Intussusception of small bowel due to metastatic tumour

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.

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.

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.

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.

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.

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.

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.

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.

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