Mouth and oesophagus

Digestion begins in the mouth where food is chewed and moistened with saliva. The salivary fluid is a cocktail of enzymes, including amylase and lingual lipase and bicarbonate and lysozyme. Saliva is secreted by the parotid, submandibular and sublingual glands, with a small contribution from the labial glands on the inner aspects of the lips.

Swallowing is controlled by a medullary centre in the brainstem which relays to and from the pharynx and oesophagus via the glossopharyngeal and vagus nerves (Fig. 7.2). There is also an intrinsic innervation within the smooth muscle of the oesophagus. There are three phases to the swallowing reflex: oral, pharyngeal and oesophageal. During the oral phase, the tongue presses the bolus up against the hard palate and drives the food into the pharynx. In the pharyngeal phase, the respiratory tract closes off, the upper pharyngeal sphincter (cricopharyngeus) relaxes and the upper, middle and lower pharyngeal constrictors propel the food into the oesophagus. In the oesophageal phase, a powerful peristaltic wave propels the bolus towards the stomach. The lower oesophageal sphincter has intrinsic tone that prevents regurgitation of the gastric contents: it relaxes in advance of the peristaltic wave and remains relaxed for a few seconds after the wave has passed.

Fig. 7.2 The innervation of the oesophagus.

Difficulty swallowing (dysphagia) may be caused by damage to the neural control, abnormalities of the oesophageal muscle or obstruction of the lumen.

Stomach

The churning action of the antrum continues the mixing process started in the mouth and prepares food for its journey into the duodenum. The parietal cells in the body of the stomach (Fig. 7.3) secrete hydrochloric acid, which sterilises the meal, and intrinsic factor, which is necessary for the absorption of vitamin B₁₂ in the terminal ileum. The chief cells secrete pepsinogen which is converted to the proteolytic enzyme pepsin by the low pH of the stomach lumen. The secretion of acid is stimulated by the vagus nerve, distension of the stomach with food and the secretion of the hormone gastrin from the G-cells of the gastric antrum (Fig. 7.4). A mucous layer coats the stomach mucosa, protecting it from self-inflicted injury by acid and pepsin.

Fig. 7.3 Cells found in the mucosa of the stomach body are responsible for the principal gastric secretions.

Fig. 7.4 The control of gastric acid secretion by food, vagal stimulation and gastrin. Pepsinogen is activated to pepsin at low pH.

Regurgitation of gastric contents into the oesophagus is prevented by an antireflux mechanism at the gastro-oesophageal junction. This includes the intrinsic tone of the lower oesophageal sphincter, the flap-valve effect of the angle of His and the squeezing effect of intra-abdominal pressure on the small segment of oesophagus that protrudes through the diaphragm into the abdomen (Fig. 7.5). If one or more of these antireflux mechanisms breaks down, gastric contents may regurgitate into the lower oesophagus, damaging the mucosa and causing heartburn.

Fig. 7.5 The antireflux mechanism comprises the intrinsic tone of the lower oesophageal sphincter, the acute angle formed at the oesophagogastric junction (angle of His) and the pressure on the intra-abdominal oesophagus.

Small intestine

The small intestine comprises the duodenum, the jejunum and the ileum. It fills most of the anterior abdomen and is framed by the ascending, transverse and descending colon. Blood is supplied by the superior mesenteric vessels (Fig. 7.6). The principal role of the small intestine is digestion and absorption, which is achieved by a combination of macroscopic and microscopic folds creating a vast absorptive area (Fig. 7.7).

Fig. 7.6 The blood supply of the small intestine, colon, sigmoid and rectum.

Fig. 7.7 The large surface area of the small intestine is formed by the duodenal folds, the villi and the microvillus membrane of the enterocyte.

Most of the enzymes necessary for the digestion of fat, protein and carbohydrate are present in the duodenum. Enterocytes develop in the base of the crypts of Lieberkuhn and migrate to the tip of the finger-shaped villi (Fig. 7.8). Both the enterocyte’s capacity to produce specialised digestive enzymes on the brush border membrane and its absorptive properties develop progressively as the cell migrates towards the villous tip, at which point these functions are maximally developed.

Fig. 7.8 Duodenal enterocytes develop in the crypts and migrate towards the villus tip.

Carbohydrate digestion is initiated by salivary and pancreatic amylase. Enzymes, such as lactase and sucrase, on the brush border membranes of the enterocytes, complete the digestion of complex polysaccharides and disaccharides to monosaccharides, which are then transported through the enterocyte by specialised transporters on the brush border and basolateral membranes (Fig. 7.9). Pancreatic lipase hydrolyses triglycerides to fatty acids and monoglycerides. These products are emulsified by bile acids which help form micelles. The micelles are then taken up at the brush border membrane and diffuse passively into the enterocyte, where the triglyceride is reconstituted (Fig. 7.9). These triglycerides, as well as absorbed cholesterol, are formed into fat aggregates (chylomicrons) that are absorbed into the lymphatics and discharged into the circulation through the thoracic duct. The fat-soluble vitamins A, D, K and E are absorbed in a similar manner to other lipids.

Fig. 7.9 Digestion in the small intestine. Digestion of complex carbohydrates occurs in the lumen and at the brush border membrane. Monosaccharides can then be absorbed through the brush border membrane into the portal circulation. Fat digestion occurs in the lumen and triglyceride is reconstituted in the enterocyte before absorption. Proteins are digested in the lumen and at the brush border membrane. Amino acids are then absorbed into the enterocyte and portal circulation.

Proteolysis is initiated in the stomach by pepsin, yet the bulk of protein digestion is mediated by trypsin and other pancreatic peptidases in the small intestine (Fig. 7.9). The action of these enzymes produces small peptides with 4–6 amino acids that undergo further processing to amino acids, dipeptides and tripeptides by oligopeptidases on the enterocyte brush border membrane. These are absorbed into the enterocytes where the final digestion to single amino acids occurs. The amino acids are transported to the liver by the portal blood.

The addition of pancreatic juice and bile, which are secreted through the ampulla of Vater, modifies and enriches the chyme (semi-liquid food) entering the duodenum from the stomach.

Absorption of nutrients occurs in the jejunum and ileum, along with the production and secretion of a range of hormones. The terminal ileum absorbs vitamin B₁₂ and bile acids.

The small intestine has a considerable functional reserve and only fails when there is less than 100 cm of bowel following surgical resection.

Table 7.1 lists the principal effects of gastrointestinal hormones.

Table 7.1 Principal effects of gastrointestinal hormones

Colon

The ileum enters the caecum through the ileocaecal valve, which prevents reflux of colonic contents into the small intestine. Whereas the small intestine is relatively microbe free, the colon is heavily colonised by bacteria. Approximately 1.5 litres of ileal fluid empties into the caecum each day. Most of this effluent is reabsorbed as it passes through the ascending, transverse and descending colon. The colon concentrates the ileal outflow so that the daily stool output on a Western diet averages 200 g; 75% of stool weight is water and the remainder is unabsorbed food and bacteria. The colonic mucosa is rich in glands producing mucus, which provides constant lubrication for the passage of faeces and protects the mucosa from bacterial enzymes. The rectum is the storage organ for stool.

Infection or inflammation of the colonic mucosa may provoke fluid and electrolyte secretion and interfere with absorption, causing diarrhoea and dehydration. Diarrhoea may also occur in small bowel disease when the volume of ileal effluent exceeds the colon’s absorptive capacity.

Liver

The liver is the largest intra-abdominal organ. The falciform ligament divides the liver into a large right lobe and a smaller left lobe (Fig. 7.10). Two smaller lobes, the anterior quadrate and posterior caudate, are squeezed between the left and right lobes on the visceral surface of the liver.

Fig. 7.10 The gross anatomy of the liver.

The liver is the focal point of intermediary metabolism and energy production and it lies in a strategic position between the gut and the systemic organs. The products of digestion are absorbed into the mesenteric veins which drain into the portal vein and ultimately into the hepatic sinusoids (Fig. 7.11). Specialised macrophages (Kupffer cells) straddle the sinusoids and mount an almost impenetrable defence against unwanted microbes or matter that has escaped the first line of defence in the bowel. Nutrient-rich plasma filters through the small holes (fenestrae) in the endothelial cells lining the sinusoids and passes into the space of Disse, which lies between the endothelial cells and hepatocytes (Fig. 7.12). The plasma filtrate bathes these highly adaptable cells, which are enriched with a range of enzymes able to metabolise the wide variety of incoming digestion products. Three hepatic veins collect the sinusoidal outflow and deliver it into the inferior vena cava.

Fig. 7.11 The anatomy of the portal venous system. The vessels drain into the liver sinusoids carrying nutrients from the intestine, pancreatic hormones from the islets of Langerhans and antibodies from the spleen.

Fig. 7.12 Microanatomy of the liver sinusoids, the space of Disse and hepatocytes. Tight junctions adjacent to the bile canaliculi bind the hepatocytes together.

Hepatocytes perform a remarkable array of synthetic and catabolic functions, with many clinical features of liver disease resulting from derangement of these processes. They convert glucose to glycogen (which can be stored and later reconverted, on demand, to glucose), synthesise a range of proteins (including albumin and the clotting factors), degrade protein to amino acids, synthesise urea from ammonia, and manufacture cholesterol and bile acids. The lateral borders of hepatocytes are modified to form bile canaliculi which interconnect and eventually converge as the left and right main hepatic ducts at the liver hilum. The liver cells secrete bile into the canaliculi. Bile is a fluid comprising bile salts, cholesterol and bilirubin. Bilirubin is a pigment derived from haemoglobin released from dead erythrocytes. It cannot be excreted in bile until it has been rendered water-soluble by conjugation with glucuronic acid in the liver (Fig. 7.13).

Fig. 7.13 Bilirubin is a product of haemoglobin catabolism.

The liver is an important storage site for iron and vitamins and plays a central role in the hydroxylation of vitamin D. Other functions include the conjugation and excretion of steroid hormones, the detoxification of drugs and the conversion of fat-soluble waste products to water-soluble substances for excretion by the kidneys.

Gallbladder

The gallbladder is a pear-shaped organ with a fundus, a body and a neck that narrows to give rise to the cystic duct. It lies protected beneath the lower surface of the liver in the gallbladder fossa that separates the right and quadrate lobes. The gallbladder concentrates and stores bile and, under the influence of cholecystokinin, it pumps the bile through the cystic duct into the common bile duct and through the ampulla of Vater into the duodenum, where it blends with the other products of digestion (Fig. 7.14).

Fig. 7.14 The gallbladder and related ducts. Bile and pancreatic juice both enter the duodenum through the ampulla of Vater.

Pancreas

The pancreas is an elongated retroperitoneal organ that lies in the transpyloric plane with its head end tucked into the C-shaped loop of the duodenum and its tail end abutting the spleen (Fig. 7.15). Its posterior position places the organ well out of reach of the examining hand and diagnosis of pancreatic diseases is largely dependent on the use of special imaging techniques such as CT scanning, magnetic resonance cholangiopancreatography (MRCP) and endoscopic retrograde cholangiopancreatography (ERCP) (Fig. 7.16).

Fig. 7.15 The anatomical relationships of the pancreas.

Fig. 7.16 (a) CT scan showing a normal pancreas and the surrounding structures; (b) the pancreatic duct visualised after ERCP injection of radio-opaque contrast medium through the ampulla of Vater.

The pancreas has mixed exocrine and endocrine functions. The duct cells secrete bicarbonate which protects the duodenum from gastric acid and ensures an optimum pH for digestive enzyme activity. The exocrine acinar cells secrete lipase, phospholipase, amylase and peptidases (trypsinogen, chymotrypsinogen, elastase and carboxypeptidase). All the pancreatic enzymes are secreted in an inactive precursor form and are only cleaved to their active forms in the duodenum by enterokinase, which is fixed on the enterocyte brush border membranes. The hormone cholecystokinin mediates pancreatic enzyme secretion, whereas secretin promotes the secretion of fluid and bicarbonate from duct cells. The mucosa of the duodenum synthesises both these hormones. The endocrine secretion of the pancreas arises from the islets of Langerhans, which secrete insulin, glucagon, somatostatin and pancreatic polypeptide into the pancreatic and portal veins.

Blockage of the main pancreatic duct by a carcinoma, or diffuse damage caused by pancreatitis, may cause maldigestion of protein, fat and carbohydrate. Patients with pancreatic exocrine failure pass pale, fatty stools that are difficult to flush (steatorrhoea).

Spleen

The spleen is a highly modified lymphoid organ which also regulates the destruction of red blood cells. Reticuloendothelial cells populate the bulk of the spleen, forming the white pulp. These cells provide an important line of defence and the organ is a major site of antibody production. The remainder of the spleen, the red pulp, consists of capillaries and venous sinuses that act as a sump for the storage of red blood cells, white blood cells and platelets. When the spleen enlarges, excessive pooling of these cells may occur, causing a fall in the peripheral blood count. The splenic venous outflow drains into the portal vein, adding a rich supply of antibodies to the portal blood entering the liver.

Kidneys

The kidneys control fluid electrolyte balance and produce the hormones erythropoietin and renin. Each kidney contains approximately 1.2 million nephrons. The structural and functional arrangement of a typical nephron is shown in Figure 7.17.

Fig. 7.17 The structure and function of a typical nephron.

The capillary loops of the glomerulus form between the afferent and efferent arterioles supplying each glomerulus; the capillary tuft is embedded in the mesangium, which consists of a matrix and specialised mesangial cells. The basement membrane of the capillary tuft impinges on the epithelium of Bowman’s capsule via foot processes (podocytes) that arise from the visceral cells. This complex anatomical relationship allows a protein-free fluid to filter under pressure from the blood into the proximal convoluted tubule, where specialised epithelium allows the reabsorption of sodium, water, bicarbonate, glucose and amino acids into the efferent arteriole. Approximately two-thirds of the glomerular filtrate is reabsorbed in the proximal convoluted tubule.

The fluid entering the descending limb of the loop of Henle is isosmotic. The proximal and distal limbs of this loop are highly differentiated in their ability to secrete water, chloride and sodium and this, together with the spatial orientation of the loop, is responsible for the progressive increase in the sodium chloride concentration gradient between the cortex and medulla. This medullary hyperosmolality is vital for the further reabsorption of water. The thin descending limb of the loop of Henle is permeable to the outflow of water but not to that of sodium and chloride, so as the filtrate approaches the hairpin bend in the loop it becomes hypertonic. The thick ascending limb of the loop is impermeable to the efflux of water, yet permeable to the efflux of sodium which follows the active secretion of chloride ions. In the ascending limb, the tubular fluid becomes hypotonic while medullary interstitium becomes hypertonic. More sodium is reabsorbed from the distal convoluted tubule in exchange for potassium under the modulating influence of aldosterone.

The final composition of urine is determined by the collecting ducts that course through the medulla. The collecting ducts are normally impermeable to water but they are rendered permeable by the action of antidiuretic hormone (ADH), which is secreted by the pituitary. This allows water to be reabsorbed passively down the osmotic gradient that exists between the duct lumen and interstitial fluid. The permeability of the collecting duct is modified in response to body water requirements and is important for the fine tuning of fluid balance. Failure to produce ADH or insensitivity of the renal tubule to ADH causes inappropriate loss of water through the kidneys and excess urine secretion (polyuria), a syndrome known as diabetes insipidus. Sodium is also actively reabsorbed in the collecting tubules under the influence of aldosterone.

Dysphagia

Difficulty in swallowing is the principal symptom of oesophageal disease. Patients can usually indicate the level of obstruction but this does not always correspond to the actual level. Determine whether the dysphagia developed suddenly or gradually over weeks or months. Enquire whether the symptom is constant or intermittent and whether the dysphagia occurs with both solids and liquids. Associated symptoms such as weight loss and pain or cough with swallowing may help you construct a differential diagnosis.

The more common causes of dysphagia include oesophageal cancer, benign stricture caused by longstanding acid reflux, and motility disorders including achalasia of the cardia (where there is increased tone in the lower oesophageal sphincter and failure of oesophageal peristalsis). The history may indicate the underlying cause, although special tests such as barium swallow, oesophagoscopy and manometry are required to make a definitive diagnosis.

Dysphagia caused by a carcinoma usually progresses rapidly over 6–10 weeks and is worse for solids than liquids. Profound weight loss results from reduced food intake and the wasting effect of the cancer.

Patients with a benign ‘peptic’ stricture often have a long history of heartburn, a slower rate of progression and less marked weight loss. In dysmotility syndromes the dysphagia often varies in intensity and is not accompanied by profound weight loss. Solids and fluids may be equally difficult to swallow. When dysphagia is caused by disease of the swallowing centre in the brainstem (e.g. pseudobulbar palsy) or damage to the vagus nerve (e.g. bulbar palsy caused by polio), the symptom is accompanied by coughing and spluttering as food spills into the larynx and trachea.

Heartburn

Malfunction of the antireflux mechanism of the gastro-oesophageal junction allows gastric acid, pepsin and bile to reflux into the oesophagus, causing damage to the mucosa, muscle spasm and pain felt behind the sternum. Most people have experienced heartburn: the pain is a scalding or burning sensation that wells up behind the sternum and radiates towards the throat. An acid or bitter taste may develop in the mouth and reflex salivation may cause it to fill with saliva (water brash). The patient’s description is often accompanied by a hand gesture that illustrates the upward radiation of the pain behind the sternum. Heartburn is rapidly relieved by antacids. Retrosternal chest pain caused by reflux or oesophageal spasm may closely mimic the pain of myocardial ischaemia.

A common cause of heartburn is a hiatus hernia, in which the oesophagogastric junction prolapses into the chest through the oesophageal hiatus (Fig. 7.18). The heartburn is often provoked by postures which raise intra-abdominal pressure, such as stooping, bending or lying down. The diagnosis may be suspected in overweight patients but confirmation relies on visualising the hernia, either by barium meal or endoscopy, and assessing the response to treatment with antacids.

Fig. 7.18 Barium meal showing a sliding hiatus hernia with the gastro-oesophageal junction and a segment of stomach prolapsing into the chest.

Heartburn may result from a particular diet and lifestyle: chocolate, alcohol consumption and cigarette smoking relax the lower oesophageal sphincter, allowing reflux to occur. It is a common symptom in the later months of pregnancy. This is due both to the increase in intra-abdominal pressure and the loss of sphincter tone caused by high oestrogen levels.

Differential diagnosis

Distinguishing clinical features of reflux and myocardial ischaemic pain

Pain on swallowing (odynophagia)

Chest pain caused by swallowing has a deep ‘boring’ quality which differs from heartburn, although both may occur together. The symptoms suggest deep inflammation or ulceration of the oesophageal wall or intense spasm of the oesophagus; it may be provoked by obstruction or an intrinsic motor disorder causing abnormal, intense and uncoordinated contraction (‘nutcracker’ oesophagus).

Loss of appetite (anorexia)

Loss of appetite is a nonspecific symptom that commonly accompanies both acute and chronic ill health; return of appetite usually heralds recovery. Prolonged or unexplained anorexia, especially when accompanied by weight loss, should alert you to a serious underlying disease. Anorexia may be a prominent feature of digestive diseases, failure of the major organs (kidneys, liver, heart and lungs) and generalised debilitating illnesses (e.g. cancer, tuberculosis).

Profound anorexia occurs in anorexia nervosa, a psychiatric disorder occurring mainly in young women. Anorexia in these patients results in marked weight loss, malnutrition and cessation of menstruation (amenorrhoea). Suspect anorexia nervosa in teenagers and young adults, otherwise healthy, who present with an eating disorder associated with depression, vomiting or purgative abuse.

Weight loss

Weight loss is an important but rather unspecific symptom of gastrointestinal and other diseases. Enquire about appetite, eating habits and average daily diet. When eating causes pain (as in gastric ulceration, mesenteric angina or pancreatitis), the inclination to eat is suppressed. Weight loss may be caused by inappropriate wastage of calories due to steatorrhoea, thyrotoxicosis or diabetes mellitus. Marked weight loss accompanies serious diseases such as chronic pancreatitis, advanced malignancy, chronic infections and failure of the major organs.

Dyspepsia and indigestion

Most people have experienced ‘indigestion’ or ‘dyspepsia’. Patients and doctors use these terms rather loosely and interchangeably to describe a range of subjective abdominal symptoms. This term applies to a sensation of pain, discomfort or fullness in the epigastrium, often accompanied by belching, nausea and early satiety. Dyspepsia should focus your attention on foregut disorders.

Nausea

Nausea describes the sensation experienced before vomiting, although it often occurs without vomiting. Nausea may last hours or days, usually comes in waves and is often associated with belching. It may be relieved by vomiting. The symptom may be provoked by unpleasant sights, smells and tastes or by abnormal stimulation of the inner ear labyrinths (motion sickness). Nausea may be accompanied by other complaints such as abdominal pain and diarrhoea (Fig. 7.19). It is a characteristic of the prodromal phase of viral hepatitis and often accompanies biliary diseases (e.g. cholecystitis). Drugs causing gastric irritation (e.g. nonsteroidal analgesics) or those stimulating the vomiting centre (e.g. digoxin, morphine and anticancer drugs) cause nausea. Early morning nausea commonly occurs during the first trimester of pregnancy.

Fig. 7.19 The causes of nausea and vomiting.

Vomiting and haematemesis

A wave of nausea usually heralds vomiting and the causes of nausea and vomiting are similar. Vomiting may occur in diseases of the gastrointestinal and biliary tracts, as well as in a variety of systemic and metabolic disorders. It may also be the presenting symptom of psychological disorders such as anorexia nervosa, bulimia and fear. Suspect an iatrogenic cause in patients taking digoxin or morphine and in individuals undergoing cancer treatment with cytotoxic drugs. Try to establish whether the vomit is bile-stained because this indicates patency between the stomach and duodenum. The presence of undigested food and a lack of bile suggest pyloric obstruction. Early morning nausea and vomiting are characteristic of early pregnancy and alcoholism.

Vomiting blood (haematemesis) indicates bleeding from the oesophagus, stomach or duodenum. If the bleeding is brisk the vomit may be heavily bloodstained but if bleeding is slower or vomiting delayed, gastric acid reacts with haemoglobin, turning it a dark brown or ‘coffee-ground’ colour. The patient’s history often yields clues to the cause of haematemesis. If the bleeding is preceded by repeated bouts of retching or vomiting, consider as the cause a Mallory–Weiss tear which results from mechanical disruption of the mucosa at the gastro-oesophageal junction. Enquire about ingestion of alcohol or other gastric irritants (e.g. aspirin). If there is evidence of coincident liver disease, consider oesophageal varices to be the cause of bleeding. Weight loss may suggest bleeding from a gastric cancer, and a history of epigastric pain or heartburn suggests bleeding from a peptic ulcer or ulcerated oesophagus.

Abdominal pain

Pain is an important symptom of abdominal disease that may present in various forms, ranging from a dull ache to cramp, colic and peritonitis. A differential diagnosis can often be constructed from the position, character and timing, the aggravating and relieving factors and other distinctive or associated features (Fig. 7.20). When taking a history of abdominal pain, aim to distinguish between visceral, parietal and referred pain.

Fig. 7.20 The characteristics of abdominal pain which may help in making a differential diagnosis.

Visceral pain is caused by stretching or inflammation of a hollow muscular organ (gut, gallbladder, bile duct, ureters, uterus). It is often described as a ‘dull ache’ or a ‘gnawing’ or ‘cramping’ sensation that is perceived near the midline, irrespective of the location of the organ. The pain can usually be localised to the epigastric, periumbilical or suprapubic areas, depending on whether the affected organ is derived from the embryological foregut, midgut or hindgut (Fig. 7.21). Pain arising from foregut is felt in the epigastrium; midgut pain is perceived around the umbilicus; pain arising from the hindgut is felt in the suprapubic area. Visceral pain may also radiate to specific sites and this helps to establish its origin (Fig. 7.22). It is commonly accompanied by nonspecific, ‘visceral’ symptoms (e.g. anorexia, nausea, pallor, sweating).

Fig. 7.21 Perception of visceral pain is localised to the epigastric, umbilical or suprapubic region according to the embryological origin of the diseased organ.

Fig. 7.22 Characteristic radiation of pain from the gallbladder, diaphragm and ureters. The pain is not always felt in the organ concerned.

Colic is a characteristic manifestation of visceral pain and is caused by concerted and excessive smooth muscle contraction. It signifies obstruction of a hollow, muscular organ, such as the intestine, gallbladder, bile duct or ureter, and consists of recurring bouts of intense, cramping, visceral pain which build to a crescendo and then fade away. When the smaller organs such as the gallbladder, bile duct or ureters are acutely obstructed by a stone, the cyclical nature of colic soon gives way to a continuous visceral pain caused by the inflammatory effect of the impacted stone or secondary infection. Movement does not aggravate visceral pain, so the patient may writhe or double-up in response to it.

Unlike the visceral peritoneum, the parietal peritoneum is innervated by pain-sensitive fibres. Therefore, pain arising from the parietal peritoneum is well localised to the area immediately overlying the area of inflammation or irritation. Parietal pain is aggravated by stretching or moving the peritoneal membrane; the patient lies as still as possible. Palpation over the area is extremely painful, with the overlying muscles contracting to protect the peritoneum (guarding). When the pressure of the examining hand is suddenly released, the pain is further aggravated and the patient winces. This sign is known as ‘rebound tenderness’.

Abdominal pain may progress from a visceral sensation to a parietal pain. Acute appendicitis provides an excellent example of this transition. When this midgut structure becomes inflamed and obstructed, a dull pain localises to the periumbilical area and the patient may feel nauseous and sweaty. As the inflammation advances through the visceral covering to the parietal peritoneum, the pain appears to shift to the right iliac fossa where it localises over McBurney’s point. The character of the pain also changes from dull to sharp. The area overlying the appendix is very tender and palpation causes reflex guarding and rebound tenderness.

Mesenteric angina

When the mesenteric arteries are stenosed by atherosclerosis the blood supply to the bowel may be impaired. The collateral supply to the bowel is well developed and the pain of bowel ischaemia usually becomes apparent only on eating, when the metabolic demands of digestion and absorption require an increase in the blood supply. Patients complain of a severe visceral periumbilical pain occurring soon after meals (mesenteric angina). The pain causes anorexia, which, together with damage to the bowel mucosa, results in considerable weight loss.

Wind

Most gas in the gastrointestinal tract is swallowed, with a smaller contribution arising from fermentation of cellulose in the colon. Small, imperceptible amounts of gas constantly escape from the bowel via the mouth and anus. Excessive belching (flatulence) or the passage of wind through the anus (flatus) are common symptoms that cause considerable distress. These symptoms are rather unspecific and occur in both functional and organic disorders of the gastrointestinal tract. Flatulence is usually caused by excessive air swallowing (aerophagy) and often occurs with a hiatus hernia, peptic ulceration and chronic gallbladder disease. The symptom may be accompanied by a feeling of abdominal distension. Intestinal gas is produced by fermentation of certain foods, especially legumes, in the colon and your history should seek to identify a possible dietary cause of excessive flatus and flatulence.

Constipation

Most people on a Western diet expect bowel actions once or twice daily. Consequently, constipation usually implies failure to produce a stool over 24 h. However, normal expectations vary between individuals and cultures; some healthy individuals evacuate every other day or even only three times a week, whereas others, particularly people on high roughage diets, expect up to three bulky bowel actions daily. Constipation is described more precisely as a disorder of bowel habit characterised by straining and the infrequent passage of small, hard stools. Constipated patients often complain that they are left dissatisfied, with a sense of incomplete evacuation (tenesmus). Patients with troublesome constipation often seek medicinal relief and a history of laxative use may be a helpful guide to the severity of the condition.

When constipation has troubled a patient for years or even decades, the cause is likely to be functional rather than obstructive and it may be attributed to diet, lifestyle or psychological make-up. Lack of exercise, inadequate fibre intake, irritable bowel syndrome and depression may all cause constipation.

When constipation presents as a recent change, and especially if it is associated with colic, suspect an organic cause such as malignancy or stricture formation. Enquire about constipating drugs (e.g. codeine-containing analgesics, aluminium-containing antacids) and about rectal bleeding, an alarm symptom that raises the suspicion of cancer. Consider hypothyroidism or electrolyte abnormalities. Anal pain caused by a fissure or a thrombosed pile may cause profound constipation because of the patient’s fear of pain at stool.

Differential diagnosis

Constipation

• Low-residue diet

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