Gastroenterology (Lecture Materials)

Gastroenterology Upper GI • General Gut structure • The mouth • Salivation • Oesophagus o Hiatus hernia o GORD • Dysphagia o Carcinoma of the oesophagus o Achalasia • General Abdominal anatomy o Stomach o Gastric secretions o Pharmacology of the upper GI tract • Peptic Ulcer disease • Gastro-intestinal haemorrhage • Gastric neoplasms • The acute abdomen Small Intestine • The intestines o Duodenum o Jejunum & Ileum o Large intestine • GI motility • Diarrhoea & Constipation • Acute Appendicitis • Meckels diverticulum • Small bowel obstruction • Malabsorption o Coeliac disease • Irritable bowel syndrome • Inflammatory Bowel disease Large Intestine • Diverticular of the colon • Carcinoma of the large bowel • Large bowel obstruction • Haemorrhoids • Perianal infection • Fissue in Ano Hepatobiliary • Hepatobiliary anatomy • Liver & Gall Bladder Function • LFTs • Gall bladder • Acute & Chronic Hepatitis • Liver neoplasms, abscesses & cysts • Chronic liver disease • Portal hypertension • Obstructive jaundice • Acute & Chronic gall bladder disease • Diagnostic studies in biliary tract 2 5 8 9 9 9 12 12 13 15 16 17 19 20 25 27 29 31 31 32 34 36 39 39 40 42 43 45 46 50 52 55 57 59 60 61 62 64 66 67 72 75 77 79 80 83 Gastro 1 Pancreas • Pancreas • Pancreatitis • Pancreatic pseudocysts • Pancreatic neoplasms • Spleen Hernias • Hernias o Inguinal o Fermoral o Umbilical o Incisional 84 86 90 91 92 94 94 96 97 98 General gut structure • Describe the arrangement that is characteristic of the tubular alimentary tract and explain how this basic pattern varies through its course. Outermost layer either serosa or adventitia Submucosa connective tissue nerves, vessels Epithelium & Lamina Propria Mucosa epithelium cellular lining lamina propria connective tissue muscularis mucosae smooth muscle layer Muscularis Mucosa Sub mucosa Muscle layer Muscular coat 2 -3 smooth muscle layers MUCOSA Folds of Kerckring Crypts, villi & Glands Microvilli on an enterocyte Folds of submucosa found in distal duodenum & proximal ileum Glands in stomach Crypts and villi in intestines (crypts of Lieberkühn) Further increase surface area for absorption – brush border on light microscopy NB: The foldings of the GI tract à increase its SA by up to 500x The oesophagus and anus are lined with non keratinising stratified squamous epithelium as their function is purely transport The stomach à sigmoid colon is lined with columnar epithelium with secretory and absorptive functions Oesophageal Mucosa – non keratinising, stratified squamous Exfoliating Prickle Granular Basal Pit / foveola (M) Isthmus / neck (P) Gastric Mucosa highly glandular mucosa forming gastric glands Base (can be up to 7 joining to none isthmus) (C) GC = mucous cells (45%) pale staining in H&E Secrete alkaline mucus P = Parietal/oxyntic cells (15%) Large, eosinophilic deep invaginations (canaliculi) produce intrinsic factor secrete hydrochloric acid missing in the pyloric mucosa (pylorus = “non-oxyntic” mucosa) C = Chief/zymogenic cells (30%) Granular, basophilic secrete pepsinogen Gastro 2 Surface of the mucosa is covered in mucous GC EEC C C P C EEC = Enteroendocrine cells small, scattered; basal granules secrete various hormones Enteric Mucosa E GC MC B E = Enterocytes (columnar cells) Brush border (microvilli), absorptive GC = Goblet cells (mucous cells) Pale staining in H&E, secrete alkaline mucus MC = M cells Dome area of lymphoid nodules, transepithelial antigen EEC Pa transport, port of entry for pathogens B = Brush cells Bottle-shaped, scattered, apical protrusions, chemosensory function EEC = Enteroendocrine cells Small, scattered, basal granules, secrete various hormones Pa = Paneth cells Base of crypts, apical eosinophilic granules, secrete antimicrobial peptides LAMINA PROPRIA The lamina propria contains: Blood vessels arteries veins capillaries- lymphatic vessels axial lacteals (lymph capillaries)- nerve fibres Cells smooth muscle cells fibroblasts immune cells myofibroblasts Lymph nodules isolated nodules - peyers patches in lower ileum opposite mesentry aggregated nodules – appendix has circumferential NERVE PLEXUS 8 10 neural crest-derived neurons (ganglion cells), glial cells and connecting nerves organized in 3 major plexus: inner submucosal plexus of Schabadasch outer submucosal plexus of Meissner myenteric plexus of Auerbach Secretory Motor MUSCLE LAYERS CAECUM & COLON * STOMACH * indicates taeniae coli 3 thickenings of the longitudinal muscle layer Oblique Circular * Longitudinal Gastro 3 * • Know the epithelial transition zones (lips and gastrooesophageal, gastroduodenal, ileocecal, rectoanal, mucocutaneous zones). Where 2 epithelial types meet there is a “transitional zone” • Lips - keratinised à non keratinised stratified squamous • Gastro-oesophageal junction – non kerat strat squamous à gastric columnar • Gastro-duodenal – gastric à enteric columnar • Ileocecal • Rectoanal – columnar à non keratinised stratified squamous • Mucocutaneous junction – non keratinised à keratinised stratified squamous Gastro-oesophageal (squamo-columnar) Non keratinised stratified squamous à gastric mucosa Barrett’s oesophagus = intestinal metaplasia in the distal oesophagus = Increased risk of developing oesophageal adenocarcinoma Gastro-dudenal Gastric mucosa à intestinal mucosa Recto-anal and mucocutaneous junctions transition from columnar to squamous epithelium anal glands and ducts with cuboidal epithelium Recto-anal Pectinate (dentate) line Hilton’s white line transition into keratinizing epithelium Gastro 4 progressive thickening of the squamous epithelium The mouth • Know the key anatomical features of the oral cavity, including the teeth and recognise their structure, and function LIPS The 1st transitional zone of the GI tract Skin Keratin layer Hair follicles with sebacious glands Sweat glands with spiral ducts Free margin – vermillion border Keratohyalin, but no keratin layer Thick stratum lucidum High dermal papillae with rich capillaries (red colour) Mucosa Keratohyalin, but no keratin layer Papillae Numerous mucous glands CHEEKS Include the lateral distensible walls and facial prominences over the zygomatic bones Main muscle is Buccinator GINGIVAE (GUMS) Fibrous tissue covered with mucous membranes Firmly attached to alveolar processes of the jaws and necks of the teeth TEETH 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. Incisive fossa Palatine process of maxilla Horizontal plate of palatine bone Greater & less palatine formamina Central incisors Lateral incisors Canines 1st Premolars 2nd premolars 1st molars 2nd molars 12. 3rd molars 2 sets of teeth 20 Deciduous (baby / milk) Erupt from 6-24 months 32 Permanent (adult) Usually all by mid teens Wisdom teeth (3rd molars) by late teens / early 20s Maxilliary teeth are innervated by the superior alveolar branches of the maxillary nerve Mandibular teeth and innervated by inferior alveolar branch of the mandibular nerve 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. Cheeks Palate Floor Crown Neck Root Enamel (substatia adamantia) Sentine & dentine tubules (substatia eburna) Dental pulp containing vessels & nerves Gingival (gum) epithelium (stratified) Peridontium (alveolar periosteum) Cement (cementum) Root (central) canals containing vessels & nerves Apical foramina Each tooth is composed of an enamel covered crown, dentine and pulp. The pulp fills a central cavity and is continuous with the root canal. Vessels, nerves etc enter through an apical foramen The root is embedded in the alveolar bone of the maxilla/ mandible and covered by cement, which is connected to the Gastro 5 alveolar bone by the periodontal ligament PALATE Forms the arched roof of the oral cavity and floor of nasal cavity Hard Palate (anterior) Separates anterior oral cavity from nasal cavities Filled with tongue at rest Formed by palatine processes of maxilla and horizontal plates of palatine bones 2 foramina – incisive, greater and lesser palatine fossa Soft palate (posterior) Separates posterior oral cavity from nasopharynx Muscular – suspended form posterior border of hard palate Extends backwards as the uvula Strengthened by palatine aponeurosis During swallowing Soft palate is initially tenses to allow tongue to press against it (moving bolus back) Then elevated posteriorly and superiorly against the wall of the pharynx (prevents food entering nasal cavity) TONSILS Palatine tonsils are 2 masses of lymphoid tissue, one each side of the oropharynx Each lies in a tonsillar sinus (fossa) • SALIVARY GLANDS Demonstrate by dissection the major salivary glands and their ducts. 1. 2. 3. 4. 5. 6. 7. Branches of the facial nerve Transverse facial artery Parotid duct Sublingual gland Submandibular duct Submandibular gland Parotid gland The parotid gland (serous) empties into the oral cavity via the parotid duct The submandibular gland (mostly serous) empties into the floor of the mouth via the submandibular duct (lies close to lingual nerve) The sublingual gland (mostly mucous) opens through several small ducts beneath the tongue TONGUE Functions of the tongue Assistance with mastication, deglutination, articulation of speech and oral cleansing • Construct diagrams illustrating the innervation of the tongue All the muscles of the tongue are innervated by the hypoglossal nerve (CN XII) Except for the palatoglossus (CN XI carried by CN X) CN XII palsy – Tongue will deviate towards the lesion Sensory innervation Anterior 2/3 of tongue - touch and temperature = lingual nerve (branch of CN V3) Anterior 2/3 of tongue – taste = chorda tympani (branch of CN VII) Posterior 1/3 of tongue – taste = glossopharyngeal (CN IX) Gastro 6 Circumv Foliate Filif or Posterior Part 1/3 Lingual tonsil Circumvallate (sensory) Ø 1-3 mm dozen, sulcus terminalis von Ebner’s glands Foliate (sensory) L 1-3 mm rare, dorsolateral Anterior Part 2/3 Papillae and taste buds filiform (mechanical) L 2-3 mm numerous, ubiquitous horny tips Taste Buds Fungiform (thermoregulatory) L 1-2 mm numerous, ubiquitous rich capillaries • Describe the importance of the lymphatic drainage of the tongue. Posterior 1/3 à superior deep cervical LN Medial anterior 2/3 à Inferior deep cervical LN Lateral anterior 2/3 à submandibular LN Apex à submental LN NB: Posterior 1/3 and midline groove drain bilateraly NB: posterior carcinomas metastasise early via lymph, Apex and anterolateral do not met until late. Once in the deep cervical nodes can spread deep into neck Gastro 7 Salivation • Outline the functions of saliva. • Salivary amylase – starts polysaccharide breakdown • Produces mucous – facilitates swallowing • Protective – lysozyme + IgA • Solvent to stimulate taste • Moisturiser – aids speech • Promotes oral hygiene • Contains HCO3- (neutralises food acid to prevent dental caries) • Name the salivary glands, and outline their structure. Parotid (cheek) 20% Serous Submandibular 70% Mainly serous Sublingual 5% Mainly mucous Simple (buccal) 5% Mucous Acinus Striated Duct Intercalated Duct • Excretory Duct Indicate how and why the electrolyte composition of saliva varies with salivary flow rate and how it compares to plasma. Resting flow rate = 0.5ml / min Maximal flow rate = 7ml / min Total = approx 1 litre / day Acinar cells Primary secretion Isotonic with plasma Some salivary proteins Duct cells Some active reabsorption of Na+ (& Cl-) Impermeable to H2O à Hypotonic in relation to plasma • Describe how salivary secretion can be modified by the autonomic nervous system. Conditioned reflex Simple Relfex Cerebral Cortex Other Inputs Salivary centre in medulla Pressure & chemoreceptors in mouth Autonomic NS Salivary Glands Taste Chew Smell Salivary Secretion Gastro 8 NB: parasympathetic stimulation of acinar cells à large volumes of serous saliva (rich in enzyme) requires an increased blood supply innervation à kalikrein à bradykinin à v/d and increased permeability sympathetic stimulation à v/c à small volume of thick, mucous rich saliva • Outline the process of swallowing Oropharyngeal phase – bolus moved to oesophagus (nasal passage sealed off by uvula & trachea by glottis) Oesophageal phase – peristaltic wave • Describe the anatomy of the oesophagus Anatomy Descends through the posterior mediastinum Usually flattened AP when not with bolus Constrictions are possible due to the arch of the aorta, the left hilum and the diaphragm Passes though the diaphragm’s oesophageal hiatus at the level of T10 (IOD,8,10,12) Opens into the stomach at the level of T11 Muscle of the diaphragm form the oesophageal sphincter Histology Lined with stratified non keratinising epithelium Oesophago-gastric junction is marked by the Z-line Wall contains striated (upper portion) and smooth (lower portion) muscle fibres Blood supply Blood supply to abdominal part is from left gastric and left inferior phrenic artery Venous drainage of the thoracic part is via oesophageal veins to azygous vein Venous drainage of the abdominal part is left gastric vein à portal circulation Lymph drainage – left gastric nodes à celiac nodes Gastro 9 OESOPHAGUS Hiatus hernia • Define hiatus hernia with regard to anatomical type (sliding and para-oesophageal). Herniation of part of the stomach into the chest Can be congential or aquired, If acquired can be traumatic or hiatal. Congenital Cause poor lung development due to numerous bowel lumps in the chest Present at US / as respirator distress after birth, regurgitation, vomiting, dysphagia, weight loss. Traumatic acquired Due to blunt chest / abdo trauma (or occasionally penetration of diaphragm e.g. stab) More common on LHS (right protected by liver Rx by surgical repair Hiatal acquired More common in obese, middle-aged & elderly M:F = 1:4 Mostly asymptomatic Symptoms Mechanical – due to stomach in chest à cough, dyspnoea, palpitations, hiccough Reflux – incompetence of cardiac sphincter à burning retrosternal/epigastric pain, worse on bending / lying, may refer to arms (Δ Δ cardiac pain). Relieved by antacids Oesophagitis à stricture formation, dysphagia, bleeding (acute / occult) Sliding (90%) Common condition – 30% of over 50s Gastrooesophageal junction slides through the hiatus and sits above the diaphragm. Anterior is covered in peritoneum, posterior is not Symptoms occur due to presence of relfux (sphincter compromised) Rx – mainly symptomatic Para-oesophageal (Rolling) (10%) Cardia remains in position The fundus rolls up though the hernia along side the oesophagus The sphincter remains below the diaphragm and therefore competent Usually asymptomatic Occasionally can cause voluvulus into chest à severe pain à surgical emergency GORD • List the anatomical and physiological factors predisposing to gastro-oesophageal reflux disease. Due to poor sphincter function If pressure in stomach > sphincter pressure Hiatus hernia, Large meals High abdominal pressures Obesity, Pregnancy Drugs & foods affecting competency Antimuscarinic, Ca2+ blockers, nitrates, Smoking Fat / chocolate / coffee / alcohol Iatrogenic Drugs + post treatment for achalasia Systemic sclerosis Gastro 10 90% have oesophageal involvement. Decreased peristalsis + decreased sphincter pressure à reflux & damage • Name three typical symptoms of reflux oesophagitis. “Heartburn” pain – worse after bending / stooping / lying down, better with antacids Indigestion Waterbrash / Vomiting / Regurgitation of food à night cough & possible pneumonia NB: degree of oesophagitis doesn’t correlate to severity of symptoms • Describe the investigations used to confirm diagnosis of reflux oesophagitis. Endoscopy & Biopsy – looking for changes in lower oesophagus Barium Swallow – observes motility and degree of reflux. Will also show hiatus hernia 24 hour oesophageal pH monitoring – proves reflux but not oesophagitis. Should always be performed before surgery Acid infusion test – dilute acid reproduces pain • List other causes of oesophagitis Fungal infections - esp. in immunocompromised (candida) Viral infection – Herpes simplex & CMV seen in AIDS / immunocompromised Irradiation Ingestion of caustic agents Pemphigus, epidermolysis bullosa, behcet’s syndrome • Describe the morphology and pathological consequences of oesophagitis. Reflux Oesophagitis = acute inflammation of the mucosa due to acid reflux. Mucose is acutely inflamed Peptic ulceration of the lower oesophagus à chronic small ulceration with fibrosis Lower oesophageal stricture – due to fibrous thickening of the wall à dysphagia. Usually 60+. Rx by dilatation & PPI Barrett’s oesophagus (CLO)– metaplasia of the mucosa epithelium from squamous to columnar = premalignant change à predisposition to adenocarcinoma à regular endoscopy to monitor Adenocarcinoma – reflux symptoms à 8 x more likely to develop adenocarcinoma of the lower oesophagus. The more severe & longer the Sx, the higher the risk • Discuss general, medical & surgical therapy available for GORD Conservative measures Weight loss & adapt diet (avoid triggers & large meals) Smoking cessation Avoid tight clothing (corsets, hernia belts) Prop head of bed up Medical management PPI (omeprazole, see later for action) – reduce acid by 90%, rebound effect on stopping H2 receptor antagonists (ranitidine) – acid suppression, available OTC Alginate antacids (gaviscon 3x daily) – acts as raft Prokinetic agents (metoclopromide, domperidone) – increase gastric emptying H.Pylori eradication – little effect on symptoms but advised as reduced peptic ulcers Surgical management Repair of any hiatus hernia + antireflux surgery (fundoplication = suture stomach fundus around lower oesophagus) à improvement in 80% Sricture dilatation / resection will cure any dysphagia Gastro 11 Dysphagia • List the common causes and discuss the main investigations for dysphagia. Lesions in the lumen Swallowed foreign bodies – esp in children Lesions in the wall Congenital atresia Benign neoplasm / CA oesophagus (see below) Fibrosis due to chronic inflammation (GORD) / caustic stricture Plummer Vinson = Oesophageal webs. Dysphagia (hyperkeratinisation of oesophagus) + iron deficient anaemia (smooth tongue, koilonycias), middle age – elderly women. = PREMALIGNANT Pharyngeal pouch – mucosal pouch between thyropharyngeus & cricopharyngeus. Gurgling sounds in neck & regurgitation of undigested food à foetor. Confirm with barium Lesions outside the wall Oesophageal diverticulum Mediastinal tumours (e.g. lung) Lymphadenopathy Thoracic aortic aneurysm Retrosternal goitre Lesions affecting function Achalasia (see below) Chagas disease Motor neurone disease Stroke Diptheria Investigations History – sudden / gradual, fluids/solids etc Examination – lymph nodes, abdomen, plummer-vinson (smooth tongue, anaemia, spooned nails, iron-deficiency anaemia, common in middle age females, increased CA risk) Bloods – FBC (anaemia), U&E (dehydration), CXR – mediastinal fluid level, absent gastric bubble, aspiration Barium swallow Endoscopy& biopsy Oesophageal malignancy • List the symptoms suggestive of an oesophageal malignancy. According to NICE GI bleeding, dysphagia, unintentional weight loss, abdominal swelling and persistent vomiting Others include: Sudden onset / increasing severity, Assoc with reflux (if Barrett’s), Hoarse voice = involvement of recurrent laryngeal nerve, Absence of neurological signs • Alarm symptoms for dyspepsia Anaemia Loss of weight Anorexia Recent onset (progressive & < 3months) Melaena & haematemesis Dysphagia Describe the pathology and natural history of a malignant lesion of the oesophagus. Most commonly squamous or adenocarcinoma M>F, Peak = 50-60 Gastro 12 Higher risk in Far East (China & Japan) Presentation Progressive dysphagia Initial difficulty with bread, meat, potato Then progresses to other solids and eventually liquids Weight loss, retrosternal chest pain = all general Upper oesophagus signs = hoarse voice, cough Squamous (most common in middle & lower oesophagus) 40-60 yrs, m>f Assoc with heavy alcohol / smoking Preceded by epithelial dysplastic change Often presents late with dysphagia Lymph node involvement at presentation is common 20% upper à cervical nodes, 50% middle à mediastinal, 30% lower à celiac Often quite responsive to radiotherapy Adenocarcinoma – lower oesophagus In areas of epithelial metaplasia (Barrett’s) Some are 1o stomach CA which has locally infiltrated If in upper oesophagus usually linked to Plummer-Vinson (mid-elderly women) Metastasise earlier than squamous (via lymph) Poorer prognosis than squamous Prognosis for both is poor – 10% 5 yr survival • List the treatment options for an oesophageal malignancy. If localised – radical oesophagectomy Otherwise – chemo-radiotherapy Paliative – stenting / laser Staging Tis = in situ T1 = lamina propria / submucosa T2 = into muscularis propria T3 = invading adventitia T4 = into adjacent structures • Nx = nodes not assessed N0 = nodes clear N1 = nodes involved M0 = no mets M1 = distant mets Discuss the pre-operative work up for carcinoma of the oesophagus and assessment of fitness for operation involving thoracotomy. CT Staging to ensure disease is suitable for surgery (i.e. no spread) Assessment to ensure the patient is fit for major surgery The surgery involves opening thorax & abdomen & collapsing a lung) Workup required: ECG (+/- echo) – long operation with significant strain on the heart Spirometry & ABGs – is the patient fit for throracotomy & having a lung collapsed Achalasia • Outline the pathology of achalasia of the cardia Gastro 13 Abnormal innervation due to the ganglion cells in the muscle plexus à aperistalisis / peristaltic spasms in oesophagus + failure of oesophageal sphincter to relax à food bolus is retained in the oesophagus à megaoesophagus NB: predisposes to CA Oesophagus Most common in middle age, Predisposes to CA Can occur due to trypanosoma in S.America = Chagas Disease Presentation Long history of intermittent dysphagia from liquids & solids Regurgitation (induced / spontaneous) Liquid intake increases (used to force food through) Can get severe retrosternal pain No weight loss Investigations CXR – may show dilated oesophagus, possibly with fluid level behind the heart Barium swallow – will show lack of peristalsis & narrowing (“swan neck deformity”) Oesophagoscopy – to ensure no tumour causing similar XR Management Endoscopic dilatation of sphincter = success in 80% Always complicated by reflux Gastro 14 General abdominal anatomy The arteries of the posterior abdominal wall 1. Inferior phrenic arteries 2. Celiac trunk à common hepatic, left gastric and splenic 3. Middle suprarenal artery 4. Renal artery 5. 1st - 4th lumbar arteries 6. Common iliac arteries 7. Internal iliac artery 8. External iliac artery 9. Inferior epigastric artery 10. Inferior mesenteric artery 11. Aorta 12. Gonadal (testicular / ovarian) artery 13. Superior mesenteric artery The veins of the posterior abdominal wall 1. Inferior phrenic veins 2. Inferior vena cava 3. Renal vein 4. 1st – 4th Lumbar veins 5. Common iliac vein 6. External iliac vein 7. Internal iliac vein 8. Common iliac vein 9. Ascending lumbar veins 10. Gonadal (testicular / ovarian) veins The autonomic nerves of the posterior abdominal wall 1. 2. 3. 4. 5. Right greater and lesser splanchnic nerves Right sympathetic trunk 2nd & 3rd lumbar splanchnic nerves Pelvic splanchnic nerves Right and left hypogastric nerves to inferior hypogastric plexus 6. Superior hypogastric plexus 7. Inferior mesenteric ganglia 8. Superior mesenteric ganglia and plexus 9. Celiac ganglia 10. Anterior and posterior vagal trunks Gastro 15 Stomach Main anatomical features of the stomach Cardia Z-line Fundus Lesser curvature Body Pyloric canal Parts of the stomach Cardia – contains cardiac glands = shallower than normal glands Fundus – dilates with food, fluid or gas Body – main section Pyloric – contains pyloric glands Angular incisure = sudden angle in the lesser curvature Greater curvature Interior Z-line – Histological junction Rugae - Longitudinal gastric folds Pyloric antrum 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Aorta Celiac trunk Left hepatic artery Cystic artery Hepatic artery proper Right gastric artery - most often arises from hepatic artery, runs along lesser curvature to anastomose with LGA Gastroduodenal artery Right gastro-omental (gastro-epiploic) artery – one of the terminal branches of the gastroduodenal artery, runs along greater curvature, anatstomoses with Left gastro-omental Common hepatic artery Left gastro-omental (gastro-epiploic) artery – from distal part of Splenic artery, runs along greater curvature, anastomoses with Right gastro-omental Short gastric arteries – also from Splenic artery, supply fundus Splenic artery Left gastric artery - runs in lesser omentum to cardia, gives off oesophageal artery, anstomoses with RGA Venous drainage of the stomach Gastric veins parallel the arteries in position and course L & R gastric veins à into portal vein Short gastric and left gastro-omental à Splenic à superior mesenteric à portal vein Lymphatic drainage of the stomach Gastric – drain lesser curvature à celiac nodes Gastro-omental – drain greater curvature à celiac nodes Pancreato-splenic - drain posterior aspect of stomach Pyloric – drain the first part of the duodenum Innervation of the stomach Parasympathetic supply from anterior & posterior vagal trunks (enter abdomen via oesophageal hiatus) Sympathetic supply T6-9 à greater splanchnic nerves à celiac plexus à plexi around the arteries • Identify the stomach and duodenum on a radiograph of a barium meal. 1. Duodenum 2. Jejunum 3. Plicae circulares (valvulae coniventes) Gastro 16 on the inside of the ileum Gastric secretions • Describe the functions of the stomach Initiation of protein digestion Kill ingested bacteria (by acid) Formation of chime (before food progresses to small intestine) Storage of food (to optimise digestion chime should be delivered to duodenum in small amounts, intragastric pressure doesn’t increase as the stomach fills due to distension of the stomach wall and vagal inhibition of smooth muscle tone) • Describe the cephalic, gastric and intestinal phases of gastric secretion. Cephalic phase Secretion stimulated prior to arrival of food in the stomach Induced by thought, sight, smell, taste, chewing & swallowing à 40% of gastric secretions Dependent on vagus nerve being intact Gastric phase When food reaches the stomach secretion increases due to: Local vago-vagal reflexes in response to mechanical stimulation to presence of food in antrum Stimulation of gastrin release from G cells by peptide fragments of partially digested proteins à 50-60% of secretions Intestinal phase Due to circulation of amino acids acting on parietal cells & gastrin produced in duodenal endocrine cells • Describe the main functional role of parietal, chief and surface epithelial cells. Mucosal gland cells (in gastric pits) • Mucous neck cells • Surface epitheium – secrete mucous • Parietal cells – secrete HCl (see below) and intrinsic factor (binds to B12 allowing absorption in terminal ileum) • Chief cells – secrete pepsinogen • Describe the production of HCl by parietal cells. Cl- Cl- Cl- Cells of the mucosal pits Function at pH 0.8-1.0 = 160mmol/l K+ A = Antiport C = Symport carrier P = Proton pump (H+ / K+ / ATPase) C A K+ HCO3- Cl- HCO3P + H H+ H2CO3 Carbonic Anhydrase CO2 H2O Gastro 17 Functions of HCl Activates pepsin & provides optimal pH Aids breakdown of connective tissue & muscle Non specific defence against microbes • Describe the interaction of the parasympathetic nervous system, histamine and gastrin in the control of HCl production GRP 2 Antral G Cell ELC 3b 1 2 3b 3 3 Gastrin Histamine 3 Inhibits Somatostatin Release 4 D Cell H2 M Prostaglandins inhibit acid production G PG H+ K+ K+ Cl- 1. Parasympathetic NS à ACh à muscarinic receptors à increase HCl 2. Parasympathetic NS à ACh à Muscarinic receptors on Endochromaffin Like Cells à histamine release à H2 receptor à increase HCl 3. Parasympathetic NS à Gastrin Releasing Polypeptide à Antral G cells à gastrin release à capillaries à gastrin receptors on parietal cells à increase HCl 3b. gastrin also à ELC à histamine release à H2 receptors à Increase HCl 4. Parasympathetic NS à inhibits D cell from producing somatostatin (NB: somatostatin inhibits gastrin release) è increases gastrin release à increased Hcl (by mechanisms in 3 and 3b) • Describe the mechanism behind inhibition of gastric secretions As meal passes into intestines secretions decrease due to: Removal of peptide fragments à gastrin release stops pH change – acid à inhibits gastrin & increases somatostatin Distension of the duodenum / presences of acid and fat à enterogasterone from duodenum wall à inhibits gastrin NB: gastric acid secretion is also reduced by cephalic influences such as fear and depression • Describe how the gastric mucosa is protected from autodigestion. • • • • Luminal membranes of cells impermeable to H+ & cells have tight junctions so no movement between the cells Negative feedback – pH <2.0 à inhibits G cells directly and via somatostatin release from D cells Mucous released from surface of epithelial cells Rapid repair of damaged mucosa (cells turnover in approx 3 days) – local production of prostaglandin ensures nourishment by causing local v/d & stimulates HCO3- production Gastro 18 Pharmacology of the upper GI tract. • Describe the pharmacological actions and therapeutic uses of: Antacids – give relief not cure HCO3- + H+ à CO2 + H2) à bloating and belching Al (OH)3 + 3HCl à AlCl3 + 3H2O à constipation Mg(OH)2 + 2HCl à MgCl2 + 2H2O à laxative Use Al and Mg together to even out effects Ca2+ salts à gastrin release so not used H2 antagonists Alginic acid + saliva à viscous foam which floats on surface protecting from reflux Proton pump inhibitors (PPI) Omeprazole(now OTC), pantoprazole, lansoprazole Widely used Irreversible inhibitors of proton pumps More effective than H2 antagonists (hits end process, not just one factor) Only act at low pH Inhibit secretion by 90% Increase risk of food poisoning Prostaglandin analogues Misoprostol Prostaglandins prevent acid production, as do their analogues Used to prevent ulceration in those taking NSAIDS H2 antagonists Cimetidine, ranitidine, famtodine Low dose available OTC, high dose = POM Complete histamine antagonist Symptomatic relief Best given at night Promote ulcer healing NB: cimetidine inhibits CYP450 (so interactions), ranitidine doesn’t Gastrin antagonists Not in use Difficult to block as also blocks muscarinic receptor à blurred vision, constipation, retention etc) Prokinetic drugs Cause gastric emptying Benefit GORD Domperidone = closure of oesophageal sphincter & opens lower sphincter Metoclopromide = local increase in gastric motility to hasten emptying • Describe the ulcerogenic effects of NSAIDS. Membrane ¼ of ulcers are associated with NSAIDs PLA2 NSAIDs are irreversible cox inhibitors Arachidonic Acid Steroids have similar effect by COX à lipocortin à inhibiting PLA2 NB: ibuprofen is preferable to aspirin as analgesic as fewer Leukotrienes Prostaglandins side effects 2 forms of COX COX1 = physiological à gastric protection COX2 = pathological à inflammation Most NSAIDs inhibit both enzymes COX2 selective e.g. clopidogrel have fewer GI side effects Gastro 19 Peptic Ulcer Disease • List the two main causes and three rarer causes of peptic ulcer disease H.Pylori NSAIDs / steroids Gastric acid hypersecretion Zollinger-ellison syndrome (rare gastrin secreting tumour of pancreas D cells) Extensive burns (Curling’s ulcer), major surgery / stress (Cushing ulcer) NB: smoking increases recurrence and decreases healing • Describe the relationship between H.Pylori, smoking and NSAIDs and peptic ulcer disease. H.Pylori 70% of peptic ulcers, 80-90% of duodenal ulcers Infection à chronic inflammation à (gastritis) à ulceration of mucosa NSAIDs Cox inhibitors (prevent arachadonic acid à prostaglandins) Prostaglandins inhibit acid production So decreased PGs à increased acid Steroids inhibit PLA2 which allows arachadonic acid release Smoking Increased infection risk à H.pylori And increases risk of inflammation by NSAIDs & alcohol Some evidence that smoking increases acid and decreases bicarbonate secretion • List the symptoms and differences between gastric and duodenal ulcer. Gastric Ulcers M=F Incidence increases with age Usually in lesser curvature Can be malignant Duodenal Ulcers M:F = 4:1 Usually in duodenal bulb (1st 1.5cm) Mostly benign Episodic, epigastric pain + indigestion / reflux Radiates to back (if erodes to retroperitoneum) Worsened by eating Improved by antacids Anorexia, weight loss Malena Vomiting, dysphagia (indicate malignancy) May be Waterbrash & heartburn • Periodic (with remissions of weeks/months) epigastric pain Radiates to back (if erodes to retroperitoneum) Hunger and night (2-3am) pain Improved by food and milk, (and antacids) Weight gain Malena Discuss the investigation of peptic ulcer disease and the role of endoscopy. Blood tests Serology for H.Pylori (see below) Anaemia WCC – infection Clotting screen Fibre optic endoscopy (gold standard) Visualise mouth to 2nd section of duodenum & Locate ulcer If gastric take 6 biopsies ALWAYS take a CLO biopsy for H.Pylori. Usually take a sample to check for Coeliac Gastro 20 Barium meal (contrast radiography) Assess stomach surface Assess emptying H.Pylori CLO test – urease test on biopsy sample CO2 breath test (ingest urea, NH3 + HCO3 à CO2 à exhaled) Serology – Ig antibody based Culture Faecal occult blood Faecal occult blood = bleeding from somewhere in GI tract • Outline a regimen for H. Pylori eradication and discuss its implications for ulcer recurrence. Triple therapy for a week, then PPI alone 2 from metronidazole, amoxycillin and clarithromycin + PPI +/- H2 antagonist Bismuth chelate – kills H-pylori, coats the ulcer, absorbs pepsin, increases PG production, increased HCO3If fully treated recurrence risk is reduced BUT increases risk of food poisoning (due to decreased acid) Requires good compliance Successful in 90% of patients, 1% recurrence Should also stop smoking to aid healing Recheck with breath test to ensure success If gastric ulcer re-endoscope at 6 weeks • Discuss the symptomatic management of peptic ulcer disease with antacids, H2 antagonists, proton pump inhibitors and misoprostol (NSAIDS). Conservative Avoid causative drugs and foods (curry etc) Prop bed up and loosen belt if GORD Stepped pharmacological treatment Antacid +/- alginate HCO3- + H+ à CO2 + H2O Al(OH)3 + 3HCl à AlCl3 + 3H2O Mg(OH)2 + 2HCl à MgCl2 + 2H2O NB: Ca salts à gastrin release so not used Alginates Forms a foam raft on gastric contents which protects from reflux H2 antagonist Cimetidine, ranitidine, famotidine Now available low dose OTC, high dose POM Best given at night NB: Cimetidine is a CytP450 inhibitor PPI Omeprazole (OTC), pantoptrazole, lansoprazole Activated by low pH Can à achlorhydria Increase risk of food poisoning Prokinetic drugs Promote gastric emptying Aids GORD Domperidone (acts on sphincters) Gastro 21 Metoclopromide (increases gastric motility & emptying) Give with analgesia to accelerate absorption • List the complications of peptic ulcer disease requiring surgical treatment and describe that treatment Haemorrhage à if ulcer erodes into vessels à haematemesis & malena à adrenalin injection / diathermy / cauterisation / laser under endoscopy. Ulcer base can be underrun / oversewn Perforation (more common if duodenal, when rate of ulceration > rate of repair) à peritonitis à surgical repair and drain the abdomen. Perforated ulcer Sudden onset, extreme pain (May have Hx of ulcer pain) Pain refers to shoulders (due to diaphragm irritation) Worsened by movement à lay still Nausea, but only occasional vomiting May be haematemesis / Melaena Shock with 12 hrs O/E Rigid, silent abdomen Reduced liver dullness due to air in peritoneum Differentials Perforated appendix Acute cholecystitis Acute pancreatitis MI Treatment NG tube à reduces further leakage to peritoneum Opiates as pain relief IV fluid resus, Abx & PPI started Surgery (50%) – omental plug + biopsy ulcer, remove if malignancy signs Penetration into pancreas à Pancreatitis à repair ulcer & monitor pancreatitis closely Pyloric stenosis – complication of duodenal ulcers. Will cause hypochloraemia, hypokalaemic methabolic acidosis (due to vomiting with renal compensation) Can be dilated with balloon & acid suppression or may require pyloroplasty Obstruction – due to inflammatory oedema (will improve with PPI) / scarring (no improvement with medical treatment). Causes vomiting, dehydration, splash and alkalosis à pyloroplasty / gastric bypass may be needed Gastrocolic fistula – ulcer may perforated through into the colon (in Zollinger Ellison) à intractable diarrhoea with faeces in stomach à requires complex surgical repair Malignant change – uncommon but all ulcers should be viewed & biopsied to check • Name the operations (past and present) for duodenal and gastric ulcers Partial gastrectomy Billroth I = remove affected part + simple anastomosis to duodenum Billroth II = duodenal stump is oversewn à blind loop & stomach anastomosed into proximal jejunum Comlications 2% recurrence of ulcers 20% dumping - fainting & sweating after eating due to food with high osmotic potential being dumped in the jejunum à rapid fluid shifts. “late dumping” is due to rebound hypoglycaemia 1-3hrs post meal Weight loss – due to poor calorie intake Bacterial overgrowth & malabsorption – in the blind loop Gastro 22 Anaemia – due to B12 deficiency from partial gastrectomy Osteomalacia à pseudofractures (look like mets) 1% diarrhoea Abdominal fullness (due to decreased stomach size, improves with time) Bilious vomiting (difficult to treat but improves with time) Increased amylase – if with abdo pain may = afferent loop obstruction (billroth II) + many metabolic complications Obsolete due to the number of complications Vagotomy & pyloroplasty Vagotomy à reduces acid production from body & fundus + reduces gastrin from antrum Affects emptying at the pyloric sphincter à requirement for drainage = pyloroplasty Complications 7% recurrence 14% dumping 4% diarrhoea + some metabolic complications Almost obsolete due to medical treatments Highly selective vagotomy Occasionally used in patients unable to tolerate medical treatment. Vagus denervated only at lower oesophagus & stomach (pylorus left in tact) Comlications >7% recurrence 6% dumping <1% diarrhoea NO metabolic complications • List the clinical features and causes of the Zollinger-Ellison syndrome. Gastrinoma (gastrin secreting adenoma) usually in the pancreas / stomach / duodenum à Excessive acid production à Multiple ulcers in stomach & duodenum Most cases are sporadic, 20% have MEN1 (multiple endocrine neoplasia type 1) 60% are malignant à LNs & Liver mets Symptoms Abdominal pain Dyspepsia – due to increased acid Chronic diarrhoea / steatorrhoea due to inactivation of pancreatic enzymes & mucosal damage Suspect if multiple ulcers / FH Investigations Raised fasting serum gastrin (need to exclude hyperchlorhydria) Gastric pH < 2 Imaging very difficult as tumour is small – use CT, EUS & scintigraphy to image Screen for MEN1 Management High dose PPIs Excise if > 2cm (as increased likelihood of malignancy) Mets Rx with chemo & interferon alpha 80% 5yr survival if single, resectable lesion. 20% if hepatic mets Gastro 23 Gastritis Acute Superficial inflammation Usually caused by ingested chemicals (alcohol, aspirin, NSAIDs) Acute erosive Focal loss of superficial endothelium à dyspepsia, vomiting, haematemesis (if numerous erosions) Due to shock / stress (burns, raised ICP, NSAIDs, binge drinking) Necrotising ulcerative Follows suicidal ingestion of acid/alkali Chronic Helicobacter – see sheet on PUD Autoimmune Assoc with pernicious anaemia Usually elderly à atrophy of mucosa Ab for parietal cells (90%) and IF (60%) à decreased acid and failure of B12 absorption à megaloblastic anaemia Body of stomach mostly affected Reactive (reflux) Bile refluxing into the stomach Assoc with previous pyloric surgery / incompetent pyloric sphincter Also seen with chronic NSAID use Gastro 24 Gastrointestinal Haemorrhage • Specify the symptoms and common causes of acute gastrointestinal bleeding. Haematemesis – bleeding proximal to duodenum Melena – black tarry stools, proximal to caecum Blood in stools – bleeding between caecum and sigmoid Blood on stools – bleeding between sigmoid and anus Shock – based on blood lost • List the common causes of acute gastrointestinal bleeding Oesophagus Oesophagitis (assoc with hernia) Varices due to portal hypertension (5-10% cases of haematemesis. 30% mortality) Stomach Ulcer (>50% cases of haematemesis. 4.3% mortality) Erosions (7.1% mortality) Mallory Weiss syndrome (tear of mucosa) Tumours Duodenum Ulcer (more common than gastric ulcers but lower haematemesis & lower mortality) Pancreatic tumour à erosions Small intestine Tumours Meckel’s diverticulum Large intestine Diverticulitis (30% of lower GI) Colitis (15% of lower GI) Tumours / Polyps (13% of lower GI) Angiodysplasia (10% of lower GI) • List the commonest presentations of chronic GI blood loss. Faecal occult blood Iron deficient anaemia Tiredness, lethargy, malaise • Outline according to priority the steps of assessment and initial management in a patient with gastrointestinal haemorrhage including the following: o o o o general systemic evaluation ABC including cannuale & monitoring. FBC, U&E, LFTs, Clotting, Antibody screen, G&S / Xmatch Catheterise for UO Consider CVP if very severe correction of hypovolaemia Aim to maintain Hb > 10g/dl (8 = transfusion trigger but 10 gives the safety net!) Use colloid until blood available If showing signs of heamodynamic problem X-match minimum 4 units verification of bleeding including rectal examination Eliminate swallowed blood (dental / nose bleed) Examine (if possible) what has been vomited / passed. Test for Hb PR should confirm lower loss & give some indication of rate of loss management triage Once stable à diagnostic tests (see below) Gastro 25 o o • If known varices – balloon Tamponade with Sengstaken-Blakemore tube + vasopressin infusion diagnostic methods to investigate upper GI haemorrhage Upper GI endoscopy - can be used to diagnose & treat (banding / adrenalin injection / sclerosant injection / diathermy / laser) Angiography – can be used if source of bleeding cannot be found diagnostic methods sequence for lower GI bleeding Procto-sigmoidoscopy / colonoscopy - can be used for visualisation and treatment if a cause can be found Barium studies – if bowel perf NOT suspected can be used to locate defects in the bowel Angiography – if source of bleeding cannot be found List the criteria for surgical intervention in a patient with gastrointestinal haemorrhage. Surgery must always be considered in terms of risk:benefit analysis Emergency – torrential bleeding Urgent – continuous bleeding / rebleeding (esp if < 45) Rockall Score is used to assess the severity of outcomes of Upper GI bleeds Higher score à worse outcome. SCORE Age Shock Co-morbidity 0 <60 yrs No None 1 60-79 yrs HR >100 Diagnosis Stigmata of recent bleed M-W tear None Benign lesion Gastro 26 2 >80 yrs BP <100 Heart failure IHD Major illness Upper GI cancer Blood Adherent clot Visible vessel 3 Liver failure Renal failure Disseminated Ca Gastric Neoplasms • Name the three main recognised causes of gastric cancer and list three symptoms that would suggest gastric cancer Associations H.Pylori (class 1 gastric carcinogen) à chronic gastritis à premalignant change Smoked and salted foods à nitrosamines Hypochlorhydria – low acid à colonisation à nitrite formation Gastric adenomatous polyps Smoking Loss of function of tumour suppressor genes (p53 etc) Pernicious anaemia, atrophic gastritic (both à achlorhydria) Previous gastric resection (2-3x increase) Chronic peptic ulcer More common in Japan, Chile, China, Portugal & Russia More common in lower socioeconomic groups Blood group A HNPCC Symptoms General features of lemon yellow tinge, anaemia & weight loss = 5 differentials Gastric carcinoma Caecal carcinoma Pancreatic carcinoma Pernicious anaemia Uraemia Pain – similar to ulcer • Describe the epidemiology, morphology and natural history of gastric cancers. Benign tumours Are rare! Occur as adenomas, leiomyomas (see stromal tumours below), tmours of connective tissue or haemangiomas Adenocarcinoma = majority of Gastric cancers Epidemiology Worldwide incidence decreasing each year (due to decline of H.Pylori) More common in far east, south America & scandinavia Increases with age (peak 50-70), Rare under 30 M>F Some links with FH Higher in blood group A & atrophic gastritis Morphology Mostly occur in the antrum Common type is intestinal 4 appearances: Malignant ulcer with raised edges, necrotic base & absent surrounding folds Polypoid tumour into the lumen – present early due to discomfort & trauma to polyp à bleeding. Has best prognosis Colloid tumour – massive gelatinous growth Leather bottle stomach (diffuse infiltrative pattern) – fibrous reaction in wall à small capacity of stomach à weight loss & food intolerance à poor prognosis Often surrounding metaplasia with H.Pylori Spread Local – to oesophagus & duodenum + direct invasion of organs (inc gastrocolic fistula) Gastro 27 Lymphatic – nodes around lesser & greater curvatures commonly. If from cardia to mediastinal nodes à virchow’s node. Also subpyloric & hepatic Blood – dissemination via portal vein à liver, lungs & spleen Trans-coelomic – peritoneal seedlings & can à krukenburg tumours Clinical features Epigastric pain – indistinguishable from ulcer, relieved by food & antacid Usually advanced disease at the time of presentation à Nausea, anorexia, weight loss Vomiting if near pylorus Dysphagia if near the fundus Anaemia from faecal occult blood is common Mets to liver (jaundice, ascites), bone, brain & lung Signs 50% have palpable epigastric mass + tenderness Occasionally palpable Virchow’s node 1/3 have signs of mets Assoc with dermatomyositis & acanthosis nigricans Stromal tumour (used to be known as leiomyomas / leiomyosarcomas but are not smooth muscle) Very slow growing but are malignant Usually asymptomatic, found by chance Occasionally can ulcerate à haematemesis Treatment – surgical removal / Tyrosine kinase inhibitor chemo if unresectable mets Lymphoma Non-hogkins, B cell type arising in the gastric mucosa lymphoid tissue Caused by H.Pylori & same presentation as adenocarcinoma Some will regress once H.Pylori treated Others require Chemo +/- radiotherapy Prognosis is good (75% 5 yr survival) • List diagnostic methods used to investigate patients with suspected gastric neoplasia FBC & LFTs OGD (Oesophogastroduodenoscoopy) for anyone over 40yrs or with weight loss / persistant symptoms - with 10 biopsies around any ulceration + brushing for cytology Barium meal (double contrast – shows filling defect with rolled egdes) Ultrasound (normal & endoscopic) to detect masses and wall thickening + liver mets CXR will help with staging • List the general principles of curative and palliative surgical procedures for gastric neoplasms and discuss the role of adjunctive/alternative therapy (chemotherapy and radiotherapy). Gastric resection with level 1 lymphadenectomy & resection of neighbouring organs as appropriate Stenting / palliative surgery to slow the disease can help palliatively Radiotherapy is usually not appropriate Combination Chemotherapy can be used and is very effective against lymphoma • Quantify the prognosis of the average patient with gastric cancer. Stage 1 Stage 2 Stage 3 Early carcinoma (confined to the wall) Perigastric LN involvement Distant (> 3cm away) nodes 72% 5yr (with resection) 32% 10% Stage 4 Mets 0% (all die before 5 yrs) Gastro 28 The Acute Abdomen • Define the acute abdomen. Conditions which cause hospital admission within a few hours on onset of pain. Accounts for approx 50% of surgical emergencies • Identify the cardinal symptoms of the acute abdomen and describe the pain patterns associated with the most common causative conditions. Pain Constant Colicky Colicky à constant Sudden onset Back pain Gradual onset Worse on movement Vomiting Persistent Blood Altered bowel habit Constipation Gynae history • - inflammation - blocked lumen (biliary tract, renal, intestinal or uterus/tubes) - strangulation - perforation, rupture, torsion, acute Pancreatitis - Pancreatitis, ruptured aneurysm, renal tract disease - inflammation - peritonitis - obstructive lesion - ulcers or varices (varices are usually painless) - obstruction - ectopic Identify and define the physical findings associated with the acute abdomen and relate these to the basic underlying pathology. Shock Pale, cold clammy Large loss of fluid volume – e.g. ulcer, ruptured aneurysm Absent bowel sounds Peritonitis with gut shutdown Increased bowel sounds Obstruction – gut working hard to try to clear obstruction Foetor Obstruction – rotting food in upper GI tract • Based on the clinical presentation of the acute abdomen, including signs, symptoms, age and sex, list and discuss a differential diagnosis, relating these to the pathology of the conditions. Right Upper Quadrant Acute cholecystitis Duodenal ulcer Hepatitis Congestive hepatomegaly Pyelonephritis Appendicitis R. Pneumonia Right Lower Quadrant Appendicitis Salpingitis / Tubo-ovarian abscess Ruptured ectopic pregnancy Renal / ureteric stone Strangulated hernia Mesenteric Adenitis Meckel’s diverticulum Crohns Perforated Caecum Psoas Abscess Epigastrium Panrceatitis MI Peptic ulcer Acute cholecystitis Perforated oesophagus Left Upper Quadrant Ruptured spleen Gastric ulcer Aortic Aneurysm Perforated colon Pyelonephritis L. Pneumonia Central Intestinal obstruction Acute pancreatitis Early appendicitis Mesenteric thrombosis Aortic Aneurysm Diverticulitis Left Lower Quadrant Sigmoid diverticulitis Salpingitis / Tubo-ovarian abscess Ruptured ectopic pregnancy Strangulated hernia Perforated colon Crohns UC Renal / ureteric stone Gastro 29 • Select appropriate laboratory and ancillary studies to further define a cause for an acute abdomen. Bloods FBC – anaemia = ulcers, diverticular, tumour (+ checking if fit for surgery) WCC – infection Increase Hb – can show dehydration Platelets – increased in crohns / inflammation, decreased in hepatoplenomegally, liver disease U&E – dehydration increases urea, increased K+ = kidney failure / increased cell death LFT’s – obstructive à increased bilirubin & Alk Phos, Hepatic à increased enzymes Amylase – 3-4 x normal = Pancreatitis, slight increase = most causes ABG’s – acidosis = any acute illness Urine Dipstick – blood, glucose, beta HCG à culture Stool C.diff toxin à culture Radiology Small bowel obstruction – banding Large bowel obstruction – haustra Calcifications - stones, AAA wall etc Air under diaphragm = perf • Outline the appropriate initial management of a patient with an acute abdomen. A B – inc O2 C – inc replace fluids Investigate, identify cause à definitive management • Identify the patient needing urgent resuscitation and operative intervention on the basis of their clinical presentation. Patients requiring urgent resuscitation Class I Class II Class III Class IV Blood loss <750ml 750-1500ml 1500-2000ml >2000ml <15% 15-30% 30-40% >40% Pulse <100 bpm > 100bpm >120bpm >140bpm BP Normal Normal Dropped Dropped Pulse Pressure Normal / up Down Down Down Resp Rate 14-20 20-30 30-40 > 35 UO >30ml/hr 20-30ml/hr 5-15ml/hr Negligible Mental State Slightly anxious Marked anxious Confused Lethargic Fluid to give Crystalloid Crystalloid Crystalloid + Blood NB: Based on 70kg man with blood volume for 5l Syndromes requiring laparotomy Rupture of an organ (spleen, aorta, ectopic) – present as shock Peritonitis (perfed ulcer, appendix, diverticulum, bowel, gall bladder) – board like rigidity, guarding, no bowel sounds Syndromes not requiring immediate laparotomy Local peritonitis (diverticulitis, cholecystitis, salpingitis, appendicitis) – check for abscess using US Colic (gut, ureter, salpinx, uterus, bile duct, gall bladder) – regular waxing & waning pain caused by muscular spasm in a hollow viscus Gastro 30 The intestines 1. 2. 3. 4. 5. 6. 7. Greater omentum (reflected upward) Transverse colon (reflected upward) Right colic (hepatic) flexure Ileum & Jejunum Ascending colon Ceacum Bladder Duodenal Anatomy 1st part (superior) – 5cm long, level of L1. 1st 2 cm has mesentery and is mobile. Remainder of duodenum is retroperitoneal 2nd part (descending) – 7-10cm, level of L2-3, curves around head of pancreas. Bile duct enters this section 3rd part (horizontal) – 6-8cm, crosses anterior to IVC and aorta, but posterior to SMA & SMV, level of L3 4th part (ascending) – 5cm, L3-2 Blood supply to the duodenum Proximal (up to entry of bile duct in 2nd section) is supplied from celiac trunk via gastroduodenal artery and its branch the superior pancreaticoduodenal artery Distal (after entry of bile duct – until left colic flexure) is supplied by SMA. 3rd & 4th parts of duodenum supplied by inferior pancreaticoduodenal artery (branch of SMA) NB: the superior and inferior pancreaticoduodenal arteries form an anastomosis with potential for collateral supply Venous drainage of the duodenum Veins follow arteries and drain to portal vein Lymphatic drainage of the duodenum Lymph vessels follow the arteries in retrograde direction Anterior vessels drain to pancreaticoduodenal lymph nodes à pyloric nodes Posterior vessels pass posterior to head of pancreas and drain to superior mesenteric nodes Innervation of the duodenum From vagus and sympathetic nerves of celiac and superior mesenteric plexuses Duodeno-jejunal flexure – acute angle where 4th part of duodenum joins jejunum Jejunum and Ileum Combined are 6-7 metres long (shorter in life due to tonic contraction) Jejunum approx 2/5 of length Terminal ileum enters caecum at ileo-caecal junction (in right iliac fossa) Entire length attached to gut wall by mesentery Blood supply Superior mesenteric artery – runs in the mesentery Arteries unite to form arterial arcades à vasa recta SMA à Intestinal - approx 15-18 forming the arcades and supplying the jejunum and ileum Middle colic - supplies transverse colon Right colic - supplies ascending colon Terminates as ileocolic Ileocolic branches to appendicular supply appendix Venous drainage All drains via mesenteric vessels to the superior mesenteric vein à hepatic portal vein Gastro 31 Lymphatic drainage All via mesenteric lymph nodes (found by the intestinal wall, throughout the mesentery and along the proximal SMA) à superior mesenteric LN Large intestine Caecum, colon (ascending, transverse, descending and sigmoid), rectum and anus Main differences between large and small intestine Teniae coli – three thickened bands of longitudinal muscle fibres Haustra – sacculations of the pouches of the colon between the teniae Omental appendices – fatty appendices of colon Calibre – internal diameter is much larger Caecum Blind ending pouch in right iliac fossa Almost entirely enveloped by peritoneum so is free, but has no mesentery Appendix – blind ending diverticulum with a triangular mesentery. Base of the appendix is usually 1/3 of way between ASIS and umbilicus = McBurney point Blood supply – ileocolic artery (terminal branch of SMA), appendix is supplied by appendicular artery (branch of ileocolic) Venous drainage – ileocolic vein drains caecum and appendix Lymphatic drainage – ileocolic nodes à superior mesenteric nodes Colon Ascending – retroperitoneal, separated from anterior abdominal wall by greater omentum. Supplied by ileocolic and right colic artery (from SMA) Transverse – has mesentery. Supplied mainly (right 2/3) by middle colic artery (from SMA) although also (left 1/3) b left colic artery (from IMA) NB: left colic flexure is higher, more acute and less mobile than the right colic flexure Descending – retroperitoneal and is continuous with sigmoid. Supplied by the left colic artery (from IMA) Sigmoid – s-shaped and has a long mesentery. The loss of the taenia signifies the rectosigmoid junction. Supplied by sigmoid artery (from IMA) Arteries of the large intestine 1. Superior mesenteric artery 2. Middle colic artery 3. Vasa recta 4. Arterial arcades 5. Right colic artery 6. Ileoceacal artery (showing colic and ileal branches) 7. Appendicular artery 8. Superior rectal artery 9. Sigmoid arteries 10. Left colic artery 11. Inferior mesenteric artery 12. Jejunal and ileal arteries SUMMARY of blood supply to the gut based on embryological origin Gut Fore Division points Proximal to ampulla of vater Somatic referral Upper abdo Gastro 32 Arterial supply Coeliac abscess Mid Hind To 2/3 of transverse colon Distal to above Middle abdo Lower abdo Superior mesenteric Inferior mesenteric Rectum Connects sigmoid to anus S-shaped and has 3 flexures as it follows the curve of the sacrum and coccyx Terminal part has sharp posterior flexure = anorectal flexure – important for faecal continence, held in place by puborectalis muscle Blood supply - superior rectal artery (continuation of IMA), middle rectal artery (from gonadal) and inferior rectal artery (from interior pudendal) Venous drainage - superior rectal vein (à portal system) and middle and inferior rectal veins (à systemic) Anal canal From upper aspect of pelvic diaphragm to anus Has internal and external anal sphincters to maintain continence External sphincter – large, voluntary, muscles blend with puborectalis muscle over inferior 2/3 Internal sphincter – involuntary around superior 2/3 – innervated by sympathetic system, inhibited by parasympathetic system Interior – anal columns = longitudinal ridge, containing artery and veins, pectineal line is the line of the valves Blood Supply - superior rectal artery superior to pectineal line, and inferior rectal arteries inferior to pectineal line. Middle rectal arteries supply between and provide anastomosis The portal venous system and anastomoses 1. Paraumbilical vein 2. Right gastric vein 3. Hepatic portal vein 4. Superior mesenteric vein 5. Middle colic vein 6. Right colic vein 7. Ileocolic vein 8. Inferior rectal vein 9. Middle rectal vein 10. Superior rectal vein 11. Left colic vein 12. Inferior mesenteric vein 13. Splenic vein 14. Left gastric vein 15. Oesophageal veins Important anastomoses Oesophageal varices Haemorrhoids Paraumbilical Gastro 33 Gastro-intestinal motility. • Explain what is meant by electrical coupling between smooth muscle cells and its importance for generating waves of activity along the gastrointestinal tract. Primed by pacemaker cells (Interstitial cells of Cajal - ICC) à a spreading Basal electrical rhythm (BER) – sensitive to stretch which stimulates gut activity Movement is co-ordinated by myenteric plexus BER à Approx 3-5 waves per minute Smooth muscle excitability controlled by Myogenic properties of smooth muscle Activity of intrinsic and extrinsic nerves Hormones and locally produced chemicals NA à B-receptors on smooth muscle cells à muscle relaxes (ahead of bolus) by release of VIP (Vasoactive intestinal polypeptide) ACh à contraction behind the bolus • Describe the main features of normal oesophageal peristalsis. Controlled by vagal nerves Contraction speed = 5cm /sec Wave lasts 7-10 sec Gravity assisted Rate of movement is proportional to viscosity If bolus doesn’t reach stomach à 2nd wave by vasovagal reflex Empty oesophagus – salivary swallowing Awake = 70 / hr Asleep = 7 / hr By small intermittent waves • Describe the mechanisms involved in the control of gastric motility. Empty stomach = feeble contractions Full stomach = weak for 1st hour, later waves more powerful Waves à mixing of contents, and some emptying of contents Neural control Vagal relaxatory fibres induce relaxation in corpus and fundus Mediated by VIP Sympathetic (NA) stimulation inhibits activation by distension of duodenum Vagal relaxatory fibres release ACh à increased motility Hormonal control Gastrin (antrum) and motilin (small intestine) are stimulatory Secretin and CCK and inhibitory • Describe factors which affect gastric emptying Meal composition Meal volume Fragment size Osmolarity Acid Fat • – liquids pass through faster than solids – increased volume à increased emptying – must be 1mm or smaller to pass through – 200mOsmolar = optimal – excess acid in duodenum slows emptying – fat in duodenum slows emptying Describe the main features of intestinal motility in the small bowel and colon. Gastro 34 Small bowel motility - 2 types of contractions Segmenting – in circular muscle, moves chime to and fro, BER in duodenum 12/min, BER in terminal ileum = 9/min à ensure movement oral à anal Peristaltic – in longitudinal muscle, over short distances, after meal MMC (migrating motility complex) = intestinal house keeping Control of small bowel motility Myogenic (stretch) mechanisms Myenteric plexus (local regulation) – stimulated by ACh, Gastrin and CCK, inhibited by VIP, opioids and NO Extrinsic nerves – both sympathetic & direct – vagus has little role Local chemicals – fat / hyperosmolarity à increased time Large bowel motility Ileal-caelcal sphincter (ZEP) prevents backwash Movement in the large bowel is generally slow and non propulsive “Haustral contractions” – segment food approx 2/hr 3-4 times daily gastrocolic reflex à drives contents towards rectum in response to food in stomach Defecation Rectum is usually empty. Sensory nerves detect faeces à internal anal sphincter relaxes Anus = tonically contracted smooth muscle ring with voluntary control Defecation reflex – myenteric plexus is weak. Parasympathetic spinal reflex is required for voluntary effort not to defecate Gastro 35 Diarrhoea & Constipation • Diarrhoea Frequency > 3/day watery / soft Causes Rotavirus (damages to small bowel villi – preventing H2O uptake) Invasive Bacteria (invade & damage epithelium) Adhesive Enterotoxigenic bacteria (e.g. cholera) – adhere to brush border & increase cAMP à Cl- and NA+ secretion à H2O loss May be 2o to drugs Antibiotics (e.g. clindamycin à super infection à pseudomembranous colitis) orlistat (lipase inhibitor) à steatorrhoea misoprostol (via cAMP) PPI’s (increase infection risk) Others include - digoxin, acarbose, metformin, Fe salts Management Oral rehydration therapy Effective yet simple treatment Dioralyte = electrolyte rich isotonic solution with glucose for Na Symport Glucose in solution allows symport of Na+ into cells Antibiotics Most simple infections are viral Should only be given if microbiology is proven Ciprofloxacin – for travellers diarrhoea Antimotility agents (opioids) Codeine, loperamide Inhibit presynaptic µ receptors à reduces release of AC à K+ efflux à neurones less excitable (hyperpolarisation) à reduce tone and peristaltic movements à increase transit time (can prolong the expulsion of infection) Loperamide doesn’t penetrate the BBB and has efficient enterohepatic cycling so is retained in the gut Codeine is used as analgesic but has constipation side effects a2 adrenoceptor antagonists (e.g. clonidine – used for HT) also cause constipation Antimotility & antimuscarinic agents Dicylovirine à decreased GI motility TCAs à constipation due to antagonis of Muscarinic receptors – advise high fibre diet • Constipation <3 / week Causes May be drug induced (e.g. opioids, TCA’s, diuretics, antimuscarinics) – reduce dose Management Best approach is balanced diet with roughage Check for any drug causes & address as necessary Osmotic laxatives e.g. lactulose – bacteria produce acids, draw H2O back to lumen by osmosis e.g. movicol – inert polymer which draws H2O into bowel lumen Magnesium – osmotic effect & CCK releaseà increases GI motility Bulking agents - ispaghula husk, methylcellulose Stimulant laxatives e.g. senna – metabolised to stimulant of GI tract e.g. dantron - irritant Gastro 36 Acute Appendicitis Incidence decreasing duet to improvement in high fibre diets Still the most common surgical emergency (approx 6% lifetime risk) Pathophysiology Appendix obstructed by a faecolith / mucus / lymphoid hyperplasia à Ulceration of mucosa & migration of bowel flora into submucosal layers à Inflammation & suppuration As blood supply is limited by a tight mesentry inflammation à occlusion à Gangrene & spreading peritonitis • List the symptoms and signs of acute appendicitis. Abdominal pain – begins central à localises to RIF RIF tender with guarding (due to local peritonitis), can be mass Pain on coughing à shallow breathing & laying still Nausea, Vomiting, Anorexia Fever (37.5 - 38.5) Raised WCC (polymorph leucocytosis) Coated tongue with fetor • Formulate a differential diagnosis of the conditions that commonly mimic acute appendicitis. GIT - Diverticulutis / meckel’s with ulcer / crohns / food poisoning / mesenteric Adenitis / Caecal ulcer or carcinoma HPB – Cholecystitis / acute pancreatitis Urinary – Cystitis / right ureteric colic / right pyelonephritis Female only - Ectopic pregnancy / salpingitis / period pain • Outline the diagnostic workup in a patient with suspected appendicitis. List the laboratory findings that would tend to confirm the diagnosis of appendicitis. On examination Rovsing’s sign – pain in RIF with LIF pressed Pain in McBurney’s point (2/3 of way from umbilicus to ASIS) May be appendix mass = abscess (if > 3 days body walls off appendix --> tender mass above inguinal ligament requiring drainage under US) DON’T RELY ON TESTS Should check FBC, U&E, CRP, Urinoscopy but don’t wait if ill & requiring surgery CT Visualise and confirm inflammation - don’t wait if ill & requiring surgery US Diagnostic and excludes other differentials Diagnostic laparotomy Should be considered in women if ectopic cannot be ruled out If the appendix appears normal ALWAYS search for a meckel’s divertuculum • List the complications of a perforated appendix. General peritonitis Risk of intra-abdominal sepsis (gut bacteria) Blood loss à shock • List and discuss the common complications following appendicectomy and explain how each can be prevented. Gastro 37 Infection of surgical wound – give Abx prophylaxis Appedicular abscess - drain and give Abx • List the common situations in which appendicitis is difficult to diagnose or manage. Infants – watery diarrhoea and vomiting Children – vague abdominal pain and decreased appetite OAP –shock, confusion, usually no pain Pregnancy – pain is higher and more lateral than usual • Discuss the pathology of causes of a mass in the right iliac fossa and outline the assessment, investigation and management. Appendix Caecal carcinoma - older, longer history, diarrhoea, anaemia Crohn’s – younger with diarrhoea Distended gall bladder Pelvic kidney – from renal transplant Common / external iliac aneurysm Retroperitoneal tumour Ileoceacal TB – common in India Psoas abscess Assess using CT / US and manage accordingly Gastro 38 Meckel’s Diverticulum • Describe the nature of a Meckel’s diverticulum and its possible pathological effects. Less than 2% of the population Less than 2” long and 2cm wide More than 2’ from the ileo-caecal junction Male : Female = 2:1 It is a true diverticulum (has a muscle coating) Most common congenital malformation of the GI tract An embryological remnant of the vitello-intestinal duct. Lies on antimesenteric border of ileum Is sometimes connected to the umbilicus by a fibrous band / as a fistula Embryology Early in embryonic life, the vitelline duct connects the midgut to the yolk sac. The duct undergoes progressive narrowing and usually disappears by week 7. If the duct fails to obliterate: A persistent vitelline duct (appearing as a draining fistula at the umbilicus) A fibrous band connecting the ileum to the inner surface of the umbilicus A patent vitelline sinus beneath the umbilicus An obliterated bowel portion A vitelline duct cyst Can be silent BUT 20% contain gastric and pancreatic tissues à can produce acid à ulcer / bleeding • Discuss the relationship between the umbilical hernias and Meckel's diverticulum. Both umbilical hernias and meckel’s diverticulum are defects of embryological development NB: a Littre’s hernia is an inguinal / femoral hernia which contains the meckel’s diverticulum • Describe the variable clinical presentations of a patient with a Meckel's diverticulum. Presentations Asymptomatic – at operation / autopsy Acute inflammation – identical to acute appendicitis Perforation by a foreign body – presenting as peritonitis Intussussception (ileo-ileal) – often ganrenous by the time of surgery Peptic ulceration – due to containing HCl producing parietal cells (often in children approx 10yrs) Patent vitello-intestinal duct – presents as umbilical fistula that discharges intestinal contents Raspberry tumour at the umbilicus – due to persistent umbilical extremity of duct Vitello-intestinal band – stretching from tip of diverticulum to umbilicus – may à obstruction or act as an apex for volvulus Symptoms Blood in stool Abdominal discomfort Iron deficiency anaemia Diagnosis Radionucleotide scan – technecium is taken up by gastric mucosa – will show stomach & meckels. Technecium will also show up any bleeding areas Barium follow through may show the diverticulum • Discuss the treatment of a Meckel's diverticulum. Surgical resection (laparoscopic) with an end-to-end anastomosis Gastro 39 Intestinal Obstruction (small intestine) • Describe the symptoms and signs in a patient with intestinal obstruction. Colicky pain Vomiting with constipation Distension of the abdomen Increased bowel sounds • List the common causes and the associated pathology of intestinal obstruction. Adhesions – 80% of adult obstruction cases Hernias Crohn’s à structure Intussusception Obstruction due to external CA • Discuss the complications of small bowel obstruction including fluid and electrolyte shifts, vascular compromise of the intestine and sepsis. Strangulation – loss of blood supply à gangrene Infection – as bacteria invade bowel wall Perforation – if bowel expands too far Electrolyte imbalance – check U&Es. Vomiting à hypochloraemic, hypokalaemic metabolic alkalosis 3rd space losses – tend to be high in potassium • List the appropriate laboratory and X-ray tests to be employed in a patient with suspected small intestinal obstruction. AXR – erect and supine to show fluid levels Ladder pattern of dilated loops, centrally places, with valvulae coniventes CXR erect – to exclude perforation (free air under the diaphragm) Barium follow through (if perf is excluded as barium in peritoneum à scarring Water soluble contrast enema (no bowel prep required) CT • Differentiate between mechanical small bowel obstruction and paralytic ileus. Mechanical obstruction is due to a physical blockage in the bowel lumen Paralytic ileus is due to a lack of intestinal motility (therefore is not assoc with colicy pain) • List the symptoms and signs suggestive of strangulation. Change in character of pain from colicky to continuous Tachycardia Pyrexia Peritonism Bowel sounds reduced / absent Leucocytosis • Outline a plan of treatment in a patient with small bowel obstruction IF NO SCARS / SURGICAL HISTORY à ARRANGE URGENT LAPAROTOMY Drip & Suck IV fluids – based on U&E results. Replace deficit + maintenance + losses NG tube – to reduce risk of aspiration Gastro 40 Analgesia - as the pain is very severe Antibiotics – usually ceph & met to cover for bowel perf & surgery Refer to the surgical team for assessment & surgery Non-Viable bowel Loss of peristalsis Loss of sheen Colour (green / black, BUT purple may recover) Loss of pulsation of vessels in the mesentry • Distinguish between small bowel and large bowel obstruction on abdominal X-ray. On AXR loops of small bowel: Valvulae conniventes Many loops Centrally placed Small radius of curvature 3-5cm No solid faeces Distended small bowel has: Dilated, gas filled loops (> 5cm) Multiple fluid levels (> 2.5cm) on erect film String of beads sign = Virtually diagnostic of SBO. Gas trapped in valvulae conniventes when bowel almost completely filled with fluid Gastro 41 Malabsorption • Outline the pathology of common causes of malabsorption in the UK Common causes Pancreatic insufficiency (e.g. chronic pancreatitis, CF) Celiac disease Resection of ileum Parasitic infestation of the gutt Frequent causes Resection of the stomach Crohn’s disease Liver disease à failure of bile secretion into gut Uncommon causes Bacterial overgrowth in blind loops / diverticulae Post infection malabsorption (tropical sprue) A-chain disease Giardiasis Disaccharise deficiency (e.g. lactase) Abetalipoproteinaemia Intestinal lymphangiectasis Whipple’s disease • Describe the clinical presentation suggesting malabsorption. Tiredness & lethargy Malaise Anaemia Diarrhoea & steattorhoea Weight loss despite good / increased appetite • Outline the deficiencies that may result from malabsorption including haematinics, fatsoluble vitamins, calcium and protein together with the clinical consequences of deficiency. Absorbed in Small intestine Jejunum Small intestine Small intestine à xeropthalmia à rickets, osteomalacia à haemoloysis & neurological deficit à clotting / bleeding disorders Vit B1(thiamine) encephalopathy Vit B2 (riboflavin) Vit B6 (pyridoxine) Vit B12 Small intestine à beri-beri / Wernicke’s Proximal small intestine Small intestine Terminal ileum Vit C Folate Nicotinamide Proximal ileum Jejunum Jejunum à angular stomatitis, cheilitis à polyneuropathy à anaemia (hypochromic, macrocytic), neuropathy, glossitis à scurvy à Macrocytic anaemia à pellagra Calcium Copper Fluoride Iodine Iron duodenum & jejunum Stomach & jejunum Stomach Small intestine Duodenum & Jejunum à hypocalcaemia à Menke’s kinky hair syndrome à dental caries à goitre, cretinism à Microcytic anaemia Vit A Vit D Vit E Vit K Gastro 42 Magnesium arrhythmias Phosphate Selenium Zinc healing Protein • Small intestine à paraesthesiae, fits, tetany, Small intestine Small intestine Jejunum à osteoporosis, anorexia, weakness à cardiomyopathy à acrodermatitis enteropathica, poor Jejunum (& Ileum) à oedema Compare and contrast the consequences of malabsorption due to extensive small bowel disease such as Coeliac disease and pancreatic disease. Pancreatic disease will affect fat digestion (no pancreatic lipase) à poor absorption of ADEK & fatty stools Extensive small bowel disease will affect all substances absorbed in the small bowel • Outline the investigation of a patient with malabsorption including endoscopy with duodenal biopsy, barium studies and microbiological assessment. Bloods Iron deficiency – macrocytic, hypochromic Decreased vit D – due to fat malabsorption Increased prothrombin time – low Vit K Coeliac Ab Ca2+, Fe2+, B12, Folate, INR, Lipid profile, Stool Sudan stain for fat globules, microscopy for infestation Barium study Diverticula, Crohns, radiation enteritis Biopsy Study samples for cellular pathology ERCP Biliary obstruction, chronic pancreatitis Breath hydrogen analysis Give glucose, take samples of expired air at ½ hr intervals – if hydrogen increases indicates bacterial overgrowth Coeliac disease • Outline the morphology, pathological consequences and clinical features of coeliac disease including advice about treatment. Gluten enteropathy Allergy to gliadin in wheat, rye and barley Most common in Pathology T cell mediated auto immune disease of small bowel Prolamin (alcohol soluble proteins) intolerance à villous atrophy & malabsorption Associations HLA DQ2 (95%), HLA DQ8 (5%) Dermatitis herpetiformis (blistering subepidermal eruption) More common in the Irish & NW Europe, rare in black Africans Occurs at any age (peaks in infancy and 50-60yrs) M>F Gastro 43 10% prevalence in 1st degree relatives, 30% siblings Presentation Loose bowel motions (steatorrhoea) Abdominal pain Bloating Nausea & Vomiting Apthous ulcers, angular stomatitis weight loss despite hearty appetite (Amenorrhoea & low body mass) Fe deficient anaemia (due to malabsorption) Osteomalacia Failure to thrive in children Psychiatric symptoms (anxiety / depression) are common 1/3 are asymptomatic Differentials Thyrotoxicosis, DM type I Diagnosis Endoscopy + Biopsy (duodenal / jejunal) – On microscopy - atrophy of villi and hypertrophy and hyperplasia of crypts + intraepithelial lymphocytes Blood tests = Endomysial Ab (EMA) and Tissue transglutaminase (tTG) Ab (95% specific unless IgA def) FBC to check anaemia All patients should have bone densitometry due to osteoporosis risk RX Life long gluten free diet (some diet items are prescribable) Rice, maize, soya, potatoes & oats are OK Check diet compliance by monitoring antibody levels Should have pneumococcal vaccine once every 5 yrs (due to splenic atrophy) Complications Anaemia 2o lactose intolerance GI T-cell lymphoma (rare, suspect if refractory / weight loss) Increase risk of cancers (gastric, oesophageal, bladder, breast, brain) More prone to osteoporosis – reduced Vit D and Ca absorption due to damage to villi Increased risk of atopy & autoimmune disease (DM, thyroid, primary biliary cirrhosis) Outcome Fairly normal if well managed Gastro 44 Irritable Bowel Syndrome • Describe symptoms that may suggest a diagnosis of IBS Abdominal pain / discomfort for at least 12 weeks of the last year: Relieved by defecation OR assoc with altered stool frequency OR change in form of stool Associated with Abnormal frequency (>3/day or <3/week) Abnormal stool (lumpy hard / watery) Abnormal passage (straining, urgency, tenesmus) Passage of mucus Bloating / abdominal distension Other Non-GI symptoms include Dysmenorrhoea, dyspareunia, PMT Urinary freq, urgency, nocturia and incomplete emptying Back pain Headaches Bad breath Poor sleep Fatigue • Outline current ideas regarding the pathophysiology of IBS Risk factors Female Severity and duration of diarrhoea Preceeding life events High hypochondriacal anxiety Anxiety and depression • Discuss possible investigations (used to rule out more serious pathology) If young with classic history FBC, ESR, LFT, Coeliac serology, urinalysis, +/- sigmoidoscopy with rectal biopsy If > 45yrs / has any marker of organic disease Add colonoscopy (or barium enema if colonoscopy unavailable) If prominent diarrhoea LFT, stool culture, B12/folate levels, antiendomysial Ab, TSH. Consider referral +/barium follow through +/- rectal biopsy Further tests are guided by symptoms Upper GI endoscopy (dyspepsia, reflux) Duodenal biopsy (if antiendomysial Ab +ve) Giardia tests Small bowel radiology (crohn’s) ERCP (chronic pancreatitis) or MRCP (if active pancreatitis) • Outline therapeutic approaches. Lactulose / loperamide for symptomatic relief Anti-spasmodic agents Antimuscarinics – inhibit parasympathetic stimulation Mebeverine – smooth muscle relaxant Amytriptyline Some pain relief Antimuscarinic effects Alters sensitivity of sensory nerves Gastro 45 Inflammatory Bowel Disease • Describe the morphology and pathological consequences of Crohn's and ulcerative colitis. Crohn’s 5-6 / 100,000 (higher in Europe & N.America) 20-60 yrs, F > M Sibilings 20-35x more likely to get Smoking increases risk (3-4x) NSAIDS may worsen disease High sugar worsens, elemental diet improved Anatomy Begins in rectum & works proximally – only to terminal ileum – no skip lesions 50% just proctitis BUT perianal disease rare 30% à left sided colitis 20% à pancolitis Never spreads proximal to ileo-caecal valve (but can get effects of backwash Anatomy Skip lesions Rectum often spared 30% small bowel involvement 30% colon 40% both 5% also stomach & duodenum 50% perianal disease Pathology TH2 response pANCA usually +ve Pathology TH1 response pANCA usually –ve Transmural inflammation Deep involvement à fistulae and sinuses Mucosa has cobblestone appearance (linear ulcers with islands of oedematous mucosa) Crypt abscesses unusual Lymphoid hyperplasia & granulomas Thickening (mucosal oedema) & narrowing of the bowel (strictures) Late stages have fibrosis, strictures à obstruction • Ulcerative colitis 10-15 / 100,000 (20-40yrs) F>M 15% prevalence in 1st degree relatives Smoking is protective (x3) 10% have milk allergy Stress can à relapse Non specific superficial inflammation Multiple minute superficial ulcers, crypt abscesses, loss of goblet cells, depletion of mucin No granulomas Red and inflamed mucosa, prone to bleeds Ulcers & pseudopolyps (islands of oedematous mucosa between ulcers) if severe Describe common presenting symptoms of Crohn’s disease and ulcerative colitis. Crohn’s Acute presentation perf with local peritonitis Chronic Sx Diarrhoea Abdominal pain – if RIF mimics appendix Weight loss Malaise & lethargy Anorexia, N&V Low fever Gastro 46 Ulcerative colitis Diarrhoea (blood, mucus, urgency & tenesmus) Discomfort Relapses and exacerbations Malaise & lethargy Anorexia Mild = rectal bleed / diarrhoea < 4/day Mod = > 4 motions / day Sev = > 4 motions / day + systemic Sx (fever, HR>90, hypoalbuminaemia < 30g/l, weight loss > 3kg) • List the extra-colonic manifestations of inflammatory bowel disease as they affect the skin, joints, liver and eyes Area Eyes Joints Skin HPB Crohn’s Uveitis 2% Conjunctivitis 5-8% Arthropathy Arthralgia 5% Ankylosing spondylitis 1% Back pain 3% Erythema Nodosum 1% Pyoderma Gangrenosum 1% Sclerosing Cholangitis 5% Fatty Liver Ulcerative colitis Uveitis 5% Conjunctivitis 3-10% Arthropathy Arthralgia 14% Ankylosing spondylitis 1% Back Pain 9% Erythema Nodosum 4% Pyoderma Gangrenosum 2% Sclerosing Cholangitis 2% Fatty Liver Gall stones 15-30% Renal stones 5-10% Venous Thrombosis 1% Renal Vascular Venous Thrombosis 5% • List the important differentials for ileitis and colonitis Ileitis – TB, yersina enterocolitica (stool culture to exclude) Colonitis – infection (food poisoning), ischaemia, microscopic colitis • Describe the clinical features suggesting toxic dilatation in patients with ulcerative colitis. Severe UC attack >6 stools / day with +++ blood >37.5oC HR > 90bpm ESR > 30 Hb < 10 Albumin < 30 Severe Crohn’s attack (merits admission) Increase Temp Increased pulse Increased ESR Increased CRP Increased WCC Decreased albumin Toxic Megacolon Systemic toxicity Colon diameter > 6cm Thin wall à liable to perforation Abdominal distension Local / general peritonitis Fever > 38o HR > 120bpm Leucocytosis > 11,000 AXR – distension with loss of contour, greatest on transverse colon • Discuss the investigation of a patient with suspected inflammatory bowel disease including sigmoidoscopy, barium studies and colonoscopy. Bloods Both Raised platelets, ESR and CRP Decreased serum albumin if severe CD – increased WCC UC - Normochromic, Normocytic anaemia, Fe deficient if severe Stool cultures To exclude infections (C.diff, Salmonella, Shigella, Campylobacter, E.coli, Amoebae) Gastro 47 Radiology CD – Barium = asymmetrical change to mucosa pattern with deep (rose-thorn) ulceration, narrowing of lumen and skip lesions. UC – check for toxic dilatation. Barium enema = loss of haustra, mucosal granularity, pseudopolyps, lead pipe colon Endoscopy with biopsy UC – procto-sigmoidoscopy + colonoscopy - diagnostic although contraindicated during severe attacks due to perf risk • Describe the medical therapy of a patient with inflammatory bowel disease including local and systemic steroids, non-steroidal anti-inflammatory agents and immunosuppressive therapy. Crohns Mild Symptomatic but systemically well Steroids are main Rx Prednisolone to bring under control, reduce dose to maintainence Severe Hospitalisation Aggressive management (IV steroids, fluid balance, TPN, correction of anemia) Mesalazine in crohn’s colitis Azothioprine / cyclosporin will à remission in resistant cases Metronidazole – helps avoid perianal disease & superadded infection Infliximab can help if steroid resistant Surgical treatment Indications Drainage of abscess Stricture resection / plasty Surgery for obstruction, bleeding, perf or fistula Fulminant colitis & perianal disease Dysplasias & invasive carcinomas in chronic cases Operations Ileocaecal resection Segmental resection Colectomy & ileorectal anastomosis Panproctocolectomy Stricturoplasty Temporary loop ileostomy Anal disease – abscess drainage, fistula repair UC Steroids to induce remission (Steroid enemas for local control) 5ASA to maintain remission Mild cases Rectal steroids (prednisolone suppository) @ night If no response give oral prednisolone / Mesalazine / 5ASA High protein diet + replace fluids & electrolytes Control diarrhoea with codeine phosphate / loperamide Moderate cases Oral Prednisolone + 5ASA + 2x daily steroid enemas Severe cases (medical emergency) Admission to hospital Fluid & electrolyte balance control IV hydrocortisone (QDS), Blood transfusion & TPN Xray to rule out toxic dilatation / perf Gastro 48 Cyclosporin / azothioprine to induce remission if steroids fail Infliximab (??) may be used to induce remission if all else fails Maintainence 5ASA (sulphasalazine, mesalazine) decrease relapse rate from 80% to 20% SEs inc – headache, nausea, anorexia, malaise, (rash, fever, haemoloysis) Therapy is life long Surgical treatment (20% require at some stage) Indications Perforation / Acute toxic dilatation Failure to respond to medical treatment / unremitting / debilitating Sx Steroid dependency & assoc problems Severe polyarthritis Severe haemorrhage / stenosis à obstruction (rare) Severe dysplasia (malignancy risk) Operations Total colectomy & ileostomy Pan-procto-colectomy & ileostomy Restorative procto-colectomy (with pouch formation & anastomosis) • Outline the risk of colonic malignancy in inflammatory bowel disease and how this should be screened for. UC for 10 yrs à increased risk of CA (5% at 20 yrs, 12% at 25yrs) Crohn’s = lower risk but still higher than the general population Should have yearly / biyearly colonoscopy with multiple biopsy after 10 yrs Also suggested that high grade dysplasia in UC = indication for colectomy Gastro 49 Diverticula of The Colon • Outline the theories on the aetiology of diverticula of the colon Low fibre diet à muscular hypertrophy à high intraluminal pressures Increasing age à cholinergic denervation à hypersensitivity à uncoordinated muscle contraction à herniation through weak points where vessels join the colon (along taenia coli) • Describe the morphology and pathological consequences of diverticula of the colon. False diverticula (do not have an outer muscle layer) Mostly occur in sigmoid (95% of complications at this site) Occur in 50% of over 50s (unusual before 40yrs) M=F Rare in developing countries Diverticulosis = presence of diverticula Diverticular disease = 95% asymptomatic – discovered on barium enema Diverticulitis = inflammation of diverticula • Describe the clinical features of diverticula of the colon, differentiating the symptoms and signs of diverticulosis from diverticulitis including signs of inflammation and bleeding. Diverticulosis 95% asymptomatic Can à colicy LHS pain Relieved by defecation / flatulence Nausea Some altered bowel habit Worsening à severe pain & constipation with narrowing of the colon Diverticulitis Severe LIF pain (with tenderness/guarding) Fever Constipation Vomiting Increase WCC, ESR, CRP Can be palpable mass Investigations Bloods – acute diverticulitis is assoc with polymorphonuclear leucocytosis & raised ESR & CRP Sigmoidoscopy / colonoscopy Double contrast barium enema Occasionally plain abdo film will show air in bladder due to fistula • Describe the management of a patient with asymptomatic diverticula of the colon. Dietary advice – high fibre diet If painful – antispasmodic (mebeverine) or surgical resection • Outline the complications of diverticula of the colon. Diverticulitis With altered bowel habit, left sided colic relieved by defecation, nausea, flatulence. Can get pyrexia, raised WCC, raised ESR & CRP, tender colon, localised / generalised peritonism. Rx: analgesia, NBV & IV fluids, Abx Perforation Into peritoneum à peritonitis Into pericolic tissues à pericolic abscess Into adjacent structures à fistula Gastro 50 à ileus & shock 40% mortality Rx: Hartman’s procedure (temp colostomy with partial colectomy) or colonic lavage with immediate anastomisis Fistuale à enterocolic, colovaginal or colovesical Can à pneumaturia, UTIs, discharge Rx: surgical resection Chronic inflammation à obstruction Inflammatory fibrosis (bowel loops adhere)à obstructive symptoms Abscess (fever & high WCC) à US to locate and drain Haemorrhage Erosion of vessel in bowel wall Usually a sudden painless PR bleed Rx: usually stops with bed rest. transfuse if req. then resect or diathermy to ablate vessels • Describe the treatment of a patient with diverticulitis including indications for antibiotics, drainage and resection. Initial management Mild attacks – can be treated at home with bowel rest (fluids only) + coamoxiclav (or metronidazole / ciprofloxacin) If oral fluids not tolerated – (or pain not tolerated) admit for analgesia, NBM & IV fluids & Abx (ceph & met) until cultures available. Most settle but some require abscess drainage / surgery for perf Imaging US – can detect perforation, free fluid & collections (but CT contrast more useful) Contrast enema – MUST use water soluble contrast incase of perf. DO NOT DO colonoscopy during an acute attack Surgery Stage 1 – Small confined pericolic abscess – surgery rarely needed Stage 2 – Larger abscesses - may resolve without surgery Stage 3 – Generalised suppurative peritonitis - surgery required Stage 4 – faecal peritonitis - surgery required For severe / recurrent diverticulitis 20% will require surgery Gastro 51 Carcinoma of the Colon, Rectum and Anus • Tumours of the small bowel Are very rare – Usually stromal (leiomyoma or lipoma) à intussussception Carcinoid (neuoendocrine) – from small intestine crypts most common in jejunum & ileum Malignant lymphomas – usually B cell, Coeliac disease à T-cell Primary adenocarcinoma – very rare. Presents as ulcerating strictures lesion • Tumours of the large bowel Benign Adnomatous polyp (elevation above the mucosal surface) = precancerous à remove & follow up in 6 months Papilloma Lipoma Neurofibroma (schwannoma) Haemangioma Malignant Primary Carcinoma (90% of colonic malignancies) Lymphoma Carcinoid tumour (in ileo-caecal region) Secondary Invasion from adjacent tumours • Describe the aetiology, morphology and pathological consequences of carcinoma of the large bowel. 2nd most common fatal malignancy Can occur at any age – most common 65-70yrs Colon F>M, Rectum M>F Sigmoid is commonest site, rectum = 1/3, 5% are multiple Risk Factors Western society - Low fibre, high fat & high meat diet (high fibre & Vit C are protective) Family history FAP (autosomal dominant) – invariably à CA. Polyps from 20, malignant before 40. Rx with total collectomy & rectum excision & form ileoanal pouch Hereditary non-polyposis coli (HNPCC) – AD inheritance à defect in DNA repair system. Tumours in right colon before 50yrs. Suspect if colon CA in 3+ relatives, spanning 2 generations, with one Dx before 50yrs. Also assoc with tumours of ovary, uterus & stomach UC & Crohns Polyps Morphology – ALL are adenocarcinomas Polyploid Ulceration Annular (ring like contriction) Large sections of wall usually involved Spread Local – to perirectal fascia, prostate, seminal vesicles, bladder, vagina & uterus Lateral – along bowel à obstruction Lymphatic – to epi & paracolic LNs à nodesa rouns vessels (venous spread is late) Blood – late. To liven, lungs & occasionally adrenals Gastro 52 Transcoelomic (peritoneal) spread • Identify five common symptoms of carcinoma of the colon, rectum and anus. Discuss the frequency of each symptom depending on the location of the carcinoma particularly with rectal and carcinoma of the caecum. By location Caecum & asc colon (30%) – iron def anaemia, pain, palpable mass, weight loss, diarrhoea (bec water not absorbed), change in bowel habit, vomiting, obstruction (uncommon) Dec colon (& transverse 20%)– Change of bowel habit, rectal bleeding & mucus, solid stool à obstruction Rectum (&sigmoid) (50%)– change in bowel habit, bleeding – with blood mixed in with faeces, feeling of incomplete emptying, tenesmus, constipation, spurious diarrhoea, weight loss, pain, obstruction 25% present as emergencies with obstruction, haemorrhage, perforation or peritonitis 2ndry deposit Liver à LFTs & Jaundice Lung à Cough & wheeze Breast Bone General malignancy Weight loss Anorexia Anaemia NB: many are asymptomatic • Describe the TNM staging system and identify possible associated findings on examination. TNM staging = Duke’s staging A = confined to colon wall (not breeching muscularis propria) B = breech of colon wall, no nodes C = lymph nodes involved D = distant spread • 90% 5 yr survival 65% 5 yr survival 30% 5 yr survival 5% 5 yr survival Discuss appropriate laboratory tests, radiological studies and endoscopic investigations to investigate a patient with a suspected carcinoma of the colon, rectum and anus. Examine – general, masses, signs of spread/complications. ALWAYS PR Bloods – FBC (anaemia), CEA, CRP, ESR, LFTs, U&Es Faecal Occult Blood Sigmoid / colonoscopy – visualise mass & biopsy Double contrast Barium enema – apple core = narrowing CT – for staging Differentials – diverticular disease, UC, other causes of altered bowel habit • Outline the treatment of carcinoma of the colon, rectum and anus and define appropriate resection levels according to lymphatic drainage. Pre-operative Phosphate enema to empty bowel Ceph & Met (or gent) as prophylactic antibiotics Check Hb – transfuse if required Gastro 53 Operative Caecum & asc colon – right hemicolectomy Transverse colon – extended right hemicolectomy / transverse colectomy Desc colon – left hemicolectomy Sigmoid – sigmoid colectomy Rectum – anterior resection (resection + anastomosis) OR perineal resection (resection + colostomy if lesion is too low) Pallative – transrectal resection with resectoscope Solitary liver mets can be resected NB: Hartman’s procedure leaves a rectal stump to which the bowel can be reanastomosed. The rectal stump may be important for those who untertake anal sex NB: Ileostomies should have a spout to allow attachment of pouches. Important as without à surrounding skin damage • Post operative Chemo (5FU & folinic acid) to all Dukes C as improves prognosis to level of B Radiotherapy – usually rectal Incurable Palliative care Outline the role of radiotherapy and chemotherapy in management. Radiotherapy good for inoperable / recurrent CA, provides good palliation for pain & rectal bleeding Adjuvant can be used per/post op (pre op can downstage large bulky tumours) Chemotherapy Used for metastatic / recurrent CA 5FU most commonly used (with folinic acid) – response is incomplete (only 20% of pats) Can be used as adjuvant in Dukes B / C at high risk Immunoadjuvant therapy Levamisole (immunostimulant) used with 5FU for high risk patients Locoregional chemotherapy 5FU instilled into portal vein to clear hepatic mets Gastro 54 Intestinal Obstruction (large intestine) • List the symptoms and signs of large bowel obstruction. Colicky lower abdominal pain Vomiting (with dehydration) Absolute constipation (no faeces or flatus with empty rectum) Dehydration – due to vomiting, poor intake, sequestration & poor absorption Distension – due to gas filled loops of bowel (air swallowing) The more distal the obstruction the greater the distension Visible peristalsis – rare as patient needs to be slim Central resonance to percussion with dull flanks (air filled bowel rises) Abdominal tenderness Abnormal bowel sounds – exaggerated, fluid movement, tinkling • • Discuss the diagnostic aids available for the diagnosis of large bowel obstruction. L Investigations i Management Resuscitate – NBM & IV fluids Examination s Bloods (FBC, U&E, G&S) AXR – supine & erect t Drip (IVI) & Suck (NG tube to Loops lie peripherally releive vomiting & calculate Haustra should be visible t some of fluid losses) (unless megacolon) h Analgesia CXR erect – to exclude perforation e Catheterise to monitor fluid balance (free air under the diaphragm) Unprepared water soluble contrast c enema a CT u s es of intestinal obstruction in children and outline the diagnostic tests most appropriate for each: list the frequency of each cause of intestinal obstruction. Neonatal Intestinal atresia – may be a septum, partial or complete gap (+/- mesentery defect). Rx by resecting stricture & anastomosis but high mortality Volvulus neonatorum – congential malrotation of the bowel. Caecum remains high, midget mesentery is narrow & drags across duodenum. Rx – untwist bowel & widen mesenteric attachment to retroperitoneum Meconium ileus – 80% will have CF. Rx by gastrograffin to attempt clearance / surgery Necrotising enterocolitis – seen in prems due to mesenteric ischemia à bacterial invasion of mucosa. Rx – resus & TPN with Abx. Resect bowel. 25% mortality Hirschprung’s disease – 80% of cases in males. Failure of development of submucosal nerve plexus à spastic section with functional obstruction & proximal distension. Rx – resect agangiolonic segment Anorectal atresia – range from imperforate rectum to complete absence. 50% are assoc with fistula (to vagina or bladder), 25% have other abnormalities. Rx – surgical reconstruction Paediatric Intussusception – prolapse of bowel into adjacent segment 75% ileocolic (can also be ileoileal, ileo-caecal and colo-colonic) 95% occur in infants / young children (usually 3-12 months) M:F = 2:1 No known cause Gastro 55 Colic, screaming & pallor with vomiting & redcurrent jelly stool (blood & mucus) In adults Adhesions (2/3 of adult cases) Carcinoma Non malignant strictures Volvulus Faecal impaction Pseudo-obstruction (ileus) – usually post operative / trauma • Describe the radiological features of large bowel obstruction On AXR - Large bowel: Haustra Fewer loops Peripheral distribution Large radius of curvature 5cm + Solid faeces may be present Large bowel obstruction Fluid levels (>5.5cm in transverse colon, >9cm in caecum) Distension of bowel Volvulus (bottom right) Long mobile mesentery Sigmoid and caecum Coffee bean sign in bowel Gastro 56 Haemorrhoids Most common cause of PR bleeding 40% of population will suffer at some point in their lives • Discuss the anatomy of haemorrhoids; differentiate internal from external haemorrhoids; describe the role of the anal sphincters in maintaining faecal continence. Continence is a function of the anal sphincters & anal cushions Anal cushions - are highly vascular tissues (supplied by rectal aa & drained by sup rectal vv) These are at 3, 7 and 11 O’clock Internal haemorrhoids – congested cushions with dilated veins External haemorrhoids – out of date term for perianal haematoma, sentinel piles or skin tags) Interno-external haemorrhoids – prolapsed haemorrhoids • State the aetiological factors in the development of haemorrhoids, including the roles of heredity, diet, pregnancy and occupation. Diet à constipation à straining à increased congestion Occupation à erect posture impairs drainage Pregnancy à increased venous pressure due to gravid uterus (or any other pelvic tumour) Cardiac failure / Portal hypertension à high BP • Describe the symptoms and complications of haemorrhoids. Symptoms Rectal bleeding – dark red blood (venous) at defecation Extensive piles à mucus, pruritus ani, impaired continence Grading of severity 1st degree – remain in rectum 2nd degree – prolapse on defecation, spontaneous return 3rd degree – require digital replacement 4th degree – persistent prolapse Differentials Rectal prolapse, IBD, anal polyp / fissure, malignant disease (biopsy if suspicious) Acute pain may be due to coexisting anal pathology Fissure, perianal haematoma, perianal / ischorectal abscess, tumour of anal margin or proctalgia fugax (benign episodic pain relived by digital dilatation of the anal sphincter) Complications Anaemia – due to chronic / severe bleeding Thrombosis – prolaspsing piles gripped by anal sphincter à occludes venous drainage à thrombus Appear swollen, red/black with pain & distress Fibrosis and cure after several weeks Rx: conservative (bed rest, elevate foot of bed, local cooling & analgesia), manual dilatation (under GA), emergency haemorrhoidectomy (if prev attacks / gangrene. Abx will help prevent portal pyaemia) • Describe the physical examination of a patient with haemorrhoids, including proctoscopy. Gastro 57 Abdominal Exclude lesions of the colon Assess aggravating factors (e.g. congested liver) Rectal If prolapsing are obvious If internal are non-palpable Proctoscopy Visualise internal haemorrhoids Barium enema If any other symptoms Colonoscopy If barium study reveals any other lesions • Outline the principles of management of patients with symptomatic haemorrhoids Conservative – Reassure & exclude serious disease. bulk laxative / stool softener & fluid intake with decreased straining. Sclerotherapy – for 1st / 2nd degree à scarring of vessels. Uses phenol in arachis oil --> chemical thrombosis & fibrosis. Can be done as outpatient Banding – strangulation of prolapsed piles (must be above dentate line to be pain free) Surgery – for 3rd degree piles (haemorrhoidectomy). Complications of surgery are: Stricture – excessive amounts of mucosa & skin excised. Should leave a bridge of epithelium between each excised haemorrhoid Post operative haemorrhage – reactionary (that night) or secondary (week later). May bleed from above the sphincter so source not obvious. Rx by transfuse if required, wash out rectum & diathermy if visible / pack the anus if not • Describe symptoms and signs associated with perianal haematoma. (aka thrombosed external haemorrhoid). Outline the management. Thrombus in inferior rectal venous plexus = tense, dark blue swelling at the anal margin Covered by squamous epithelium Painful for 2-3 days – somatic nerves in epithelium Acute onset (post defecation) with smooth tense dark blue lump at anal verge Treatment Untreated will resolve or rupture Usually reassure & give analgesia if already ruptured advise hot baths If large – excise under LA Gastro 58 Perianal Infection • Discuss the role of anal crypts in perianal infection. Infection often begins in the epithelial lining of the anal canal Internal anal sphincter is breached by anal crypts allowing infection to pass into perirectal spaces More common in med (esp. if penetrative anal sex) Can be 1st indication of Crohn’s, UC or TB • Describe the various types of perianal infections, including perianal, perirectal, ischeorectal and pelvirectal infection. Perianal (45%) – infected hair follicle, sebaceous gland or perianal haematoma Ischiorectal (30%) – ischiorectal fossa. Infection of an anal gland --> submucosa & surrounding tissue. May track to opposite side Intersphincteric(20%) Submucosal (1%) – infected fissure / laceration of anal canal Pelvirectal – spread from pelvic abscess = rare • Outline the symptoms of patients with perianal infections including pain, fever and a mass. Perianal Dull perianal discomfort – worsened by movement, sitting & defecation Pruritus Small erythematous well defined fluctant mass Ischiorectal Systemic fever, chills Severe perirectal pain Erythema & fluctuance • Describe the physical examination of patients with perianal infections, Under anaesthetic / large amounts of analgesia Usual finding: include mass, tenderness, cellulitis, fistula and drainage. MRI & US to assess extent • Outline the principles of management of patients with perianal infections. Surgical drainage early prevents fistulae formation Gastro 59 Fissure In Ano • Define fissure in ano. A painful linear ulcer at the anal margin 90% are posterior in men (70% in women) – peak age 20-30 years Appears as a crack / slit in the mucous membrane Very painful & difficult to heal • Describe the symptoms of patients with fissure-in-ano including pain and bleeding. Pain on defecation “like passing broken glass” Mostly due to hard faeces Onset following passage of a hard stool Can also be due to trauma, syphilis, herpes, Crohn’s or CA Acute anal pain – stinging Slight bleeding • Describe the physical examination of patients with fissure-in-ano. Anal sphincter in spasm Posterior tears are not visible PR often not possible without LA Sigmoidoscopy if sever or suspect other suspicious symptoms • Outline the principles of management of patients with fissure-in-ano Small early fissures may self heal Give dietary advice RE keeping stool soft and high fibre diet (+ drink lots of water) Offer stool softners (e.g. fybogel) Local anaethetic & laxatives give symptomatic relief GTN cream relaxes anal sphincter increases healing If very severe consider surgical anal dilatation, internal anal sphincterotomy (but does compromise continence) Gastro 60 Hepato-biliary system 1. Coronary ligament 2. Fissure for ligamentum venosum 3. Portal Triad (porta hepatis) a. Bile duct b. Hepatic portal vein c. Hepatic artery 4. Gall Bladder 5. Quadrate lobe of liver 6. Bare surface of liver 7. Round ligament (ligamentum teres, from unbilical vein à free border of the falciform ligament) 8. Falciform ligament Gastro 61 Liver and gall bladder function. • Describe the structure of the liver. Periportal Hepatocytes are more prone to an adapted to cope with high toxin levels Centrilobular Hepatocytes are more prone to and adapted to cope with hypoxia Classical Lobule Portal Lobule area drained by a bile ductule area drained by a central vein Acinus area supplied by a terminal branch of the hepatic artery/portal vein A B PV L portal canal lobules CV hepatocyte strands Gastro 62 central vein • Describe the cell types found in the liver 2/3 epithelial cells 1/3 non-epithelial cells 60% hepatocytes large polygonal cells, often binucleate polarized with three different surfaces: - 50% intercellular face - 37% sinusoidal face; microvilli - 13% canalicular face; microvilli connected by tight junctions 05% cholangiocytes 25% endothelial cells 10% others Kupffer cells Pit cells Ito cells intrasinusoidal macrophages intrasinusoidal NK cells perisinusoidal fibroblasts • Describe the hepatic portal blood supply. 30% hepatic artery = oxygenated blood 70% hepatic portal vein = deoxygenated blood • Name the major constituents of bile & describe the excretion of bile pigments. Bile consists of cholesterol and bile pigments Bile pigments are breakdown products of haemoglobin Haemoglobin à bilirubin (insoluble) à Conjugated by addition of glucaronic acid (increases polarity and solubility) à excreted into intestine à Acted on by bacteria in colon à urobilinogens à reabsorbed into blood à liver via portal circulation à kidney à excreted in urine as urobilinogen (golden yellow pigment) AND some converted to stercobillin = brown pigment in faeces • Explain the phrase eneterohepatic recycling. Recycling through liver by excretion in bile, reabsorption from intestines into portal circulation, passage back into liver, and re-excretion in bile • Describe the role of the gall bladder in storing and releasing bile. Rate of bile production depends on the rate of hepatocyte secretions In resting conditions the sphincter of oddi closes à bile forced into gall baldder After a mean neural and CCK à spincter relaxation and build up of pressure à bile towards duodenum • Describe the detoxification role of the liver. Multiple enzyme secretion à modification of chemicals à increased water solubility Phase I = oxidation / reduction Phase II = methylation / conjugation (by adding of AA/sulphate/glucaronic acid/acetic acid • Peripheral signs of hepatic disease Palmar erythema (oestrogen?) Leukonychia (low albumin) Clubbing (cirrhosis – rarely) Bruising (coagulopathy) >2/3-spider naevi (oestrogen?) Parotid enlargement (unknown) Gynaecomastia/testicular atrophy (oestrogen?) Peripheral oedema (hypoalbuminaemia) Gastro 63 Liver function tests • Distinguish the concepts of liver damage (hepatitis), biliary obstruction and liver failure, and describe which abnormalities of liver function tests characterise each. True tests of liver function Albumin – should be 30-48 g/l Clotting – INR 1-1.2 (measure of synthetic activity of the liver & long term change) Bilirubin – 5-17 micromol / l. Increase in cholestasis, hepatocellular damage & haemolysis. > 30 = clinically detectable, > 60 = clinically obvious Urea Tests of liver damage Transaminases – found in hepatocytes – leaks out if cells damaged ALT (alanine) <45 iU/l (more specific than AST) AST (aspartate) < 50iU/l NB: alcohol never puts ALT over 200, ALT >1000 = inflammation Tests of biliary obstruction GGT – 0-70 iU/L (male), 0-40 iU/l (female) – increased by induction Alcohol, carbemazepine, barbiturates, phenytoin, rifampicin Also increased with cholestasis and cellular damage Alk Phos (ALP) – 39-117 iU/l – marked increase in cholestasis • List the important drug classes requiring LFT monitoring. Stains Fibrates Amiodarone Isotretionoin Rifampicin Glitazones Valproate Sulfasalazine • Name three types of jaundice and describe the typical pattern of liver function tests associated with each. Prehepatic Jaundice Increase in amount of pigment being produced E.g. due to haemolytic anaemia, thalassaemia etc Urine darker yellow but liver function is normal Intrahepatic (hepatocellular) Jaundice Liver cells damaged – increased alanine transaminase E.g. in hepatitis Cells not able to process bilirubin effectively à paler stools Results show increased bilirubin (unconjugated) and increased ALT Post Hepatic Jaundice E.g. obstructive due to gall stone / cancer of head of pancreas Soluble bilirubin unable to leave gall bladder à blood à kidneys à brown urine & pale fatty stools (no bile à fat malabsorption), hypercholesterolaemia (à CHD) and bile acids in skin à itching Results show high urine uroblinogen + high GGT and Alk Phos in blood NB: high GGT alone = alcoholism, high Alk Phos alone = bone defects • Name the derangements of normal liver function affecting glucose, albumin, clotting factors, and hormone and drug metabolism associated with compensated cirrhosis. Cirrhosis Scaring with regenerative nodules à disorganised architecture Gastro 64 Linked to Hepatitis B & C in chronic form & alcoholism Metabolic changes Albumins (protein synthesis) decreased albumin Glycogen (carbohydrate storage) altered glucose tolerance Fat storage and metabolism Fatty liver Clotting factors Bruising and bleeding Urea (protein breakdown) decreased urea Altered drug metabolism paracetamol OD at lower levels Oestrogen (decreased uptake by liver) increases oestrogen Aldosterone (decreased uptake) retain NCl Altered insulin and glucagons levels affects carbohydrates Signs Palmar erythema (excess oestrogens) Dupytrens contractures Spider naevii • Name three clinically important consequences of portal hypertension and describe the pathophysiological derangements which lead to them. Consequences of cirrhosis Portal hypertension à increased flow through anastomoses à variceal bleeding & splenomegaly Na+ retention (higher circulating aldosterone) & Low oncotic pressure (low albumins) à Ascites Higher circulating oestrogen à breast development Portal systemic encephalopathy à drowsiness & coma with parietal lobe dysfunction DEATH due to GI bleed / coma Gastro 65 Gall bladder • Relate the typical appearance of the gall bladder mucosa to its function. The gall bladder has a mucosa layer, but no submucosa. The surface can appear wrinkled when it is empty – these are not villi The mucosa - Simple, tall columnar epithelium Lamina propria No goblet cells No muscularis mucosae The muscularis externa Irregular strands of smooth muscle Function of the gall bladder Storage of continuously formed bile Concentration of the stored bile Secretion of bile when required • Understand the formation and course of the common bile duct. Canaliculi à Cholangioles Interlobular ducts Intrahepatic Left Hepatic Duct Common hepatic duct GB Common bile duct Extrahepatic Cystic Duct Gastro 66 Acute and Chronic Hepatitis • Describe the infective causes of acute hepatitis including viral, bacterial and protozoal organisms. Viral Hep A – RNA virus Faeco-oral spread (can get small epidemics in nurseries / watersports in contaminated water / infected shell fish), Immunity after 1st infection. 2-4 week incubation à fever, malaise, jaundice (1 week later, lasts 2 weeks) à complete recovery with normal LFTs Serological markers: IgM anti-HAV antibody Hep B – DNA virus Spread by body fluids (can get vertical transmission). 5 clinical patterns of infection Acute self limited (majority) – recovery after jaundice, malaise & anorexia à immune. Incubation 6-8 weeks à rise in HbsAg (peaks before clinical disease & undetectable in 6 months). Serum transaminase will be elevated during symptomatic illness Fulminant acute – very rare à massive necrosis of liver cells Chronic hepatitis – may à cirrhosis / recovery. Arises if failure to eliminate virus from liver Asymptomatic carrier state à may later develop chronic hepatitis Clinically inapparent asymptomatic – may à recover / chronic / carrier NB: Carriers are at risk of developing hepatocellular CA Serological markers – HBsAg – Surface antigen – appears 6 wks after infection, gone by 3 mths HBeAg – Internal component antigen – occurs similar to HBsAg & = high infectivity HBcAg – Core antigen = immunity (if not present = carrier) Hep C – RNA virus Spread by body fluids. Clinically similar to Hep B. 2 month incubation à acute hepatitis with fever, malaise, anorexia & jaundice. Some recover within 2 months, others à chronic à remission & relapses. NB: Risk of hepatocellular CA. Extrahepatic manifestations common (arthritis, agranularcytosis) Serological markers – Anti HCV antibody, HCV RNA Hep D – RNA virus Requires infection by hep B. Common in drug users & dialysis patients. If chronic then seldom resolves & 60% à cirrhosis Serological markers – IgM anti D, with IgM anti HBc Hep E Spread by water (faeco-oral). Similar to Hep A. Causes self limiting epidemics. Incubation 1 month à mild jaundice. Can à fulminant hepatitis if pregnant Gastro 67 EBV – a rare cause of clinical hepatitis CMV – mainly in immuno-compromised Yellow Fever – carried by mosquitoes Herpes Simplex – usually in immuno-compromised / pregnant Protozoa Entamoeba Histolytica – causes amboebic abscesses containing necrotic material (like anchovy paste). May rupture into abdomen or perforated the diaphragm to cause disease in the chest Malaria – causes enlarged liver. Kupffer cells become hyperplastic & contain malaria pigment Visceral Leishmaniasis – liver is enlarged, Kupffer cells contain leishmania which appear as Donovan bodies ? Toxoplasma gondii Helminths Ascariasis lumbricoides – eggs from worms in the biliary tract à cholangitis Schistosoma – eggs from worms cause fibrosis in portal tracts Liver Flukes – colonise the biliary tree & cause chronic inflammation & biliary obstruction. Predisposes to carcinoma of the biliary tree Hydatid disease (echinococcus) – liver cysts develop containing the scolices of developing worms Bacteria Leptospiri icteroheamorrhagia (weils disease) – fever, jaundice, purpuric skin rash & renal failure. Focal hepatocyte necrosis & cholestasis. Syphylis – may affect liver in congenital infection à diffuse fibrosis or in tertiary disease à gummatous necrosis ? Coxiella burnetii (Q-fever) (intracellular bacteria) • Describe the features of liver damage resulting from drug therapy including that due to paracetamol overdose. Can be predictable – i.e. dose related or unpredictable Can be due to Disruption of Ca2+ homeostasis Disruption of bile canalicular transport Formation of drug-enzyme complexes à autoimmune attack Induction of apoptosis Inhibition of mitochondrial function Paracetamol à cell necrosis Asymptomatic for 24 hrs Damage begins to show in LFTs after 18 hrs Halothane / volatile anaesthetics à hepatitis is repeated exposures Hypersensitivity reaction à fever Steroids Affect bile flow à cholestasis Anti TB chemotherapy Increase aminotransferase Can cause hepatic necrosis and jaundice • Describe the causes of chronic hepatitis including hepatitis B/C infection, autoimmune hepatitis and non-alcholic steatohepatitis Any hepatitis over 6 months duration Can be detected in 3 ways Gastro 68 Follow up from acute hepatitis shows continues raised serum transaminase Patient is symptomatic (anorexia, malaise, weight loss) with abnormal LFTs (raised transaminase), liver disease is found & the disease persists for > 6 months Asymptomatic but present incidentally (routine screening). Investigations the suggest chronic hepatitis Causes Viral – Hep B, Hep C, Hep D, Chronic viral hepatitis of unknown origin Autoimmune – more common in women. Can be: Autoimmune hepatitis (lupoid hepatitis) - women 20-40. Assoc with other immune disorders (thyroid, arthritis & sjogren’s syndrome). Can have antismoothmuscle (anti-SM) and antinuclear antibodies Primary biliary cirrhosis – F:M = 10:1. Important cause of liver disease in women over 50. Destruction of intrahepatic bile ducts à pruritus & hyperbilirubinaemia with progression to cirrhosis. Usually have antimitochondrial antibodies . Sufferers get Osteodystrophy due to Vit D deficiency + osteoporosis Primary sclerosing cholangitis – M>F, 25-40. 60% cases assoc with UC. Progressive obstructive jaundice with inflammation & fibrosis of bile ducts. Classic beaded appearance on introducing contract to the ducts. Cirrhosis within 10 yrs. Increased risk of cholangiocarcinoma Drug induced – often females in OD attempt Fatty change – methatrexate, tetracyclines, Valproate Hepatitc granulomas – sulphonamides, allopurinol Acute hepatitis – isoniazid, halothane Chronic hepatitis – isoniazid, methyldopa Cholestasis – steroids, chlorpromazine Central vein occlusion – cytotoxics Tumours – oral contraceptives (adenomata), anabolic steroids (carcinomas) Acute necrosis - paracetamol Metabolic damage - Wilson’s disease, Alpha 1 antitrypsin deficiency Non alcoholic steatohepatitis (fatty liver disease) - Risk factors include obesity, high BP, type II DM, increase lipids Unknown – detected by routine LFT screening • Describe the effects of alcohol and the different types of alcoholic liver disease. Alcoholism 21 units (male), 14 units (female) 35 units + becomes hazardous Control addiction with disulfiram / acromprosate Control withdrawal seizures with Benzox Avoid wernicke’s encephalopathy with Vit B1 Alcohol is the most common cause of liver disease in the west Fatty change (hepatic steatosis) Asymptomatic Elevated GGT Reversible with abstinence Alcholic hepatitis Fatty change and inflammation Often asymptomatic but can à signs of chronic liver disease Treat based on S&S + stop drinking In severe cases mortality upto 90% Alcholic cirrhosis In 15% of heavy drinkers 90% 5Yr survival if abstinence 35% 5Yr survival if severe disease Gastro 69 • Describe the morphology and pathological consequences of acute and chronic hepatitis. Liver cell necrosis & inflammatory cell infiltrate = pathological features Resolution is complete with return to normal structure & function Can progress to massive cell necrosis à death Viral hepatitis Swollen hepatocytes à apoptosis à eosinophilic Councilman bodies Focal infiltration of liver by lymphoid cells assoc with necrosis Increased lymphoid cells in portal tracts Regeneration à lobular disorganisation Mild cholestasis may be seen • Outline the clinical presentation of a patient with acute hepatitis including relevant features in the medical history. Nausea, anorexia Low-grade pyrexia & general malaise Palpable tender liver Jaundice (peaks at 10 days) Gradual recovery within 3-8 weeks Increase bilirubin (mostly conjugated) Increased ALT and AST – high early and fall with recovery • Outline the clinical presentation of a patient with chronic hepatitis including relevant features in the history. Patient follow up - LFTs still high Anorexia, malaise, weight loss à diagnosis & symptoms persist for >6 months Asymptomatic – incidental finding with investigations showing signs of chronic hepatitis Severity assessed by staging & grading. Requires biopsy as histology based (see below) • Discuss the diagnosis of a patient with jaundice including relevant blood tests, and radiological investigations. For jaundice to be clinically seen must be > 50 micro mols / l Can be Haemolytic – increased bilirubin for liver to deal with Congenital – enzyme defect / anatomical defect Cholestatic Investigations Seek a cause Travel – viral Duration of illness (short = hepatic, long could be malignancy) Recent local outbreak Shellfish – Hep A IVDU – Hep B / C Blood transfusion Alcohol / drug use Recent anaesthetic FH Surgery Hepatomegaly – smooth = hepatitis, irregular = mets Splenomegaly – chronic liver disease Gastro 70 Ascities – cirrhosis / CA Viral markers – Hep A / B / C LFTs US – size of ducts, level of obstruction Fine needle aspiration of any mass found • Outline the indications for liver biopsy and discuss the contraindications to this procedure. Indications Confirmation of diagnosis, & to stage & grade disease Suspected neoplasm Diagnosis of cholestatic liver disease Evaluation of infiltrative / granulomatous disease To evaluate unexplained jaundice To assess drug reactions Contraindications Increased prtrombin time (INR > 1.6) Throbocytopenia (<60,000) Ascites Suspected Heamangioma Suspected enchinococcal disease Complications (usually within 24 hrs) Abdominal / shoulder pain Intraperitoneal bleed Haemothorax Peritonitis Septicaemia • Outline the treatment options for hepatitis due to autoimmunity, hepatitis B or C Autoimmune hepatitis Immunosupressive therapy is successful in most cases 80% respond to steroids (+/- azothioprine) Failure to respond required orthoptic liver transplant Hep B Treatment with alpha-interferon + reverse transcriptase inhibitor à viral DNA & & HBeAg dissapear from serum tests Immunisation – uses recombinant HBsAg. 3 Doses (0, 1 and 6 months, boster every 5 years) If infected – give HBIg (Hep B immunoglobulin) with vaccine Hep C 40% respond to alpha interferon + ribavirin à sustained fall in transaminase levels All patients with chronic Hep C should be vaccinated against Hep A (as can cause fulminant failure if co-infected) & Hep B (as common risk factors) Gastro 71 Liver Neoplasms, Abscess and Cysts • Discuss the pathology, natural history, presentation, investigation and treatment of liver, abscesses, cysts and neoplasms. Liver abscess Uncommon Most commonly due to portal pyaemia from intra-abdominal sepsis Usually E.coli. Also sterp milleri, bacteroides, enterococcus faecalis, proteus vulgaris & staph aureus Presentation Some are not acutely ill – long history of malaise If acute – fever, rigors, vomiting, anorexia, weight loss & abdominal pain. Can get Gr-ve septicaemia O/E may be little to find. Can be toxic, febrile, jaundice, with tender, enlarged liver. Can also be signs of pleural effusion / rub Investigations Usually investigated as PUO – with most investigations normal. Only usual clue is raised serum alk phos 25% cases have raised serum bilirubin Can also be normochromic, normocytic anaemia with polymorphonuclear leucocytosis Serum Alk Phos & ESR are often raised Serum B12 is high (B12 is stored in liver) Blood cultures +ve in 30% of cases Imaging US CT if multiple / complex lesions CXR may show raised R hemidiaphragm (+ pleural effusion if severe) Management Aspiration of the abscess under US control Abx to cover Gr+, Gr- and anaerobic until cause found Further drainage may be required if slow / difficult Prognosis After drainage & Abx a single lesion has 85% survival Scattered multiple abscesses have 20% survival Entamoeba histolytica causes amoebic abscesses Contracted from ingestion of cysts from contaminated food / water Amoebiasis usually only affects the intestine but if it reaches the liver à abscess Liver Cysts Simple cysts Solitary, non-neoplastic cysts. Believed to be congenital in origin. Lined by biliary epithelium which produces the cystic fluid. The fluid is usually similar to plasma in composition. Needle aspiration is not curative Mostly asymptomatic. Usually found incidentally on imaging If large can à dull RUQ pain, bloating & early satiety On rupture can à 2o infection à abdominal pain,fever & leucocytosis Treat only if symptomatic Polycystic liver disease Multiple cysts Congenital & usually associated with AD polycystic kidney disease (medullary sponge kidney). The kidney cysts usually occur first. The kidney cysts can à renal failure but the hepatic ones rarely cause fibrosis & liver failure Gastro 72 Liver cysts usually appear around puberty & increase in adulthood More common in women (cyst number and size is associated with oestrogen) Treat only if symptomatic Parasitic (Hydatid) cysts Caused by Echinococcus granulosus (dog/wolf tapeworm) Eggs are released in stool of host à inadvertently ingested by hosts (sheep, cattle or humans) à Egg larvae invade the bowel wall & mesenteric vessels à circulation to the liver à in the liver the larvae grow & become encysted à cyst has outer inflammatory layer and inner germinal layer producing daughter cysts à carnivore eats intermediate host à scolices of daughter cysts are released into small intestine à grow to adult worms à lay eggs & released in stool Pain may develop as the cyst grows – may à palpable mass Cysts may rupture into the biliary tree, through diaphragm or into peritoneum à jaundice, cholangitis or shock Investigations Causes eosinophilia in 40% of patients On US daughter cysts are visible Should ALWAYS be treated – Abx, drainage / resection 1 = in bowel of host 2 = eggs in stool 3 = eggs ingested & attach to host bowel wall 4 = hydatid cysts form thoughout body 5 = protoscolex ingested from host body 6 = scolex finds definitive host Benign tumours Hepatic adenomata – well circumscribed nodules upto 20cm. Usually in women on reproductive age (predisposed by oestrogen contraceptives). Very similar to normal liver except no portal structures. May rupture à bleeding Bile duct adenomata – very common (probably hamartomas). Small white nodules beneath the liver capsule & composed of normal bile ducts in a collagenous stroma. Can be mistaken for mets at laparoscopy Haemangioma – common. Dark (almost black) lesion 2-3cm under capsule. Abnormal vascular channels in a collagenous stroma Gastro 73 Malignant tumours Metastatic is most common. Arrive by portal circulation (GI malignancy) or by systemic circulation (others) Hard craggy liver on palpation Lung, breast, colon and stomach are most common Can get malignant lymphomas & leukaemias Primary hepatocellular carcinoma (80% of primary) Predisposed by cirrhosis (80% of cases), Hep B (causing the cirrhosis) & mycotoxins (e.g. from aspergillus in food) High incidence in Africa & far east due to Hep B & high mycotoxins in food Either forms a large solitary mass or multiple foci Presentation depends on the size & site of the tumour Diagnosis - Raised alpha-fetoprotein (although also high in cirrhosis), MRI & hepatic angiography can show nodules Very poor prognosis (approx 6 months from diagnosis) as usually spread via portal vessels Treatment – in the absence of cirrhosis if confined to one lobe then liver resection can be successful. The only alternative is transplant Cholangiocarcinoma (20% of primaries) Adenocarcinoma from the intrahepatic bile duct epithelium Predisposed by chronic inflammatory disease of bile ducts (esp sclerosing cholangitis & liver flukes) Presents with jaundice May be single or multifocal lesions Very poor prognosis (usually 6 months) Treatment – stenting of the bile duct (palliative) Angiosarcomas Highly malignant tumours derived from vascular endothelium Cause multifocal haemorrhagic nodules in the liver Due to exposure to environmental agents (thorotrast (radiological contrast used until 1950’s), vinylcholoride monomer (PVC industry), arsenic (in tonics) or anabolic steroids) Gastro 74 Chronic Liver Disease • Define cirrhosis in pathological terms. Irreversible change to liver structure Normal architecture of the liver is diffusely replaced with nodules of regenerated liver cells separated by bands of fibrosis Long-standing destruction of liver cells Chronic inflammation & fibrosis Regeneration of hepatocytes à nodules • Describe the morphology and pathological consequences of cirrhosis. Decreased hepatocyte function (decreased synthesis & detox) Disturbance of blood flow à portal hypertension Decreased immune competence à increased susceptibility to infection Increased risk of hepatocellular carcinoma Increased risk of portal venous thrombosis Can à acute liver failure • Discuss how to establish the diagnosis of the cause of cirrhosis including alcohol, posthepatitis B/C infection, immunological, drugs and metabolic diseases (Wilson's disease and haemochromatosis). Chronic alcohol abuse (10-15% will progress to cirrhosis) Diagnosis: Check patient history. FBC – will show anaemia, LFTs show High GGT Chronic Hep B / C infection Diagnosis: Check hepatitis serology markers Autoimmune Primary billiary sclerosis – Dx: 90-95% have anti-mitochondrial Ab Primary sclerosing cholangitis – Dx: LFTs will be off. Main diagnosis from CT / MRI Autoimmune liver disease Genetic Alpha 1 antitrypsin deficiency - assoc with CF & COPD. May manifest in neonate or later (adulthood). Diagnosis based on plasma electrophoresis showing lack of alpha 1 antitrypsin. Wilson’s disease – AR - causes copper to accumulate in liver & brain. Initially causes hepatitis à cirrhosis. In brain à psych disorders & movement disorders. Diagnosis: Kayser-Fleischer rings, ceruloplasmin levels of less than 20 mg/dL, elevated urine copper excretion, high levels of copper on liver biopsy Haemochromatosis – excessive iron accumulation à chronic damage to liver cells Primary – AR – excessive absorption of iron from the gut. Iron accumulates as heamosiderin in liver, pancreas, pituitary, heart & skin. Tissues appear rusty brown & cells die. Secondary – excessive iron acculation due to other diseases (e.g. alcoholism) or repeated transfusions due to blood disorders Diagnosis – check serum ferritin & transferring saturation Drugs – e.g. amidoarone, methyldopa, methotrexate Due to biliary obstruction – primary biliary cirrhosis, sclerosing cholangitis Others – budd-chiari syndrome • Outline the pathophysiology underlying the clinical features of cirrhosis Jaundice – due to decreased conjugation Gynaecomastia, testicular atrophy & spinder nevi – altered metabolism of oestrogens Ascites & ankle oedema – decreased albumin production + Na retention due to 2o hyperaldosteronism Gastro 75 3 mechanisms produce ascites: Increased transudation due to hydrostatic pressure in portal system Increased transudation due to low plasma oncotic pressure (low albumin) Sodium & water retention due to abnormal renal retention Splenomegally, caput medusae, oesophageal varices – portal hypertension Easy bruising – decreased production of clotting factors • Describe the investigation of a patient with suspected cirrhosis. To assess severity LFTs & U&E, Clotting & Albumin (index of synthetic function) To confirm diagnosis Liver biospsy To find cause Viral markers Serum Ab & immunoglobulins Iron indices & ferritin Coper Alpha 1 antitrypsin MRI To look for complications US / CT / endoscopy • Describe the clinical features of complications of cirrhosis and portal hypertension including oesophageal varices, ascites and encephalopathy and outline their management. Jaundice Rx with colestryramine (increases bile excretion) Pruritus Menthol in aq. Cream is cooling Antihistamines reduce itching Naloxone can help ?? Ascites Rx with paracentesis & drain fluid Na restrict diet Spironolactone (diuretic) amiloride (K sparing) Avoid fluid retaining drugs (steroids, antacids, Nsaids) If infected – Abx Encepalopathy (with confusion & à coma) Due to build up of nitrogenous products à Protein restrict diet Eradicate gut bacteria (neomycine / metronidazole) Lactulose – clears toxins from gut beware centrally acting drugs (benzos, antipsychotics, opioids) Impaired coagulation Give Vit K Avoid anticoagulants Ranitidine reduces risk of GI bleed Bleeding oesophageal varices Vasopressin à V/c Octreotide – somatostatin analogue à v/c B blocker – reduces portal pressure Gastro 76 Portal Hypertension • Define portal hypertension and classify its causes. Portal hypertension is any increase in the portal vein pressure Causes Pre hepatic (pre-sinusoidal) Portal vein thrombosis (due to local sepsis, polycythaemia & pre existing portal HT due to cirrhosis. Occlusion of intrahepatic branches à venous infacrt (wedge shaped red/Zahn infarcts) Splenic vein thrombosis Intrahepatic (sinusoidal) Cirrhosis – distortion & destruction of hepatic vascular architechture Schistosomiasis – portal tract fibrosis Sarcoidosis Myeloproliferative disease Congenital hepatic fibrosis Idiopathic portal hypertension Polycyctic disease of the liver Post hepatic (post sinusoidal) Budd-chiari syndrome – due to occlusion of the main hepatic vein à severe acute disease with massive vascular congestion à acute portal hypertension & jaundice, painful enlargement & rapid ascites. Fatal unless portosystemic vascular anastomosis performed Right heart failure (nutmeg liver, pulsatile hepatomegaly) Constrictive pericarditis Venoocculsive disease – ingestion of plants (found in Africa & jamaca) containing toxic alkaloids / having undergone irradiation of the liver à fibrosis around central veins à obliteration by fibrosis • Review the portal circulation and describe the pathological changes that occur in portal hypertension. The portal vein drains the splenic, gastic and all colic and ileal veins Anastomoses – Gastric à oesophageal à varices Superior rectal à inferior rectal à haemorrhoids Paraumbilical à epigastic veins of abdo wall à caput medusae Colic veins à retroperitoneal veins • Describe the clinical manifestations of portal hypertension. Collaterals (see above) Splenomegaly à leucopenia & throbocytopenia Ascites Manifestations of severe hepatic failure (jaudice & encephalopathy) • List the complications of portal hypertension. Bleeding oesophageal varices Gastro 77 Ascites Encephaloopathy (due to blood bypassing liver) Splenomegaly • Outline the treatment methods available for bleeding oesophageal varices. Haemorrhage from varices à hypotensives liver damage + systemic anaemia Large protein load entering GI tract can à encephalopathy Prophylaxis B-blockers reduce splanchnic blood flow à lower portal venous pressure Large varices can be band ligated or injected with sclerosant Diagnosis & management Fibreoptic OGD should be arranged immediately to confirm if varices / ulcer Fluid resuscitate – with gelofusin then blood once available Give enema to reduce protein absorption (reduces encephalopathy) Stopping the haemorrhage Endoscopic ligation / sclerotherapy – NB risk of perf oesophagus IV vasopressin/octreotide infusion – reduces portal venous pressure à reduces bleeding & prevents clots blowing off Balloon Tamponade – using sengstaken tube à inflation à pressure on varices. Rebleeding after decompression is common but this buys time Transjugular intrahepatic portosystemic shunt (TIPS) – connects hepatic vein to portal vein à decompression Oesophageal transection – cardio-oesophageal junction divided to prevent communication of varices Portocaval shunt – works but precipitates encephalopathy as liver is bypassed. Patients must be maintained on a low protein diet • Describe the prognosis for patients with portal hypertension. The Child-Pugh classification system indicates prognosis: Score 1 Score 2 Score 3 Serum Albumin (g/dL) Serum Bilirubin (mg/dL) Prothrombin time (secs) Ascites Encephalopathy >3.5 >2 1-4 none none 3.0-3.5 2.0-3.0 4-6 moderate mild <3.0 >3.0 >6 severe severe Class A Class B Class C Score 5-6 Score 7-9 Score >9 80% 5-years survival 70% 5-years survival 50%1-year survival Gastro 78 Obstructive Jaundice • Classify causes of cholestatic jaundice with a brief outline of underlying pathology. Intrahepatic – failure to secrete bile § autoimmune - primary biliary cirrhosis, sclerosing cholangitis § infective - acute phase of Hepatitis A § drug related causes - including Alcoholic hepatitis --> Cirrhosis § others – Pregnancy, Recurrent idiopathic cholestasis, Congenital disorders Extrahepatic – obstruction to bile flow § intraductal - gallstones, carcinoma of pancreas § intramural - cholangiocarcinoma, carcinoma of ampulla of Vater, stricture § extramural - porta hepatis, lymphadenopathy • Describe the classical clinical features of obstructive jaundice including dark urine, pale stools and itching and outline why they are present. Jaundice – deposition of bilirubin in the skin due to increased blood levels Pale stools – bile is unable to enter the GI tract Dark Urine – conjugated bilirubin excreted in the urine Pruritus – due to accumulation of bile salts in the skin Steatorrhoea – disturbance of fat absorption due to no bile – also affects ADEK absorption Pain - RUQ • Describe the laboratory and radiological investigation of a patient presenting with obstructive jaundice. Urine Faeces FBC Serum bilirubin Conjugated bilirubin ALP (Alk Phos) Serum proteins Haptoglobin ALT / AST GGT Prothrombin time Prehepatic á uribilinogen á urobilinogen Haemolysis < 100 micro mol / l Mostly unconjugated Normal Normal â normal Hepatic Post hepatic á Bilirubin Absence of bile Infection (raised WCC) > 100 micro mol / l mixed picture mostly conjugates Raised VERY HIGH Decreased Normal á in acute viral hepatitis indicates liver disease long non-correctable long (correctable with Vit K) US – shows gallstones CT / MRI - show obstructive masses AXR – only 10 % are radio-opaque MRCP – non invasive imaging of the biliary tree ERCP – show & define nature of obstruction + can be used to treat • Discuss endoscopic or transcutaneous methods of draining an obstructed common bile duct. ERCP – Endoscopic Retrograde CholangioPancreatography Ampulla of vater is canulated using an endoscope passed via the mouth A stent can be introduced to decompress the jaundice If gall stones are present these can be removed at the same time Often involves a sphincterotomy PTC - Percutaneous Transhepatic Cholangioography A needle is passed percutaenously into the liver substance to canulate a dilated bile duct A stent can be introduced to decompress the jaundice Gastro 79 Acute and Chronic Gallbladder Disease, Carcinoma Of The Biliary Tract • List the common types of gallstones and describe the pathophysiology involved in their formation. Cholesterol stones – 80% Form when bile becomes super saturated (insufficient bile to keep cholesterol in solution) Assoc with decreased bile acids (due to oestrogens or malabsorption (Crohn’s, CF) and high cholesterol – obese, old, female Pigment stones – 20% Largely calcium bilirubinate Assoc with increased RBC breakdown, cirrhosis & ileal resection (affects recycling) & chronic biliary infections • List several diseases known to predispose to gallstones. Predisposing conditions High cholesterol High oestrogen levels - inc COCP & pregnancy. ? due to low gall bladder motility Haemolysis à increased haemoglobin breakdown Cirrhosis – due to abnormal metabolism of haemoglobin Infections – esp in the liver and gall bladder – provide a nexus for stone formation • List the common pathological consequences of gallstones. Stones in biliary tract à hypertrophy & thickening of the GB wall Cholecystitis (inflamed GB) Cholangitis (inflamed duct) Acute pancreatitis CA gall bladder • Describe the symptoms and signs in a patient with biliary colic and contrast these features with acute cholecystitis. Acute cholecystitis (stone in neck of GB) Continuous epigastric / RUQ pain Vomiting, fever (empyema), local peritonism +ve murphy’s sign (2 fingers over RUQ, breath in & pain à arrest of breathing) Billiary colic Intense spasmodic pain in RUQ (radiating to back) +/- jaundice NB: no features of inflammation • List the common tests used in the diagnosis of calculus biliary tract disease. Urine / bloods / stool as for jaundice US – presence of stones / thickened wall / dilated ducts AXR – 10% of stones visible / Calcified GB Upper GI endoscopy – to exclude hiatus hernia or peptic ulcer MRCP / ERCP • Outline the medical management of a patient with acute cholecystitis/cholelithiasis including appropriate antibiotic regimen. Initially ALL gallstones should be managed medically until the patient is stable NBM, IV fluids, opiate analgesics, IV Abx (e.g. cefotaxime) Most patients then progress to cholecystectomy once stable Medical management is infrequently used (mainly only if unfit for surgery) Gastro 80 Chenodeoxycholic acid & Urosdeoxycholic acid - can be used to increase the bile content of the bile. This will dissolve cholesterol stones (< 10mm if functioning GB). Can take several months Adding HMG-CoA-reductase inhibitors (statins) will increase cholesterol excretion • Discuss the indications for surgical and endoscopic management of gall bladder disease including laparoscopic cholecystectomy. Acute cholecystitis – resolve on bed rest & analgesia à Elective cholecystectomy 6 weeks later to prevent recurrence Laparoscopic surgery if possible as faster recovery Empyema of GB – emergency drainage required with cholecystecomy Perforation – rare – requires urgent surgery (high mortality) Stones – ERCP removal f.b. cholecystectomy • Define the following o Murphy's sign Pain & arrest of inspiration as the GB brushes against a hand placed at the costal margin in the mid clavicular line NO pain on repeating the manoeuvre on the left hand side o Courvoisier's sign / law In the presence of a palpable GB, jaundice is unlikely to be caused by gall stones (stones form over a long period of time à fibrotic, shrunken GB which doesn’t distend easily) The GB is more likely to be enlarged in pathologies which cause obstruction over a shorter period of time (e.g. pancreatic malignancy) o T-tube, including purpose and circumstances of use Historically, it was used for decompression of the biliary tree to allow spasm and oedema of the sphincter to settle, to obtain postoperative cholangiography to detect retained stones and to develop a track along which percutaneous removal of a retained stone could be achieved. Also helps reduce bile leakage into the peritoneum (therefore avoids peritonitis) In modern times is used for similar reasons following liver transplant or choledochectomy (removal of part of the CBD) o Gallstone ileus Infrequent cause of mechanical bowel obstruction Caused by an impaction of a gall stone in the terminal ileum by passing through a billiray-enteric fistula Presents as episodic subacute obstruction. Abdominal pain & vomiting intermiitent based on the progress of the stone. Haematemesis can be due to haemorrhage at the biliary fistula O/E patient is febrile and appear dehydrated with distended abdomen & increased bowel sounds. Jaundice only occurs in 15% Diagnosis – plain abdo film – signs of partial / complete small bowel obstruction, air in the biliary tree, the stone may be visible Management – Fluid replacement à Enterolithotomy (localise & extract the gall stone), cholecystectomy & fistula division if patient is fit • Contrast carcinoma of the gallbladder, bile duct and ampulla of Vater with regard to survival and presenting symptoms. Gall Bladder Carcinoma (adenocarcinoma) Usually in 60’s, 3x more common in women Some links show more common if chronic gallstones / diffuse calcification (porcelain GB) Can be detected at cholecystectomy but spreads early via lymph to liver 5 yr survival < 5% Cholangiocarcinoma Gastro 81 Assoc with choledochal cysts, chronic infection & auto-immune disease (PSC) Usually presents with jaundice Resectable if detected early – requires aggressive resection including part of the liver Adenocarcinoma of the Ampulla of Vater Arises from distal 2cm of CBD Uncommon tumour 50% will have distant spread at presentation Treat by whipples procedure (Pancreaticoduodenectomy) Palliative surgery involves stenting of the ampulla 5yr survival 40% Gastro 82 Diagnostic Studies in Biliary Tract Disease • Contrast the liver enzyme abnormalities in obstructive jaundice with those of viral hepatitis Obstructive Jaundice High ALP Smaller increase in ALT • Viral Hepatitis Small increase in ALP High ALT List the most common bacteria found in acute cholecystitis. e.coli klebsiella enterococci • Describe the indications for and risks of ultrasound scanning, transhepatic cholangiogram and ERCP. Ultrasound of the biliary tree Used to look for dilated ducts (CBD > 8mm), the structure & thickness of the GB wall, any obvious gall stones and the liver structure (may detect cysts) Transhepatic cholangiogram Indications Jaundice - obstruction, infection, scarring, stones, or carcinoma Perforation in bile duct --> peritonitis Contraindications Patients at increased risk of bleeding Biliary tract sepsis Non availability of prompt surgical facilities Hydatid disease Complications Cholangitis Haemorrhage Subphrenic abscess Shock Bacteraemia / septicaemia Contrast allergy ERCP Indications Cholangitis Jaundice with normal calibre ducts & non diagnostic liver biopsy Recurrent pancreatitis Post cholecystectomy pain Sphincterotomy for CBD stones Stenting of malignant strictures Complications Contrast allergy Pancreatitis Bleeding Cholangitis Perforation Gastro 83 Pancreas • Describe the structure of the pancreas. Islets of Langerhans • Describe pancreatic exocrine and endocrine functions and identify the cells underlying these functions. Enzymes – amylase HCO3 - neutralises acid à Optimum pH for digestive enzymes à Micelle formation to aid fat absorption à Protects duodenal mucosa from acid Gastro 84 Is dependent to Cl- ion exchange – Channel absent in CYSTIC FIBROSIS Insulin and glucagon – islets of langerhans (see endocrine notes) • Describe the influence of cholecystokinin and secretin on pancreatic secretions. Vagus nerve à Conditioned stimuli for cephalic phase à Presence of food for gastric phase ACh also potentiates the actions of secretin and cholecystokinin (CCK) Secretin Release into response to acid in duodenum à stimulates HCO3- production CCK --> enzyme rich secretion – released in response to fat and protein in duodenum • Describe how carbohydrate, protein and lipid are digested in the small intestine. Carbohydrate digestion Begins in the mouth (salivary amylase) Continues in small intestine (pancreatic alpha amylase) Enzymes in brush border Matose à acted on by maltase à glucose and glucose Sucrose à acted on by sucrase à glucose and fructose Lactose à acted on by lactase à glucose and galactose Transfer into lumen of capillary is reliant on Na+ co transport Protein digestion Begins in stomach (pepsin has 15% activity until alkali) Pancreatic enzymes are proteolytic Endopeptidase – interior bonds Exopeptidases – exterior bonds Secreted into duodenum and inactive precursors Trypsinogen à acted on by enterokinase/trypsin à trypsin Chymotrypsinogen à acted on by trypsin à chymotrypsin Pro-elastase à acted on by trypsin à elastase Procarboxypeptidase A/B à acted on by trypsin à carboxypeptidase A/B Mono, di and tri peptidases can be taken up by cells Absorption is passive / facilitated diffusion Digestion is completed by intracellular peptidases Fat digestion Pancreatic lipase is H2O soluble so cant be taken up by lipid Required conjugated bile acids from gall bladder to emulsify fats Products are mostly insoluble – absorbed by forming a micelle Also important for ADEK (fat soluble vitamins) Once absorbed monoglycerides and glycerol are resynthesised to triglyceride à chylonmicron à transported in lymphatics as too large for capillary • Describe the following abnormalities of the digestive system and detail their consequences: Lactase insuffiency Unable to break down lactose à lactose enters large intestine à osmotic diarrhoea & flatulence Gluten enteropathy (celiac disease) Gluten in diet causes mucosal damage à Decreased surface area of villi for absorption à increased nutrients to large intestine à osmotic diarrhoea & flatulence Pancreatitis Acute – autodigestion of the pancreas by enzymes (due to blockage / alcohol binge) Chronic – usually alcohol abuse Symptoms include steartorrhoea (fat malabsorption) & diabetes Gastro 85 Pancreatitis • Classify pancreatitis on the basis of the severity of injury to the organ. Acute – occurs in previously normal pancreas, can return to normal after resolution More information below Chronic – continuing inflammation, irreversible structural damage Usually presents with pain and symptoms of loss of function, or of GI or biliary tract obstruction. May have abdominal skin discolouration Can get calcification of the pancreatic ducts – visible on AXR & CT Complications (left) are related to loss of function Rx is to reconnect the bowel to the pancreatic ducts bypassing the obstruction – i.e. using a Lateral Pancreato-jejunostomy (right) • Describe the aetiology and pathology of pancreatitis. NOT alcoholism! G – Gallstones (45-60%) Usually a genetic E – Ethanol (35%) susceptibility. T – Trauma / Tumour Continued drinking S – Steroids usually à chronic M – Mumps (& Coxsaccie B) pancreatitis A – Autoimmune S – Scorpion venom H – Hyperlipideamia / Hypothermia / Hypercalcaemia (triggers 2nd messenger enzymes) E – ERCP / Emboli D – Drugs (azothioprine, oestrogens) Upto 20% of cases are idiopathic – onsetting after a fatty meal. These are most likely due to gallstones which cannot be detected Pathogenesis Increased intracellular Ca2+ à activation of intracellular proteases à cellular necrosis Gallstones à occlude drainage à ductal hypertension à increased intracellular Ca2+ Duct obstruction Necrosis takes place in acinal cells adjacent to ducts. Seen in duct obstruction assoc with gallstones & ethanol à oedema & poor blood flow in acinus à defective exocytosis of proteolytic enzymes à predominant periductal necrosis Gastro 86 Acinar damage (drugs, virus, metabolic, alcohol) Necrosis affecting all parts of pancreatic lobule. May be due to spread from initial periductal or perilobular necrosis à direct cytopathic damage to acinar cells à release of hydrolytic enzymes à panlobular necrosis Hypoperfusion (shock, hypothermia, vascular disease) Necrosis in the periphery of the lobules. Pathogenesis is poor vascular perfusion à acinar necrosis à reduced perfusion to acinar cells à cell necrosis with release of hydrolases à predominant perilobular necrosis • Describe the clinical presentation of a patient with Pancreatitis Back pain – which eases on sitting forward à more intense as inflammation increases Prominent N&V May have history of gall stones / previous similar episodes of this pain Can follow alcoholic binge On examination Pain & tenderness Peritonism Peripheral vasoconstriction, cold pale extremities If severe Tachycardia, hypotension, oligouria Widespread tenderness & guarding Absent bowel sounds Necrotising pancreatitis Cullens sign – periumbilical bruising (can also occur with ectopic) Grey Turners sign – flank bruising due to retroperitoneal haemorrhage (inc AAA) NB: Cullens & Grey Turners are only present in 3%. The mortality if they are present increases from 10% to 40% • Outline the appropriate diagnostic approach for a patient with acute pancreatitis, emphasising the timing, interpretation and reliability of various studies Serum amylase – 3-4x normal (>1000U/ml) within 24 hrs of pain, falls to normal by 3-5 days Amylase is also increased by: Mumps / parotitis – salivary amylase Dehydration Ovarian Ca Salpingitis & ectopics (as made by fallopian tubes) Perfed gut (see below) Urine amylase – remains higher for longer Serum lipase – increases & remains high ABG – repeat at 24 & 48 hrs. To monitor oxygenation & acid-base balance Erect CXR to exclude gastroduodenal perforation NB: will only show 80% of perfs. Gut perf will cause pain + release amylase containing fluid into peritoneum à absorption to blood Supine AXR for gallstones / calcification. No psoas shadow if retroperitoneal fluid Abdo US – screen for stones & assess size of pancreas (if gallstones & increased AST) Contrast CT – within 2-3 days to assess necrosis Gastro 87 ERCP if LFTs worsen as may mean duct obstruction To assess severity FBC, U&E, CRP, Glucose, LFT, Ca2+ + monitoring • Discuss the management of acute pancreatitis, including the specific conservative management of the initial phase and the indications for surgical intervention. Get expert help! NBM & NG tube IV fluids – lots of 0.9% saline to replace 3rd space losses (until urine output satisfactory) Insert catheter & consider CVP monitoring to check fluid status Analgesia – pethidine / morphine (although do à contraction of sphincter of oddi) Hourly monitoring – BP, UO Daily monitoring – FBC, U&E, Ca2+, Glucose, Amylase, ABG Nutrition - TPN initially to reduce pancreatic secretions, restart with NG à fluids & then solids If deterioration - à ITU (consider abscess / necrosis) ERCP – if progressive jaundice Repeat imaging to track progress • Discuss the criteria used to predict the prognosis for acute pancreatitis. 25% of acute pancreatitis is severe! 10% of cases are fatal (same mortality as acute GI bleed) PaO2 Age Neutrophils Calcium Renal function Enzymes Albumin Sugar < 8.0 kPa > 55yrs WBC > 15 x 109 / l < 2mmol/l Urea > 16mmol / l LDH > 600iu / l, AST > 200 iu / l < 32g / l (serum) blood glucose > 10mmol / l 3 or more +ve factors sugest severe pancreatic à ITU / HDU • Discuss the potential early complications of acute pancreatitis. Immediate Shock ARDS Renal failure DIC Sepsis Low Ca2+ High glucose (usually transient) Within 1-2 weeks Fluid collections Acute Fluid Collections (MILD) Early event, lack distinct wall Most resolve spontaneously NOT life-threatening Pancreatic Necrosis (SERIOUS) Diffuse area, non-viable parenchyma, often with peri-pancreatic (fat) necrosis Pathological diagnosis or CT Gastro 88 Infection quadruples mortality Renal impairment with acute tubular necrosis Hypoxia with basal atelectasis, ARDS & pleural effusion Myocardia depression with CCF & arrhythmias SIRS & MODS Bleeding – if elastase erodes into a major vessel (e.g. splenic artery). Requires embolisation to save life Thrombosis – in splenic / gastroduodenal aa à bowel necrosis 2-6 weeks Pancreatic Abscess Circumscribed pus in/near pancreas Little or no pancreatic necrosis Viable organisms not invariable Over 6 weeks Pseudocyst formation (fluid in the lesser sac, with temp, mass, increased amylase & LFT) See later section for more information on pseudocysts • Outline the metabolic complications of pancreatitis Malabsorption due to pancreatic insufficiency required enzyme supplements (CREON) Hyperglycaemia requires insulin replacement Gastro 89 Pancreatic Pseudocysts • Discuss the mechanism of pseudocyst formation with respect to the role of the pancreatic duct. Pancreatic pseudocyst is a circumscribed collection of fluid rich in amylase, other pancreatic enzymes, blood & necrotic tissue, located in the lesser sac Its surface is non-epithelialised – made of granulation tissue (hence it is not a true cyst) Acute Pancreatitis / trauma (disruption to the parenchyma & ductal system) à extravasation of enzymes à digestion of adjacent tissues including necrosis especially of fat à collection of pancreatic enzymes, blood and necrotic debris necrosis is converted to serosanguinous fluid surrounded by granulation tissue = pancreatic pseudocyst (found 6 weeks after illness) • List and discuss the symptoms and signs of a pseudocyst. Persistently raised amylase Epigastric Pain Fever Epigastric mass Usually no sooner than 2nd week post pancreatitis • In a patient with a pancreatic mass suspected to be a pseudocyst, discuss the indications for and sequence of diagnostic methods including laboratory, radiological and invasive studies. US: of little use as patient is often in pain & pancreas may be obscured by gas in stomach CT: gold standard Large cyst cavity in and around the pancreas Pancreas may appear irregular or have calcifications The CT scan provides a very good appreciation of the wall thickness of the pseudocyst, which is useful in planning therapy. MRCP: will establish relationship of pseudocyst to the ductal system • Discuss the natural history of an untreated pancreatic pseudocyst. Those < 6cm diameter frequently resolve without treatment Larger cysts usually persist à risk of infection & intraperitoneal bleeding. These larger cysts are usually drained either percutaenously, endoscopically or surgically • Describe the medical and surgical treatment of a pancreatic pseudocyst. Endoscopic trans-gastric drainage Imaging guided percutaneous drainage Laparoscopic / open cystogatrostomy Gastro 90 Pancreatic Neoplasms • List the common pancreatic neoplasms; describe the pathology of each with reference to cell type and function. Benign – are very rare. Cystadenomas are most common Malignant – one of the most common causes of cancer death Typical patient = women > 60yrs Assoc with smoking, alcohol, DM & chronic pancreatitis, FH Mostly ductal adenocarcinoma (60% head, 10% body, 10% tail, 20% diffuse) Routes of spread Local à obstructive jaundice / invasion of duodenum Lymphatic à adjacent LNs Hematogenous à to liver • Describe the symptoms and physical signs of pancreatic cancer on the basis of location of the tumour within the gland. At head of the pancreas Present earlier Painless obstructive jaundice à “Courvoisier’s sign” Hepatomegally Can present with pancreatitis if drainage is blocked Migratory thrombophlebitis in superficial veins (trousseau’s sign) In body / tail of pancreas Present late - Anorexia & weight loss Abdominal pain – dull, radiating to back, decreases if sat forward • Outline the diagnostic approach for pancreatic masses, including the laboratory, radiological and invasive methods. Bloods – cholestatic jaundice Transabdominal US – to confirm dilation obstructed ducts & masses present Contrast CT – to confirm mass and assess metastasis Laparascopy – pre-op assessment Tumour markers NOT - ERCP & percutaneous needle biopsy (discouraged as can à spread) • Describe the indications for surgical treatment of pancreatic neoplasms and operations available. Discuss non-surgical techniques of management available. If fit, <3cm tumour with no mets then consider surgery Pancreatoduodenectomy (Whipples) – requires removal of duodenum as shared blood supply NB: Post op morbitiy is very high Non curative resections offer no benefit (stenting may help palliatively) Post op chemotherapy delays disease progression • On the basis of pathology and cell type discuss the long-term prognosis of pancreatic cancers. Extremely poor – 90% of patients die within 6 months of diagnosis 5 yr survival < 2% without surgery 5 yr survival with whipples 5-14% Ampullary and islet cell tumours have better prognosis Gastro 91 The Spleen Structure The spleen lies retroperitoneally in the LUQ Entirely surrounded by peritoneum except at the hilum where the splenic vessels enter and leave Usually 12cm x 7cm Normal spleen should not protrude from under the rib cage Relations Hilum of the spleen sits in contact with the tail of the pancreas = boundary of the omental bursa Posterior Relations = 9-11th ribs separated by diaphragm & costodiaphragmatic recess Connected to stomach by gastrosplenic ligament, and to kidney by spenorenal ligament Splenic artery – largest branch of celiac trunk runs along pancreas & divides into 5+ proper splenic vessels Splenic vein – from several tributaries from hilum, joined by IMV & runs posterior to pancreas à joins with SMV to form portal vein Lymphatic vessels pass to pancreaticosplenic lymph nodes Red pulp – consists of sinuses lined by endothelial macrophages & cords (spaces) White pulp – has a stucture similar to lymphoid follicles Blood enters & is delivered to the red & white pulp. The blood is ‘skimmed’ with leucocytes & plasma preferentially passing to the white pulp. Some red cells pass rapidly to the venous system while others are trapped in the red pulp Function Sequestration & phagocytosis – normal red cells which are flexible pass through to the venous system without difficulty. Old or abnormal cells are damaged by the hypoxia, low glucose and low pH of the red pulp & are removed by the phagocytes with other circulating foreign matter Extramedullary haemopoiesis – pluripotent stem cells are present in the spleen & proliferate during severe haematological stress such as haemolytic anaemia or thalassaemia major Immunological function – 25% of T lymphocytes and 15% of B lymphocytes live in the spleen. The tissues of the spleen produces antibodies Blood pooling – upto 1/3 of the body’s platelets are in the spleen and can be rapidly mobilised as required • List the common causes of splenomegaly including portal hypertension, lymphoreticular disease and chronic infection. Infection Acute – sepsis, infective endocarditis, typhoid, infective mononucleosis Chronic – TB, brucellosis Parasitic – malaria, schistosomiasis Inflammation Rheumatoid arthritis Sarcoidosis Gastro 92 SLE Haematological Haemolytic anaemia Haemoglobinopathy Autoimmune thrombocytopenia Neoplastic Leukaemias Lymphomas Extramedullary haemopoeisis – as seen in Myeloproliferative disease Portal hypertension Liver disease • Outline the haematological abnormalities correctable by splenectomy. Splenectomy is performed for 4 groups of reasons Trauma ITP Haemolytic anaemias including hereditary spherocytosis; thalassemia major; myeloproliferative disorders; thrombotic thrombocytopenic purpura (TTP) and hairy-cell leukemia unresponsive to other treatment strategies Hypersplenism • Discuss the potential causes of splenic rupture. Injured by blunt trauma to ribs / abdomen causing an increase in intra-abdominal pressure An enlarged spleen (due to EBV etc) is more likely to rupture Once the capsule is ruptured the spleen bleeds profusely as the capsule is thin and the parenchyma is soft Rupture à severe intraperitoneal haemorrhage & shock Repair is difficult so splenectomy is performed to achieve haemostasis Presentations Immediate massive bleeding (à rapid death) = rare Peritonism from progressive blood loss Signs of blood loss + peritonism over several hours Delayed rupture – several days after the trauma. Initial pain at injury then settles. Returns a few days later after the haematoma reaches a size to rupture the capsule Spontanous rupture – usually due to disease e.g. malaria, glandular fever or leukaemia • Discuss the potential adverse consequences associated with removal of the spleen; discuss ways of reducing these risks. Problems post splenectomy Increased platelets (600-1000 x 109 / l) lasts for 2-3 weeks Thromboembolic events may occur Increased risk of infections – esp pneumococcus OPSS – overwhelming post splenectomy sepsis NB: patients should be pre-vaccinated (2-3 weeks) if elective splenectomy Pneumococcus – repeat every 5 yrs Men C Annual flu vaccine HiB Long term penicillin if problems NB: if emergency splenectomy due to trauma then vaccinate 10-14 days after Gastro 93 Hernias • Define the terms reducible, irreducible, strangulated and sliding with respect to the description of hernias. Hernia - A protrusion of an organ or tissue through an abnormal opening Reducible – contents of the sack can be reduced to their normal location Irreducible – contents cannot be returned to normal location without surgery Sliding – an abdominal organ forms part of the sac • Outline the principles on management of patients with hernias including preparation for surgery and treatment of bowel obstruction if present. Some require no treatment Use of truss, or external method to maintain reduction Surgery Open / keyhole Use nylon mesh to reinforce abdominal wall Strangulated Lack of blood supply to contents Surgical emergency due to ischaemia & bowel obstruction Inguinal Herniae • Revise the relevant anatomy in relation to the inguinal canal Inguinal canal lies between the superficial and deep inguinal rings Deep ring lies deep to the mid-inguinal point In men it contains vas deferens and testicular artery and veins In women it contains the round ligament Anterior border is the external oblique aponeurosis Posterior border is the transversalis fascia Inferior border is the inguinal ligament Superior border is the conjoint tendon - the lower fibres of internal oblique and transversus abdominis • Define indirect and direct inguinal herniae. Direct – 20% Always acquired Through the posterior wall of the canal Medial to the epigastric aa & vv Rarely strangulates (wide neck) Rarely enters scrotum Spontaneously reduces on lying down • Indirect - 80% (60% RHS, 20% LHS, 20% bilat) Can be congenital Through deep inguinal ring Lateral to inguinal aa & vv Commonly strangulate Commonly enter scrotum Does not reduce on lying down List the factors that predispose to the development of inguinal herniae Male Family history Chronic cough (CF, COPD or smoking) Gastro 94 Chronic constipation Important triad of symptoms to ask Straining at micturition (prostatism) Excess weight Pregnancy Occupation (heavy lifting, standing all day) Premature birth Previous hernia And other increased intra abdominal pressure / wall weakness • Discuss the relative frequency of indirect, direct and femoral herniae in children, women, young men and elderly men. Men : Women = 10 : 1 Increase with increasing age Can occur in children, more common in males • Describe the physical examination of patients with reducible inguinal herniae, including examination of the external ring and descent to the scrotum, and incarcerated inguinal herniae including the signs of bowel obstruction and possible strangulation. History – duration, causes (see above), reducible? Exaination – groin + testes / labia standing and laid down + cough Observe stood Ask the patient to point to the swelling Ask the patient to cough to see if it enlarges Palpate stood The testicles to see if any scrotal swelling is inguinal or scrotal Ask the patient to lay down Observe – has it reduced Can you / the patient reduce the hernia If it reduces occlude the deep ring and ask the patient to cough – if it returns then its direct NB: an irreducible hernia will only have a weak (if any) cough impulse Inguinal - If above groin crease Direct – unlikely to be in scrotum Indirect - towards / in scrotum (controlled by pressure over deep inguinal ring) Deep inguinal ring is at mid inguinal point Femoral - If below / lateral to groin crease You should NOT be able to feel above the hernia as it enters the scrotum – if you can then it’s a scrotal swelling You should NOT be able to transilluminate a hernia You should be able to hear bowel sounds in the hernia if it contains bowel Signs of obstruction Vomiting, constripation and abdominal distension Pain Fever & leukocytosis • Outline the principles on management of patients with strangulated inguinal hernias, including preparation for surgery, treatment of bowel obstruction and hernia repair. Gastro 95 Resuscitate the patient to be fit for theatre IV fluid NG tube – to relieve obstruction Prophylactic Abx Check FBC, clotting etc Arrange for emergency repair Will involve removal of ischaemic bowel May require a (temporary) stoma if anastomosis is not possible at repair • Outline the principles of management of patients with reducible inguinal herniae. Medical management Reduce risk factors – treat cough, constipation & prostatism, loose weight etc If unfit for surgery consider a Truss – often difficult to keep in place & uncomfortable to wear Surgical repair If due to patent processus vaginalis (usually in children) – then herniotomy (remove hernial sac) In adults – hernia repair by plicating the transversalis muscle or using a mesh to reinforce Femoral Herniae • Define a femoral hernia. Passes through femoral canal More common in females (increases with increasing obesity) Always aquired Usually middle aged / elderly (rare in children) NB: should ALWAYS be repaired due to high risk of strangulation • Define incarcerated femoral hernia, strangulated hernia and Richter's hernia. Incarcerated The tissue / organ is trapped in hernial sac Often due to adhesions Irreducible Strangulated Incarcerated à lack of perfusion à ischaemia Surgical emergency Richter’s hernia Only part of the small intestine wall herniates & strangulates No symptoms of obstruction because lumen not occluded Can perforate into sac – due to necrosis of wall • Describe the symptoms of patients with femoral hernias, including local pain, mass, and possible bowel obstruction. Symptoms depend on the degree of herniation and if it is complicated Gastro 96 • Describe the physical examination of patients with femoral herniae, including a mass below the inguinal ligament and possible signs of bowel obstruction. Globular swelling below & lateral to the pubic tubercle Enlarges on standing and coughing May disappear when supine Pain & bowel obstruction indicates strangulation Umbilical Herniae • Define an umbilical hernia and relate it to the embryological origin of the umbilicus. An abnormal protrusion of the internal abdominal contents into a defect in the umbilical area Common in the newborn & usually resolves with age Exomphalos Midgut fails to return to the abdominal cavity during fetal life Bowel is contained in a translucent sac protruding through the defective abdominal wall Untreated à rupture à peritonitis Should be repaired immediately if possible or protected in a sterile dressing for later repair Congenital umbilical hernia From failure of umbilical cicatrix to close More common in black children Usually spontaneously closes by the age of 2 Should be surgically repaired if it persists Paraumbilical hernia Acquired – just above / below umbilicus Contents are momentum +/- small bowel / transverse colon Prone to become irreducible / strangulated Requires surgical repair • List the factors that predispose to the development of umbilical hernias, including congenital factors, increased intra-abdominal pressure and ascites. Congenital Black, low birth weight, prematurity Acquired Ascites, any cause of raised intrabdominal pressure (cough, constipation, CCF, peritoneal dialysis) • Describe the symptoms of patients with umbilical hernias. Presence of large central abdominal protrusion Enlarges of coughing and standing Reduces on laying down Signs of strangulation • Describe the physical examination of patients with umbilical hernias, differentiating reducible and nonreducible hernias; recognise the signs of strangulation. Examination – assess standing & laid down Can use US / CT / MRI Gastro 97 Incisional Herniae • Discuss the incidence of incisional hernias according to the original incision and indication for operation. 11-20% of surgical cases Risk factors Male Old Factors increasing intraabdominal pressure (Smoker, Obese) Any factor affecting wound healing (Arteriosclerosis, DM) Size of incision = increases risk Any person undergoing emergency surgery (as linea alba is used) • Describe the risks of complications of incisional hernias including bowel obstruction and strangulation. As for all hernias – obstruction & strangulation If soon post op – re-opening of ward • Describe the symptoms of patients with incisional hernias including distension and pain and, in patients with irreducibility, symptoms of bowel obstruction. Swelling / distension @ site of previous surgery Irreducible / strangulation signs • Describe the physical examination of patients with ventral hernias including mass and tenderness in those with incarcerated hernias and estimation of the size of the defect in patients with reducible hernias. Assess symptoms Assess hernia for size Palpate edges of incision if possible Assess for contents, strangulation etc • Outline the risk factors for recurrence after repair, including the size of the defect, obesity and chronic cough. Size of hernia & incision Obseity Increased intraobdominal pressure (cough, constipation etc) Poor wound healing ( DM, smoking etc) Gastro 98