The upper GI tract plays a pivotal role in digestion, absorption, and gastrointestinal regulation. A thorough understanding of its anatomy and physiology is essential for diagnosing conditions ranging from GORD to pernicious anaemia.
🔬 Key Structures & Functions
🦷 Mouth & Pharynx
✨ Digestion begins with mastication, breaking food into smaller particles. Salivary glands (parotid, submandibular, sublingual) produce saliva, which contains amylase, initiating carbohydrate digestion.
🧠 The pharynx serves as a conduit for food and air, coordinating swallowing via the cranial nerves (V, VII, IX, X, XII).
🔒 The upper oesophageal sphincter (UES) controls entry into the oesophagus, ensuring airway protection during swallowing.
🚇 Oesophagus
💪 A muscular tube (approximately 25cm) propels food via peristalsis, regulated by the enteric nervous system.
🚫 The lower oesophageal sphincter (LES) prevents gastric reflux. Weakness here leads to gastro-oesophageal reflux disease (GORD), which can predispose patients to Barrett’s oesophagus and oesophageal adenocarcinoma.
🔥 Pathophysiology of GORD
🚶♂️ Transient relaxation or incompetence of the LES allows acidic gastric contents to reflux into the oesophagus. Several mechanisms contribute:
⚡ Reduced LES tone – Triggered by factors such as obesity, smoking, alcohol, pregnancy, and medications (e.g. calcium channel blockers, nitrates).
🕰️ Impaired oesophageal clearance – Reduced peristaltic contractions hinder acid neutralisation and clearance.
🔄 Delayed gastric emptying – Conditions like gastroparesis or high-fat meals prolong gastric retention, increasing the likelihood of reflux.
🏔️ Hiatus hernia – Weakening of the diaphragmatic oesophageal hiatus disrupts LES function, exacerbating reflux.
🚨 Chronic mucosal injury – Persistent acid exposure leads to oesophagitis, ulceration, and metaplasia (Barrett’s oesophagus), increasing cancer risk.
🥼 Stomach
🏺 The stomach acts as a reservoir, mixing food with gastric acid (HCl), pepsin, and intrinsic factor. Acid secretion is regulated by gastrin, histamine (H2 receptors), and acetylcholine.
🛡️ The mucosal barrier, including prostaglandins and bicarbonate, protects against autodigestion. Disruptions can result in peptic ulcers, often associated with Helicobacter pylori infection or NSAID use.
⚡ Gastric motility is mediated by interstitial cells of Cajal, acting as pacemakers for coordinated contractions.
🔄 Duodenum (First section of the small intestine)
💧 The primary site of chemical digestion, where bile (from the liver) emulsifies fats, and pancreatic enzymes break down macronutrients.
🛡️ Brunner’s glands secrete alkaline mucus to neutralise gastric acid and protect the intestinal lining.
💊 Dysfunction here affects nutrient absorption, particularly vitamin B12, essential for erythropoiesis.
🩸 Pernicious Anaemia & Clinical Relevance
⚔️ Pernicious anaemia results from vitamin B12 deficiency due to autoimmune destruction of gastric parietal cells, leading to reduced intrinsic factor production and impaired B12 absorption in the ileum.
⚡ Symptoms include macrocytic anaemia, neurological changes (peripheral neuropathy, cognitive impairment), and glossitis (inflamed tongue).
💉 Treatment involves lifelong vitamin B12 supplementation, typically via intramuscular injection, bypassing the defective absorption mechanism.
🔬 Understanding these key structures enhances diagnostic precision and informs targeted management strategies for upper GI disorders.
💬 What are your burning questions on upper GI pathology? Let’s discuss! 👇
#MedicalEducation #UpperGIT #UOWmedicine #FutureDoctors #Gastroenterology
No comments:
Post a Comment