The hormone that increases gallbladder contraction is Cholecystokinin (CCK). It is secreted by I cells in the upper small intestine, particularly in response to a high-fat meal. Although it has many functions, its role in increasing gallbladder contraction may exacerbate biliary colic caused by gallstones in the patient described.

Gastrin, insulin, and secretin are also hormones that can be released in response to food intake, but they do not have any known effect on gallbladder contraction. Therefore, CCK is the most appropriate answer.

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.

Coeliac disease typically presents in children around the age when they start consuming wheat and cereal, but some individuals may not show symptoms until later in life. It is crucial for healthcare professionals to be able to identify this condition, both in clinical settings and for exams.

Coeliac Disease in Children: Causes, Symptoms, and Diagnosis

Coeliac disease is a condition that affects children and is caused by sensitivity to gluten, a protein found in cereals. This sensitivity leads to villous atrophy, which causes malabsorption. Children usually present with symptoms before the age of 3, coinciding with the introduction of cereals into their diet. The incidence of coeliac disease is around 1 in 100, and it is strongly associated with HLA-DQ2 and HLA-DQ8. Symptoms of coeliac disease include failure to thrive, diarrhoea, abdominal distension, and anaemia in older children. However, many cases are not diagnosed until adulthood.

Diagnosis of coeliac disease involves a jejunal biopsy showing subtotal villous atrophy, as well as screening tests for anti-endomysial and anti-gliadin antibodies. The biopsy shows complete atrophy of the villi with flat mucosa and marked crypt hyperplasia, as well as dense mixed inflammatory infiltrate in the lamina propria. Another biopsy may show flat mucosa with hyperplastic crypts and dense cellular infiltrate in the lamina propria, as well as an increased number of intraepithelial lymphocytes and vacuolated superficial epithelial cells. Overall, coeliac disease is a serious condition that requires early diagnosis and management to prevent long-term complications.

To address recurrent variceal haemorrhage despite optimal medical therapy, a TIPS procedure may be performed. This involves linking the hepatic vein to the portal vein, which helps to alleviate the complications associated with portal hypertension.

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.

Zollinger-Ellison syndrome (ZES) is the most likely diagnosis for the patient due to their persistent epigastric pain, diarrhea, and high levels of serum gastrin, which cannot be explained by peptic ulcer disease alone. ZES is caused by a gastrin-secreting tumor in the pancreas or duodenum, and is often associated with MEN 1. Diagnosis is confirmed by elevated serum gastrin levels at least 10 times the upper limit of normal, reduced gastric pH, and a secretin stimulation test if necessary.

Carcinoid syndrome is an incorrect diagnosis as it presents with different symptoms such as diarrhea, wheezing, flushing, and valvular lesions due to serotonin secretion.

Although celiac disease can cause epigastric pain and diarrhea, the elevated gastrin levels make ZES a more likely diagnosis. Celiac disease is diagnosed by measuring levels of anti-TTG and anti-endomysial IgA.

Gastric carcinoma is unlikely as there are no risk factors, constitutional symptoms, or elevated fasting gastrin levels.

H. pylori infection has been ruled out by a negative stool antigen test.

Understanding Zollinger-Ellison Syndrome

Zollinger-Ellison syndrome is a medical condition that is caused by the overproduction of gastrin, which is usually due to a tumor in the pancreas or duodenum. This condition is often associated with MEN type I syndrome, which affects around 30% of cases. The symptoms of Zollinger-Ellison syndrome include multiple gastroduodenal ulcers, diarrhea, and malabsorption.

To diagnose Zollinger-Ellison syndrome, doctors typically perform a fasting gastrin level test, which is considered the best screening test. Additionally, a secretin stimulation test may also be performed to confirm the diagnosis. With early diagnosis and treatment, the symptoms of Zollinger-Ellison syndrome can be managed effectively.

The initial management approach for mild diverticulitis typically involves a combination of oral antibiotics, a liquid diet, and analgesia.

Understanding Diverticulitis

Diverticulitis is a condition where an out-pouching of the intestinal mucosa becomes infected. This out-pouching is called a diverticulum and the presence of these pouches is known as diverticulosis. Diverticula are common and are thought to be caused by increased pressure in the colon. They usually occur in the sigmoid colon and are more prevalent in Westerners over the age of 60. While only a quarter of people with diverticulosis experience symptoms, 75% of those who do will have an episode of diverticulitis.

Risk factors for diverticulitis include age, lack of dietary fiber, obesity (especially in younger patients), and a sedentary lifestyle. Patients with diverticular disease may experience intermittent abdominal pain, bloating, and changes in bowel habits. Those with acute diverticulitis may experience severe abdominal pain, nausea and vomiting, changes in bowel habits, and urinary symptoms. Complications may include colovesical or colovaginal fistulas.

Signs of diverticulitis include low-grade fever, tachycardia, tender lower left quadrant of the abdomen, and possibly a palpable mass. Imaging tests such as an erect chest X-ray, abdominal X-ray, and CT scan may be used to diagnose diverticulitis. Treatment may involve oral antibiotics, a liquid diet, and analgesia for mild cases. More severe cases may require hospitalization for intravenous antibiotics. Colonoscopy should be avoided initially due to the risk of perforation.

In summary, diverticulitis is a common condition that can cause significant discomfort and complications. Understanding the risk factors, symptoms, and signs of diverticulitis can help with early diagnosis and treatment.

The chief cells responsible for producing Pepsi cola are not to be confused with the chief cells found in the stomach. In the stomach, chief cells secrete pepsinogen, while parietal cells secrete HCl, Ca, Na, Mg, and intrinsic factor. Additionally, surface mucosal cells secrete mucus and bicarbonate.

Understanding Gastric Secretions for Surgical Procedures

A basic understanding of gastric secretions is crucial for surgeons, especially when dealing with patients who have undergone acid-lowering procedures or are prescribed anti-secretory drugs. Gastric acid, produced by the parietal cells in the stomach, has a pH of around 2 and is maintained by the H+/K+ ATPase pump. Sodium and chloride ions are actively secreted from the parietal cell into the canaliculus, creating a negative potential across the membrane. Carbonic anhydrase forms carbonic acid, which dissociates, and the hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter pump. This leaves hydrogen and chloride ions in the canaliculus, which mix and are secreted into the lumen of the oxyntic gland.

There are three phases of gastric secretion: the cephalic phase, gastric phase, and intestinal phase. The cephalic phase is stimulated by the smell or taste of food and causes 30% of acid production. The gastric phase, which is caused by stomach distension, low H+, or peptides, causes 60% of acid production. The intestinal phase, which is caused by high acidity, distension, or hypertonic solutions in the duodenum, inhibits gastric acid secretion via enterogastrones and neural reflexes.

The regulation of gastric acid production involves various factors that increase or decrease production. Factors that increase production include vagal nerve stimulation, gastrin release, and histamine release. Factors that decrease production include somatostatin, cholecystokinin, and secretin. Understanding these factors and their associated pharmacology is essential for surgeons.

In summary, a working knowledge of gastric secretions is crucial for surgical procedures, especially when dealing with patients who have undergone acid-lowering procedures or are prescribed anti-secretory drugs. Understanding the phases of gastric secretion and the regulation of gastric acid production is essential for successful surgical outcomes.

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.

The femoral artery can be located using the mid inguinal point, which is positioned halfway between the anterior superior iliac spine and the symphysis pubis.

Understanding the Anatomy of the Femoral Triangle

The femoral triangle is an important anatomical region located in the upper thigh. It is bounded by the inguinal ligament superiorly, the sartorius muscle laterally, and the adductor longus muscle medially. The floor of the femoral triangle is made up of the iliacus, psoas major, adductor longus, and pectineus muscles, while the roof is formed by the fascia lata and superficial fascia. The superficial inguinal lymph nodes and the long saphenous vein are also found in this region.

The femoral triangle contains several important structures, including the femoral vein, femoral artery, femoral nerve, deep and superficial inguinal lymph nodes, lateral cutaneous nerve, great saphenous vein, and femoral branch of the genitofemoral nerve. The femoral artery can be palpated at the mid inguinal point, making it an important landmark for medical professionals.

Understanding the anatomy of the femoral triangle is important for medical professionals, as it is a common site for procedures such as venipuncture, arterial puncture, and nerve blocks. It is also important for identifying and treating conditions that affect the structures within this region, such as femoral hernias and lymphadenopathy.

Coeliac disease is characterized by villous atrophy, which leads to malabsorption. This patient’s symptoms are typical of coeliac disease, which can affect both males and females in their 50s. Patients often experience non-specific abdominal discomfort for several months, similar to irritable bowel syndrome, and may not notice correlations between symptoms and specific dietary components like gluten.

Aphthous ulceration is a common sign of coeliac disease, and patients may also experience nutritional deficiencies such as iron and folate deficiency due to malabsorption. Histology will reveal villous atrophy and crypt hyperplasia. Iron and folate deficiency can lead to a normocytic anaemia and conjunctival pallor. Positive anti-transglutaminase antibodies are specific for coeliac disease.

Ulcerative colitis is characterized by crypt abscess and mucosal ulcers, while Crohn’s disease is associated with non-caseating granulomas and full-thickness inflammation. These inflammatory bowel diseases typically present in patients in their 20s and may have systemic and extraintestinal features. Anti-tTG will not be positive in IBD. Ovarian cancer is an important differential diagnosis for females over 40 with symptoms similar to irritable bowel syndrome.

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.

Large bowel obstruction is the most likely diagnosis based on the pattern of symptoms, which include abdominal distension, absence of passing flatus or stool, and late onset or no vomiting.

Large bowel obstruction occurs when there is a blockage in the passage of food, fluids, and gas through the large intestines. The most common cause of this condition is a tumor, accounting for 60% of cases. Colonic malignancy is often the initial presenting complaint in approximately 30% of cases, especially in more distal colonic and rectal tumors due to their smaller lumen diameter. Other causes include volvulus and diverticular disease.

Clinical features of large bowel obstruction include abdominal pain, distention, and absence of passing flatus or stool. Nausea and vomiting may suggest a more proximal lesion, while peritonism may be present if there is associated bowel perforation. It is important to consider the underlying causes, such as recent symptoms suggestive of colorectal cancer.

Abdominal x-ray is still commonly used as a first-line investigation, with a diameter greater than the normal limits of 10-12 cm for the caecum, 8 cm for the ascending colon, and 6.5 cm for recto-sigmoid being diagnostic of obstruction. CT scan is highly sensitive and specific for identifying obstruction and its underlying cause.

Initial management of large bowel obstruction includes NBM, IV fluids, and nasogastric tube with free drainage. Conservative management for up to 72 hours can be trialed if the cause of obstruction does not require surgery, after which further management may be required if there is no resolution. Around 75% of cases will eventually require surgery. IV antibiotics are given if perforation is suspected or surgery is planned. Emergency surgery is necessary if there is any overt peritonitis or evidence of bowel perforation, involving irrigation of the abdominal cavity, resection of perforated segment and ischaemic bowel, and addressing the underlying cause of the obstruction.