Secretin is a hormone that is released by the duodenum in response to acidity. Its primary function is to decrease gastric acid secretion. It should be noted that the secretin stimulation test involves administering exogenous secretin, which paradoxically causes an increase in gastrin secretion. Secretin does not play a role in carbohydrate digestion, stimulation of gallbladder contraction, stimulation of gastric acid secretion (which is the function of gastrin), or stimulation of pancreatic enzyme secretion (which is another function of CCK).

Overview of Gastrointestinal Hormones

Gastrointestinal hormones play a crucial role in the digestion and absorption of food. These hormones are secreted by various cells in the stomach and small intestine in response to different stimuli such as the presence of food, pH changes, and neural signals.

One of the major hormones involved in food digestion is gastrin, which is secreted by G cells in the antrum of the stomach. Gastrin increases acid secretion by gastric parietal cells, stimulates the secretion of pepsinogen and intrinsic factor, and increases gastric motility. Another hormone, cholecystokinin (CCK), is secreted by I cells in the upper small intestine in response to partially digested proteins and triglycerides. CCK increases the secretion of enzyme-rich fluid from the pancreas, contraction of the gallbladder, and relaxation of the sphincter of Oddi. It also decreases gastric emptying and induces satiety.

Secretin is another hormone secreted by S cells in the upper small intestine in response to acidic chyme and fatty acids. Secretin increases the secretion of bicarbonate-rich fluid from the pancreas and hepatic duct cells, decreases gastric acid secretion, and has a trophic effect on pancreatic acinar cells. Vasoactive intestinal peptide (VIP) is a neural hormone that stimulates secretion by the pancreas and intestines and inhibits acid secretion.

Finally, somatostatin is secreted by D cells in the pancreas and stomach in response to fat, bile salts, and glucose in the intestinal lumen. Somatostatin decreases acid and pepsin secretion, decreases gastrin secretion, decreases pancreatic enzyme secretion, and decreases insulin and glucagon secretion. It also inhibits the trophic effects of gastrin and stimulates gastric mucous production.

In summary, gastrointestinal hormones play a crucial role in regulating the digestive process and maintaining homeostasis in the gastrointestinal tract.

Pseudomembranous colitis is caused by the gram-positive bacillus Clostridium difficile, which can overgrow in the intestine following broad-spectrum antibiotic use. A patient recovering from a total hip replacement who develops signs of infection and is treated with clindamycin may develop severe abdominal pain and diarrhea, indicating a diagnosis of pseudomembranous colitis. Treatment options include metronidazole or oral vancomycin for more severe cases. Staphylococcus bacteria are gram-positive, catalase-positive cocci that can be differentiated based on coagulase positivity and novobiocin sensitivity. Listeria, Bacillus, and Corynebacterium are gram-positive aerobic bacilli, while Campylobacter jejuni, Vibrio cholerae, and Helicobacter pylori are gram-negative, oxidase-positive comma-shaped rods with specific growth characteristics.

Clostridium difficile is a type of bacteria that is commonly found in hospitals. It produces a toxin that can damage the intestines and cause a condition called pseudomembranous colitis. This bacteria usually develops when the normal gut flora is disrupted by broad-spectrum antibiotics, with second and third generation cephalosporins being the leading cause. Other risk factors include the use of proton pump inhibitors. Symptoms of C. difficile infection include diarrhea, abdominal pain, and a raised white blood cell count. The severity of the infection can be determined using the Public Health England severity scale.

To diagnose C. difficile infection, a stool sample is tested for the presence of the C. difficile toxin. Treatment involves reviewing current antibiotic therapy and stopping antibiotics if possible. For a first episode of infection, oral vancomycin is the first-line therapy for 10 days, followed by oral fidaxomicin as second-line therapy and oral vancomycin with or without IV metronidazole as third-line therapy. Recurrent infections may require different treatment options, such as oral fidaxomicin within 12 weeks of symptom resolution or oral vancomycin or fidaxomicin after 12 weeks of symptom resolution. In life-threatening cases, oral vancomycin and IV metronidazole may be used, and surgery may be considered with specialist advice. Other therapies, such as bezlotoxumab and fecal microbiota transplant, may also be considered for preventing recurrences in certain cases.

Pancreatic cancer is a type of cancer that is often diagnosed late due to its non-specific symptoms. The majority of pancreatic tumors are adenocarcinomas and are typically found in the head of the pancreas. Risk factors for pancreatic cancer include increasing age, smoking, diabetes, chronic pancreatitis, hereditary non-polyposis colorectal carcinoma, and mutations in the BRCA2 and KRAS genes.

Symptoms of pancreatic cancer can include painless jaundice, pale stools, dark urine, and pruritus. Courvoisier’s law states that a palpable gallbladder is unlikely to be due to gallstones in the presence of painless obstructive jaundice. However, patients often present with non-specific symptoms such as anorexia, weight loss, and epigastric pain. Loss of exocrine and endocrine function can also occur, leading to steatorrhea and diabetes mellitus. Atypical back pain and migratory thrombophlebitis (Trousseau sign) are also common.

Ultrasound has a sensitivity of around 60-90% for detecting pancreatic cancer, but high-resolution CT scanning is the preferred diagnostic tool. The ‘double duct’ sign, which is the simultaneous dilatation of the common bile and pancreatic ducts, may be seen on imaging.

Less than 20% of patients with pancreatic cancer are suitable for surgery at the time of diagnosis. A Whipple’s resection (pancreaticoduodenectomy) may be performed for resectable lesions in the head of the pancreas, but side-effects such as dumping syndrome and peptic ulcer disease can occur. Adjuvant chemotherapy is typically given following surgery, and ERCP with stenting may be used for palliation.

The patient is diagnosed with gastric adenocarcinoma, which is a type of cancer that originates in the stomach lining. The presence of signet ring cells in the biopsy is a concerning feature, indicating an aggressive form of adenocarcinoma.

Chief cells are normal cells found in the stomach lining and are not indicative of any pathology in this case.

Megaloblast cells are abnormally large red blood cells that are not expected to be present in a gastric biopsy. They are typically associated with conditions such as leukaemia.

Merkel cells are benign cells found in the skin that play a role in the sensation of touch.

Mucous cells are normal cells found in the stomach lining that produce mucus.

Gastric cancer is a relatively uncommon type of cancer, accounting for only 2% of all cancer diagnoses in developed countries. It is more prevalent in older individuals, with half of patients being over the age of 75, and is more common in males than females. Several risk factors have been identified, including Helicobacter pylori infection, atrophic gastritis, certain dietary habits, smoking, and blood group. Symptoms of gastric cancer can include abdominal pain, weight loss, nausea, vomiting, and dysphagia. In some cases, lymphatic spread may result in the appearance of nodules in the left supraclavicular lymph node or periumbilical area. Diagnosis is typically made through oesophago-gastro-duodenoscopy with biopsy, and staging is done using CT. Treatment options depend on the extent and location of the cancer and may include endoscopic mucosal resection, partial or total gastrectomy, and chemotherapy.

The majority of colonic polyps mentioned earlier are adenomas, which can be accompanied by dysplasia. The severity of dysplasia is directly proportional to the level of clinical apprehension.

Understanding Colonic Polyps and Follow-Up Procedures

Colonic polyps can occur in isolation or as part of polyposis syndromes, with greater than 100 polyps typically present in FAP. The risk of malignancy is related to size, with a 10% risk in a 1 cm adenoma. While isolated adenomas seldom cause symptoms, distally sited villous lesions may produce mucous and electrolyte disturbances if very large.

Follow-up procedures for colonic polyps depend on the number and size of the polyps. Low-risk cases with 1 or 2 adenomas less than 1 cm require no follow-up or re-colonoscopy for 5 years. Moderate-risk cases with 3 or 4 small adenomas or 1 adenoma greater than 1 cm require a re-scope at 3 years. High-risk cases with more than 5 small adenomas or more than 3 with 1 of them greater than 1 cm require a re-scope at 1 year.

Segmental resection or complete colectomy may be necessary in cases of incomplete excision of malignant polyps, malignant sessile polyps, malignant pedunculated polyps with submucosal invasion, polyps with poorly differentiated carcinoma, or familial polyposis coli. Screening from teenager up to 40 years by 2 yearly sigmoidoscopy/colonoscopy is recommended. Rectal polypoidal lesions may be treated with trans anal endoscopic microsurgery.

The development of Crohn’s disease is connected to a genetic abnormality in the NOD-2 gene.

Phenylketonuria is linked to the PKU mutation.

Cystic fibrosis is associated with the CFTR mutation.

Ehlers-Danlos syndrome is connected to the COL1A1 mutation.

Understanding Crohn’s Disease

Crohn’s disease is a type of inflammatory bowel disease that can affect any part of the digestive tract, from the mouth to the anus. The exact cause of Crohn’s disease is unknown, but there is a strong genetic component. Inflammation occurs in all layers of the affected area, which can lead to complications such as strictures, fistulas, and adhesions.

Symptoms of Crohn’s disease typically appear in late adolescence or early adulthood and can include non-specific symptoms such as weight loss and lethargy, as well as more specific symptoms like diarrhea, abdominal pain, and perianal disease. Extra-intestinal features, such as arthritis, erythema nodosum, and osteoporosis, are also common in patients with Crohn’s disease.

To diagnose Crohn’s disease, doctors may look for raised inflammatory markers, increased faecal calprotectin, anemia, and low levels of vitamin B12 and vitamin D. It’s important to note that Crohn’s disease shares some features with ulcerative colitis, another type of inflammatory bowel disease, but there are also important differences between the two conditions. Understanding the symptoms and diagnostic criteria for Crohn’s disease can help patients and healthcare providers manage this chronic condition more effectively.

Understanding Peutz-Jeghers Syndrome

Peutz-Jeghers syndrome is a genetic condition that is inherited in an autosomal dominant manner. It is characterized by the presence of numerous hamartomatous polyps in the gastrointestinal tract, particularly in the small bowel. In addition, patients with this syndrome may also have pigmented freckles on their lips, face, palms, and soles.

While the polyps themselves are not cancerous, individuals with Peutz-Jeghers syndrome have an increased risk of developing other types of gastrointestinal tract cancers. In fact, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.

Common symptoms of Peutz-Jeghers syndrome include small bowel obstruction, which is often due to intussusception, as well as gastrointestinal bleeding. Management of this condition is typically conservative unless complications develop. It is important for individuals with Peutz-Jeghers syndrome to undergo regular screening and surveillance to detect any potential cancerous growths early on.

Acute pancreatitis can be caused by azathioprine.

It is important to note that the symptoms and blood tests suggest acute pancreatitis. The most common causes of this condition are gallstones and alcohol, but these have been ruled out through patient history. Although there is a possibility of retained stones in the common bile duct after cholecystectomy, it is unlikely given the time since the operation.

Other less common causes include trauma (which is not present in this case) and sodium valproate (which the patient has not been taking).

Therefore, the most likely cause of acute pancreatitis in this case is azathioprine, an immunosuppressive medication used to treat rheumatoid arthritis, which is known to have a side effect of acute pancreatitis.

Acute pancreatitis is a condition that is primarily caused by gallstones and alcohol consumption in the UK. However, there are other factors that can contribute to the development of this condition. A popular mnemonic used to remember these factors is GET SMASHED, which stands for gallstones, ethanol, trauma, steroids, mumps, autoimmune diseases, scorpion venom, hypertriglyceridaemia, hyperchylomicronaemia, hypercalcaemia, hypothermia, ERCP, and certain drugs. It is important to note that pancreatitis is seven times more common in patients taking mesalazine than sulfasalazine. CT scans can show diffuse parenchymal enlargement with oedema and indistinct margins in patients with acute pancreatitis.

The most likely diagnosis for the patient is a perforated peptic ulcer, which may have been caused by their use of ibuprofen. The recommended first-line treatment according to NICE guidelines is endoscopic intervention, which can confirm the diagnosis and stop the bleeding. This involves injecting adrenaline into the bleeding site and using cautery and/or clip application. Helicobacter pylori eradication therapy is not appropriate in this case, as the patient’s symptoms suggest a perforated peptic ulcer rather than peptic ulcer disease caused by H. pylori. IV proton-pump inhibitor infusion may be considered later, but the patient requires immediate management with endoscopic intervention.

Managing Acute Bleeding in Peptic Ulcer Disease

Peptic ulcer disease is a condition that can lead to acute bleeding, which is the most common complication of the disease. In fact, bleeding accounts for about three-quarters of all problems associated with peptic ulcer disease. The gastroduodenal artery is often the source of significant gastrointestinal bleeding in patients with this condition. The most common symptom of acute bleeding in peptic ulcer disease is haematemesis, but patients may also experience melaena, hypotension, and tachycardia.

When managing acute bleeding in peptic ulcer disease, an ABC approach should be taken, as with any upper gastrointestinal haemorrhage. Intravenous proton pump inhibitors are the first-line treatment, and endoscopic intervention is typically the preferred approach. However, if endoscopic intervention fails (which occurs in approximately 10% of patients), urgent interventional angiography with transarterial embolization or surgery may be necessary. By following these management strategies, healthcare providers can effectively address acute bleeding in patients with peptic ulcer disease.

The posterior fundus of the stomach is located while the inferolateral position is occupied by the pylorus. In order to access the proximal stomach and abdominal esophagus during a total gastrectomy, it is helpful to divide the ligaments that hold the left lobe of the liver. However, this maneuver is not usually necessary during a distal gastrectomy.

Structure and Relations of the Liver

The liver is divided into four lobes: the right lobe, left lobe, quadrate lobe, and caudate lobe. The right lobe is supplied by the right hepatic artery and contains Couinaud segments V to VIII, while the left lobe is supplied by the left hepatic artery and contains Couinaud segments II to IV. The quadrate lobe is part of the right lobe anatomically but functionally is part of the left, and the caudate lobe is supplied by both right and left hepatic arteries and lies behind the plane of the porta hepatis. The liver lobules are separated by portal canals that contain the portal triad: the hepatic artery, portal vein, and tributary of bile duct.

The liver has various relations with other organs in the body. Anteriorly, it is related to the diaphragm, esophagus, xiphoid process, stomach, duodenum, hepatic flexure of colon, right kidney, gallbladder, and inferior vena cava. The porta hepatis is located on the postero-inferior surface of the liver and transmits the common hepatic duct, hepatic artery, portal vein, sympathetic and parasympathetic nerve fibers, and lymphatic drainage of the liver and nodes.

The liver is supported by ligaments, including the falciform ligament, which is a two-layer fold of peritoneum from the umbilicus to the anterior liver surface and contains the ligamentum teres (remnant of the umbilical vein). The ligamentum venosum is a remnant of the ductus venosus. The liver is supplied by the hepatic artery and drained by the hepatic veins and portal vein. Its nervous supply comes from the sympathetic and parasympathetic trunks of the coeliac plexus.

The infant in this scenario is displaying symptoms of intussusception, including red current jelly stools and shock. Malrotation, which typically causes obstruction, can be ruled out as there is evidence of the passage of red stools. Meckel’s diverticulitis does not cause the infant to draw their knees up and is not typically associated with shock. Pyloric stenosis is characterized by projectile vomiting and not bloody stools. Acute appendicitis is not a likely diagnosis based on this presentation.

Understanding Intussusception

Intussusception is a medical condition where one part of the bowel folds into the lumen of the adjacent bowel, usually around the ileocecal region. This condition is most common in infants between 6-18 months old, with boys being affected twice as often as girls. Symptoms of intussusception include severe, crampy abdominal pain, inconsolable crying, vomiting, and bloodstained stool, which is a late sign. During a paroxysm, the infant will draw their knees up and turn pale, and a sausage-shaped mass may be felt in the right upper quadrant.

To diagnose intussusception, ultrasound is now the preferred method of investigation, which may show a target-like mass. Treatment for intussusception involves reducing the bowel by air insufflation under radiological control, which is now widely used first-line compared to the traditional barium enema. If this method fails, or the child has signs of peritonitis, surgery is performed. Understanding the symptoms and treatment options for intussusception is crucial for parents and healthcare professionals to ensure prompt and effective management of this condition.

Jaundice becomes visible when bilirubin levels exceed 35 umol/l. Therefore, the correct option is the one with a bilirubin level of 40 umol/l, as this is typically the range where jaundice becomes visible. Furthermore, all other liver function values in this option are within the normal range. The other options are incorrect because they have bilirubin levels that are too low to cause visible jaundice, and the liver function results are usually normal in cases of Gilbert’s syndrome.

Understanding Bilirubin and Its Role in Jaundice

Bilirubin is a chemical by-product that is produced when red blood cells break down heme, a component found in these cells. This chemical is also found in other hepatic heme-containing proteins like myoglobin. The heme is processed within macrophages and oxidized to form biliverdin and iron. Biliverdin is then reduced to form unconjugated bilirubin, which is released into the bloodstream.

Unconjugated bilirubin is bound to albumin in the blood and then taken up by hepatocytes, where it is conjugated to make it water-soluble. From there, it is excreted into bile and enters the intestines to be broken down by intestinal bacteria. Bacterial proteases produce urobilinogen from bilirubin within the intestinal lumen, which is further processed by intestinal bacteria to form urobilin and stercobilin and excreted via the faeces. A small amount of bilirubin re-enters the portal circulation to be finally excreted via the kidneys in urine.

Jaundice occurs when bilirubin levels exceed 35 umol/l. Raised levels of unconjugated bilirubin may occur due to haemolysis, while hepatocyte defects, such as a compromised hepatocyte uptake of unconjugated bilirubin and/or defective conjugation, may occur in liver disease or deficiency of glucuronyl transferase. Raised levels of conjugated bilirubin can result from defective excretion of bilirubin, for example, Dubin-Johnson Syndrome, or cholestasis.

Cholestasis can result from a wide range of pathologies, which can be largely divided into physical causes, for example, gallstones, pancreatic and cholangiocarcinoma, or functional causes, for example, drug-induced, pregnancy-related and postoperative cholestasis. Understanding bilirubin and its role in jaundice is important in diagnosing and treating various liver and blood disorders.

Colorectal cancer can be classified into three types: sporadic, hereditary non-polyposis colorectal carcinoma (HNPCC), and familial adenomatous polyposis (FAP). Sporadic colon cancer is believed to be caused by a series of genetic mutations, including allelic loss of the APC gene, activation of the K-ras oncogene, and deletion of p53 and DCC tumor suppressor genes. HNPCC, which is an autosomal dominant condition, is the most common form of inherited colon cancer. It is caused by mutations in genes involved in DNA mismatch repair, leading to microsatellite instability. The most common genes affected are MSH2 and MLH1. Patients with HNPCC are also at a higher risk of other cancers, such as endometrial cancer. The Amsterdam criteria are sometimes used to aid diagnosis of HNPCC. FAP is a rare autosomal dominant condition that leads to the formation of hundreds of polyps by the age of 30-40 years. It is caused by a mutation in the APC gene. Patients with FAP are also at risk of duodenal tumors. A variant of FAP called Gardner’s syndrome can also feature osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma, and epidermoid cysts on the skin. Genetic testing can be done to diagnose HNPCC and FAP, and patients with FAP generally have a total colectomy with ileo-anal pouch formation in their twenties.

The renal artery provides branches that supply the proximal ureter, while other feeding vessels are described in the following.

Anatomy of the Ureter

The ureter is a muscular tube that measures 25-35 cm in length and is lined by transitional epithelium. It is surrounded by a thick muscular coat that becomes three muscular layers as it crosses the bony pelvis. This retroperitoneal structure overlies the transverse processes L2-L5 and lies anterior to the bifurcation of iliac vessels. The blood supply to the ureter is segmental and includes the renal artery, aortic branches, gonadal branches, common iliac, and internal iliac. It is important to note that the ureter lies beneath the uterine artery.

In summary, the ureter is a vital structure in the urinary system that plays a crucial role in transporting urine from the kidneys to the bladder. Its unique anatomy and blood supply make it a complex structure that requires careful consideration in any surgical or medical intervention.

The patient’s symptoms and laboratory findings suggest a cholestatic disease, specifically primary biliary cholangitis, which is an autoimmune condition of the biliary tract. This disease is more common in middle-aged women and can present with symptoms such as fatigue and pruritus. Non-alcoholic steatohepatitis is a metabolic syndrome-related condition characterized by triglyceride accumulation and myofibroblast proliferation, while primary sclerosing cholangitis is characterized by bile duct inflammation and sclerosis. Alcoholic hepatitis is caused by long-term alcohol misuse and is characterized by macrovesicular fatty change, spotty necrosis, and fibrosis.

Primary biliary cholangitis is a chronic liver disorder that affects middle-aged women. It is thought to be an autoimmune condition that damages interlobular bile ducts, causing progressive cholestasis and potentially leading to cirrhosis. The classic presentation is itching in a middle-aged woman. It is associated with Sjogren’s syndrome, rheumatoid arthritis, systemic sclerosis, and thyroid disease. Diagnosis involves immunology and imaging tests. Management includes ursodeoxycholic acid, cholestyramine for pruritus, and liver transplantation in severe cases. Complications include cirrhosis, osteomalacia and osteoporosis, and an increased risk of hepatocellular carcinoma.

Hyposplenism is a possible complication of coeliac disease. The patient’s symptoms and positive tissue transglutaminases support the diagnosis of coeliac disease, which can lead to malabsorption of important nutrients like iron, folate, and vitamin B12. Hyposplenism may occur due to autoimmune processes and loss of lymphocyte recirculation caused by inflammation in the colon. However, hepatomegaly, pancreatitis, and polycythaemia are not associated with coeliac disease.

Understanding Coeliac Disease

Coeliac disease is an autoimmune disorder that affects approximately 1% of the UK population. It is caused by sensitivity to gluten, a protein found in wheat, barley, and rye. Repeated exposure to gluten leads to villous atrophy, which causes malabsorption. Coeliac disease is associated with various conditions, including dermatitis herpetiformis and autoimmune disorders such as type 1 diabetes mellitus and autoimmune hepatitis. It is strongly linked to HLA-DQ2 and HLA-DQ8.

To diagnose coeliac disease, NICE recommends screening patients who exhibit signs and symptoms such as chronic or intermittent diarrhea, failure to thrive or faltering growth in children, persistent or unexplained gastrointestinal symptoms, prolonged fatigue, recurrent abdominal pain, sudden or unexpected weight loss, unexplained anemia, autoimmune thyroid disease, dermatitis herpetiformis, irritable bowel syndrome, type 1 diabetes, and first-degree relatives with coeliac disease.

Complications of coeliac disease include anemia, hyposplenism, osteoporosis, osteomalacia, lactose intolerance, enteropathy-associated T-cell lymphoma of the small intestine, subfertility, and unfavorable pregnancy outcomes. In rare cases, it can lead to esophageal cancer and other malignancies.

The diagnosis of coeliac disease is confirmed through a duodenal biopsy, which shows complete atrophy of the villi with flat mucosa and marked crypt hyperplasia, intraepithelial lymphocytosis, and dense mixed inflammatory infiltrate in the lamina propria. Treatment involves a lifelong gluten-free diet.

The lining of the oesophagus is composed of stratified squamous epithelium that is not keratinised. Metaplastic processes in reflux can lead to the transformation of this epithelium into glandular type epithelium.

Anatomy of the Oesophagus

The oesophagus is a muscular tube that is approximately 25 cm long and starts at the C6 vertebrae, pierces the diaphragm at T10, and ends at T11. It is lined with non-keratinized stratified squamous epithelium and has constrictions at various distances from the incisors, including the cricoid cartilage at 15cm, the arch of the aorta at 22.5cm, the left principal bronchus at 27cm, and the diaphragmatic hiatus at 40cm.

The oesophagus is surrounded by various structures, including the trachea to T4, the recurrent laryngeal nerve, the left bronchus and left atrium, and the diaphragm anteriorly. Posteriorly, it is related to the thoracic duct to the left at T5, the hemiazygos to the left at T8, the descending aorta, and the first two intercostal branches of the aorta. The arterial, venous, and lymphatic drainage of the oesophagus varies depending on the location, with the upper third being supplied by the inferior thyroid artery and drained by the deep cervical lymphatics, the mid-third being supplied by aortic branches and drained by azygos branches and mediastinal lymphatics, and the lower third being supplied by the left gastric artery and drained by posterior mediastinal and coeliac veins and gastric lymphatics.

The nerve supply of the oesophagus also varies, with the upper half being supplied by the recurrent laryngeal nerve and the lower half being supplied by the oesophageal plexus of the vagus nerve. The muscularis externa of the oesophagus is composed of both smooth and striated muscle, with the composition varying depending on the location.

The inferior mesenteric artery is responsible for supplying blood to the hindgut, which includes the distal third of the colon and the rectum superior to the pectinate line. In this case, the patient’s sudden onset of severe abdominal pain and history of atrial fibrillation suggest acute mesenteric ischemia, with the affected artery being the inferior mesenteric artery. Therefore, if a thrombus were to block this artery, the distal third of the colon and superior rectum would experience ischaemic changes. It is important to note that the ascending colon, caecum, ileum, appendix, greater omentum, and stomach are supplied by different arteries and would not be affected by a thrombus in the inferior mesenteric artery.

The Inferior Mesenteric Artery: Supplying the Hindgut

The inferior mesenteric artery (IMA) is responsible for supplying the embryonic hindgut with blood. It originates just above the aortic bifurcation, at the level of L3, and passes across the front of the aorta before settling on its left side. At the point where the left common iliac artery is located, the IMA becomes the superior rectal artery.

The hindgut, which includes the distal third of the colon and the rectum above the pectinate line, is supplied by the IMA. The left colic artery is one of the branches that emerges from the IMA near its origin. Up to three sigmoid arteries may also exit the IMA to supply the sigmoid colon further down the line.

Overall, the IMA plays a crucial role in ensuring that the hindgut receives the blood supply it needs to function properly. Its branches help to ensure that the colon and rectum are well-nourished and able to carry out their important digestive functions.

Individuals with Gilbert’s syndrome exhibit a decrease in the amount of UDP glucuronosyltransferase, an enzyme responsible for conjugating bilirubin in the liver. This deficiency leads to an accumulation of unconjugated bilirubin, which cannot be eliminated through urine, resulting in jaundice. Although symptoms may arise during periods of stress, the condition is generally not clinically significant.

HMG-CoA reductase is an enzyme involved in cholesterol synthesis, while lipoprotein lipase plays a central role in lipid metabolism and is associated with various conditions such as hypertriglyceridemia. G6PD deficiency, on the other hand, affects the pentose phosphate pathway by reducing the production of NADPH.

Gilbert’s syndrome is a genetic disorder that affects the way bilirubin is processed in the body. It is caused by a deficiency of UDP glucuronosyltransferase, which leads to unconjugated hyperbilirubinemia. This means that bilirubin is not properly broken down and eliminated from the body, resulting in jaundice. However, jaundice may only be visible during certain conditions such as fasting, exercise, or illness. The prevalence of Gilbert’s syndrome is around 1-2% in the general population.

To diagnose Gilbert’s syndrome, doctors may look for a rise in bilirubin levels after prolonged fasting or the administration of IV nicotinic acid. However, treatment is not necessary for this condition. While the exact mode of inheritance is still debated, it is known to be an autosomal recessive disorder.

The causative organism in pseudomembranous colitis following recent broad-spectrum antibiotic use is Clostridium difficile, a gram-positive bacillus. This woman’s clinical presentation is consistent with C. diff infection, as she has experienced multiple episodes of loose stool with abdominal pain and has risk factors such as residing in a care home and recent antibiotic use for chest infections. While gram-negative comma-shaped bacteria like Vibrio cholerae can cause cholera, it is not found in the UK and is therefore unlikely to be the cause here. Gram-negative rods like Escherichia coli or Campylobacter jejuni can cause diarrhoeal illnesses, but are more associated with bloody diarrhoea and food poisoning, which do not match this woman’s symptoms. Gram-positive rods like Bacillus cereus can cause vomiting or diarrhoeal illness from contaminated food, but antibiotics are not beneficial and vancomycin would not be needed. Given the woman’s risk factors and symptoms, C. diff is the most likely cause.

Clostridium difficile is a type of bacteria that is commonly found in hospitals. It produces a toxin that can damage the intestines and cause a condition called pseudomembranous colitis. This bacteria usually develops when the normal gut flora is disrupted by broad-spectrum antibiotics, with second and third generation cephalosporins being the leading cause. Other risk factors include the use of proton pump inhibitors. Symptoms of C. difficile infection include diarrhea, abdominal pain, and a raised white blood cell count. The severity of the infection can be determined using the Public Health England severity scale.

To diagnose C. difficile infection, a stool sample is tested for the presence of the C. difficile toxin. Treatment involves reviewing current antibiotic therapy and stopping antibiotics if possible. For a first episode of infection, oral vancomycin is the first-line therapy for 10 days, followed by oral fidaxomicin as second-line therapy and oral vancomycin with or without IV metronidazole as third-line therapy. Recurrent infections may require different treatment options, such as oral fidaxomicin within 12 weeks of symptom resolution or oral vancomycin or fidaxomicin after 12 weeks of symptom resolution. In life-threatening cases, oral vancomycin and IV metronidazole may be used, and surgery may be considered with specialist advice. Other therapies, such as bezlotoxumab and fecal microbiota transplant, may also be considered for preventing recurrences in certain cases.

After passing the inguinal ligament, the external iliac artery transforms into the femoral artery. This means that the other options provided are not accurate. Here is a brief explanation of their anatomical importance:

– The medial edge of the sartorius muscle creates the lateral wall of the femoral triangle.
– The medial edge of the adductor longus muscle creates the medial wall of the femoral triangle.
– The femoral vein creates the lateral border of the femoral canal.
– The pectineus muscle creates the posterior border of the femoral canal.

The inguinal canal is located above the inguinal ligament and measures 4 cm in length. Its superficial ring is situated in front of the pubic tubercle, while the deep ring is found about 1.5-2 cm above the halfway point between the anterior superior iliac spine and the pubic tubercle. The canal is bounded by the external oblique aponeurosis, inguinal ligament, lacunar ligament, internal oblique, transversus abdominis, external ring, and conjoint tendon. In males, the canal contains the spermatic cord and ilioinguinal nerve, while in females, it houses the round ligament of the uterus and ilioinguinal nerve.

The boundaries of Hesselbach’s triangle, which are frequently tested, are located in the inguinal region. Additionally, the inguinal canal is closely related to the vessels of the lower limb, which should be taken into account when repairing hernial defects in this area.

The inferior mesenteric artery supplies the distal 1/3 of the transverse colon, while the proximal two thirds are supplied by the middle colic artery, a branch of the SMA. The left colic artery, a branch of the IMA, supplies the remaining distal portion. Although the left colic artery is the primary supplier, collateral flow from branches of the middle colic artery also contributes. The left colic flexure, located between the end of the SMA and the start of the IMA’s blood supply, is a watershed region that can be susceptible to ischemia due to atherosclerotic changes or hypotension.

The splenic artery directly supplies the spleen and also has branches that supply the stomach and pancreas. There is no such thing as the AMA or PMA.

The Transverse Colon: Anatomy and Relations

The transverse colon is a part of the large intestine that begins at the hepatic flexure, where the right colon makes a sharp turn. At this point, it becomes intraperitoneal and is connected to the inferior border of the pancreas by the transverse mesocolon. The middle colic artery and vein are contained within the mesentery. The greater omentum is attached to the superior aspect of the transverse colon, which can be easily separated. The colon undergoes another sharp turn at the splenic flexure, where the greater omentum remains attached up to this point. The distal 1/3 of the transverse colon is supplied by the inferior mesenteric artery.

The transverse colon is related to various structures. Superiorly, it is in contact with the liver, gallbladder, the greater curvature of the stomach, and the lower end of the spleen. Inferiorly, it is related to the small intestine. Anteriorly, it is in contact with the greater omentum, while posteriorly, it is in contact with the descending portion of the duodenum, the head of the pancreas, convolutions of the jejunum and ileum, and the spleen. Understanding the anatomy and relations of the transverse colon is important for medical professionals in diagnosing and treating various gastrointestinal conditions.

Annual colonoscopy is recommended for individuals who have both ulcerative colitis and PSC.

Colorectal Cancer Risk in Ulcerative Colitis Patients

Ulcerative colitis patients have a significantly higher risk of developing colorectal cancer compared to the general population. The risk is mainly related to chronic inflammation, and studies report varying rates. Unfortunately, patients with ulcerative colitis often experience delayed diagnosis, leading to a worse prognosis. Lesions may also be multifocal, further increasing the risk of cancer.

Several factors increase the risk of colorectal cancer in ulcerative colitis patients, including disease duration of more than 10 years, pancolitis, onset before 15 years old, unremitting disease, and poor compliance to treatment. To manage this risk, colonoscopy surveillance is recommended, and the frequency of surveillance depends on the patient’s risk stratification.

Patients with lower risk require a colonoscopy every five years, while those with intermediate risk require a colonoscopy every three years. Patients with higher risk require a colonoscopy every year. The risk stratification is based on factors such as the extent of colitis, the severity of active endoscopic/histological inflammation, the presence of post-inflammatory polyps, and family history of colorectal cancer. Primary sclerosing cholangitis or a family history of colorectal cancer in first-degree relatives aged less than 50 years also increase the risk of cancer. By following these guidelines, ulcerative colitis patients can receive appropriate surveillance and management to reduce their risk of developing colorectal cancer.

The presentation of symptoms related to the conjugation of bilirubin varies depending on where the process is disrupted, such as pre-hepatic, hepatic, or post-hepatic. In this case, a mass in the pancreatic head has caused an obstruction of the common bile duct, which is post-hepatic. This obstruction results in less conjugated bilirubin reaching the intestinal tract and more being absorbed into the systemic circulation. As a result, there is a decrease in stercobilin production, leading to paler stools.

Pancreatic cancer is a type of cancer that is often diagnosed late due to its non-specific symptoms. The majority of pancreatic tumors are adenocarcinomas and are typically found in the head of the pancreas. Risk factors for pancreatic cancer include increasing age, smoking, diabetes, chronic pancreatitis, hereditary non-polyposis colorectal carcinoma, and mutations in the BRCA2 and KRAS genes.

Symptoms of pancreatic cancer can include painless jaundice, pale stools, dark urine, and pruritus. Courvoisier’s law states that a palpable gallbladder is unlikely to be due to gallstones in the presence of painless obstructive jaundice. However, patients often present with non-specific symptoms such as anorexia, weight loss, and epigastric pain. Loss of exocrine and endocrine function can also occur, leading to steatorrhea and diabetes mellitus. Atypical back pain and migratory thrombophlebitis (Trousseau sign) are also common.

Ultrasound has a sensitivity of around 60-90% for detecting pancreatic cancer, but high-resolution CT scanning is the preferred diagnostic tool. The ‘double duct’ sign, which is the simultaneous dilatation of the common bile and pancreatic ducts, may be seen on imaging.

Less than 20% of patients with pancreatic cancer are suitable for surgery at the time of diagnosis. A Whipple’s resection (pancreaticoduodenectomy) may be performed for resectable lesions in the head of the pancreas, but side-effects such as dumping syndrome and peptic ulcer disease can occur. Adjuvant chemotherapy is typically given following surgery, and ERCP with stenting may be used for palliation.

The patient is experiencing acute pancreatitis, possibly due to excessive alcohol consumption. As this is his first visit to the emergency department, it is unlikely to be a sudden attack on top of chronic pancreatitis. The presence of tachycardia and hypotension suggests that he is also experiencing blood loss. The correct answer should identify an acute condition associated with blood loss.

a. Bulky, greasy stools are a long-term complication of chronic pancreatitis, indicating that the pancreas has lost its exocrine function and is unable to properly digest food.

b. Grey Turner’s sign is a sign of blood pooling in the retroperitoneal space, which can occur due to inflammation of the retroperitoneal pancreas.

c. This is a complication of long-term diabetes or chronic pancreatitis.

d. Ascites is not typically associated with an acute first-time presentation of pancreatitis, although it can have many causes.

e. This description is typical of an abdominal obstruction, which may cause nausea and vomiting.

The retroperitoneal structures are those that are located behind the peritoneum, which is the membrane that lines the abdominal cavity. These structures include the duodenum (2nd, 3rd, and 4th parts), ascending and descending colon, kidneys, ureters, aorta, and inferior vena cava. They are situated in the back of the abdominal cavity, close to the spine. In contrast, intraperitoneal structures are those that are located within the peritoneal cavity, such as the stomach, duodenum (1st part), jejunum, ileum, transverse colon, and sigmoid colon. It is important to note that the retroperitoneal structures are not well demonstrated in the diagram as the posterior aspect has been removed, but they are still significant in terms of their location and function.

The stones in the ureter can be seen at the anterior of L2 to L5, as well as over the sacro-iliac joints.

Anatomy of the Ureter

The ureter is a muscular tube that measures 25-35 cm in length and is lined by transitional epithelium. It is surrounded by a thick muscular coat that becomes three muscular layers as it crosses the bony pelvis. This retroperitoneal structure overlies the transverse processes L2-L5 and lies anterior to the bifurcation of iliac vessels. The blood supply to the ureter is segmental and includes the renal artery, aortic branches, gonadal branches, common iliac, and internal iliac. It is important to note that the ureter lies beneath the uterine artery.

In summary, the ureter is a vital structure in the urinary system that plays a crucial role in transporting urine from the kidneys to the bladder. Its unique anatomy and blood supply make it a complex structure that requires careful consideration in any surgical or medical intervention.

Helicobacter pylori uses urease to survive in the stomach by neutralizing gastric acid. This enzyme produces ammonia, which creates a more suitable environment for bacterial growth. The patient’s CLO positive peptic ulcer is consistent with a Helicobacter pylori infection. It is important to note that Helicobacter pylori does not use arginase, beta-lactamase, protease, or trypsin to neutralize stomach acid.

Helicobacter pylori: A Bacteria Associated with Gastrointestinal Problems

Helicobacter pylori is a type of Gram-negative bacteria that is commonly associated with various gastrointestinal problems, particularly peptic ulcer disease. This bacterium has two primary mechanisms that allow it to survive in the acidic environment of the stomach. Firstly, it uses its flagella to move away from low pH areas and burrow into the mucous lining to reach the epithelial cells underneath. Secondly, it secretes urease, which converts urea to NH3, leading to an alkalinization of the acidic environment and increased bacterial survival.

The pathogenesis mechanism of Helicobacter pylori involves the release of bacterial cytotoxins, such as the CagA toxin, which can disrupt the gastric mucosa. This bacterium is associated with several gastrointestinal problems, including peptic ulcer disease, gastric cancer, B cell lymphoma of MALT tissue, and atrophic gastritis. However, its role in gastro-oesophageal reflux disease (GORD) is unclear, and there is currently no role for the eradication of Helicobacter pylori in GORD.

The management of Helicobacter pylori infection involves a 7-day course of treatment with a proton pump inhibitor, amoxicillin, and either clarithromycin or metronidazole. For patients who are allergic to penicillin, a proton pump inhibitor, metronidazole, and clarithromycin are used instead.

The facial nerve’s chorda tympani branch is responsible for providing taste sensation to the anterior two-thirds of the tongue. Bell’s palsy is a condition characterized by unilateral facial nerve weakness or paralysis, which can result in impaired taste sensation in the anterior tongue.

Upper motor neuron lesions typically spare the forehead, as alternative nerve routes can still provide innervation. In contrast, lower motor neuron lesions like Bell’s palsy can cause forehead paralysis.

While ptosis may occur in Bell’s palsy, it typically presents unilaterally rather than bilaterally.

Although patients with Bell’s palsy may complain of tearing eyes, tear production is actually decreased due to loss of control of the eyelids and facial muscles.

The facial nerve controls the motor aspect of the corneal reflex, so an abnormal corneal reflex may be observed in Bell’s palsy.

Nerve Supply of the Tongue

The tongue is a complex organ that plays a crucial role in speech and taste. It is innervated by three different cranial nerves, each responsible for different functions. The anterior two-thirds of the tongue receive general sensation from the lingual branch of the mandibular division of the trigeminal nerve (CN V3) and taste sensation from the chorda tympani branch of the facial nerve (CN VII). On the other hand, the posterior one-third of the tongue receives both general sensation and taste sensation from the glossopharyngeal nerve (CN IX).

In terms of motor function, the hypoglossal nerve (CN XII) is responsible for controlling the movements of the tongue. It is important to note that the tongue’s nerve supply is essential for proper functioning, and any damage to these nerves can result in speech and taste disorders.

A non-cardioselective β blocker (NSBB) is the appropriate medication for prophylaxis against oesophageal bleeding in patients with varices. NSBBs work by causing splanchnic vasoconstriction, which reduces portal blood flow. Omeprazole, warfarin, and unfractionated heparin are not suitable options for this purpose.

Variceal haemorrhage is a serious condition that requires prompt and effective management. The initial treatment involves resuscitation of the patient, correction of clotting abnormalities, and administration of vasoactive agents such as terlipressin or octreotide. Prophylactic IV antibiotics are also recommended to reduce mortality in patients with liver cirrhosis. Endoscopic variceal band ligation is the preferred method for controlling bleeding, and the use of a Sengstaken-Blakemore tube or Transjugular Intrahepatic Portosystemic Shunt (TIPSS) may be necessary if bleeding cannot be controlled. However, TIPSS can lead to exacerbation of hepatic encephalopathy, which is a common complication.

To prevent variceal haemorrhage, prophylactic measures such as propranolol and endoscopic variceal band ligation (EVL) are recommended. Propranolol has been shown to reduce rebleeding and mortality compared to placebo. EVL is superior to endoscopic sclerotherapy and should be performed at two-weekly intervals until all varices have been eradicated. Proton pump inhibitor cover is given to prevent EVL-induced ulceration. NICE guidelines recommend offering endoscopic variceal band ligation for the primary prevention of bleeding for people with cirrhosis who have medium to large oesophageal varices.

To manage bleeding caused by liver injury or a challenging cholecystectomy, a vascular clamp can be utilized at the epiploic foramen. This opening is defined by the following borders: the bile duct on the right, the portal vein at the back, and the hepatic artery on the left, all of which are located in the free edge of the lesser omentum.

Structure and Relations of the Liver

The liver is divided into four lobes: the right lobe, left lobe, quadrate lobe, and caudate lobe. The right lobe is supplied by the right hepatic artery and contains Couinaud segments V to VIII, while the left lobe is supplied by the left hepatic artery and contains Couinaud segments II to IV. The quadrate lobe is part of the right lobe anatomically but functionally is part of the left, and the caudate lobe is supplied by both right and left hepatic arteries and lies behind the plane of the porta hepatis. The liver lobules are separated by portal canals that contain the portal triad: the hepatic artery, portal vein, and tributary of bile duct.

The liver has various relations with other organs in the body. Anteriorly, it is related to the diaphragm, esophagus, xiphoid process, stomach, duodenum, hepatic flexure of colon, right kidney, gallbladder, and inferior vena cava. The porta hepatis is located on the postero-inferior surface of the liver and transmits the common hepatic duct, hepatic artery, portal vein, sympathetic and parasympathetic nerve fibers, and lymphatic drainage of the liver and nodes.

The liver is supported by ligaments, including the falciform ligament, which is a two-layer fold of peritoneum from the umbilicus to the anterior liver surface and contains the ligamentum teres (remnant of the umbilical vein). The ligamentum venosum is a remnant of the ductus venosus. The liver is supplied by the hepatic artery and drained by the hepatic veins and portal vein. Its nervous supply comes from the sympathetic and parasympathetic trunks of the coeliac plexus.