Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Describe the pathophysiology, clinical features, and management principles of inflammatory bowel disease (IBD). Recognise and differentiate the causes, clinical presentation, and initial management of upper and lower gastrointestinal bleeding. Summarise the causes and key features of viral hepatitis, alcoholic liver disease (ALD), and non-alcoholic fatty liver disease (NAFLD). Interpret liver function tests (LFTs) to distinguish between patterns of hepatocellular injury, cholestasis, and synthetic dysfunction. Immune system Microbe s Over-reactive or sensitive Immune System Untrained gut NOD2 mutation/ Genetics Dysbiosis Antibiotic use Dietary change Leaky Gut Barrier Age: IBD can occur at any age, but most commonly starts in young adults (15–35 years) with second peak in older adults (60–80 years). Geography: More prevalent in Western countries like the UK, US, and Northern Europe. Incidence is increasing globally—including in newly industrialized countries. Ethnicity & Genetics: More common in Caucasian populations, especially those of Ashkenazi Jewish descent. Around 10–25% of patients have a first-degree relative with IBD. Crohn’s disease is slightly more common in women. Ulcerative colitis affects both genders equally.Netter's Integrated Review of Medicine, E-Netter's Integrated Review of Medicine, E-History and Physical Exam We ask about symptoms—how many times do you pass stools a day? Do you get up at night ? Is there blood? Do you feel cramping, pain, urgency, or the feeling of not being fully done (tenesmus)? Beyond the gut: IBD doesn’t just affect the gut—it can also cause skin problems, joint pains, eye issues, or liver problems. Lifestyle and family: Do you smoke? Does anyone in your family have IBD or cancer? Body check: We check for weight loss and in children, if growth or puberty is delayed• Blood tests: ⚬ Inflammation: CRP, ESR ⚬ Anaemia: full blood count ⚬ Malnutrition: vitamin D, B12, iron ⚬ Liver: alkaline phosphatase (↑ may suggest PSC) • Stool tests: ⚬ Fecal calprotectin (↑ indicates gut inflammation, esp. colonic) ⚬ Infection screen: stool culture, ova & parasite exam, C. difficile assay• Abdominal X-ray: Detects severe IBD complications—bowel obstruction (dilated loops, air-fluid levels), toxic megacolon, or perforation. • CT Enterography (CTE): IV and oral contrast imaging; ~90% sensitive for identifying Crohn’s bowel-wall thickening. • MR Enterography (MRE): Radiation-free counterpart to CTE, preferable for long-term follow-up. • Pelvic MRI: Gold standard for perianal Crohn’s evaluation (fistulas, abscesses). • Ultrasound: Evaluates bowel-wall thickening and strictures; ideal for pediatric cases or where MRI isn’t available.Netter's Integrated Review of Medicine, E-Netter's Integrated Review of Medicine, E-• Control Inflammation: Reduce the chronic gastrointestinal inflammation that defines both Crohn’s disease and ulcerative colitis. • Induce Remission: Rapidly alleviate symptoms during flare-ups to bring about remission. • Maintain Remission: Continue therapy to prevent relapse and keep patients symptom-free. • Manage Complications: Address disease-related issues—medical or surgical—to avert or treat complications. • Provide Nutritional Support: Correct malabsorption and deficiencies—especially in ileal Crohn’s—through tailored diet and supplements.MEDICAL SCHOOL COUNCILS OFFICIAL UKMLA AKT PRACTISE TESTGastrointestinal Bleeding Case Discussion: A 68-year-old man presents to the Emergency Department with two episodes of large-volume haematemesis and one episode of melaena over the past 6 hours. He feels dizzy on standing and reports a history of peptic ulcer disease. His medications include ibuprofen for osteoarthritis and omeprazole 20 mg daily. He drinks 20 units of alcohol per week and has a 40 pack-year smoking history. Observations: Heart Rate: 110 bpm Blood pressure 95/60 mmHg (drops to 80/50 on standing) Pale, clammy Examination: Abdomen soft, non-tender, no organomegaly PR exam: melaena on gloveHb 85 g/L (13.5–17.5) Platelets 220 × 10⁹/L PT 13 s (10–14) Urea 12 mmol/L (2.5–7.8) Creatinine 95 µmol/L (60– 110) 1) Differential Diagnosis ? 2) What is the most appropriate immediate management step? 3) Which risk score is most useful at presentation to predict need for intervention GI Bleed What is it? Upper GI This ligament of treitz serves as a landmark for differentiating upper and Lower GI lower gastrointestinal tract issues, including identifying the source of bleeding.Why does it Happen? How are you going to treat it? 1)ABCDE Approach: Airway- Assess and maintain airway patency. Consider intubation in high-risk patients (Eg: Significant haematemesis, altered consciousness Breathing Circulation: -Assess heart rate, blood pressure, capillary refill, and skin colour. -Resuscitation is paramount • Insert two large-bore IV cannulae, • Administer IV crystalloids (normal saline) *Avoid over-resuscitation* • Consider early blood transfusion if hemodynamically unstable. • In emergencies, consider O-negative blood **Activate Major Haemorrhage Protocol** Disability: GCS Exposure: Full Examination ) Investigations Risk Stratification 1)Full blood Count Blatchford Score (or Glasgow-Blatchford 2) Coagulation Screen - Especially Score): important in patients on antioagulatants or liver disease. • Calculated before endoscopy. • Uses clinical and laboratory parameters (Hb, urea, 3)Liver Functions heart rate >100, systolic BP, melaena, syncope, 4)Renal Functions (Blood urea raised in UGIB) liver disease, heart failure). 5)Group and Save/ Crossmatch: • A score of 0 suggests a low risk patient potentially suitable for outpatient management. Essential for blood transfusion • Higher scores indicate increased risk and need for 6)VBG/Lactate 7) Oesophago-Gastro- Endoscopy**** inpatient management and likely endoscopic intervention. Rockall Score: • Calculated after endoscopy. • Predicts prognosis, including risk of re-bleeding and mortality. ENDOSCOPY Cornerstone of diagnosis and treatment Urgent Upper Endoscopy (Oesophagogastroduodenoscopy OGD) Endoscopic Therapy for Variceal Bleeding Non-Variceal Bleeding: Treatment is guided by Endoscopic findings • Injection therapy: Adrenaline injection to induce vasoconstriction (not monotherapy). • Thermal therapy: Cauterisation of bleeding vessels. • Mechanical therapy: Application of clips to bleeding vessels. Variceal Bleeding High Clinical Suspicion in Patients with Liver Disease: Pre-Endoscopy Management: Urgent administration of antibiotics (prophylaxis against Spontaneous Bacterial Peritonitis - SBP in cirrhosis). Vasoactive drugs: Terlipressin: Preferred first-line vasopressin analogue, causes splanchnic vasoconstriction. Octreotide: Somatostatin analogue, also reduces portal pressure. Endoscopic Therapy: • Oesophageal Variceal Ligation or banding: Placement of rubber bands around bleeding varices to achieve haemostasis. • Gastric varices requires N-butyl-2-cyanoacrylate Management of Refractory Bleeding: Consider early Transjugular Intrahepatic Portosystemic Shunt (TIPS) in high-risk patients or if bleeding is uncontrolled. Balloon tamponade (Sengstaken-Blakemore tube) as a temporary measure in severe, refractory bleeding. Case 2: 68-year-old man presents with a 2-day history of painless bright red rectal bleeding, which he noticed on the toilet paper and in the bowl. He reports no abdominal pain, change in bowel habit, or systemic symptoms such as weight loss or fatigue. His past medical history includes hypertension and diverticulosis diagnosed five years ago via colonoscopy. He is on amlodipine and aspirin 75 mg daily. He quit smoking five years ago after a 30-pack-year history and drinks around 10 units of alcohol weekly. There is a family history of bowel cancer—his father was diagnosed at age 72 On examination, he is hemodynamically stable with a soft, non-tender abdomen and bright red blood on rectal examination but no palpable massesABCDE Approach: As with UGIB, focus on resuscitation if unstable. Oakland Score History and Examination: helps to categorise Detailed history of bowel habits, patients as major/minor bleed abdominal pain, medications (especially to guide initial management. anticoagulants/antiplatelets). Digital rectal examination is Shock index (>1, essential. heart rate/systolic Blood Tests: FBC, coagulation BP) indicates instability. screen, U&Es, group and save.The British Society of Gastroenterology Treatment of LGIB: Resuscitation: As needed based on stability. Endoscopic Therapy: Haemostatic techniques (e.g., clips, cautery) can be applied during colonoscopy if the bleeding source is identified. Mesenteric Embolisation: Can be effective for stopping persistent arterial bleeding identified on angiography. Surgery: Reserved for massive, uncontrolled bleeding unresponsive to endoscopic and radiological interventions. May involve segmental or subtotal colectomy. Management of Anticoagulants and Antiplatelets: Discuss with haematology regarding temporary cessation and potential reversal based on the clinical context and bleeding severity. Consider the risks and benefits of restarting these medications post-bleed.Feature Upper GI Bleed Lower GI Bleed Location Proximal to Ligament of Distal to Ligament of Treitz Treitz Peptic ulcers, varices, Diverticular disease, Common Causes angiodysplasia, Mallory-Weiss tear haemorrhoids Haematochezia (bright Typical Presentation Haematemesis, melaena red) Initial Investigation Upper endoscopy (OGD) Colonoscopy (stable), CTA (unstable/ongoing) Mortality Generally higher Generally lowerA 58-year-old man presents with black, tarry stools for the past 2 days. He has no history of vomiting. His medications include aspirin and ramipril. On examination, he is hypotensive and tachycardic. Which of the following investigations is the most appropriate initial step? A. Colonoscopy B. CT angiography C. Upper GI endoscopy D. Faecal occult blood test E. Capsule endoscopyA 58-year-old man presents with black, tarry stools for the past 2 days. He has no history of vomiting. His medications include aspirin and ramipril. On examination, he is hypotensive and tachycardic. Which of the following investigations is the most appropriate initial step? A. Colonoscopy B. CT angiography C. Upper GI endoscopy D. Faecal occult blood test E. Capsule endoscopy A patient with known oesophageal varices presents with an acute upper gastrointestinal bleed. Initial management should include: A) Urgent upper endoscopy as the sole priority. B) Administration of intravenous proton pump inhibitor. C) Administration of terlipressin and consideration for early upper endoscopy with endoscopic band ligation. D) Immediate surgical consultation. E) Initiation of broad-spectrum antibiotics only after endoscopy confirms variceal bleeding. A patient with known oesophageal varices presents with an acute upper gastrointestinal bleed. Initial management should include: A) Urgent upper endoscopy as the sole priority. B) Administration of intravenous proton pump inhibitor. C) Administration of terlipressin and consideration for early upper endoscopy with endoscopic band ligation. D) Immediate surgical consultation. E) Initiation of broad-spectrum antibiotics only after endoscopy confirms variceal bleeding.You have a 53 year old man presenting to you at the GP, with a 4-week history of RUQ pain, abdominal distension, increased bruising and fatigue He has a PMH of T2DM, HTN and has been trying to lose weight to help both of these. He has recently come back from holiday with his family, and has a high-stress job. He had some diarrhoea whilst away on holiday, but this resolved. Differentials? Investigations B Physical examination; reduced appetite, diarrhoea, nutritional deficiencies (B12, thiamine), withdrawal symptoms and features of CLD L LFafld; causes, symptoms, presentation and management I Abdominal USS “transient elastography/fibroscan) S Biopsy (Gold standard but not usually required), AFP (hepatocellular carcinoma) S Hepatology r/v Investigations B Physical examination; reduced appetite, diarrhoea, nutritional deficiencies (B12, thiamine), withdrawal symptoms and features of CLD L LFafld; causes, symptoms, presentation and management I Abdominal USS “transient elastography/fibroscan) S Biopsy (Gold standard but not usually required), AFP (hepatocellular carcinoma) S Hepatology r/v Investigations B Physical examination; reduced appetite, diarrhoea, nutritional deficiencies (B12, thiamine), withdrawal symptoms and features of CLD L LFafld; causes, symptoms, presentation and management I Abdominal USS “transient elastography/fibroscan) S Biopsy (Gold standard but not usually required), AFP (hepatocellular carcinoma) S Hepatology r/v Investigations B Physical examination; reduced appetite, diarrhoea, nutritional deficiencies (B12, thiamine), withdrawal symptoms and features of CLD L LFT; AST > ALT, GGT, Bilirubin, FBC and clottingment I Abdominal USS “transient elastography/fibroscan) S Biopsy (Gold standard but not usually required), AFP (hepatocellular carcinoma) S Hepatology r/v Management 1) Lifestyle modification 2) Alcohol abstinence +/- withdrawl management afld; causes, symptoms, presentatio an management ScoringSystems (normally chlordiazepoxide or diazepam) AUDIT - 10 Q’s for screening • b. Deficiencies - Thiamine/multivitamins • >5 in 3Qs - progress to full 10Q’s • c. Seizure Treatment – Benzodiazepines. Antiepileptics should not be used • >8 = hazardous alchol use • 4-6 = alchohol dependence routinely. SAD-Q - 60Q’s Degree of dependence and withdrawl • >20 = requires assisted withdrawl • >30 = severe dependence Investigations B Physical examination; hepatomegaly, metabolic syndrome features, acanthosis nigricans, chronic liver disease stigmaafld; causes, symptoms, presentation and management L LFT; ALT > AST, high fasting lipids, high fasting glucose, FBC, clotting I Abdominal USS “transiet elastography/fibroscan) S Biopsy (Gold standard but not usually required) S Hepatology r/v ScoringSystems Enhanced Liver Fibrosis Score (ELF) • >10.51 = advanced • <10.51 = Every 3-years Investigations B Physical examination; hepatomegaly, metabolic syndrome NAFLD Fibrosis Score (NFS) features, acanthosis nigricans, chronic liver disease • Age/BMI/AST:ALT/Platelets/Albumin stigmata. Diabetes afld; causes, symptoms, presentation and management L LFT; ALT > AST, high fasting lipids, high fasting glucose, • >-1.455 = advancee FBC, clotting I Abdominal USS “transiet elastography/fibroscan) Fibrosis 4 (FIB-4) S Biopsy (Gold standard but not usually required) • Age/AST:ALT/Platelets S Hepatology r/v • >2.67 = advanced Management 1) Lifestyle modification 2) Pioglitazone (thiazolidinedione; reduces peripheral afld; causes, symptoms, presentation and management insulin resistance) 3) Vitamin E 4) Bariatric surgery 5) Liver transplant IgM - Acute phase Ab IgG - Immunity Ab D A B C Co-infects with B E Transmission Faecal/oral Blood Blood Blood Faecal/oral Hep C Ab - Hep A IgM - Acute Hep D IgM - Acute Hep E IgM - Acute Serology Hep A IgG - Immunity HBsAg infection at some Hep D IgG - Immunity Hep E IgG - Immunity point Chronic infection No Yes (<20%) Yes (75%) Yes (<50%) No Childhood Vaccination target Travellers and high- No No No groups risk IgM - Acute phase Ab IgG - Immunity Ab A B C D E 2 4 6 8 20 2 Week 5 sIgM - Acute phase Ab IgG - Immunity Ab HBsAg HBcAg HbeAg Anti-HBs Anti-HBc Anti-HBe Acute + + + - + (IgM) - Carrier/Chronic + + + - + (IgG) + Recovered - - - + + (IgG) + Vaccination - - - + - - Acute Chronic Key Management No chronic A Supportive No treatment infection Antivirals (Tenofovir, B Supportive Vaccination Entecavir), PEG- IFN Direct-acting C Supportive antivirals (DAAs) Screening PEG-IFN, Liver D Supportive Hep B vaccine transplant Ribavirin/PEG-IFN E Supportive (immunocompro Hygiene mised)A 25-year-old medical student is found to have: HBsAg: negative Anti-HBs: positive (120 mIU/mL) Anti-HBc: negative What is the most likely explanation? A. Past natural infection B. Current infection C. Window period D. Immunity due to vaccination E. Chronic hepatitis B carrier Correct Answer: D Rationale: Isolated anti-HBs with no anti-HBc indicates vaccine-induced immunity HBsAg HBcAg HbeAg Anti-HBs Anti-HBc Anti-HBe Acute + + + - + (IgM) - Carrier/Chronic + + + - + (IgG) + Recovered - - - + + (IgG) + Vaccination - - - + - - A 25-year-old woman presents with a 1-week history of fatigue, nausea, and right upper quadrant discomfort. She recently returned from travelling, where she ate street food daily. Her ALT is 2200 U/L, and bilirubin is elevated. What is the most likely diagnosis? A. Hepatitis A infection B. Hepatitis B infection C. Drug-induced liver injury D. Autoimmune hepatitis E. Gallstone hepatitis Correct Ans.er: A Teaching point: Travel history + feco-oral transmission = Hep A A B C D E Co-infects with B Transmission Faecal/oral Blood Blood Blood Faecal/oral Hep A IgM - Acute Hep C Ab - Hep D IgM - Acute Hep E IgM - Acute Serology HBsAg infection at some Hep E IgG - Hep A IgG - Immunity point Hep D IgG - Immunity Immunity Chronic infection No Yes (<20%) Yes (75%) Yes (<50%) No Childhood Vaccination target groups Travellers and high- No No No risk Liver Pre-hepatic e.g. haemolysis Bilirubin Spleen Hepatic e.g. acute hepatitis Post-hepatic e.g gallstones i i Alcohol misuse t Liver Drug induced p AST Cardiac muscle Skeletal Ischaemic hepatitis e muscle Acute/Chronic liver disease H Non-GI e.g. MI or Myositis s t Alcohol misuse t Drug induced a ALT Liver Ischaemic hepatitis e Acute/Chronic liver disease H Non-GI e.g. MI or Myositis - c Cholestatic liver disease e.g. PBC l t Liver Biliary obstruction e.g. gallstones h t ALP Bones Drugs C s Placenta Non-GI e.g. heart failure, bone disease, metastasis, pregnancy Drugs * GGT Liver Fatty Liver Alcohol Liver Chronic liver disease Albumin Non GI e.g. nephrotic syndrome, sepsis * GGT allows us to see if increased AST or ALP is due to the liver, and not other organs ↑ALP + ↑GGT = Cholestasis = e.g. gallstones ↑Bilirubin + ↑AST + ↑ALT + ↑ALP = Cholestatic + Hepatic = e.g. Sepsis or drug side- effects due to inflammation and destruction of bile flow ↑ALP + normal GGT = Bone cause ** AST < ALT = Viral or NAFLD hepatitis AST > ALT = alcohol hepatitis * GGT allows us to see if increased AST or ALP is due to the liver, and not other organs ↑ALP + ↑GGT = Cholestasis = e.g. gallstones ↑Bilirubin + ↑AST + ↑ALT + ↑ALP = Cholestatic + Hepatic = e.g. Sepsis or drug side- effects due to inflammation and destruction of bile flow ↑ALP + normal GGT = Bone cause i Unconjugated (pre-liver) - haemolysis, gilberts, crigler-naijar u l Conjugated (post liver) - biliary disease, rotor and dubin- B johnson syndromeWhat is the liver pathology? AST ↑↑ ALT ↑ ALP ↑ Bili ↑↑↑ (conjugated) GGT ↑↑ What is the liver pathology? AST ↑↑ - hepatitis ALT ↑ - hepatitis ALP ↑ Bili ↑↑↑ - liver injury GGT ↑↑ - liver injury We can see this is a liver injury, specifically fitting a hepatitis more than a cholestatic picture. As AST > ALT, this is more indicative of an ALCOHOL related hepatitis.What is the liver pathology? AST ↑ ALT ↑ ALP ↑↑↑ Bili ↑↑ (conjugated) GGT ↑↑ What is the liver pathology? AST ↑ ALT ↑ ALP ↑↑↑ - cholestatic Bili ↑↑ (conjugated) - ?obstruction GGT ↑↑ - liver We can see these results fit a CHOLESTATIC picture due to the raised ALP, specific to the liver due to the raised GGT. The presence of CONJUGATED BILIRUBIN indicates a possible obstruction, making gallstones a differential. Slides and recordings to be found on MedAll @teaching.frontie