmotility-like;
•          non-specific.

Symptoms alone do not differentiate between organic and non-organic disease. Hence history does not always predict the underlying cause of dyspepsia and for this reason investigation by endoscopy is necessary for certain

groups:

•          patients who are H. pylori positive;
•          patients with a history of using non-steroidal anti-inflammatory drugs (NSAIDs);
•          patients with alarm/sinister symptoms (loss of appetite, weight loss, bleeding).

Alarm symptoms

Loss of appetite, weight loss, recent-onset dyspepsia, constant upper abdominal pain and evidence of bleeding are regarded as alarm or sinister symptoms and thus require urgent endoscopy, particularly if the patient is over 40 years of age. Weight loss and loss of appetite associated with early satiety/abdominal discomfort are suspicious of a gastric neoplasm.

Investigations

Endoscopy and radiology

Upper gastrointestinal endoscopy is necessary for the following

groups of patients.

•         Individuals > 45 years old testing positive for H. pylori, with persistent symptoms despite eradication treatment.

•         Individuals > 45 years old, never investigated, H. pylori-negative and no intake of NSAIDs, with persistent symptoms despite acid-lowering treatment.

•         Individuals > 45 years old with a previous history of gastric ulcer, no H. pylori testing or H. pylori test negative, with persistent symptoms despite acid-lowering drugs.

•         Gastrointestinal bleeding: acute and chronic. Contrast swallow and meal examination is seldom used in the investigation of patients with dyspepsia because endoscopy has a higher diagnostic yield and permits biopsy with histological diagnosis. However, contrast radiology is needed in:

•         patients with gastric cancer undergoing surgery (precise location of lesion);

•         patients with hiatus hernia undergoing surgery (type and size of hernia);

•         suspected perforation/anastomotic leak (water-soluble contrast must be used). Barium studies are unreliable in the assessment of a patient with acute upper gastrointestinal bleeding. Endoscopy is the preferred investigation in this situation.

Tests for H. pylori infection

The most commonly performed are the rapid ureasetests, which are carried out on endoscopic biopsies. These tests use kits such as the Campylobacter-like organism (CLO), Hpfast and Pyloritec and provide a result within 3 h of endoscopy. Other tests include culture in a microaerobic environment, polymerase chain reaction, histology of the antrum and corpus (Giemsa or Warthin-Starry silver stain), 13C urea breath test, and serology for detection of H. pylori-specific antibodies.

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WEIGHT LOSS IN GERIATRIC

Weight loss improves many of the adverse health outcomes associated with obesity, including preventing or delaying the onset of diabetes, improving blood sugar control in those with diabetes, reducing low-density lipoprotein (bad cholesterol), raising high-density lipoprotein (good cholesterol), improving hypertension, improving symptoms of osteoarthritis, and providing an improved sense of well-being. Individuals must only lose a small percentage of their weight (B5–10%) to begin seeing these improved health outcomes. As many people know from their personal experiences, weight loss is difficult and lost weight is often regained for a variety of reasons. Returning to the original concept of energy balance, the formula for weight loss is predictable. To lose weight, energy expenditure must be greater than energy consumption.

The first recommendation therefore is lifestyle modification with a combination of increased exercise and decreased intake (diet modification). The amount of exercise needed to lose weight is variable. Current recommendations from the US Surgeon General is for adults to engage in an activity of moderate intensity (such as brisk walking) for 30 min daily or more strenuous activities (such as jogging) for 15–20 min daily. Additional exercise will increase energy expenditure and may result in further favorable health outcomes. Caloric restriction through dieting is also essential for losing weight. The ideal diet has not yet been established, but the principle of reducing caloric intake along with ease of long-term compliance remains the cornerstone of any diet. The American Dietetic Association currently changes their recommendation periodically in an effort to determine the most helpful, practical diet, based on current data. The problem with short-term dieting is that weight loss can rarely be maintained once the diet has ended. Exercise may help maintain some of the weight loss.

Some medications exist for weight loss. These medications are moderately effective, although they often have side effects that limit their widespread use. The history of diet medications has been plagued with adverse health outcomes, including valvular heart disease and heart arrhythmias. Many of these medications have focused on increasing the metabolic rate or suppressing appetite. One such medication that has been approved for use in the United States for weight loss is orlistat. This medication uses a novel mechanism to prevent the body from digesting a portion of the fat that has been ingested, thereby lowering the number of 280 Obesity calories absorbed. The undigested fat is excreted out of the body via bowel movements. This medication has minimal systemic side effects since there is little absorption; however, it results in uncomfortable changes in bowel movements such as oily discharge and increased frequency of bowel movements. Another medication available for weight reduction is sibutramine. The mechanism of action is inhibition of norepinephrine, dopamine, and serotonin reuptake, resulting in weight loss from appetite suppression, possibly combined with an increase in thermogenesis from stimulation of adipose tissue. Use of this medication combined with diet and exercise results in modest reduction (B7%) in weight at 1 year, although sustained weight loss at 2 years is less robust. Because of the high failure rates of lifestyle modification and medical therapies, surgical approaches for weight loss are becoming widely available. The most successful of these surgeries is the gastric bypass. It works by decreasing the size of the stomach, to achieve satiety earlier, as well as by bypassing part of the small intestine, which results in fewer calories being absorbed. This surgery is very effective in achieving weight loss and improving many of the obesity-related diseases. Complications include nutritional deficiencies, postoperative wound infections, leaks at the surgical sites, and postoperative mortality (B1.5%). Due to these risks, this therapy should be reserved for patients who are morbidly obese (BMI 440 or BMI 435), who have obesityrelated diseases, and who have failed behavioral modification therapies.

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THE IMMUNE MECHANISM

The actual body's defence mechanism is a remarkable safeguard procedure. That creates quick, particular, and also safety responses from the range likely pathogenic microbes in which inhabit the entire world by which we reside. The tragic examples of acquired immunodeficiency syndrome (AIDS) and the inherited severe combined immunodeficiencies (SCID) graphically show the outcomes of a nonfunctional adaptive body's defence mechanism. HELPS individuals and also young children using SCID frequently tumble unwilling recipient to be able to attacks which might be of minimal end result to be able to individuals with normally functioning immune system techniques. The actual body's defence mechanism even offers a role in the rejection of growths and also, when dysregulated, may well promote a few autoimmune illnesses, which include insulin-dependent diabetes mellitus, several sclerosis, rheumatism, systemic lupus erythematosus, and also inflammatory intestinal illnesses, and the like.

Fundamental Immunology offers since its goal this authoritative presentation with the simple portions of this body's defence mechanism, with the implies through which this mechanisms of protection take action throughout many clinical problems, which include healing coming from infectious illnesses, rejection of growths, transplantation of structure and also internal organs, autoimmunity as well as other immunopathologic problems, and also allergy, and also how the mechanisms of protection may be marshaled by means of vaccination to offer security versus microbial pathogens.

The objective of this kind of beginning page is always to produce audience having a basic launch to the existing perception of this body's defence mechanism. It should be of unique relevance for anyone having a constrained backdrop throughout immunology, offering all of them using the preparing meant for succeeding chapters with the book. Instead of offering comprehensive sources on this page, each one of the theme headings will certainly reveal this chapters in which cope in more detail using the theme under conversation. People chapters is not going to provide an prolonged treatment with the theme, nevertheless will even provide this readers having a extensive research listing.

Major Guidelines of Immunity

The actual key rules with the immune system reaction are generally:

•           Elimination of the many microbial agencies throughout the nonspecific safety mechanisms with the inborn body's defence mechanism.

•           Cues on the inborn body's defence mechanism advise this tissues with the adaptive body's defence mechanism regarding unique appropriate to manufacture a reaction and also the type of respond to produce.

•           Cells with the adaptive body's defence mechanism show exquisitely particular recognition of unusual antigens and also mobilize effective mechanisms pertaining to removal of microorganisms displaying such antigens.

•           The body's defence mechanism displays memory space of its past responses.

•           Tolerance of self-antigens.

The others on this starting page will certainly illustrate temporarily this molecular and also cellular time frame with the program and also how most of these key traits with the immune system reaction may be discussed.

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