At the superior part of the pancreas, the gastroduodenal artery splits into the pancreaticoduodenal and gastro-epiploic arteries.

Anatomy of the Pancreas

The pancreas is located behind the stomach and is a retroperitoneal organ. It can be accessed surgically by dividing the peritoneal reflection that connects the greater omentum to the transverse colon. The pancreatic head is situated in the curvature of the duodenum, while its tail is close to the hilum of the spleen. The pancreas has various relations with other organs, such as the inferior vena cava, common bile duct, renal veins, superior mesenteric vein and artery, crus of diaphragm, psoas muscle, adrenal gland, kidney, aorta, pylorus, gastroduodenal artery, and splenic hilum.

The arterial supply of the pancreas is through the pancreaticoduodenal artery for the head and the splenic artery for the rest of the organ. The venous drainage for the head is through the superior mesenteric vein, while the body and tail are drained by the splenic vein. The ampulla of Vater is an important landmark that marks the transition from foregut to midgut and is located halfway along the second part of the duodenum. Overall, understanding the anatomy of the pancreas is crucial for surgical procedures and diagnosing pancreatic diseases.

The omental branches of the right and left gastro-epiploic arteries provide the blood supply to the omentum, while the colonic vessels do not play a role in this. The left gastro-epiploic artery originates from the splenic artery, and the right gastro-epiploic artery is the final branch of the gastroduodenal artery.

The Omentum: A Protective Structure in the Abdomen

The omentum is a structure in the abdomen that invests the stomach and is divided into two parts: the greater and lesser omentum. The greater omentum is attached to the lower lateral border of the stomach and contains the gastro-epiploic arteries. It varies in size and is less developed in children. However, it plays an important role in protecting against visceral perforation, such as in cases of appendicitis.

The lesser omentum is located between the omentum and transverse colon, providing a potential entry point into the lesser sac. Malignant processes can affect the omentum, with ovarian cancer being the most notable. Overall, the omentum is a crucial structure in the abdomen that serves as a protective barrier against potential injuries and diseases.

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.

Mesenteric infarcts can be caused by various factors such as prolonged atrial fibrillation, ventricular aneurysms, and post myocardial infarction.

Understanding Mesenteric Vessel Disease

Mesenteric vessel disease is a condition that affects the blood vessels supplying the intestines. It is primarily caused by arterial embolism, which can result in infarction of the colon. The most common type of mesenteric vessel disease is acute mesenteric embolus, which is characterized by sudden onset abdominal pain followed by profuse diarrhea. Other types include acute on chronic mesenteric ischemia, mesenteric vein thrombosis, and low flow mesenteric infarction.

Diagnosis of mesenteric vessel disease involves serological tests such as WCC, lactate, CRP, and amylase, as well as CT angiography scanning in the arterial phase with thin slices. Management of the condition depends on the severity of symptoms, with overt signs of peritonism requiring laparotomy and mesenteric vein thrombosis being treated with medical management using IV heparin. In cases where surgery is necessary, limited resection of necrotic bowel may be performed with the aim of relooking laparotomy at 24-48 hours.

The prognosis for mesenteric vessel disease is generally poor, with the best outlook being for acute ischaemia from an embolic event where surgery occurs within 12 hours. Survival rates may be as high as 50%, but this falls to 30% with treatment delay. It is important to seek medical attention promptly if symptoms of mesenteric vessel disease are present.

After a splenectomy, the blood film may show the presence of Howell-Jolly bodies, Pappenheimer bodies, target cells, and irregular contracted erythrocytes due to the absence of the spleen’s filtration function.

Blood Film Changes after Splenectomy

After undergoing splenectomy, the body loses its ability to remove immature or abnormal red blood cells from circulation. This results in the appearance of cytoplasmic inclusions such as Howell-Jolly bodies, although the red cell count remains relatively unchanged. In the first few days following the procedure, target cells, siderocytes, and reticulocytes may be observed in the bloodstream. Additionally, agranulocytosis composed mainly of neutrophils is seen immediately after the operation, which is then replaced by a lymphocytosis and monocytosis over the next few weeks. The platelet count is typically elevated and may persist, necessitating the use of oral antiplatelet agents in some patients.

Intestinal diverticula are more likely to develop in individuals with a low fibre diet. This patient’s diet appears to be lacking in fruits and vegetables, which increases their risk. While smoking has been linked to diverticulosis, there is no evidence to suggest that alcohol consumption is a risk factor. Although obesity is associated with an increased risk, this patient’s BMI is not in the obese range. Diverticulosis is more prevalent in men than women, and abdominal surgery is not a known risk factor.

Diverticulosis is a common condition where multiple outpouchings occur in the bowel wall, typically in the sigmoid colon. It is more accurate to use the term diverticulosis when referring to the presence of diverticula, while diverticular disease is reserved for symptomatic patients. Risk factors for this condition include a low-fibre diet and increasing age. Symptoms of diverticulosis can include altered bowel habits and colicky left-sided abdominal pain. A high-fibre diet is often recommended to alleviate these symptoms.

Diverticulitis is a complication of diverticulosis where one of the diverticula becomes infected. The typical presentation includes left iliac fossa pain and tenderness, anorexia, nausea, vomiting, diarrhea, and signs of infection such as pyrexia, raised WBC, and CRP. Mild attacks can be treated with oral antibiotics, while more severe episodes require hospitalization. Treatment involves nil by mouth, intravenous fluids, and intravenous antibiotics such as a cephalosporin and metronidazole. Complications of diverticulitis include abscess formation, peritonitis, obstruction, and perforation.

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.

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.

It is not recommended to use metoclopramide as an antiemetic in cases of bowel obstruction. This is because metoclopramide works by blocking dopamine receptors and stimulating peripheral 5HT3 receptors, which promote gastric emptying. However, in cases of intestinal obstruction, gastric emptying is not possible and this effect can be harmful. The choice of antiemetic should be based on the patient’s individual needs and the underlying cause of their nausea.

Understanding the Mechanism and Uses of Metoclopramide

Metoclopramide is a medication primarily used to manage nausea, but it also has other uses such as treating gastro-oesophageal reflux disease and gastroparesis secondary to diabetic neuropathy. It is often combined with analgesics for the treatment of migraines. However, it is important to note that metoclopramide has adverse effects such as extrapyramidal effects, acute dystonia, diarrhoea, hyperprolactinaemia, tardive dyskinesia, and parkinsonism. It should also be avoided in bowel obstruction but may be helpful in paralytic ileus.

The mechanism of action of metoclopramide is quite complicated. It is primarily a D2 receptor antagonist, but it also has mixed 5-HT3 receptor antagonist/5-HT4 receptor agonist activity. Its antiemetic action is due to its antagonist activity at D2 receptors in the chemoreceptor trigger zone, and at higher doses, the 5-HT3 receptor antagonist also has an effect. The gastroprokinetic activity is mediated by D2 receptor antagonist activity and 5-HT4 receptor agonist activity.

In summary, metoclopramide is a medication with multiple uses, but it also has adverse effects that should be considered. Its mechanism of action is complex, involving both D2 receptor antagonist and 5-HT3 receptor antagonist/5-HT4 receptor agonist activity. Understanding the uses and mechanism of action of metoclopramide is important for its safe and effective use.

Amylase is an enzyme that converts starch into sugars.

Enzymes play a crucial role in the breakdown of carbohydrates in the gastrointestinal system. Amylase, which is present in both saliva and pancreatic secretions, is responsible for breaking down starch into sugar. On the other hand, brush border enzymes such as maltase, sucrase, and lactase are involved in the breakdown of specific disaccharides. Maltase cleaves maltose into glucose and glucose, sucrase cleaves sucrose into fructose and glucose, while lactase cleaves lactose into glucose and galactose. These enzymes work together to ensure that carbohydrates are broken down into their simplest form for absorption into the bloodstream.