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GLASGOW NEURO SOCIETY BEYOND THE BRAIN YEAR 2 GI ATTIKA CHAUDHARY 2437808C@STUDENT.GLA.AC.UK INTRODUCTION The aim of the group is to provide undergraduate students with an interest in neuroscience/neurological medicine, the opportunity to improve upon their knowledge and understanding of the nervous sytem. We host talks, workshops, clinical skills sessions and this year we are organising this teaching series. Our most popular event is the annual conference held at Royal College of Physicians & Surgeons of Glasgow - on 5th November this year!WHAT WILL A LOT! WE COVER? UPPER GI MIDDLE STUFF LOWER GI OESPHAGUS LIVER TOP TIPS STOMACH GALLBLADDER CLINICAL BILIRUBIN CONDITIONS METABOLSIM JAUNDICE HISTOLOGY AND LFTS ANATOMY PANCREAS IRON METABOLISM COELIAC DISEASE DISCLAIMER: I AM ONLY A STUDENT OESOPHAGUS ANATOMY Fibromuscular tube that transports food from the pharynx to the stomach Blood supply Originates at C6 and extends to T11 (enters the Thoracic Oesophagus Arterial supply – inferior thyroid abdomen at the oesophageal hiatus at T10) artery (branch of thoracic aorta) Venous drainage – inferior thyroid vein and azygos vein Divided into three regions: Cervical, Thoracic and Abdominal Abdominal Oesophagus Arterial supply – left gastric artery 2 Sphincters: and inferior phrenic artery Venous drainage – left gastric vein Upper sphincter – anatomical, striated muscle at (portal circulation) and azygos vein junction between pharynx and oesophagus (systemic circulation) Lower sphincter – physiological HISTOLOGY Adventitia Outer layer of connective tissue (not serosa as we not in peritoneum yet) Muscularis externa Upper 1/3 – striated muscle Middle 1/3 – mixed (striated and smooth) Lower 1/3 - smooth Submucosa Contains oesophageal mucous glands (lubricates food) Mucosa Lined by NON-KERATINISED STRATIFIED SQUAMOUS https://webpath.med.utah.edu/webpath.html **Gastro oesophageal junction** Underneath is columnar - stomach Above is squamous - oesophagus CLINICAL CONDITION Factors to stop Barret's oesophagus acid reflux GORD Retrograde passage of Angle at which the Metaplasia of the lower acidic gastric contents oesophagus enters the into oesophagus oesophagus from stomach - ANGLE OF HIS Causes can include squamous epithelium to The functional LOS columnar hiatus hernia, obesity, sphincter alcohol Caused by chronic The diaphragm Symptoms - heartburn, backflow of acid which surrounding the irritates the lining epigastric pain oesophagus at the Treatment - lifestyle, Detected via endoscopy oesophageal hiatus drugs: PPIs and H2 antagonists STOMACH ANATOMY Answer the poll Intraperitoneal organ Found in the left 1 hypochondrium/epigastric region Two sphincters located at each 7 orifice to control the passage of material in and out of the stomach inferior oesophageal sphincter 6 pyloric sphincter - lies between 2 pylorus and first part of duodenum. An anatomical sphincter Functions 3 · Mixing chamber 5 · Storage space for ingested food 4 STOMACH ANATOMY Blood supply Arterial supply Image Venous drainage: Drains into the portal venous system. Veins run parallel to arteries Short gastric vein, and L. and R. gastro-omental veins drain into the superior mesenteric vein Lymphatic Drainage Nerve supply: Autonomic nervous system · Gastro-omental lymph nodes at the greater curvature · Gastric lymph nodes at the lesser curvature GREATER AND LESSER OMENTUM Peritoneum - supports the abdominal cavity Greater omentum -> large fold of peritoneum hanging down from the stomach attached to the greater curvature of the stomach (can be lifted/reflected up), blood supply from gastroepiploic artery. Transverse colon is stuck to back of it. It is moblile (policeman function) Lesser omentum -> sheet of tissue that connects stomach to the liver – connected from lesser curvature to groove on underside of liver. Not mobile. HISTOLOGY Serosa - outermost layer Muscularis layer Innermost – oblique Inner – circular Outer – longitudinal Submucosa Mucosa Simple columnar epithelium Gastric pits and gastric glands Ruggae - longitudoinal folds Gastric glands contains - chief cell (secrete pepsinogen), enteroendocrine cell (secrete gastrin) and parietal cell (secrete HCL)HISTOLOGYPeptic Ulcer Disease Break in the mucosal lining of the stomach or duodenum LIVER AND GALLBLADDER REQUIRES A WHOLE SESSION ON ITS OWN! We will cover: anatomy function bilirubin metabolism clinical conditions / context LIVER ANATOMY •Intraperitoneal •Found in the right hypochondrium and epigastric region Macroscopic: 4 lobes - right, left, caudate and quadrate Diaphragmatic surface - anteriosuperior surface, the posterior aspect not covered by peritoneum and known as "bare area of the liver" Visceral surface - posterioinferior surface and covered by peritoneum Porta hepatis - hilum of the liver Encompasses the hepatic portal vein, hepatic artery proper and common bile duct LIVER ANATOMY Microscopic: liver cells are known as hepatocytes arranged in lobules A lobule is hexagonal-shaped and is drained by a central vein At the periphery of the hexagon are three structures collectively known as the portal triad: Arteriole – a branch of the hepatic artery entering the liver. Venule – a branch of the hepatic portal vein entering the liver. Bile duct – branch of the bile duct leaving the liver. LIVER ANATOMY Ligaments: coronary - attaches superior surface of liver to inferior surface of diaphragm Falciform - attaches the anterior surface of the liver to the anterior abdominal wall Triangular - right and left which attach liver to diaphragm Hepatic recess: anatomical spaces clinically important as risk of infection Dual blood supply 75% deoxygenated from hepatic portal vein – nutrients from GI tract 25% oxygenated from hepatic artery proper - coeliac trunk Hepatic veins drain into IVC Referred pain: C4 supplies the diaphragm but also the skin of the shoulder. Hence, infection/pain in the space under diaphragm may cause referred pain to shoulder GALLBLADDER ANATOMY Will definitely be asked at some point in the exams! Anatomical (surface) landmark for fundus of gallbladder: Can be palpated where lateral edge of rectus abdominus muscle meets the costal margin (9th costal cartilage) Gallbladder is at level of 9th costal cartilage This landmark is useful in surgery for gallbladder disease (cholecystectomy) Right hepatic duct + left hepatic duct Common hepatic duct Gallbladder Cystic duct Common bile duct + Pancreatic duct Ampulla of vater 2/3 of the descending part of duodenum GALLBLADDER ANATOMY Arterial supply Cystic artery 1.Branch of right hepatic artery (which itself is a branch of common hepatic artery, a branch of coeliac trunk) 2.Cystic artery - R. hepatic artery - common hepatic artery - coeliac truck Venous drainage Cystic veins (neck) Drains blood from neck of gallbladder Drains directly into portal vein Hepatic sinusoids (fundus and body) Drainage of blood from the fundus and body flows into the hepatic sinuosids Bile content: made up of bile acids, cholesterol, phospholipids, bile pigments i.e. bilirubin and biliverdin, and electrolytes and water Bile secretion After eating, the hormone cholecystokinin is released from the duodenum. CCK causes gallbladder contraction and relaxes the sphincter of Oddi, thus allowing bile to flow into the duodenum. Formation of bilirubin It is formed by: 1.the breakdown of haem -> biliverdin by haem oxygenase 2.biliverdin broken to -> bilirubin by biliverdin reductase 3.At this point, we have UNCONJUGATED BILIRUBIN (water-insoluble) 4. when albumin bound, is secreted into blood stream, taken up by hepatocytes and conjugated by UDP GLUCONYL TRANSFERASE Bilirubin excretion Conjugated bilirubin is excreted into the duodenum in bile Once in the colon, colonic bacteria deconjugate bilirubin and convert it into urobilinogen. 80% is further oxidised by intestinal bacteria and converted to stercobilin and then excreted through faeces. It is stercobilin which gives faeces their colour. The other 20% is reabsorbed into the bloodstream as part of the enterohepatic circulation. It is carried to the liver where some is recycled for bile production, while a small percentage reaches the kidneys. Here, it is oxidised further into urobilin and then excreted into the urine. JAUNDICE PRE-HEPATIC HEPATIC POST-HEPATIC haemolysis liver damage obstructive / drainage unconjugated bilirubin problem Cause: excessive red cell breakdown,Cause: hepatocellular dysfunctioCause: obstruction of drainage overwhelming ability of liver to resulting in: poor uptake of U- •Intra-luminal: gallstones conjugate BILIRUBIN, impaired conjugation of •Mural: cholangiocarcinoma, •Tropical diseases e.g. Yellow feverBILIRUBIN, or impaired transportstrictures, drug-induced malaria C-BILIRUBIN cholestasis •Drug adverse effects e.g. quinines •Alcoholic liver disease •Extra-mural: pancreatic cancer, •Genetic disorders: sickle cell •Genetic: Gilbert’s, HH abdominal masses anaemia •Illnesses: Viral or autoimmune •Neonatal jaundice – physiological hepatitis, PBC, PSC and haemolyticdisease of newborn •Iatrogenic Key lab findings The combination of the colour of urine and stools can give an indication as to the cause of jaundice: • Normal urine + normal stools = pre-hepatic cause • Dark urine + normal stools = hepatic cause • Dark urine + pale stools = post-hepatic cause (obstructive) • Obstructive picture = pale stools (reduced levels of stercobilin entering the GI tract, which normally colours the stool.) LFTs Components: Alanine transaminase (ALT) Aspartate aminotransferase (AST) Alkaline phosphatase (ALP) Gamma-glutamyltransferase (GGT) Bilirubin Albumin Prothrombin time (PT) Isolated raised ALP in the abscence of raised GGT = Non-hepatobiliary cause e.g. bone disease The AST/ALT ratio can be used to determine the likely cause of LFT derangement: • ALT > AST is associated with chronic liver disease • AST > ALT is associated with cirrhosis and acute alcoholic hepatitisPOLL TIME!5 MINUTE BREAK PANCREAS ▯The pancreas is an organ with both exocrine and endocrine functions – exocrine cells are arranged in clusters known as acini and endocrine cells are arranged in islets of Langerhans ▯It is mostly retroperitoneal with only the tail being intraperitoneal ▯It has 5 sections – head, neck, uncinate process, body and tail ▯Superior mesenteric vessels pass posteriorly to the neck and anteriorly to the uncinate process. ▯Head lies within the C-shaped curve created by the duodenum PANCREAS Vasculature • Arterial supply Pancreatic branches of the splenic artery – Arteria Pancreatica Magna - Wrap around the body and tail of the pancreas Head has additional blood supply from superior and inferior pancreaticoduodenal artery which are branches of the gastroduodenal artery (from coeliac trunk) and superior mesenteric artery • Venous drainage Superior mesenteric branches of the hepatic portal vein -> Drainage of the head of pancreas Pancreatic veins -> Drain the rest of the pancreas via the splenic vein IRON METABOLISM Hepcidin = low iron hormone Iron absorption occurs in the duodenum 1.Non-haem iron is converted to ferrous (Fe2+) from ferric by duodenal cytochrome B1 2.Fe2+ is taken up into the enterocyte by DMT1 3.Iron can be stored as ferritin or circulate in the plasma as ferroportin and once in the blood it is bound by transferrin 4.Transported to bone marrow and some is taken up by marcophages for the RES Regulation: Primarily regulated by hepcidin (binds to ferroportin and degrades it) IRON DEFICIENCY Iron deficiency is a SYMPTOM not a diagnosis **HH is an autosomal recessive condition Microcytic, hypochromic anaemia = smaller and paler red blood cellsg iron overload** GOLDEN RULE In males and post-menopausal women = IDA is caused by GI blood loss until proven otherwise In young women due to menstrual blood loss or pregnancy COELIAC DISEASE Coeliac disease (Gluten-sensitive enteropathy) is a condition in which there is inflammation of the mucosa of the upper small bowel that improves when gluten is withdrawn from the diet and relapses when gluten is reintroduced. Gene linked to coeliac -> HLA DQ2/8 Condition linked with coeliac -> dermatitis herpetiformis Serology shows: IgA tTG (tissue transglutaminase Ab) IgA EMA (anti-endomysial Ab) Endoscopy is GOLD STANDARD and used for small bowel biopsy which shows LOWER GI **Top Tips** Make sure you understand anatomy (blood supply and parts of bowel) Comparison of the small and large bowel - can make up to 4 marks! Ensure you have covered the workshops and PBLs in depth https://w- radiology.com/abdomin al_ct/ Good resources for practicing imagingFINISHED!
