Finals Lecture Series 2024/25 - Upper GI Slides
Summary
In this on-demand teaching session, medical professionals will gain upper gastrointestinal (GI) expertise through the presentation of relevant symptoms, diagnostic criteria, and management strategies. The session covers a broad spectrum of conditions such as abdominal pain, achalasia, acute pancreatitis, GORD, hepatitis, intestinal obstruction, gall stones, gastric cancer, and liver abscess among others. The lecture explores in-depth the management of presenting symptoms using case scenarios and encourages attendees to think critically about the most appropriate treatment approach. Using an interactive method, attendees will learn about the idiosyncrasies of related conditions. This session is best suited for professionals who frequently diagnose and treat upper GI conditions.
Learning objectives
- Understand and describe common symptoms and causes of Upper GI distress, as well as related conditions such as Achalasia, Acute Pancreatitis, and Cholecystitis.
- Be able to correctly identify, diagnose, and manage cases of upper GI symptoms based on case study examples.
- Gain insight into the typical clinical presentation, complications, and management of Primary Biliary Cirhossis and Primary Sclerosing Cholangitis.
- Understand and describe the causes of liver cirrhosis, and learn about the different states of liver disease and their respective care bundles.
- Develop critical thinking skills by completing session-based assessments to evaluate the severity and type of liver diseases, and manage conditions such as Ascites effectively.
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Sanjana Murali sanjana.murali@doctors.org.uk Menti Code: 3987 5967 Upper GI A MedED LECTURE THE MLA REQUIREMENTS Abdominal pain/distension Achalasia Acute pancreatitis Bleeding froConditionsr GI tract Symptoms Cholecystitis • Abdominal pain (acute and chronic) Chronic • Gall bladder stuff: Cholangitis, Cholecystitis, Cirrhosis • Change in stool colour Gall sGastric Cancerstones, colic, PBC, PSC • Dysphagia Gastro-int• Liver stuff: Cirrhosis, hepatitis, hepatocellular GORD • Decreased appetite Hepatitisa, liver abscess, liver failure, Hepatocellular carcinoma • GI bleeds Hiatus herniaochromatosis, Wilson’s disease • Jaundice Intestinal obstruction and ileus Achalasia, gastric Jaundice • Malaena Liver abscesscer, perforation, GORD, Hiatus hernia, • Nausea Liver faPUD/gastritis, oesophageal cancer, Barrett’s • Vomiting Malabsorption Mesenteric adenitisgus, Mallory-Weiss tear, Nauseacreatic stuff: acute/chronic pancreatitis, Necrotising enterocolitis Oesophageal canceratic cancer Pancreatic cancer PepPrimary biliary cholangitisitis Primary sclerosing cholangitis Vomiting SBA 1 You are the F1 working in A&E. You have been asked to see Michelle Roberts, a 53 year old woman who comes in complaining of pain in her stomach. She says that is used to be intermittent but now it is constant sharp pain. It is the right upper part of her stomach. She has been worried that she has a stomach problem and has been feeling nauseous all day. On examination she is tender in the right upper quandrant, but is not notably jaundiced. No changes to urine or stool. No recent travel abroad or changes to diet. Hb 100 WBC 17.2 Heart rate 110 bpm CRP 150 Blood pressure 105/70 ALT 35 Respiratory rate 22 AST 44 SpO2 99% roomair ALP 100 Temperature 38.3 degrees Bilirubin 0.9 What is the most likely diagnosis? Albumin 4.0 Amylase 140RUQ painChole-??? CholedocChPancl lith a is Liver Common hepatic duct Gall bladder Cystic duct Common bile duct Pancreas Gall stone management Asymptomatic gall Cholecysitis Cholangitis stones Management Expectantly IV Abx and analgesia IV Abx and analgesia Early laparoscopic cholecystectomy ERCPafter 24-48 within 1 week of diagnosis hours Complications Becomes Necrosisof the gallbladder wall Acute pancreatitis symptomatic Perforation ofthe gallbladder Inadequate biliary Biliary peritonitis drainage Pericholecystic abscess Hepatic abscess Fistula (between the gallbladder and duodenum). Jaundice (due to inflammation of adjoining biliary ducts — Mirizzi's syndrome) Sepsis Pancreatitis Idiopathic Gallstones – 85% Ethanol – 85% Trauma Steroids Mumps Autoimmune Scorpion bites Hypothermia, hypercalcaemia, hyperkalaemia ERCP - Endoscopic retrograde cholangiopancreatography Drugs: azathioprine, mesalazine*, Modified Glasgow-Imrie criteria predicts the severity of didanosine, bendroflumethiazide, pancreatitis furosemide, pentamidine, steroids, sodium valproate Pancreatitis Management • ADMIT ALL CASES o In severe cases, HDU/ ITU input is required (level 2 monitoring bed) • O2 to keep SaO2 > 95% • IV fluids to keep urine output > 0.5ml/kg/h – immediately • Urinary catheter (consider CVP monitoring) • IV analgesia, morphine 5-10mg (cause Oddi’s sphincter to contract more) IM/IV with anti-emetics (10mg metoclopramide) - pethidine 75mg-100mg/4hour • IV Abx – infected pancreatic necrosis and/or associated cholangitis-> Not routinely offered • Keep NBM o If not improving and able to eat and drink in 5-10 days, start naso-jejunal or NG feeding. If these are not tolerated, start TPN • Start an insulin sliding scale is CBG > 12mmol/L • NG tube (Ryle’s tube) may be required if ongoing vomiting • Start VTE prophylaxis • Early nutritional support Peripancreatic fluid collections Pseudocysts ARDS PSC vs PBC Primary Billiary Cirrhosis Primary Sclerosing Cholangitis Demographic F > M M > F Middle age 20-40s Presenting sx Fatigue and pruritus Progressive obstructive jaundice Site of involvement Intrahepatic Intrahepatic and extrahepatic Cause of obstruction Granulomatous inflammation Fibrosis (onion-skin) around bile (florid duct lesion) ducts Diagnostic Anti-mitochondrial antibodies Beaded appearance of bile ducts on cholangiogram/ERCP/MRCP Associations Other autoimmune disorders Ulcerative colitis e.g. Sjogren’s, RA Complications Cirrhosis Cirrhosis Cholangiocarcinoma SBA 1 You are the F1 working in A&E. You have been asked to see Michelle Roberts, a 53 year old woman who comes in complaining of pain in her stomach. She says that is used to be intermittent but now it is constant sharp pain. It is the right upper part of her stomach. She has been worried that she has a stomach problem and has been feeling nauseous all day. On examination she is tender in the right upper quandrant, but is not notably jaundiced. No changes to urine or stool. No recent travel abroad or changes to diet. Hb 100 WBC 17.2 Heart rate 110 bpm CRP 150 Blood pressure 105/70 ALT 35 Respiratory rate 22 AST 44 SpO2 99% roomair ALP 100 Temperature 38.3 degrees Bilirubin 0.9 What is the most likely diagnosis? Albumin 4.0 Amylase 140 Cholecysitis SBA 2 You are the F1 working in Gastroenterology. You are bleeped to come and see a patient presenting with jaundice and acute confusion. Their history indicates that they drink up to 60 units of alcohol a asking for the menu. His friend tells you that he’s been like this all day, and it was a bit worrying. A&E have already started him on IV pabrinex and are commencing chlordiazepoxide reducing regimen for alcohol detoxification. What would be the single most prognostically beneficial medication to help with his confusion? Liver problems What are the causes of liver cirrhosis? Alcohol Non-alcoholic fatty liver disease (NASH): diabetes and obesity Infection: Hepatitis B and C Malignancy: HCC Metabolic: alpha-1 antitrypsin deficiency, haemochromatosis, Wilson’s disease, glycogen storage disease Autoimmune: Primary biliary cirrhosis, autoimmune hepatitis, primary sclerosing cholangitis Vascular: Chronic Budd-Chiari syndrome Drugs: Amiodarone, methotrexateChronic Stable Liver Disease Portal HypertensionDecompensated liver diseaseThe Decompensated Liver Care Bundle Investigations •Bloods cultures and ascitic taps •CT scan/fibroscan Alcohol? – CIWAr score •IV pabrinex (2 pairs) Infections (including SBP) •ABx, treat source •Consider HAS 20% (IV albumin) AKI/hyponatraemia •Suspend diuretics and nephrotoxic drugs •Fluid restrict, daily weights GI bleeding •IV terlipressin, Vitamin K if prolonged PT, FFP, transfusion •Early endoscopy Encephalopathy •Lactulose (traps ammonia in gut) – 3 soft stools/day •Nutritional support (high calorie diet) VTE prophylaxis Ascites SAAG > 11g/L or SAAG <11g/L or 1.1mg/dl Conservative: 1.1mg/dl - not portal hypertension Reducing dietary sodium +/- fluid restrict (if sodium <125) (indicates portal hypertension) Liver (most common): Hypoalbuminaemia: Medical: cirrhosis, alcoholic liver nephrotic syndrome, Prophylactic oral ciprofloxacin (if ascitic disease, acute liver failure, severe nutritional protein <15g/L) mets deficiency e.g. Kwashikor Aldosterone antagonists e.g. spironolactone Cardiac: right heart failure, Peritoneal carcinomatosis Procedural constrictive pericarditis Tuberculosis peritonitis Others: portal-vein Pancreatitis Therapeutic paracentesis: usually for tense thrombosis, venous Bowel obstruction ascites. occlusive disease, Biliary ascites Large volume drainage (5L<) will require myxoedema Post-operative lymphatic albumin cover due to the risk of paracentesis- leak induced circulatory dysfunction and mortality Serositis in connective Transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients tissue disordersParacetamol OD Aetiology: Examination: Differentials Investigations: ❖ Liver conjugation ✶ Jaundice ✶ Viral hepatitis Bloods: pathway becomes Paracetamol overloaded causing ✶ Oliguria ✶ Alcohol paracetamol to be levels at 4h post- metabolised in a ✶ Encephalopathy ✶ Acute fatty ingestion unless different pathway liver of >4h ODD or 0-24 hours – N+V or asymptomatic staggered ODD ❖ Produces NAPQI (toxic24 hours – hepatic necrosisnancy metabolite) begins History: Management: Following up: ❖ Ask about ✶ Activated charcoal (<1hr of ingestion) ✶ Consider discharge if: ❖ How many tablets ❖ INR is 1.3 or less AND ❖ When ✶ NAC (depends on local guidelines) – ❖ ALT is less than two times the upper limit of immediate if staggered dose, normal AND ❖ Alcohol (acute ❖ ALT is not more than double the admission alcohol reduced otherwise check 4h post-dose measurement NAPQI, chronic use increases it) ✶ Liver transplant: Depends on Kings ❖ Intention College Criteria ✶ Bloods 8-16 hours later to check LFTs and INR Viral hepatitis HBsAg Anti-HBs Anti-HBc HBeAg Unexposed - - - - Acute + - IgM+ + infection Past - + + - infection Chronic + - IgG+ - infection Vaccinated - + - - Wilson’s and Hemochromatosis Copper overload Iron overload ✶ Neurological features ✶ Bronzed diabetes ✶ Psychiatric features ✶ Hypogonadism ✶ Fanconi syndrome ✶ Heart failure ✶ Hypoparathyroidism ✶ Arthritis Low serum ceruloplasmin concentration and high High ferritin with a high transferrin saturation 24h urinary copper excretion Haemosiderin deposits in hepatocytes Reduced bound serum copper and increased free HFE gene testing shows Chr 6 AR C282Y mutation serum copper Liver biopsy with rhodanine stain is diagnostic 1. Weekly phlebotomy/venesection to keep ferritin <50 Penicillamine (chelates copper) 2. Desferrioxamine Complications: hepatocellular carcinoma SBA 2 You are the F1 working in Gastroenterology. You are bleeped to come and see a patient presenting with West-Haven Criteria jaundice and acute confusion. Their history indicates that they drink up to 60 units of alcohol a day. You speak to 1. Change in behaviour /altered him and his speech is slurred and he seems to think he’s sleep wake cycle (diurnal at a restaurant and is asking for the menu. His friend tells sleeping pattern disturbance - you that he’s been like this all day, and it was a bit earliest sign) /slurred worrying. A&E have already started him on IV pabrinex speech/mild confusion and are commencing chlordiazepoxide reducing regimen 2. Lethargy/moderate confusion, for alcohol detoxification. asterixis, drowsiness What would be the single most prognostically 3. Marked confusion/incoherent beneficial medication to help with his confusion? speech/sleeping but rousable 4. Coma Lactulose SBA 3 You are the F1 working in GP. Your next patient is a 61 year old lady who is concerned about her swallowing. She has noticed that it has been getting progressively worse over the last six months, and due to the difficulty. She mentions that she has been having more difficulty with liquids more than solids and she feels like something is ‘stuck in her throat’. When asked, she mentions that she feels that her clothes do feel a bit looser, but she suspects that it is because she has not been able to eat. She has previously been treated for reflux disease and says that the medication doesn’t help. What is the single more important investigation that needs to be done next?Dysphagia System Condition Key investigation Neurological Stroke CT/MRI brain Bulbar palsy Electromyogram Myasthenia gravis ACHr antibodies MND Parkinson’s ENT Throat cancer Nasal endoscopy Pharyngeal pouch List some causes of dysphagia Achalasia Barium swallow CREST Oesophageal manometry Chagas disease Serology (Chagas disease) Scl-70, anticentromere and ANA for CREST Structural Malignancy Barium swallow Benign stricture OGD + biopsy Hiatus hernia FBC Gastrointestinal Stomach cancer OGD Gastritis Caeruloplasin GORD Peptic ulcer Wilson’s disease External Thyroid (goitre/cancer) FNA + biopsy/USS/TFTs compression Heart (MS, LAH, Aneurysm) Echocardiogram Lung cancer CXR Mediastinal lymphadenopathy CT chestRuling in and out Weight loss Loss of appetite Haematemesis Melaena Onset: sudden/gradual Progressive and persistent Character: fluids/solids Time: duration, intermittant/continous/progressive Level: where does food/liquid feel like it is getting stuck (throat/gullet/stomach) Alleviating/exacerbating facotrs Which stage: when initiating swallowing/ after swallowing has been initiated Pain Trauma/foreign body Lump in the throat Other symptomsSpot diagnosis Spot diagnosis Diffuse oesophageal spasm Hiatus hernia Oesophageal cancer AcBird beak SBA 3 You are the F1 working in GP. Your next patient is a 61 year old lady who is concerned about her she feels that she can’t swallow very well. It has impacted her eating habits as she feels she eats less due to the difficulty. She mentions that she has been having more difficulty with liquids more than solids and she feels like something is ‘stuck in her throat’. When asked, she mentions that she feels that her clothes do feel a bit looser, but she suspects that it is because she has not been able to eat. She has previously been treated for reflux disease and says that the medication doesn’t help. What is the single more important investigation that needs to be done next? OGD SBA 4 You are the F1 working in ED. Tim Green, a 62 year old gentleman, is rushed in as he’s vomiting frank blood. He is known to alcohol rehabilitation services, but has recently relapsed. His wife, who is with vomiting blood and she called the ambulance. When you see him, he is pale, responding to voice with a vomit bowl on the side of the bed. His blood pressure is 110/70, HR 124, SpO2 97% on room air, RR 24, Temperature 35.8 degrees. He has vomited two bowls full of blood. You fast bleep the gastro team on call to come and see the patient for an OGD. What is the most appropriate initial management for this gentleman? Bleeding from the Upper GI tract The acutely unwell patient: A-E assessment ----FBC, U&E, LFT, glucose, clotting screen, X-match 4-6 units ----1L Hartman’s to restore intravascular volume, aim for urine output >30mls/hr (catheter) !remember not to overhydrate ----Correct any clotting abnormalities e.g. blood transfusion (Hb<70), platelet transfusion (<50 and actively bleeding), FFP (Actively bleeding and clotting studies >1.5x upper limit of normal), stop NSAIDs Notify surgeons of any severe bleeding Vitals every 15 minutes (enhanced obs) Bleeding from the Upper GI tract Bleeding peptic ulcer Perforated peptic ulcer Variceal bleeding Upper GI endoscopy: IV antibiotics: prophylactic (e.g. IV terlipressin (1-2mg IV repeated - Clipping and adrenaline cefotaxime and metronidazole) every 4-6h for ≤3d - Thermal coagulation with adrenaline Analgesia (morphine 5-10mg/2h max ± Check INR, give vitamin K if prolonged - Sclerotherapy (fibrin or thrombin cyclizine) PLUS Prophylactic Abx: e.g. injection) with adrenaline NG tube insertion (to decompress ciprofloxacin or 2nd/3rd gen High-dose PPI (40mg/12h IV/PO): stomach, reduce further peritoneal cephalosporin, may ↓ mortality in severe administered post-endoscopy to reduce contamination and facilitate omental haemorrhage rebleeding patch) 2nd line = surgery or embolisation by If uncontrolled bleeding: Balloon Surgery (either laparoscopic or open) IR: reserved for cases where adequate Primary suture repair and thorough tamponade with a 4-lumen haemostasis is not achieved at abdominal lavage Sengstaken-Blakemore/Minnesota endoscopy (notified surgeons) Addition of an omental patch may tube Endoscopy unsuccessful after 2 provide further protection (gold Oesophageal varices: Endoscopic treatments then laparotomy and surgical variceal band ligation (BVL), superior to standard) exploration – acute GI bleed sclerotherapy Large ≥2cm gastric ulcer: resect and Gastric: endoscopic sclerotherapy send for histology - to exclude Ca Transjugular intrahepatic Large ≥2cm duodenal ulcer: resect or portosystemic shunt (TIPS) if repair (more commonly benign) endoscopic treatment failsAfter care Non-selective beta blocker (e.g. propranolol or carvedilol 20-40mg/12h PO) Endoscopic variceal band ligation (EVL): as primary prevention performed at 2-weekly intervals until all varices eradicated, alongside PPI to prevent EVL-induced ulceration SBA 4 You are the F1 working in ED. Tim Green, a 62 year old gentleman, is rushed in as he’s vomiting frank him, says that he was recently fired from his job and got incredibly depressed. She found him at hometh vomiting blood and she called the ambulance. When you see him, he is pale, responding to voice with a vomit bowl on the side of the bed. His blood pressure is 110/70, HR 124, SpO2 97% on room air, RR 24, Temperature 35.8 degrees. He has vomited two bowls full of blood. You fast bleep the gastro team on call to come and see the patient for an OGD. What is the most appropriate initial management for this gentleman? Bloods and Fluid rehydrationTHANK YOU FOR COMING! PL EA SE FILL IN THE FEED BACK FORM!