CHI335 GI System Lecture II PDF

CHI335 Diagnosis I Lecture II Coeliac Disease aka gluten-sensitive enteropathy Gluten malabsorption due to a T-cell–mediated hypersensitivity in persons with a genetic predisposition Consistent with malabsorption: Fatigue Weight loss Diarrhea Flatulence Borborygmus (loud stomac...

CHI335 Diagnosis I Lecture II Coeliac Disease aka gluten-sensitive enteropathy Gluten malabsorption due to a T-cell–mediated hypersensitivity in persons with a genetic predisposition Consistent with malabsorption: Fatigue Weight loss Diarrhea Flatulence Borborygmus (loud stomach or intestinal rumbling) Abdominal bloating and pain Steatorrhea, Malodorous stools Coeliac Disease – Diagnosis Based on clinical manifestations Laboratory studies Serum detection of antibodies against Gliadin (Endomysial) Tissue transglutaminase Diagnosis can be confirmed by a small bowel biopsy Obesity Excessive body fat (BMI ≥30 kg/m2) Types Hypertrophic: adipose cells increased in size Hyperplasic: adipose cells increased in number (in kids and adolescents mainly) Highly complex, multifactorial pathophysiology Risk factors Lifestyle (diet and exercise) Genetics Neurologic mechanisms and hormones Leptin, estrogen, thyroid hormone, insulin, melanocortin, ghrelin Obesity Distribution of body fat Truncal-abdominal or gluteofemoral fat deposition Health risk and complications (also next slide) Diabetes, CVD and heart attack, hypertension, hyperlipidaemia, CVA and stroke, osteoarthritis, liver disease, gall stones, poor wound healing, obstructive sleep apnoea, and certain cancers Obesity – Complications Obesity – Diagnosis Body mass index – Note: there is variability in body composition and adipose tissue distribution between individuals with the same BMI BMI Categories 18.5 to 24.9 kg/m2 Normal 25 to 29.9 kg/m2 Overweight 30 to 39.9 kg/m2 Obese ≥40 kg/m2 Severely (morbid) obese  Waist-to-hip ratio (WHR) seems to have the most robust association with mortality risk from obesity Men Women Health risk 0.95 or lower 0.80 or lower Low 0.96-1.0 0.81-0.85 Moderate 1.0 or higher 0.86 or higher High Gastritis Caused by bacteria or viruses, some medications, alcohol, caffeine, spicy foods, excessive eating, poisons, and stress Nausea, lack of appetite, heartburn, vomiting, and abdominal cramps Avoid foods or medications that irritate the stomach lining, treatment with medications to reduce the production of stomach acids GORD Gastroesophageal Reflux Disease Transient relaxations of LOS (Lower Oesophageal Sphincter) occur more frequently in GORD Between swallows, the LOS remains closed due to the unique property of the muscle and relaxes (transiently) when swallowing is initiated GORD – Risk factors Hiatus Hernia GORD – Management Investigation Upper GI Endoscopy & biopsy (for histology and H. pylori) Lifestyle changes Stop smoking Small meals, losing weight, elevating head & chest when lying down, repairing hiatus hernia Avoid aggravating foods Avoid alcohol Medication PPI/H2 blockers H. pylori eradication treatment (if indicated) GORD Complications Oesophagitis (strictures) Painful swallowing (odynophagia) Bleeding (anaemia) ± Nocturnal asthma and cough Adenocarcinoma due to long-lasting GORD: Chronic Oesophagitis → Barrett's oesophagus → Oesophageal adenocarcinoma GORD Peptic Ulcer Disease (PUD) Ulceration in the upper GI tract Types Gastric ulcer (GU) Duodenal ulcer (DU is 4 x more common than GU) S & S Epigastric pain (less likely chest pain) Worse with food or relieved by food Improves with antacids Epigastric tenderness on palpation Bloating & fullness with food ± Hx of Reflux ± Pain radiating to the back ± Haematemesis (fresh blood or coffee grounds) PUD Investigation H. pylori Urea Breath Test (UBT) Serology (blood) Faecal Ag test Upper GI Endoscopy (Bx, Rapid urease test) Management The same as GORD PUD Risk factors H. pylori infection NSAIDs (± oral corticosteroids) Smoking Alcohol FHx Complications Perforation Bleeding Gastric outlet obstruction PUD PUD Inflammatory Bowel Disease (IBD) IBD includes ulcerative colitis (UC) and Crohn’s disease Unknown aetiology An interaction between genetic susceptibility, environment, intestinal microbiota and host immune response Relapsing and remitting diseases High incidence rates and prevalence in Northern Europe, UK and North America UC vs Crohn’s IBD – Systemic Manifestations IBD – Complications Toxic megacolon A life-threatening condition Haemorrhage Fistula (crohn’s only) Cancer (UC predominantly) Irritable Bowel Syndrome (IBS) Is a “functional GI disorder” Sometimes referred to as “spastic colon” Is a syndrome comprising abdominal signs and symptoms for which no structural cause can be found! Most likely an intestinal motility problem (physiological) Up to 20% prevalence Irritable Bowel Syndrome (IBS) Triggers Affective disorders, e.g. depression, anxiety Psychological stress and trauma Gastrointestinal infection Antibiotic therapy Sexual, physical, verbal abuse Pelvic surgery Eating disorders Irritable Bowel Syndrome (IBS) Features 20-40 yrs old, F>M Central or lower abdominal pain/discomfort, relieved by defecation Abdominal bloating, tenesmus, urgency Alternating constipation & diarrhoea is very common Presence of mucus within faeces (but NO bleeding) NO constitutional signs or symptoms Exacerbated by stress, menstruation,… Diarrhea Caused by bacterial, viral, or parasitic infections; ingestion of toxins; food allergies; ulcers; Crohn’s disease; laxative use; antibiotics; chemotherapy; and radiation therapy Frequent passage of faeces (including watery feces), abdominal cramps Drink clear fluids to prevent dehydration and antidiarrheal medications (not usually indicated) Constipation Risk factors are a lack of physical activity, lack of adequate fibre and water in the diet, side effects of certain medications Infrequent bowel movements (including hard faeces), abdominal pain, formation of haemorrhoids, and pain during bowel movements Increase in dietary fibre, adequate fluid intake, regular exercise, and the use of stool softeners, laxatives, and enemas (if indicated) Acute appendicitis – Pathophysiology 1. Obstruction of the lumen Infection IBD (inflammation) Faecal stasis/faecaliths Parasites Foreign body (very rarely) 2. Increase intraluminal pressure Continuous secretion of fluids and mucus Bacterial overgrowth and pus formation 3. Venous outflow obstruction due to  pressure (congestion and thrombosis) 4. Ischemia of appendiceal wall (necrosis) Acute appendicitis Can occur at any age but usually affects children of school age or adolescence or adults between 20-30 years Clinical presentation Acute onset of anorexia, nausea and vomiting Diarrhoea Fever (not always) Pain, umbilical initially, then shifts to the right iliac fossa within hours Elevated WBC Acute appendicitis Possible Risk factors Low-fibre, high-sugar diet IBD FHx Infection Complications Perforation Peritonitis Management/treatment Immediate Referral to ED Appendectomy Colorectal Cancer (CRC) Bowel cancer is the fourth most commonly diagnosed cancer in Australia Incidence increases with age (over 50) It is estimated that one in 20 people will be diagnosed by the time they are 85 Non-invasive screening test is available for Australians who turn 50 Colonoscopy is both a screening and diagnostic procedure CRC Risk factors Age Type of diet (low-fibre & high-fat, high in meat/processed meat) Smoking, obesity, & alcohol IBD Colorectal polyps Family history of colorectal cancer or polyposis Frequent pelvic/abdominal radiology Prevention Fruits and vegetables Calcium, vitamin D, & folic acid Exercise CRC – Regional Incidence CRC Clinical presentation Altered bowel habits Melaena / haematochezia Abdominal pain / LBP Anaemia and weight loss Unsatisfactory defecation (mass perceived as faeces) Obstruction or perforation (rare) Investigation Abdominal examination (palpable mass) Sigmoidoscopy / colonoscopy Imaging Hepatitis Liver inflammation associated with hepatocyte damage in an acute or chronic setting Two major causes are alcohol and viruses Viral hepatitis is a major health problem worldwide, causing millions of deaths each year Mild fever, nausea, vomiting, abdominal pain, jaundice, hepatomegaly, bloating, lack of appetite, weakness, pruritus, dark urine Complications include Existence of a chronic carrier state  Risk of further liver disease  Cirrhosis  Liver cancer Hepatitis Abnormal LFTs Alcoholic liver disease Cells utilise ethanol (alcohol) by first converting it to acetaldehyde and then to acetate (acetyl-CoA) Can be used both for aerobic energy generation and as a substrate for the synthesis of fatty acids When supplied with alcohol as a major fuel Hepatocytes make excess amount of triglyceride and, at the same time, Utilise less than usual amounts of fatty acids as fuels Triglyceride and fatty acids accumulate in the liver, causing fatty liver Fatty liver Liver is slightly enlarged and has a pale yellow appearance, seen both on the capsule and cut surface. Source: © Dr Peter Anderson, University of Alabama at Birmingham, Department of Pathology. Cirrhosis Irreversible liver damage (degeneration) Necrosis of liver cells followed by fibrosis and nodule formation Causes (common) Alcohol Hepatitis B (± D), Hepatitis C Genetic hemochromatosis Fatty liver disease And many others! Signs & symptoms of chronic liver disease (previous lecture) Complications Impaired liver function Hepatic failure Portal hypertension Risk of hepatocellular carcinoma Effects of chronic liver disease Reduced metabolic activity of the liver Portal hypertension Impeded excretion of bile Pain Gallstone (Cholelithiasis) Cholecystitis Occurs most commonly because of an obstruction of the cystic duct from cholelithiasis. Uncomplicated cholecystitis has an excellent prognosis; complications such as perforation or gangrene indicate less favourable prognosis Risk factors Age (>40) Female sex Obesity or rapid weight loss Certain ethnic groups Drugs (especially hormonal therapy in women) Diabetes Sickle cell disease Pregnancy Cholecystitis Acute Acute abdominal pain, esp. RUQ pain (referred to Rt shoulder) Positive Murphy’s sign N+V, ± Palpable mass, ± Peritoneal signs Steatorrhea Pale, bulky, floating and malodorous stools Chronic cholecystitis Milder symptoms of above ± colic Self-directed Study Topics  Anorexia nervosa S&S, complications Pancreatitis Acute & chronic Causes and presentation Diverticular disease Causes & clinical feature Wilson disease Clinical presentation & management Alcoholism and CAGE questionnaire