Digestive Pathology

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Pedunculated Adenoma of the Colon
Clinical HistoryA 50-year old male underwent a colonoscopy after testing positive for faecal occult blood during a screening test. Colonoscopy revealed a pedunculated tumour in the descending colon, which was later resected.Pathology This specimen is the resected segment of descending colon. There is a single dark lobulated mass visible arising from the mucosal surface. It is attached to a stalk which is 4cm in length. Histologically, the mass comprises a core of connective tissue covered with hyperplastic glandular epithelium of colonic type, with focal nuclear atypia. This is an example of a tubular colonic adenoma.Further InformationColorectal adenomas are intraepithelial neoplasms that characteristically display epithelial dysplasia. They are benign but are precursors to adenocarcinoma. Not all adenomas evolve into adenocarcinoma. They produce polyps (sometimes pedunculated) or sessile lesions or variable size. They occur predominantly in males and are more common in Western countries due to diet and lifestyle. They are present in about 30% of people over the age of 60 years in the West. There is an increased risk in patients with a positive family history of colorectal adenocarcinoma. Regular surveillance colonoscopy in at risk groups with polyp removal reduces incidence of adenocarcinoma. There are three classifications of colonic adenomas based on their architecture: tubular (>75% have a tubular morphology), tubulovillous (25-75% villous morphology) and villous (>75% have villous morphology). Histologically, they may have epithelial dysplasia characterized by nuclear hyperchromasia, elongation and stratification. Tubular adenomas tend to be small, pedunculated polys composed of rounded or tubular glands. Pedunculated adenomas have a slender fibromuscular stalk with blood vessels derived from the submucosa. The stalk is usually non-neoplastic epithelium. The size of the adenoma is the biggest predictor of progression to adenocarcinoma. Progression is rare in adenomas <1cm in diameter. However, up to 40% of lesions larger than 4cm in diameter progress to adenocarcinoma.Most adenomas are asymptomatic and slow growing. Large polyps may present with symptoms of anaemia from occult bleeding. Villous adenomas occasionally secrete large amounts of mucoid protein and/or potassium rich fluid, leading possibly to hypokalemia.

Mesenteric Metastases from Cutaneous Malignant Melanoma
Clinical HistoryA 44-year-old man had a skin lesion on his back that grew slowly. At presentation at A&E several years later, he complained of bone pain, and had hepatomegaly and a pleural effusion. He died shortly afterwards.PathologyThe specimen is a loop of small intestine mounted to display the mesentery, which contains numerous small dark brown, circumscribed nodules varying from pin head size to approximately 1 cm in diameter. Histology confirmed the diagnosis of metastatic melanoma.Further InformationThe most common form of melanoma is cutaneous melanoma, which develops from the pigment-producing cells known as melanocytes. In women, they most commonly occur on the legs, while in men they most commonly occur on the back. About 25% of melanomas develop from moles. Changes in a mole that can indicate melanoma include an increase in size, irregular edges, change in colour, itchiness or skin ulceration.Skin melanoma is associated with exposure to UV radiation in sunlight or tanning beds. Other risk factors for developing melanoma include fair complexion, presence of large number of melanocytic naevi (moles), severe sunburn as a child, and immunosuppression. It accounts for around 5% of all skin cancer diagnosis but has the highest mortality rate of all skin cancers. Melanomas typically occur in sun exposed areas as a pigmented lesion with irregular borders, variegated colour, an asymmetrical shape and which evolves with time.There are multiple mutations common in melanoma. Loss of cell cycle control gene from mutation in CDKN2A gene. Mutations in pro-growth signalling pathways, such as BRAF and PI3K mutations, are seen frequently in melanomas as well as mutations that activate telomerase, such as the TERT gene. Recognition that melanoma antigens activate host immune responses has led to promising immunotherapy, which enhances host T-cell identifying of these antigens.The most common sites for metastasis of melanoma are the lungs, liver, brain and bone as well as regional lymph nodes, and is highly dependent on the site of the primary tumour. Metastatic melanoma involving the gastrointestinal tract may present with anaemia, overt bleeding, pain, obstruction, or intussusception. The jejunum and ileum are the most commonly involved sites, followed by the colon, rectum, and stomach. Surgery has usually been reserved for patients with the above complications.The probability of metastatic spread from skin melanoma depends on the stage of the primary tumour, which is based on tumour depth, mitotic activity and ulceration of the skin as well as node and solid organ involvement. Diagnosis of melanoma is made with excisional biopsy. Investigation for bone metastasis is done using blood test (raised Alkaline phosphatase, calcium and LDH), and radiological investigations most commonly X-ray and CT but MRI and PET scans may also be used. Treatment depends on the stage or the tumour as well as the genetic and immune profiles of the melanoma. Treatment usually involves surgical resection, chemotherapy, targeted therapies (e.g. BRAF inhibitors), immunotherapy , radiotherapy or more commonly a combination of treatments.

Cholecystitis and Cholelithiasis
Clinical HistoryA 60-year-old man head a history of four episodes of severe gripping abdominal pain during the previous year, each lasting two hours and associated with meals. He presented with a similar attack associated with vomiting and fever. This last attack did not resolve spontaneously, and he underwent cholecystectomy.Pathology A thick-walled gallbladder has been opened to display a thickened haemorrhagic mucosa and many irregular faceted calculi. A large calculus is impacted in the neck of the gallbladder. The serosal surface of the gall bladder is congested and has lost its normal sheen. This is an example of cholecystitis complicating cholelithiasis (gallstones).Further InformationAcute cholecystitis is characterised by the clinical syndrome of right upper quadrant pain, fever and jaundice. Gallstones account for the vast majority of acute cholecystitis, with only 5 - 10% of cases being due to other pathology. Chronic cholecystitis may occur, resulting from recurrent attacks and causing fibrosis and thickening of the gallbladder wall. 6-11% of patients with symptomatic gallstones will go on to develop acute cholecystitis. Serum biochemistry will demonstrate leucocytosis with or without obstructive liver function tests. Ultrasound will demonstrate gallstones in the gallbladder, along with wall thickening and a sonographic Murphy’s sign (tenderness from the pressure of the ultrasound probe). Other imaging modalities include nuclear medicine cholescintography scans, MRCP (magnetic cholangiopancreatography) and CT. Endoscopic Retrograde Cholangiopancreatography (ERCP) will provide diagnostic information regarding biliary obstruction and may also be therapeutic. Causative organisms (if present) will be from the gut flora, commonly E coli, Enterococcus, Klebsiella and Enterobacter. Complications include gangrenous cholecystitis, perforation, cholecystoenteric fistula or gallstone ileus. Definitive treatment is surgical cholecystectomy.

Gall Stone Ileus
Clinical HistoryA 54-year-old man presented to hospital with 12 hours of severe colicky pain, nausea and vomiting. On history, he was noted to have had a 3-year history of intermittent right subcostal pain for which he had not seen a doctor. He was diagnosed as having an acute bowel obstruction and a laparotomy was performed.Pathology This segment of small bowel has been opened to display a large pigmented, ovoid gall stone with a roughened surface. This is an example of gall stone ileus.Further InformationGallstone disease is an uncommon cause of bowel obstruction - accounting for only 0.5% of cases with a preponderance for older and female patients. It most commonly secondary to biliary-enteric fistulae (can be to proximal or distal portions of bowel) but can also occur after sphincterotomy. Stones are usually over 2-2.5cm and 70% impact in the ileum, while others obstruct at sites of stricture/narrowing. History may include episodic obstructive symptoms. Diagnosis is confirmed either radiologically (often on CT scan) or at time of removal. Rigler’s triad is typical for gallstone ileus and consists of: (1) small bowel obstruction, (2) a gallstone outside the gallbladder, and (3) air in the bile ducts (pneumobilia) seen on imaging and gallstone presence on plane XR. Treatment usually surgical with removal of the obstructing stone, closure of the fistula and cholecystectomy to stop recurrence. These procedures may need to be staged.

Multiple Polyposis Coli
Clinical HistoryThere are no details of the clinical history.PathologyThe specimens from this case consists of two segments of sigmoid colon. The mucosa of the bowel is studded with numerous sessile and pedunculated partially pigmented polyps up to 1.5 cm in maximum diameter. There is no macroscopic evidence of malignant change.NoteMicroscopically, the polyps are most commonly tubular adenomas (>75% have a tubular structure; also called adenomatous polyps). Less frequently, they are villous adenomas (>75% have villous morphology) or tubulovillous adenomas (25-75% villous). They can have varying grades of dysplasia. The histological appearances are identical to sporadic colonic adenomas.Patients with familial adenomatous polyposis (FAP; a form of hereditary colon cancer syndrome involving the APC gene located on chromosome 5q21) are offered prophylactic colectomy because invasive adenocarcinoma is almost certain to develop in one or more of the polyps, usually about 15 years after the onset of the adenomatosis. This condition is transmitted as an autosomal dominant trait.

Villous adenoma of colon
Clinical HistoryA 70-year old man was admitted for investigation of muscular weakness and the passage of large amounts of mucus per rectum. The patient was found to be hypokalaemic. A tumour of sigmoid colon was discovered and later resected.PathologyA 15 cm long segment of colon has been opened longitudinally to display a large sessile tumour with a velvety surface. The tumour measures 11 x 7 cm. in diameter and approaches to within 2 cm of the distal resection margin. The mucosa is otherwise normal. The serosal surface is unremarkable. Histological examination confirmed the presence of a villous adenoma.Further InformationVillous adenomas occasionally secrete large amounts of mucoid protein and/or potassium rich fluid, sufficient to result in hypoalbuminaemia or hypokalaemia. Villous adenoma is the least common but most ominous type of adenomatous polyp. Invasive carcinoma is present in up to 30% of cases at the time of resection.

Fatty Liver
Clinical HistoryNo clinical details are available.PathologyA slice of liver reveals the characteristic yellow/grey and greasy appearance on one side. On the other side the appearance is restricted to the outer margin whilst the central area displays darker colouration possibly due to cirrhosis. This is an example of fatty change in the liver.NoteCauses of fatty change (steatosis) or accumulations of triglycerides in the liver include obesity, diabetes, alcohol abuse, starvation, Kwashiorkor, drugs and toxins. Alcoholism is the commonest cause in most communities.

Liver cirrhosis
Clinical HistoryThis 63-year old man had several previous admissions to hospital for bleeding from oesophageal varices. On admission he was noted to be mildly febrile, jaundiced with severe flapping tremor of his hands. He had a constellation of other findings included ascites, prominent periumbilical veins and haemorrhoids. He had a massive haematemesis and died.PathologyA slice of liver has been mounted to display the cut surface, which shows multiple well demarcated nodules varying in size from 1 to 7 mm in diameter. The external surface of the liver is also nodular and irregular. This is an example of cirrhosis of the liver, with a mixed micro- and macro- nodular pattern and marked fatty change.Further InformationThe commonest cause of cirrhosis and fatty change is chronic alcoholism.

Ulcerative Colitis
Clinical HistoryA 36-year old female was admitted to hospital with a 3-week history of bloody diarrhoea and lower abdominal pain. Further history taking revealed 4 similar episodes of diarrhoea and abdominal pain of over the past 7 years. Sigmoidoscopy showed a erythematous, ulcerated and oedematous rectal mucosa. She was commenced on steroid treatment but her symptoms failed to improve. She underwent a total colectomy.Pathology The resected colon has been sliced open longitudinally to show the mucosal surface. There is extensive confluent ulceration separated by oedematous islands of residual mucosa. The ulcers have necrotic bases with overhanging edges some of which form ‘pseudo’-polyps. Histology of the bowel mucosa showed acute inflammatory changes with crypt abscesses, focal necrosis and ulceration. This is an example of acute ulcerative colitis (UC).Further InformationUlcerative colitis is a chronic ulcero-inflammatory disease that usually involves the rectum and can extend proximally in a continuous pattern to involve other parts to the colon. The inflammatory process is diffuse but is generally limited to the mucosa and superficial submucosa. The triggering factor for UC in unknown. It most commonly begins between the ages of 15-25 years and is slightly more common in females.UC patients can present with diarrhoea, which may contain blood or mucus, faecal urgency, faecal frequency, tenesmus, colicky abdominal pain, as well as weight loss, anaemia and fatigue. Colonic inflammation can lead to toxic megacolon, colonic perforation or colon cancer. Extraintestinal manifestations include anterior uveitis, migrating polyarthritis, sacroileitis, ankylosing spondylitis, erythema nodosum, pyoderma gangrenosum and primary sclerosing cholangitis.Treatments of UC include use of anti-inflammatory drugs such as steroids, disease modifying rheumatoid drug and TNF (tumor necrosis factor) inhibitors. Colectomy essentially cures intestinal symptoms of UC but extraintestinal manifestations of the disease may persist.

Hepatocellular Carcinoma
Clinical HistoryA 60-year old male is admitted with jaundice, melena and abdominal distension. He has a past medical history of untreated Hepatitis C infection from previous intravenous drug use. Further questioning reveals a 9-month history of significant fatigue, weight loss, nausea and intermittent dull right upper quadrant pain. Liver ultrasound demonstrated two large lesions within the liver. Soon after admission the patient dies from a suspected oesophageal variceal haemorrhage.Pathology This is the liver specimen of the patient on postmortem examination. The cut surface of the liver has a multinodular appearance consistent with macronodular cirrhosis. These multiple nodules are of varying size up to 2cm in diameter, and are separated by narrow bands of fibrous tissue. There are two large round tumours also visible. These are 8cm and 6cm in diameter with a variegated cut surface due to focal necrosis, haemorrhage and bile staining. This is an example of hepatocellular carcinoma that has developed on the background of a cirrhotic liver.Further InformationHepatocellular carcinoma is the most common primary malignant liver cancer. HCC arises from hepatocytes in the liver. Risk factors for developing HCC include viral infections (Hepatitis B and Hepatitis C), liver cirrhosis, aflatoxin exposure, Non Alcoholic Fatty Liver Disease (NAFLD), haemochromatosis and Wilson‘s Disease. The latter is an inherited disorder in which excessive amounts of copper accumulate in the body, particularly in the liver, brain, and eyes. HCC incidence is highest in Asia and sub Saharan Africa. There is a higher risk of developing HCC in males. HCC is associated with acquired driver mutation in oncogenes and tumour suppressor genes. The two most common driver mutations that can lead to HCC are gain-of-function mutations in beta-catenin and loss-of-function mutations in p53.Clinically HCC can present with abdominal pain, fatigue, weight loss, abdominal fullness and less commonly jaundice, gastrointestinal or variceal bleeding. HCC metastatic spread is haematogenous with lung, abdominal lymph nodes and bones being the most common extrahepatic sites. Death usually occurs from cachexia, haemorrhage or liver failure. Treatment varies on the stage of the tumour and the patient’s underlying general status and co-morbidities. Treatment can include surgical resection of ablation of the tumour, chemotherapy and liver transplantation can be curative.

Cholelithiasis (Gallstones)
Clinical HistoryA middle-aged woman was investigated for recurrent bouts of epigastric pain. Endoscopy failed to reveal any peptic ulceration. A cholangiogram demonstrated a non-functioning gallbladder. She died from a myocardial infarction Unfortunately, the patient dies at a later stage after this procedure from a myocardial infarction”.Pathology The specimen is a portion of liver with attached gallbladder, which has been opened to display six large faceted mixed calculi. This is an example of cholelithiasis (gallstones).Further InformationGallstones contain a mixture of cholesterol, calcium salts, bilirubin, proteins, and mucin. There is a high prevalence in fair-skinned populations. Risk factors are age (greater than 50) and female sex, along with genetic factors1, pregnancy, diabetes mellitus and dyslipidaemia. Lifestyle factors, such as rapid weight loss and certain medications (e.g. erythromcyin, ampicillin, octreotide, cephalosporin), can also promote gallstone formation.Gallstones may be asymptomatic or may present with a spectrum of disease ranging from uncomplicated biliary colic through to infection, cholecystitis, pancreatitis or gallstone ileus. The typical symptoms include bouts of epigastric or right upper quadrant pain, sometimes associated with eating, and often with sweating, nausea and vomiting. Pain is usually caused by the gallbladder or biliary tract contracting forcefully against a stone, thereby causing increased pressure in the gallbladder, and pain. The risk of developing complications of gallstones is approximately 2-3 percent per year once biliary colic develops. Diagnosis is generally via transabdominal ultrasound, which has largely replaced oral cholecystography studies. Cholescintigraphy (HIDA Scan) can be used distinguish biliary colic from acute cholecystitis. Treatment of attacks are initially with simple analgesia, and subsequently definitive management usually includes elective laparoscopic cholecystectomy. Very severe cases can be life threatening, but deaths from gallstone disease are rare.It should be noted that epigastric pain can also be caused by myocardial ischemia, particularly in females, who do not necessarily present with the classic ‘left shoulder tip pain’ of an acute myocardial infarct. Therefore, should gallbladder stones be excluded in a patient presenting with epigastric pain, an ECG should always be performed, to help rule out cardiac disease[1].References1. Portincasa P; Moscheta A; Palasciano G (2006) Cholesterol gallstone disease. Lancet. 2006; 368(9531):230-9

Chronic Gastric Ulcer
Clinical HistoryThis elderly patient had a long history of "indigestion". He collapsed and died after a massive stoke.PathologyThe specimen is a 2cm coronal slice of tissue, which incorporates a portion of stomach diaphragm, liver and pancreas. The specimen has been opened to display a large ulcer at the upper end of the lesser curvature near the gastro-oesophageal junction. Macroscopically, the loss of substance at the site of the ulcer is oval, has 5-6cm in diameter and slightly elevated borders. The base is clean and smooth with no evidence of haemorrhage. The gastric wall surrounding the ulcer is indurated, because of the fibrosis that involves the base of the ulcer and spreads beneath the surrounding mucosa. Being retractile, the fibrosis manages to "pull" the gastric mucosa towards the base of the ulcer, so that gastric mucosal folds converge radially around the loss of substance (this feature is not seen in ulcerated malignant gastric tumours). This is evident on the inferior aspect of the ulcer and less so superiorly.Further InformationPatients with a gastric ulcer may experience pain worsening with eating, often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. Complications may include bleeding, perforation, and blockage of the stomach. Common causes include the bacteria Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs).H. pylori was first identified as causing peptic ulcers by Barry Marshall and Robin Warren of the University of Western Australia in the late 20th century, a discovery for which they were awarded the Nobel Prize in 2005. Other, less common causes include tobacco smoking, stress due to serious illness, Behçet’s disease, Zollinger-Ellison syndrome, Crohn’s disease, and liver cirrhosis[1]. Older people are more sensitive to the ulcer-causing effects of NSAIDs[1].The diagnosis is typically suspected due to the presenting symptoms with confirmation by either endoscopy or barium swallow[1]. H. pylori can be diagnosed by testing the blood for antibodies, a urea breath test, testing the stool for signs of the bacteria, or a biopsy of the stomach[1]. Other conditions that produce similar symptoms, include stomach cancer, coronary heart disease, and inflammation of the stomach lining (gastritis) or gallbladder inflammation (cystitis) [1].Treatment includes stopping smoking, stopping use of NSAIDs, reducing or preferably stopping alcohol consumption, and taking medications to decrease stomach acid[1]. Ulcers due to H. pylori are treated with a combination of medications, such as amoxicillin, clarithromycin, and a proton pump inhibitor (PPI). The medication used to decrease acid is usually either a PPI or an H2 blocker (histamine H2-receptor antagonists). Bleeding ulcers may be treated by endoscopy, with open surgery typically only used in cases in which it is not successful. Peptic ulcers are present in around 4% of the population[1].Reference:1. Najm WI (2011). "Peptic ulcer disease". Primary Care. 38 (3): 383–94.

Intussusception of small bowel due to metastatic tumour
Clinical HistoryA 66-year-old woman suffered sudden onset of severe colicky central abdominal pain, somewhat relieved by drawing up her knees. She passed a stool containing mucus and blood ("like redcurrant jelly"). On examination, there was a mass in the left hypochondrium, which hardened with each spasm of pain. The specimen was resected at laparotomy.Pathology The specimen is a segment of small bowel, approximately 20 cm in length, with attached mesentery up to 2 cm in width (more evident on the uncut aspect of the specimen). About 5 cm from the proximal surgical resection margin (which is at the left hand of the specimen), a polypoid tumour 3 cm in diameter has become invaginated into the lumen of the bowel, and has been propelled distally, forming an intussusception 13 cm in length. The tumour is seen at the apex of the intussusception (near the right hand side of the specimen). The congestion and exudate seen on the mucosal surface of the intussusception (invaginated portion) are features considered with early ischaemic necrosis. The histological diagnosis is not recorded in this case; however, the macroscopic appearance is consistent with a metastatic malignant tumour, although the possibility of a primary tumour cannot definitely be excluded.Further InformationIntussusception of the small bowel is most common in children, in whom it is usually due to invagination of swollen lymphoid tissue (Peyer‘s patches) in the wall of the distal ileum. In adults, it is rare, causing only between 1 - 5 percent of cases of bowel obstruction. The usual cause a polypoid tumour, as seen in this specimen, acting as a pathological lead point being pulled forward by peristalsis, and thereby causing telescoping of the affected portion of bowel distally. Presentation may be of intermittent symptoms of bowel obstruction and in some cases excruciating pain. Classification of intussusception can be by causal pathology or by location. Abdominal CT scan will typically demonstrate a typical “target sign” with alternating hyper/hypodense layers.

Hirschsprung&#x2018;s Disease
Clinical HistoryA 5-year old male presents with a history of constipation since birth. A barium enema showed a constricted rectum with a dilated sigmoid colon. Surgical resection of constricted section of bowl was attempted but the patient died during the surgery.Pathology This postmortem section of sigmoid colon has been opened to display the internal surface shown here. There is large dilation of the proximal section of bowel (sigmoid ) with loss of the normal mucosal pattern. The distal section of bowel (rectum) has a normal diameter and a normal mucosal pattern but an absence of ganglion cells in the myenteric plexus. This is an example of Hirschsprung‘s disease, also known as congenital aganglionic megacolon.Further InformationHirschsprung‘s disease is characterised by lack of coordinated peristaltic contraction in a segment of bowel, due to a lack of parasympathetic ganglia. It mainly affects the rectum but the length of the aganglionic sections vary. It is caused by defective proximal to distal migration of neural crest cells from the caecum to rectum during embryogenesis, which leads to development of a distal bowel segment lacking both a myenteric and submucosal plexus. This causes an obstruction with hypertrophy and dilation of the proximal normally innervated colon, which can lead to perforation, peritonitis, enterocolitis and electrolyte imbalances.It occurs in 1 in 5000 live births. It is more common in males, those with siblings with Hirschsprung’s disease and those with other developmental disorders, such as Down Syndrome. Mutations in the receptor tyrosine kinase RET, which is necessary for neural crest cell migration, account for a majority of the familiar cases and 15% of the sporadic cases.Patients typically present with failure to pass meconium within 48 hours of birth. Less severe cases present later with chronic constipation, vomiting, abdominal pain and distension. Treatment involves resection of the aganglionic section of bowel with anastomosis of the normal sections of bowel to the rectum.

Adenocarcinoma of the stomach
Clinical HistoryAn 82-year old female presents with an episode of melena (dark tarry faeces). She had a 6-month history of dyspepsia and nausea. Recently she had noted weight loss and early satiety. Soon after admission she had a large melena episode and died.Pathology This is a post mortem specimen sliced to include a sagittal view of the oesophagus, stomach, proximal duodenum and pancreas. A large 7x5cm ulcer is evident on the lesser curve of the stomach. The ulcer is shallow and broad with raised rolled edges and necrotic debris at the base. There is loss of gastric rugae radiating along the mucous from the ulcer. Dissection of the ulcer reveals elevation of the edge by pale homogenous tumour tissue. There were two eroded arteries present within the ulcer crater with evidence of recent haemorrhage. The pancreas is adherent to the serosal aspect of the ulcer. Histology taken from the lesion (sites visible as regular 3cm defects) demonstrated an ulcerating, well-differentiated adenocarcinoma of the stomach with direct invasion into the pancreas.Further InformationGastric adenocarcinoma is the most common malignancy of the stomach. The incidence varies widely with geography: with a much higher incidence in Japan, Chile, Eastern Europe when compared to North America, Africa, South East Asia and Northern Europe. Risk factors include smoking, high salt diets, H. Pylori infection, Gastro Esophageal Reflux Disease (GERD), atrophic gastritis and intestinal metaplasia of the gastric mucosa.There are two distinct classifications: intestinal and diffuse gastric adenocarcinoma. Intestinal adenocarcinoma resembles glandular tissue similar to colonic or oesophageal adenocarcinoma. Intestinal types tend to be bulky: growing as either an ulcerated or exophytic tumour. Intestinal type occur most frequently in endemic areas, has a male predominance and a mean age of 55 years at presentation. Intestinal type can occur from precursor lesions, such as dysplasia and/or adenomas with dysplasia. Diffuse type gastric cancers have an infiltrative growth pattern and are composed of ‘signet ring’ cells – i.e. cells that have large vacuoles full of mucin leading to displacement of the nucleus to the cell‘s periphery. The cells appear to have lost adhesion between each other, and can therefore be widely distributed within the stomach mucosa. A mass may not be appreciated in this diffuse type as a desmoplastic reaction can occur around the tumour cells, causing a thickened and rigid stomach wall with loss of rugae, creating a “leather bottle” appearance also know of linea plastica. Diffuse type has equal incidence across sexes and countries, and does not have precursor lesions. Germ line mutations in CDH1, which causing loss of function of E-cadherin leading to the loss of cell adhesion, can result in an increased risk of diffuse gastric cancer, which can be familial. Patients with Familial Adenomatous Polyposis (FAP) with germ line mutation in adenomatous polyposis coli (APC) gene have an increased risk in developing intestinal type gastric adenocarcinoma.Early symptoms include dyspepsia, dysphagia and nausea. Later symptoms include weight loss, anorexia, early satiety, fatigue, anaemia and haemorrhage. Treatment depends on tumour stage with surgical resection for early tumours and chemotherapy for later stage cancers.

Hepatic duct calculi and Obstructive Biliary Cirrhosis
Clinical HistoryAn 85-year old male presented with urinary retention due to benign prostatic hypertrophy. On admission it was noted that he was jaundiced with cholestatic derangement of his liver function tests. He underwent a transurethral prostate resection but died from pneumonia 5 days post-operative.Pathology The specimen is a slice of liver mounted to display the cut surface. The capsule is slightly thickened and the liver substance has a finely nodular appearance. Intrahepatic bile ducts are dilated. When the posterior or inferior surface is viewed an irregular pigmented calculus, 10 mm in diameter, is seen impacted in a distended hepatic duct. Another smaller calculus 3 mm in diameter has been dislodged. This specimen represents an example of secondary biliary cirrhosis due to large duct obstruction from hepatic calculi.Further InformationHepatolithiasis is characterised by the presence of intrahepatic gallstones. These calculi can lead to cholangitis, progressive hepatocyte atrophy and destruction, and an increased risk of cholangiocarcinoma. It is common in East Asia but rare in Western countries. There is no difference in incidence between genders. The stones are most commonly made up of pigmented calcium bilirubinate stones.These stones cause intrahepatic bile duct obstruction. Proximal to the obstructing stone distension and dilation of the bile ducts is evident. There is also bile duct proliferation at the portal-parenchymal interface with stromal oedema and infiltrating neutrophils, indicating an acute-chronic inflammation. If untreated this inflammation leads to periportal fibrosis and eventually obstructive biliary cirrhosis. Microscopic appearance would show feathery degeneration of periportal hepatocytes, cytoplasmic swelling often with Mallory Denk bodies (i.e. an inclusion found in the cytoplasm of liver cells with twisted-rope appearance caused by damaged intermediate filaments within the hepatocytes) and bile infarcts from extravasated bile. Chronic inflammation can lead to biliary dysplasia which may develop into cholangiocarcinoma.Patients may present with repeated cholangitis, intermittent abdominal pain, jaundice or frequently no symptoms. Treatment is usually surgical removal of the calculi.


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