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The alimentary system includes the mouth and its associated salivary glands, the oesophagus, stomach, small and large bowels, appendix and anus. The function of the alimentary tract is the ingestion, digestion and absorption of nutrients, along with the storage and expulsion of waste products. A wide range of congenital and acquired diseases may affect all parts of the tract.
The mouth and associated structures can be involved in a wide variety of disease states that may be loosely divided into three categories. First, many systemic diseases, particularly dermatological conditions, exhibit oral manifestations, e.g. lichen planus (see Fig. 21.7 ) and syphilis (see Fig. 5.11 ). Second, all oral tissues may be subject to acute or chronic inflammatory states, the most common being dental caries and its sequelae, periapical abscess formation and periodontal disease (i.e. inflammation of the gums). Of more general interest is inflammation of the salivary glands leading to chronic sialadenitis ( Fig. 13.3 ). Third, many benign and malignant tumours may arise in the oral tissues, the most common being squamous cell carcinomas of the lips, oral mucosa, tongue and oropharynx ( Fig 13.1 and 13.2 ). A wide range of salivary tumours, both benign ( Figs 13.4 and 13.5 ) and malignant ( Fig 13.6 and 13.7 ), can arise in both major and minor salivary glands. A fascinating but fairly esoteric range of benign and malignant tumours arises in the jaws.
Sialadenitis may also be caused by viral infections (most commonly mumps), bacterial infections ( Staphylococcus aureus and Streptococcus viridans ), autoimmune disease (Sjögren’s syndrome) and sarcoidosis , as well as other rarer causes such as IgG4 disease. A dry mouth due to dehydration, drugs or Sjögren’s syndrome also predisposes to bacterial sialadenitis, as do calculi as mentioned above.
A acini B basaloid tumour cells C capsule D duct Ep epithelium F fibrosis/fibrous tissue G gland K keratinisation L lymphoid follicle S stroma
Infections of the oesophagus are rare in healthy individuals, but in debilitated or immunosuppressed patients, infection with herpes simplex virus (see Fig. 5.12 ) or Candida albicans (see Fig. 5.15 ) can occur. The lower oesophagus frequently becomes inflamed as a result of gastric acid reflux, producing either oesophagitis or sometimes chronic peptic ulceration , analogous to that seen in the stomach and duodenum (see Figs 4.2 and 13.10 ). This condition is known as gastro-oesophageal reflux disease ( GORD or GERD , depending on how you spell oesophagus). In response to reflux of acid, the squamous mucosa of the lower oesophagus may undergo metaplastic transformation into a form of glandular epithelium similar to that seen in the stomach or small intestine. This metaplastic condition is termed Barrett’s oesophagus ( Fig. 13.8 ).
A acinus E epidermoid (squamous) elements GC germinal centre F fibrous stroma L lymphoid tissue M mucous (glandular) elements S spaces in tumour cell masses
AM atypical mitoses G glandular mucosa GC goblet cell HG high grade dysplasia L lymphoid aggregate M mitotic figures N dirty necrosis SS stratified squamous epithelium
The most common oesophageal neoplasm used to be squamous cell carcinoma , which is similar to squamous cell carcinomas at other sites (see Figs 7.3 and 17.8 ). However, the incidence of adenocarcinomas arising in Barrett’s oesophagus at the lower end of the oesophagus is increasing and comprises almost 50% of oesophageal carcinomas in developed countries. Both adenocarcinoma and squamous cell carcinoma of the oesophagus have a very poor prognosis. The lower oesophagus may also be involved by local spread of adenocarcinoma of the upper stomach.
Patients with longstanding GORD/GERD are at risk of developing adenocarcinoma of the oesophagus. The sequence of events appears to be oesophagitis → Barrett’s oesophagus without dysplasia → low grade dysplasia → high grade dysplasia → invasive carcinoma. High grade dysplasia is a premalignant condition and oesophagectomy often reveals co-existing superficially invasive carcinoma. Because of the grim prognosis of oesophageal carcinomas, Barrett’s oesophagus is usually regularly monitored by endoscopy and biopsy. High grade dysplasia and superficially invasive carcinomas can be locally resected or ablated by photodynamic therapy (PDT), laser therapy or other means before reaching an advanced stage.
Inflammation of the stomach is termed gastritis and may be divided into acute and chronic forms.
Acute gastritis may be associated with the use of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) and excessive alcohol consumption and also occurs in severely debilitated patients. It may present with nausea and vomiting but is also an important cause of haematemesis. Although not uncommon, acute gastritis rarely requires biopsy.
Chronic gastritis can be divided into distinct subtypes, each of which has particular histological features ( Fig. 13.9 ):
Chronic infection: Helicobacter pylori is the usual infective agent.
Chronic chemical gastritis (also known as reactive or reflux gastritis ) is associated with reflux of bile or alkaline duodenal secretions into the stomach, especially following surgical procedures, and with chronic alcohol consumption or with use of gastrotoxic drugs such as NSAIDs.
Chronic autoimmune gastritis is associated with autoantibodies to various components of gastric parietal cells and with pernicious anaemia.
Less common causes include Crohn’s disease , graft-versus-host disease and gastric outlet obstruction .
The histological details of chronic peptic ulceration in the stomach are described in Ch. 4 (see Fig. 4.2 ). Acid-induced necrosis of the gastric wall, the acute inflammatory response, organisation, granulation tissue formation and fibrous scarring occur concurrently. H. pylori infection is almost always present in chronic duodenal ulceration and most cases of chronic gastric ulceration ( E-Fig. 13.5 G ) and must be eradicated for permanent healing. The outcome of this dynamic process depends on which is the dominant element, i.e. the damaging stimulus or the attempts of the body to heal the damage.
There are three main complications of chronic peptic ulceration:
Perforation: If tissue destruction outstrips attempts to confine or repair it, the process may extend rapidly through the wall, leading to perforation ( Fig. 13.10A ).
Haemorrhage: Tissue necrosis may extend deeply enough to involve the wall of a large artery. This is most common in long-standing chronic gastric ulcers on the posterior wall, in the region of the left gastroepiploic artery. This vessel tends to become incorporated in the fibrous scar on the serosal aspect of a chronic gastric ulcer and may then be eroded during a subsequent acute exacerbation of ulceration ( Fig. 13.10B ). This may produce torrential haemorrhage, presenting as haematemesis and/or melaena , which may be fatal.
Obstruction: Persistent attempts at repair lead to progressive fibrous scarring, which undergoes shrinkage and ultimately causes distortion and thickening of the wall of the viscus, commonly at the lower end of the oesophagus or in the pyloric region of the stomach. The narrowing may cause stricture formation with partial or even complete obstruction of the lumen. When the ulcerative process is still active, obstruction may be compounded by inflammatory oedema of the mucosa surrounding the ulcer.
A artery Ex inflammatory exudate F fibrous scar tissue G glands H H. pylori organisms Hy foveolar hyperplasia In inflammatory cells M intestinal metaplasia MP muscularis propria Mu mucosa N neutrophils S smooth muscle spurs SM submucosa V vasodilatation
Chronic gastritis is very common and, in untreated patients, was often associated with the development of peptic ulceration and its complications (see Fig. 13.10 ). However, the recognition and treatment of H. pylori infection as well as the widespread use of proton pump inhibitors (PPIs) to reduce gastric acid secretion, has greatly changed the incidence of serious complications. Gastric adenocarcinoma, which is usually preceded by intestinal metaplasia and dysplasia (see Figs 13.11 and 13.12 ) is known to have a strong association with H. pylori gastritis but may also occur with any other form of chronic gastric inflammation. H. pylori is also associated with gastric lymphoma (MALT lymphoma) (see Fig. 16.7 ).
By far the most common malignant tumours of the stomach are adenocarcinomas (90%–95%). These may assume a variety of gross morphological forms, including malignant ulcers with heaped-up edges, fungating polypoid tumours or diffuse infiltration of the wall (linitis plastica) , giving rise to the so-called leather bottle stomach . Gastric adenocarcinomas are classified histologically as intestinal type ( Fig. 13.12A and B ), often arising on a background of intestinal metaplasia and dysplasia, or diffuse type ( Fig. 13.12C and D ). Gastric lymphoma (see Fig. 16.7 ) and neuroendocrine tumours (previously known as carcinoid tumours ) ( Fig. 13.13 ) make up a small percentage of stomach malignancies. Both adenocarcinoma and gastric lymphoma are associated with H. pylori infection. Of the benign tumours, gastric adenomas comprise only a small proportion of gastric polyps, most of which are inflammatory or regenerative. Mesenchymal tumours occur in the stomach and other parts of the gastrointestinal tract including lipomas, leiomyomas and gastrointestinal stromal tumours (GIST) ( Fig. 13.14 ), which are mainly found in the gastrointestinal tract; rare examples occur at other sites such as the mesentery, the retroperitoneum and the pelvis.
There are large differences in incidence of gastric cancer in different parts of the world. As well as different rates of H. pylori infection, the other major aetiological factor appears to be diet and in particular high consumption of smoked and salted foods. Diffuse type carcinomas seem to have different risk factors and, unlike the intestinal type, are not thought to be associated with preceding inflammation, atrophy, metaplasia or dysplasia. Carcinoma of the stomach may be staged histologically as early or late , with early carcinomas infiltrating into the submucosa but not into the muscularis propria. Early gastric carcinomas have an excellent prognosis in contrast to late gastric carcinomas.
In patients with advanced gastric carcinoma, a variety of conventional chemotherapeutic agents may be used. A small but important subset of these tumours over-express the HER-2 gene and these patients may benefit from treatment with drugs targeting the her-2 protein, similar to those used in the management of breast carcinoma (see Ch. 18 ). HER-2 amplification status can be determined on biopsies of the tumour, using immunohistochemical methods and/or fluorescence in situ hybridisation (FISH). This testing allows therapy to be tailored for individual patients and avoids unnecessary, potentially toxic treatments in patients who will not benefit from them.
D high grade dysplasia G malignant glands I intestinal metaplasia M muscularis propria N nucleus T tumour cells V mucin vacuole
These tumours can arise at various sites and they are usually well differentiated. They may secrete a range of hormone products, typically including 5-HT (serotonin) and other vasoactive compounds. These products can cause clinical vasomotor symptoms described as carcinoid syndrome . In the past, the term carcinoid tumour was used for all of these tumours, reflecting the fact that they have some similarities to conventional carcinomas, but their behaviour can be difficult to predict. This nomenclature has been by replaced by a classification system that aims to reflect the likely biological behaviour and prognosis of the tumours. The criteria for classification vary at different sites in the GI tract but the terms used range from well differentiated neuroendocrine tumour through to poorly differentiated neuroendocrine carcinoma , the latter having aggressive biological behaviour and a poorer prognosis. For gastrointestinal tumours, the term carcinoid tumour alone should be avoided as this fails to convey the relevant prognostic information. In contrast, this term is still used for well differentiated tumours in the lung, with more aggressive variants described as atypical carcinoid tumours (see Ch. 12 ).
E neuroendocrine cell F fascicle N nest of tumour S spindle cells T tumour cells Tr trabeculae
GISTs have a wide spectrum of clinical behaviour. About a quarter of gastric GISTs and half of small intestinal GISTs are malignant. The most useful pathological features that predict malignant behaviour are site, size of tumour and high mitotic rate. Most are treated by complete excision but, where this is not possible, treatment with a specific monoclonal antibody, imatinib, is indicated. c-kit is a membrane receptor protein for stem cell factor. When stem cell factor binds to c-kit, it is activated and acts as a tyrosine kinase, an enzyme that activates other intracellular proteins by phosphorylation of the amino acid tyrosine. Mutations in c-kit lead to constitutional activation of this signalling pathway, resulting in cell proliferation and, in time, formation of tumours. Imatinib is a tyrosine kinase inhibitor and so blocks the activity of the mutated c-kit protein. Most GISTs are responsive to imatinib initially, although with time many become resistant and the tumour recurs. A small proportion of tumours have no c-kit mutation but have activating mutations in a very similar cell surface receptor/tyrosine kinase enzyme, called platelet derived growth factor receptor-α (PDGFR α); this acts, and is treated, in the same way.
Inflammation of the small intestine due to self-limiting infections is very common but rarely biopsied. Giardiasis (see Fig. 5.19 ) is a common infective cause of inflammation in some countries and is often diagnosed on biopsy. Other inflammatory conditions affecting the small intestine include coeliac disease ( Fig. 13.15 ) and Crohn’s disease ( Fig. 13.16 ). Appendicitis ( Fig. 13.17 ) is extremely common and is a classic example of acute inflammation.
Primary tumours of the small intestine and appendix are very rare, with the exception of neuroendocrine tumours ( Fig. 13.13 ) and lymphomas , which may be MALT lymphomas (see Fig. 16.7 ), enteropathy-associated or occasionally of Burkitt lymphoma type (see Fig. 16.8 ). Neuroendocrine tumours occur in the appendix, as do rare adenomas . Although broadly similar in appearance to colonic adenomas, these mucin-producing tumours (called low grade or high grade appendiceal mucinous neoplasms ) often distend the appendix, producing the macroscopic appearance of a mucocoele . If tumours of this type rupture, mucin and neoplastic mucin-secreting epithelium may be released into the peritoneal cavity, causing a form of mucinous ascites called pseudomyxoma peritoneii . Rarely, these tumours may become frankly malignant.
C crypts G granuloma In inflammatory cells L intraepithelial lymphocytes SM submucosa P plasma cells U ulcer V villus
Chronic inflammatory bowel disease is a group of conditions including Crohn’s disease and ulcerative colitis . These are chronic inflammatory conditions of unknown aetiology with a typically relapsing course. Both conditions may lead to surgical removal of large parts of the bowel. Other conditions may mimic these two diseases such as diverticulosis-related colitis, radiation colitis and ischaemic colitis. Infections, including TB, must also be ruled out before a diagnosis of chronic inflammatory bowel disease is made. Ulcerative colitis and Crohn’s disease can occasionally be very difficult to differentiate from each other clinically and pathologically and often the distinction can only be made at the time of colectomy. Unlike ulcerative colitis, Crohn’s disease may affect any part of the gastrointestinal tract, so diagnostic difficulty only arises when disease is limited to the colon and rectum. In this situation, the term indeterminate colitis may be used until there is enough information for a definitive diagnosis; thus the term indeterminate colitis does not indicate a specific disease, only that there is idiopathic chronic inflammatory bowel disease that cannot yet be fully classified. The distinction is important, as different treatment options are appropriate for the different conditions. Both ulcerative colitis and Crohn’s disease may have extra-intestinal manifestations such as arthritis, sacroileitis and sclerosing cholangitis. Both may be associated with the development of adenocarcinoma of the bowel, but this risk is particularly high in long-standing ulcerative colitis.
A range of intra-abdominal diseases may present with features similar to those of acute appendicitis. These include mesenteric adenitis, gallstone disease, kidney and ureteric stones, acute urinary tract infections, ectopic pregnancy, acute salpingitis, ovarian cysts and tumours, diverticular disease, inflamed Meckel’s diverticulum and perforation of gastric and duodenal ulcers. Careful history taking, examination and targeted investigation is essential.
The colon and rectum are subject to various viral, bacterial and parasitic infections that are usually short-lived and readily diagnosed by microbiological methods; important exceptions are amoebic colitis (see Fig. 5.22 ), and various infections in immunosuppressed individuals, which are often diagnosed in biopsy specimens. Of great importance is chronic inflammatory bowel disease, i.e. ulcerative colitis ( Fig. 13.18 ) and Crohn’s disease. Other causes of chronic diarrhoea include microscopic colitis ( Fig. 13.19 ), radiation-induced colitis, ischaemic colitis and diverticulitis-associated colitis among others. Raised intraluminal pressure in the colon, probably as a result of a low residue diet, may lead to saccular herniation of mucosa through the muscle layers of the bowel wall; the diverticula so formed may become inflamed, giving rise to diverticulitis ( Fig. 13.25 ), which may have serious sequelae. The large intestine may undergo infarction, either as a result of mesenteric artery occlusion by thrombus or embolus, or, more commonly, by venous infarction following hernial strangulation or volvulus (see Fig. 10.5 ).
Colonic polyps are very common. By far the most common is the hyperplastic polyp ( Fig. 13.20 ), a benign lesion typically seen in the left colon and thought to have no malignant potential. Less common non-neoplastic polyps include inflammatory pseudopolyps as seen in ulcerative colitis ( Fig. 13.18A ) and polypoid hamartomas such as Peutz-Jeghers’ polyps . Neoplastic benign polyps can be divided into two main groups: conventional adenomas and serrated lesions . The first of these groups is characterised by typical epithelial dysplasia and these lesions are well recognised as an important precursor of colorectal adenocarcinoma via the traditional adenoma–carcinoma sequence . These conventional adenomas are further classified according to their architecture as tubular , villous and tubulovillous adenomas ( Fig. 13.21 ) and may show low or high grade epithelial dysplasia, reflecting their likely malignant potential. Serrated lesions ( Fig 13.22 and 13.23 ). are a distinct group of polyps with some similarities in appearance to hyperplastic polyps, having star-shaped, irregular crypt outlines. The role of these lesions in colorectal carcinogenesis has been established more recently as these lesions generally lack typical cytological dysplasia. They are associated with specific defects in DNA mismatch repair and are linked to cancers in which there are high levels of microsatellite instability (see Ch. 1 ). Nomenclature for the polyps within this group continues to evolve but important subtypes include the sessile serrated lesion (sometimes called sessile serrated polyp or sessile serrated adenoma ), the sessile serrated lesion with dysplasia and the traditional serrated adenoma (which shares some features of conventional adenoma but with serrated crypt architecture).
Malignant tumours of the colon and rectum are very common and almost all are adenocarcinomas ( Fig. 13.24 ); most appear moderately differentiated with a clearly defined glandular pattern. The anal canal, lined by squamous epithelium, is occasionally the site of squamous cell carcinoma identical to squamous cell carcinomas at other sites (see Fig. 7.3 ), although local invasion of the anal canal by adenocarcinoma of the lower rectum also occurs.
Ex inflammatory exudate F fibrinous exudate G glands M muscularis propria Mu smooth muscle fibres N neutrophils Ne necrosis P pus S serosa SM submucosa U ulceration
A crypt abscess B branched crypt C collagen band G colonic glands In inflammation in lamina propria L intraepithelial lymphocytes LP lamina propria M muscularis propria P Paneth cell metaplasia
C complex gland architecture G malignant glands N necrosis S saw tooth outline T tubular adenoma V villous adenoma
The recognition and investigation of various hereditary colorectal cancer syndromes such as familial adenomatous polyposis (FAP), hereditary non-polyposis colon cancer (HNPCC, also known as Lynch syndrome) and hyperplastic polyposis syndrome has led to huge advances in the understanding of the development of adenocarcinoma in the large bowel. It has long been understood that adenomas may develop into adenocarcinomas through the stepwise accumulation of genetic mutations. In the case of typical adenomas, the first step seems to be the loss of both copies of the APC gene. Individuals with FAP already have one copy of this gene inactivated as a germ line mutation (the ‘first hit’ according to Knudson’s hypothesis; see Ch. 7 ); individuals with sporadic carcinomas must lose both copies to develop disease. Activation of the oncogene KRAS is also an early event, as is inactivation of P53 .
A second, more recently discovered, pathway is the serrated pathway . In this pathway, serrated polyps with increasing degrees of dysplasia develop into invasive adenocarcinoma. Other characteristic features include increased DNA methylation and high levels of microsatellite instability (MSI-H) due to mutations in mismatch repair genes. This is a fast-advancing field and further pathways and subtypes of carcinoma are under investigation. Apart from the intrinsic fascination of these mechanisms, they may prove useful in determining optimal methods of treatment for different types of adenocarcinoma.
Around 15% of colorectal carcinomas show defects in their DNA mismatch repair machinery, either due to a germ line mutation in a mismatch repair gene (as seen in Lynch syndrome , an inherited disease associated with a high risk of colorectal and other malignancies, also known as hereditary non-polyposis colorectal cancer, HNPCC ) or, in sporadic cases, due to epigenetic mechanisms such as MLH1 gene promoter hypermethylation. These sporadic cases often also harbour a BRAF mutation.
These mutations can be detected using immunohistochemical methods (see Ch. 1 ), which demonstrate loss of expression of the protein products of the mismatch repair genes. The gene MLH1 is paired with PMS2 and the gene MSH2 with MSH6 and hence their loss of staining usually occurs in pairs ( E-Fig. 13.15 H ). A molecular test for microsatellite instability can also be performed, with tumours described as ‘MSI-high’ or ‘unstable’ for a positive result.
Until recently, testing by clinical geneticists has typically been used to identify patients with Lynch syndrome/HNPCC but there is now growing recognition that a subset of sporadic cancers can have MSI and this is associated with a more favourable prognosis. It is therefore recommended that all colorectal cancer patients have their tumours tested, not only to check for Lynch syndrome but also to identify the cases with sporadic MSI, who have a better outcome but respond less well to 5-fluorouracil based chemotherapy regimens.
C horizontal crypts D dilated crypt base GC goblet cells MM muscularis mucosae S saw tooth outline
As described above, cancers with microsatellite instability respond poorly to chemotherapy using conventional 5-FU based regimens. BRAF sequencing is part of the molecular test for MSI as it identifies spontaneous mutations and is also a poor prognostic marker. Testing for mutations in EGFR and KRAS is also useful in guiding therapy and predicting prognosis. Patients with mutations in KRAS are typically treated with standard chemotherapy, whilst those with wild-type KRAS benefit from the addition of antibody-based drugs such as cetuximab that act to inhibit the epidermal growth factor receptor.
CM circular muscle layer D diverticulum F perirectal fat L lymphoid tissue M muscularis propria N normal rectal mucosa SM submucosa T tumour
|Disorder||Clinical presentation||Main features||Figure|
|Mouth and oropharynx|
|Squamous cell carcinoma||Non-healing ulcer, erythroplakia, leukoplakia||Nests of epithelial cells with eosinophilic cytoplasm, intercellular bridges, squamous pearls, keratinisation||13.1|
|HPV-associated oropharyngeal carcinoma||Often tonsillar ulcer or mass Younger age group; associated with high risk HPV; better prognosis.||Typically basaloid squamous cell carcinoma with small, dark cells and abrupt keratinisation. P16 positive||13.2|
|Sialadenitis|| Pain and swelling, often after food if there is a calculus
|Chronic inflammatory cell infiltrate, fibrosis, atrophy of gland tissue||13.3|
|Pleomorphic adenoma||Painless swelling, mainly parotid||Mixed epithelial and connective tissue components||13.4A|
|Basal cell adenoma||Painless swelling, often male smokers, mainly parotid||Epithelial cells forming nests, trabeculae and glands||13.4B|
|Warthin’s tumour||Painless swelling, may be cystic, almost exclusively parotid||Glandular element consisting of tall columnar cells with lymphoid tissue, including reactive germinal centres||13.5|
|Adenoid cystic carcinoma||Initial painless swelling, later nerve pain||Epithelial cells arranged in cribriform pattern with hyalinised, fibrotic stroma, perineural invasion common||13.6|
|Mucoepidermoid carcinoma||Painless swelling, usually parotid or minor glands||Mixed squamous and glandular (mucus- producing) components||13.7|
|Barrett’s oesophagus||Heartburn||Metaplastic glandular (intestinal) epithelium at lower end of oesophagus||13.8A|
|Dysplasia||Heartburn||Atypical epithelial cells with pleomorphic nuclei, architectural distortion, increased mitotic activity||13.8B and C|
|Carcinoma||Obstruction, dysphagia||May be squamous cell carcinoma or adenocarcinoma|| Like 7.3
Like 13.8D and E
|Chronic gastritis – H. pylori associated||Dyspepsia, haemorrhage||Chronic inflammation of lamina propria with neutrophils infiltrating glands, H. pylori in surface mucus||13.9A and B, 4.2|
|Chronic gastritis – autoimmune type||Megaloblastic (macrocytic) anaemia||Atrophic body of stomach with reduction or absence of parietal cells, intestinal metaplasia||13.9C|
|Chronic gastritis – reflux or chemical type||Dyspepsia, haemorrhage||Foveolar hyperplasia of glands with saw tooth outline, minimal inflammation, smooth muscle bundles in lamina propria||13.9D|
|Peptic ulceration ( E-Fig. 13.5 G )||Dyspepsia, haemorrhage, perforation||Discontinuity of epithelial surface with necrotic slough, granulation tissue and fibrosis lining the defect||13.10|
|Gastric dysplasia||Dyspepsia||Atypical epithelial cells with pleomorphic nuclei, architectural distortion, increased mitotic activity||13.11|
|Gastric carcinoma – intestinal type||Dyspepsia, weight loss abdominal pain, anaemia||Atypical invasive glands with atypical epithelial cells, mucus production||13.12A and B|
|Gastric carcinoma – diffuse type ( E-Fig. 13.7 G )||Dyspepsia, weight loss abdominal pain, anaemia||Malignant signet ring cells forming sheets with no gland formation (linitis plastica appearance)||13.12C and D|
|Coeliac disease||Anaemia, weight loss, steatorrhoea||Blunting/flattening of small bowel villi, increased lymphocytes and plasma cells in the lamina propria, increased intraepithelial lymphocytes, crypt hyperplasia||13.15|
|Giardiasis||Diarrhoea, steatorrhoea||Mucosa normal or inflamed with villous atrophy, sickle-shaped parasitic Giardia lamblia organisms on epithelial surface||5.19|
|Acute appendicitis||Right iliac fossa pain, fever, vomiting||Ulceration of mucosa, transmural acute inflammatory infiltrate||13.17|
|Enterobius vermicularis (pinworm)||Incidental finding||Pinworm sections seen within lumen of appendix||5.24|
|Microscopic colitis (lymphocytic and collagenous colitis)||Watery, non-bloody diarrhoea with normal colonoscopy||Subtle inflammation of lamina propria, increased lymphocytes and apoptotic bodies in epithelium, subepithelial collagen band n collagenous subtype||13.19|
|Ulcerative colitis ( E-Fig. 13.12 G )||Bloody diarrhoea, pain, fever, toxic megacolon||Inflammation and ulceration of mucosa, crypt abscesses, distortion of crypt architecture||13.18|
|Diverticular disease ( E-Fig. 13.17 G )||Altered bowel habit, pain in left iliac fossa, rectal bleeding, often asymptomatic||Herniation of mucosa through muscularis propria with surrounding inflammation and fibrosis||13.25|
|Hyperplastic polyp||Incidental finding, bleeding||Polypoid glandular lesion with saw tooth architecture but no dysplasia||13.20|
|Tubular adenoma ( E-Fig. 13.13 G )||Incidental finding, bleeding||Polyp, usually with stalk, glandular architecture with variable dysplasia||13.21A|
|Villous adenoma ( E-Fig. 13.14 G )||Incidental finding, bleeding||Polyp, usually sessile, villous architecture with variable dysplasia||13.21B|
|Tubulovillous adenoma||Incidental finding, bleeding||Polyp, glandular and villous architecture with variable dysplasia||13.21C|
|Serrated lesions||Incidental finding, bleeding||Polypoid glandular lesion with saw tooth architecture and variable dysplasia||13.22, 13.23|
|Adenocarcinoma ( E-Fig. 13.16 G )||Haemorrhage, obstruction, anaemia||Invasive glands with atypical epithelial cells, mucus production, ‘dirty’ necrosis in lumina||13.24|
|Various sites throughout GI tract|
|Gastrointestinal stromal tumour (GIST)||GI haemorrhage, mass lesion, incidental finding, usually stomach or small intestine||Mainly spindle cells in collagenous stroma, less commonly epithelioid or pleomorphic||13.14|
|Neuroendocrine tumour||Usually incidental finding, commonly appendix, or small bowel obstruction, rarely carcinoid syndrome|| Small uniform cells with round nuclei, stippled chromatin and pinkish, granular cytoplasm
High grade forms include small cell carcinoma
|Crohn’s disease ( E-Fig. 13.9 G )||Diarrhoea, weight loss, obstruction, fistula formation, usually small bowel/colon but can affect mouth to anus||Transmural inflammation, granulomas, fibrosis, fissuring ulceration, skip lesions||13.16|
A 68-year-old male smoker presents with a lump in the right parotid gland. He undergoes excisional biopsy and a section from the mass is shown above. The features are those of: (choose ONE correct answer)