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ЗмістInvestigation of gastrointestinal disease
Table 1. Ultrasound scanning, CT and MRI in gastroenterology.
Table 2. Table 2. Table 3.
Table 3. Endoscopic retrograde cholangiopancreatography (ERCP)
Tests of infection
Tests of function
Table 4. Causes of vomiting.
Table 5. Extraintestinal causes of chronic or recurrent abdominal pain.
Table 6. Chronic or relapsing diarrhoea.
Table 8. Causes of lower gastrointestinal bleeding.
Table 9. Mechanisms producing jaundice.
Table 12. Causes of portal hypertension according to site of abnormality.
Table 13. Complication of portal hypertension.
Table 14. Causes of ascites.
Table 15. Appearance and causes of ascites.
Table 16. Factors precipitating hepatic encephalopathy.
Gastro-oesophageal reflux diseas
Fig. 4 Barrett's oesophagus
5 Treatment of gastro-oesophageal reflux disease: a 'step-down' approach
Table 1. Common cause of gastritis
Sumy State University
Internal Medicine Department
for 4th course students, 7 semester
Prepared by Orlovsky A. V., assistant, c.m.s.,
Murenets N. A., assistant
Sumy - 2009
Methodological Instruction to Lesson № 1.
Propedeutics in gastroenterology.
Working place: classroom, hospital wards.
Examples of Tests
Prepared by Orlovsky A. V., assistant, c. m. s.,
Murenets N. A., postgraduate
Short theoretic material
A wide range of tests are available for the investigation of patients with gastrointestinal symptoms. These can be classified broadly into tests of structure, tests of infection and tests of function.
TESTS OF STRUCTURE: IMAGING
Plain radiographs of the abdomen show the distribution of gas within the small and large intestines and are useful in the diagnosis of intestinal obstruction or paralytic ileus where dilated loops of bowel and (in the erect position) fluid levels are seen. The outlines of soft tissues such as liver, spleen and kidneys may be visible, and calcification of these organs as well as pancreas, blood vessels, lymph nodes and calculi may be detected. A chest radiograph shows the diaphragm, and erect films may detect subdiaphragmatic free air in cases of perforation. Unexpected pulmonary problems such as pleural effusions will also be revealed.
Barium sulphate is inert and provides good mucosal coating and excellent opacification. Water-soluble contrast is used to opacify bowel prior to abdominal computed tomography and in cases of suspected perforation but is less radio-opaque and is also irritant if aspirated into the lungs. Contrast studies are carried out under fluoroscopic control, which allows assessment of motility and correct patient positioning. The double contrast technique improves mucosal visualisation by using gas to distend the barium-coated intestinal surface.
Barium studies are useful for detecting filling defects, which may be intraluminal (e.g. food or faeces), intramural (e.g. carcinoma) or extramural (e.g. lymph nodes). Strictures, erosions, ulcers and motility disorders can all be detected.
Ultrasound, computed tomography (CT) and magnetic resonance imaging (MRI)
These are increasingly used in the evaluation of intra-abdominal disease. They are non-invasive and offer detailed images of the abdominal contents.
In recent years video endoscopy has replaced fibreoptic endoscopes. Images are displayed on a colour monitor. An increasing array of instruments can be passed down the endoscope to allow both diagnostic and therapeutic procedures.
Upper gastrointestinal endoscopy
After the patient has fasted for at least 4 hours, this is performed under light intravenous benzodiazepine sedation, or using only local anaesthetic throat spray. With the patient in the left lateral position the entire oesophagus (excluding pharynx), stomach and first two parts of duodenum can be seen. Indications, contraindications and complications are given in ^
Table 2. Table 3.
Using a longer endoscope (enteroscope) it is possible to visualise a large portion of the small intestine. Enteroscopy is of special value in the assessment of obscure, recurrent gastrointestinal bleeding.
Sigmoidoscopy can be carried out either in the outpatient clinic using a 20 cm rigid plastic sigmoidoscope or in the endoscopy suite using a 60 cm flexible instrument following a disposable enema for bowel preparation. When sigmoidoscopy is combined with proctoscopy, accurate detection of haemorrhoids, ulcerative colitis and distal colorectal neoplasia is possible. After full bowel cleansing it is possible to examine the entire colon and often the terminal ileum using a longer colonoscope. Indications, contraindications and complications of colonoscopy are listed in ^
Endoscopic retrograde cholangiopancreatography (ERCP)
Using a side-viewing duodenoscope, it is possible to cannulate the main pancreatic duct and common bile duct. The procedure is valuable in defining the ampulla of Vater, biliary tree and pancreas. Its main uses include investigation of obstructive jaundice, biliary pain and suspected pancreatic disease, such as chronic pancreatitis and pancreatic cancer. Obstruction of the common bile duct by stones can be treated by stone extraction after sphincterotomy, and strictures may be stented. The procedure is technically demanding and carries a significant risk of pancreatitis (3-5%), haemorrhage (4% after sphincterotomy) and perforation (1%).
Stool cultures are essential in the investigation of diarrhoea, especially when it is acute or bloody, to identify pathogenic organisms.
Detection of antibodies plays a limited role in the diagnosis of gastrointestinal infection caused by organisms such as Helicobacter pylori, Salmonella species and Entamoeba histolytica.
Non-invasive breath tests for H. pylori infection (detection of the radioisotope in expired air).
A number of dynamic tests can be used to investigate aspects of gut function, including digestion, absorption, inflammation and epithelial permeability. In the assessment of suspected malabsorption, blood tests (full blood count, erythrocyte sedimentation rate (ESR), folate, B12, iron status, albumin, calcium and phosphate) are essential.
A range of diverse radiological, manometric and radioisotopic tests exist for investigation of gut motility but many are research tests of limited value in daily clinical practice.
A careful barium swallow can give useful information about oesophageal motility. Oesophageal manometry, often in conjunction with 24-hour pH measurements, is of value in diagnosing cases of refractory gastro-oesophageal reflux, achalasia and non-cardiac chest pain.
Delayed gastric emptying (gastroparesis) may be responsible for some cases of persistent nausea, vomiting, bloating or early satiety. Endoscopy and barium studies are often normal.
The most common complaints of gastrointestinal diseases are:
Dysphagia is defined as difficulty in swallowing.
It should be distinguished from both globus sensation (in which anxious people feel a lump in the throat without organic cause) and odynophagia (which refers to pain with swallowing, usually resulting from oesophagitis due to gastrooesophageal reflux or candidiasis).
Dysphagia can be classified into oropharyngeal and oesophageal causes.
Oropharyngeal dysphagia: Difficulty in transferring food from the mouth to the esophagus, often associated with symptoms of nasopharyngeal regurgitation and pulmonary aspiration. It is typically caused by neuromuscular or structural disorders involving the oropharynx and proximal esophagus.
Esophageal dysphagia: The sensation of difficulty in passage of food down the esophagus. Oesophageal causes include structural disease (benign or malignant strictures) and dysmotility of the oesophagus.
Fig. 1. Investigation of dysphagia.
Heartburn is a specific burning sensation behind of sternum associated with regurgitation of gastric contents into the inferior portion of the esophagus.
Occasional heartburn is common in normal person, but frequent and severe heartburn is generally a manifestation of esophageal dysfunction.
Heartburn is most often associated with gastroesophageal reflux. It arises also in various diseases of the alimentary tract with hyperacidity – gastritis, peptic ulcer disease, cholecystitis, hiatus hernia, and in pregnancy.
Regurgitation is return of the part of swallowed food into the mouth due to backward movement of esophagus with open cardia without contraction of diaphragm and abdominal muscles.
Indigestion (dyspepsia) is a symptom that includes epigastric pain, heartburn, distension, nausea or 'an acid feeling' occurring after eating or drinking. The symptom is subjective and frequent. In many patients there is no demonstrable cause, but it may be associated with Helicobacter infection, peptic ulceration, acid reflux, and occasionally upper gastrointestinal malignancy.
Flatulence describes excessive wind. It is associated with belching, abdominal distension and the passage of flatus per rectum. It is only infrequently associated with organic disease of the gastrointestinal tract, but usually represents a functional disturbance, some of which is due to excessive swallowed air. In some patients it is clearly related to certain foods, such as vegetables.
Nausea and Vomiting
This term refers to loss of appetite, although some patients with GI disease have an appetite for food but feel full after just a few mouthfuls. It often indicates important pathology, particularly in the upper GI tract.
Abdominal pain is important and the leading symptom in diseases of digestive system.
Important factors in the assessment of abdominal pain:
Diarrhoea is the passage of more than 200 g of stool daily.
Acute diarrhea – this is extremely common and usually due to faecal-oral transmission of bacterial toxins, viruses, bacteria or protozoan organisms. Infective diarrhea is usually short-lived and patients who present with a history of diarrhea lasting more than 10 days rarely have an infective cause. A variety of drugs, including antibiotics, cytotoxic drugs, proton-pump inhibitors and NSAIDs, may be responsible for acute diarrhea.
Chronic diarrhoea – the most common cause is irritable bowel syndrome, which can present with increased frequency of defaecation and loose, watery stools. Diarrhoea rarely occurs at night and is most severe before and after breakfast. At other times the patient is constipated. The stool often contains mucus but never blood, and 24-hour stool volume is less than 200 g.
Table 7. Causes of constipation.
Constipation is defined as infrequent passage of hard stools. Patients may also complain of straining, a sensation of incomplete evacuation and either perianal or abdominal discomfort. Constipation may be the end result of many gastrointestinal and other medical disorders.
The onset, duration and characteristics are important, e.g. a neonatal onset suggests Hirschsprung's disease, while a recent change in bowel activity in middle age should raise the suspicion of organic disorders such as colonic carcinoma.
Weight loss may be 'physiological' due to dieting, exercise, starvation, or the decreased nutritional intake which accompanies old age. Alternatively, weight loss may signify disease; that greater than 3 kg over 6 months is significant.
Fig. 2. Some important causes of weight loss.
Gastrointestinal disease. Almost any disease of the gastrointestinal tract can cause weight loss. Dysphagia and gastric outflow obstruction cause defective dietary intake. Malignancy at any site may cause weight loss by mechanical obstruction, anorexia or cytokine-mediated systemic effects. Malabsorption from pancreatic diseases or small bowel causes may lead to profound weight loss with specific nutritional deficiencies. Inflammatory diseases such as Crohn's disease or ulcerative colitis cause anorexia, fear of eating and loss of protein, blood and nutrients from the gut.
Acute upper gastrointestinal haemorrhage
This is the most common gastrointestinal emergency, accounting for 50-120 admissions to hospital per 100 000 of the population each year in the United Kingdom.
Figure 3.Causes of acute upper gastrointestinal haemorrhage.
Haematemesis may be red with clots when bleeding is profuse, or black ('coffee grounds') when less severe. Syncope may occur and is due to hypotension from intravascular volume depletion. Symptoms of anaemia suggest chronic bleeding.
Melaena is the term used to describe the passage of black, tarry stools containing altered blood; this is usually due to bleeding from the upper gastrointestinal tract, although haemorrhage from the right side of the colon is occasionally responsible. The characteristic appearance is the result of the action of digestive enzymes and of bacteria upon haemoglobin. Severe acute upper gastrointestinal bleeding can sometimes cause maroon or bright red stool.
Lower gastrointestinal bleeding
This may be due to haemorrhage from the small bowel, colon or anal canal. It is useful to distinguish those patients who present with profuse, acute bleeding from those who present with chronic or subacute bleeding of lesser severity
Occult gastrointestinal bleeding
'Occult' means that blood or its breakdown products are present in the stool but cannot be seen. Occult bleeding may reach 200 ml per day, cause iron deficiency anaemia and signify serious gastrointestinal disease. Any cause of gastrointestinal bleeding may be responsible but the most important is colorectal cancer, particularly carcinoma of the caecum which may have no gastrointestinal symptoms.
In clinical practice, investigation of the gastrointestinal tract should be considered whenever a patient presents with unexplained iron deficiency anaemia.
Digestion and absorption of nutrients is a complex, highly coordinated and extremely efficient process; normally, less than 5% of ingested carbohydrate, fat and protein is excreted in the faeces. Diarrhoea and weight loss in patients with a normal diet should always lead to the suspicion of malabsorption.
The symptoms of malabsorption are diverse in nature and variable in severity. A few patients have apparently normal bowel habit but diarrhoea is usual and may be watery and voluminous. Bulky, pale and offensive stools which float in the toilet (steatorrhoea) signify fat malabsorption. Abdominal distension, borborygmi, cramps, weight loss and undigested food in the stool may be present. Some patients complain only of malaise and lethargy. In others, symptoms related to deficiencies of specific vitamins, trace elements and minerals (e.g. calcium, iron, folic acid) may occur.
Aetiology and pathogenesis
Malabsorption results from abnormalities of the three processes which are essential to normal digestion:
1. Intraluminal maldigestion occurs when deficiency of bile or pancreatic enzymes results in inadequate solubilisation and hydrolysis of nutrients. Fat and protein malabsorption results. This may also occur in the presence of small bowel bacterial overgrowth.
2. Mucosal malabsorption results from small bowel resection or conditions which damage the small intestinal epithelium, thereby diminishing the surface area for absorption and depleting brush border enzyme activity.
3. 'Postmucosal' lymphatic obstruction prevents the uptake and transport of absorbed lipids into lymphatic vessels. Increased pressure in these vessels results in leakage into the intestinal lumen, leading to protein-losing enteropathy.
Fig. 4. Possible physical consequences of malabsorbtion.
Major manifestation of liver disease
Investigation of patients with abnormal liver function tests starts with a clinical history and physical examination. Non-specific symptoms such as fatigue and weakness are common in patients with chronic liver disease. Clinical feature of jaundice, pruritus, ascites, gastrointestinal bleeding and hepatic encephalopathy should be sought. The patient should be questioned regarding alcohol intake and previous drug exposure. The physical examination specifically addresses whether or not there are cutaneous manifestations of chronic liver disease such as palmar erythema, spider telangiectasia. Abdominal examination may reveal hepatosplenomegaly and ascites. Often patients are truly asymptomatic or at most suffer from the non-specific symptoms.
Peripheral stigmata (signs) of chronic liver disease
Skin, nails and hands
Endocrine - due to excess oestrogens
Jaundice refers to the yellow appearance of the skin, sclerae and mucous membranes resulting from an increased bilirubin concentration in the body fluids. It is usually detectable clinically when the plasma bilirubin exceeds 50 µmol/l.
Unconjugated bilirubin is produced (425-510 mmol, 250-300 mg daily) from the catabolism of haem after removal of its iron component. Bilirubin in the blood is normally almost all unconjugated and, as it is not water-soluble, it is bound to albumin and does not pass into the urine. Further metabolism of bilirubin is shown in Figure 5.
Unconjugated bilirubin is conjugated by the endoplasmic reticulum enzyme, glucuronyl transferase, into bilirubin mono- and diglucuronide. These bilirubin conjugates are water-soluble and exported into the bile via specific carriers on the hepatocyte membrane. Conjugated bilirubin is metabolised by colonic bacteria to form stercobilinogen, which may be further oxidised to stercobilin. Both stercobilinogen and stercobilin are then excreted in the stool. A small amount of stercobilinogen (4 mg/day) is absorbed from the bowel, passes through the liver and is excreted in the urine, where it is known as urobilinogen or, following further oxidisation, urobilin.
This results from increased destruction of red blood cells, or their precursors in the marrow, causing increased bilirubin production. Jaundice due to haemolysis is usually mild because a healthy liver can excrete a bilirubin load six times greater than normal before unconjugated bilirubin accumulates in the plasma. Increased excretion of bilirubin and hence stercobilinogen leads to normal-coloured or dark stools, and increased urobilinogen excretion causes the urine to turn dark on standing as urobilin is formed. Pallor due to anaemia and splenomegaly due to excessive reticulo-endothelial activity are usually present. The plasma bilirubin is usually less than 100 µmol/l and the liver function tests are otherwise normal. There is no bilirubinuria because the hyperbilirubinaemia is predominantly unconjugated. The blood count and film may show evidence of haemolytic anaemia.
Hepatocellular jaundice results from an inability of the liver to transport bilirubin into the bile, occurring as a consequence of parenchymal liver disease. Bilirubin transport across the hepatocytes may be impaired at any point between uptake of unconjugated bilirubin into the cells and transport of conjugated bilirubin into the canaliculi. In addition, swelling of cells and oedema resulting from the disease itself may cause obstruction of the biliary canaliculi. In hepatocellular jaundice the concentrations in the blood of both unconjugated and conjugated bilirubin increase, perhaps because of the variable way in which bilirubin transport is disturbed.
In unrelieved cholestasis jaundice tends to become progressively more and more severe because conjugated bilirubin is unable to enter the bile canaliculi and passes back into the blood, and also because there is a failure of clearance of unconjugated bilirubin arriving at the liver cells.
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