Gastro enterology ebook

GASTROENTEROLOGY Dr G P Kandel Karen Bensoussan, Winnie Lee, and Rajani Vairavanathan, chapter editors Harriette Van Spall, associate editor APPROACH TO GASTROINTESTINAL (GI) LIVER 30 EXAM Hepatitis Acute Viral Hepatitis DIFFERENTIAL DIAGNOSIS OF COMMON Chronic Hepatitis PRESENTING COMPLAINTS Drug-Induced Liver Disease Abdominal Distension Wilson’s Disease Acute Abdominal Pain Hemochromatosis Chronic/Recurrent Abdominal Pain Alcoholic Liver Disease Acute Diarrhea Fatty Liver Chronic Diarrhea Cirrhosis Constipation Hepatic Encephalopathy Dysphagia Portal Hypertension Gastrointestinal (GI) Bleeding Ascites Heartburn Renal Failure in Cirrhosis Nausea/Vomiting Hepatopulmonary Syndrome Haematologic Changes in Cirrhosis ESOPHAGUS Major Symptoms of Esophageal Disorders BILIARY TRACT 41 Gastroesophageal Reflux Disease (GERD) Jaundice Esophageal Motor Disorders Gilbert’s Syndrome Esophageal Structural Disorders Primary Biliary Cirrhosis (PBC) Infectious Esophagitis Secondary Biliary Cirrhosis Sclerosing Cholangitis STOMACH AND DUODENUM Gastritis PANCREAS 45 Peptic Ulcer Disease (PUD) Acute Pancreatitis Chronic Pancreatitis SMALL AND LARGE BOWEL 13 Acute Diarrhea CLINICAL NUTRITION 48 Chronic Diarrhea Recommended Nutrient Intake Maldigestion and Malabsorption Carbohydrates Celiac Disease Lipids Bacterial Overgrowth Protein Irritable Bowel Syndrome (IBS) Kwashiorkor and Marasmus Inflammatory Bowel Disease (IBD) Determination of Nutritional Status Crohn’s Disease (CD) Enteral Nutrition Ulcerative Colitis (UC) Parenteral Nutrition Constipation REFERENCES 51 GASTROINTESTINAL BLEEDING 26 Upper GI Bleeding Bleeding Peptic Ulcer Esophageal Varices Mallory-Weiss Tear Lower GI Bleeding Colon Cancer Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G1 APPROACH TO THE GASTROINTESTINAL EXAM ❏ history • pain • location, onset, palliative/provoking factors, quality, radiation, severity, timing • constitutional symptoms • fever, chills, night sweats, weight loss • associated symptoms • jaundice, pruritus, pale stools, dark urine • anorexia, nausea, vomiting, hematemesis, food intolerance • diarrhea, constipation, melena, hematochezia, change in bowel movement • urinary: frequency, urgency, dysuria, hematuria • sexual history • first day of last menstrual period (LMP), birth control, sexually transmitted diseases (STD’s), vaginal discharge, spotting/bleeding • past medical history • major illnesses, prior hospitalization, surgeries • prior investigations for abdominal problems • diet, medications (NSAIDs, steroids, ulcer medications), alcohol • travel / exposure history ❏ physical examination (see General Surgery Chapter) ❏ investigations (see General Surgery Chapter) DIFFERENTIAL DIAGNOSIS OF COMMON PRESENTING COMPLAINTS ABDOMINAL DISTENSION Table Differential Diagnosis of Common Presenting Complaints Symptoms Differential Diagnosis ABDOMINAL DISTENSION 5Fs: • Fat • Feces • Fetus • Flatus • Fluid Ascites Gas/Bloating Other Cirrhosis Right heart failure Hypoalbuminemia Hepatic vein thrombosis Portal vein thrombosis Ovarian cancer Intra-abdominal metastases Tb peritonitis Chylous effusion Aerophagia (functional) Gastric dilation Small bowel obstruction (SBO) Irritable bowel syndrome Diet (fatty food, lactose intolerance, carbonated drinks) Pregnancy Distended bladder Obesity Obstipation ACUTE ABDOMINAL PAIN RUQ = right upper quadrant RLQ = right lower quadrant LUQ = left upper quadrant LLQ = left lower quadrant Generalized/Periumbilical Gastroenteritis Obstipation SBO Large bowel obstruction (LBO) Mesenteric ischemia Peritonitis Abdominal aortic dissection Sickle cell crisis CHRONIC/RECURRENT ABDOMINAL PAIN PUD Gastric cancer Cholecystitis Chronic pancreatitis ACUTE DIARRHEA Inflammatory Bacterial Shigella Salmonella typhi Campylobacter Yersinia E coli (EHEC 0157:H7) C difficile Protozoal E histolytica (amebiasis) Strongyloides G2 – Gastroenterology RUQ Hepatitis Bilary colic Acute cholecystits PUD Pyelonephritis RLQ Appendicitis IBD Ureteral stone Salpingitis Ruptured corpus luteum cyst Ovarian tosion Ruptured ectopic Pregnancy LUQ Myocardial infarction (MI) Pancreatitis Splenic infarciton Pyelonephritis Irritable bowel syndrome Endometriosis (IBS) Mittleschmertz Inflammatory bowel disease (IBD) Recurrent bowel obstruction Mesenteric ischemia Non-inflammatory Bacterial Salmonella enteritidis Staph aureus B cereus C perfringens Vibrio cholerae Protozoal Giardia lamblia LLQ IBD Diverticulitis Sigmoid volvulus Ureteral stone Salpingits Ruptured corpus luteum cyst Ruptured ectopic pregnancy Radiculopathy Porphyria Sickle cell anemia Lead poisoning Viral Rotavirus Norwalk Cytomegalovirus (CMV) Drugs Antacids (Magnesium) Antibiotics Laxatives, lactulose Colchicine Toronto Notes - MCCQE 2002 Review Notes DIFFERENTIAL DIAGNOSIS OF COMMON COMPLAINTS CONT Table Differential Diagnosis of Common Presenting Complaints (continued) Symptoms Differential Diagnosis CHRONIC DIARRHEA (a) ORGANIC Inflammatory IBD Ischemic Secretory Cryptosporidiosis Malignancy Villous adenoma Zollinger-Ellison (ZE) Carcinoid VIP secreting tumour of pancreas Diabetes mellitus Steatorrhea Giardia Celiac sprue Chronic pancreatitis Osmotic Drugs Lactose intolerance (b) FUNCTIONAL IBS Anal sphincter dysfunction CONSTIPATION GI IBS Colon cancer Anorectal pathology Mechanical obstruction Systemic Electrolyte (K+, Ca2+) Hypothryroidism Scleroderma + other collagen vascular diseases Neurological diseases (MS, Parkinson’s, etc.) Psych/Social Drugs Voluntary retention Lifestyle Depression DYSPHAGIA GI Esophagitis Stricture Zenker’s diverticulum Transfer dysphagia Diffuse esophageal spasms Achalasia Esophageal cancer Schatzki ring Systemic Scleroderma Myasthenia gravis Other Foreign body External compression Globus hystericus GI BLEEDING UGI = upper GI LGI = lower GI UGI Epistaxis Esophagitis Mallory-weiss tear Esophageal varices Gastritis PUD Esophageal cancer LGI Anal fissure Hemorrhoids Diverticulosis IBD Arteriovenous malformation (AVM) of colon Colon cancer Gastric cancer Aortoenteric fistula Mesenteric ischemia Infectious diarrhea HEARTBURN GI Aerophagia Reflux esophagitis Infectious esophagitis Others Drugs Pregnancy Scleroderma JAUNDICE Unconjugated Hyperbilirubinemia Hemolysis Gilbert’s syndrome Crigler-Najjar syndrome Neonatal jaundice Drugs (e.g rifampin, radiographic contrast agents, chloramphenicol) NAUSEA/VOMITTING Presenting Symptoms Inferior MI Diabetic ketoacidosis (DKA) Hepatitis Adrenal insufficiency Uremia Pregnancy Psychogenic Drugs Toronto Notes - MCCQE 2002 Review Notes Conjugated hyperbilirubinemia Familial disorders (Rotor/Dubin-Johnson syndrome) Hepatocellular disease Drugs (oral contraceptive (OCP), chlorpromazine) Primary biliary cirrhosis (PBC) Sepsis Post-operative Gallstones Biliary stricture Infection Malgnancy (cholangiocarcinoma, pancreatic cancer, lymphoma) Sclerosing cholangitis Inflammation (e.g pancreatitis) With Abdominal Pain Viral gastroenteritis Food poisoning PUD Pancreatitis Cholecystitis Appendicitis SBO Peritonitis Pyelonephritis Renal colic With Neurological Signs Migraine H/A Vestibular disturbance Increased intracranial pressure (ICP) Cerebellar hemorrhage Hypercalcemia Autonomic dysfunction Gastroenterology – G3 ESOPHAGUS Anatomy and Physiology ❏ mucosa: stratified squamous epithelium submucosa: connective tissue, lymphocytes, plasma cells, nerve cells muscularis propria: inner circular, outer longitudinal muscle ❏ muscle: upper 1/3 striated muscle, lower 2/3 smooth muscle; innervation: vagus nerve ❏ upper esophageal sphincter (UES) • cricopharyngeus + caudal fibers of inferior pharyngeal constrictor muscle ❏ lower esophageal sphincter (LES) • internal muscles - intrinsic muscle of distal esophagus sling fibers of proximal stomach • external muscles - crural diaphragm • normal resting pressure = 15-30 mm Hg • starts to relax at onset of swallowing • contraction = cholinergic (via vagus nerve) • relaxation = non-adrenergic, non-cholinergic (nitric oxide and VIP) ❏ peristalsis - rhythmic contractions that propel contents onward • neuronal control via brainstem "swallowing center" (cranial nerve nuclei) • primary = induced by swallowing • secondary = induced by esophageal distention (e.g during reflux) • tertiary = spontaneous (abnormal) MAJOR SYMPTOMS OF ESOPHAGEAL DISORDERS DYSPHAGIA Definition ❏ difficulty in swallowing, with a sensation of food “sticking” after swallowing ❏ distinct syndromes: oropharyngeal and esophageal dysphagia ❏ oropharyngeal • inability to transfer food from mouth to esophagus (i.e difficulty in initiating swallowing) • food sticks immediately after swallowing • often associated with coughing, choking, nasal regurgitation +/– dysarthria or nasal speech • neurological • cortical: pseudobulbar palsy (upper motor neuron (UMN) lesion), due to bilateral stroke • bulbar: ischemia (stroke); syringobulbia; tumour (lower motor neuron (LMN) lesion); multiple sclerosis (MS) • peripheral: polio; atrophic lateral sclerosis (ALS) • muscular • muscular dystrophy; polymyositis; myasthenia gravis • cricopharyngeal incoordination (failure of UES to relax with swallowing), sometimes seen with gastroesophageal reflux disease (GERD) • structural • Zenker's diverticulum (pharyngeal diverticulum formed when cricopharyngeal muscle fails to relax) • extrinsic compression (thyromegaly, cervical spur) • surgical resection of oropharynx • neoplasms ❏ esophageal (see Figure 1) • inability to move food down the esophagus • dysphagia occurs several seconds after initiating swallowing ESOPHAGEAL DYSPHAGIA Solid Food Only Solid or Liquid Food Mechanical Obstruction Neuromuscular Disorder Intermittent Progressive Heartburn Lower Esophageal Ring/Web Peptic Stricture Intermittent Age > 50 Carcinoma Diffuse Esophageal Spasm (DES) Progressive Reflux Symptoms Respiratory Symptoms Scleroderma Achalasia Figure Approach to Esophageal Dysphagia G4 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes ESOPHAGUS CONT HEARTBURN (Pyrosis) (see GERD section) ❏ most common complaint CHEST PAIN ❏ may be indistinguishable from angina pectoris, but not predictably elicited by exertion, and often occurs spontaneously ❏ most common esophageal cause of chest pain is GERD ODYNOPHAGIA ❏ pain on swallowing ❏ causes – usually due to ulceration of esophageal mucosa • infection - Candida, Herpes, CMV (common only in immunosuppressed, especially AIDS) • inflammation/ulceration (ex caustic damage) • drugs: doxycycline, wax-matrix potassium chloride, quinidine, iron, vitamin C, various antibiotics • radiation GASTROESOPHAGEAL REFLUX DISEASE (GERD) Definition ❏ reflux of stomach/duodenal contents severe enough to produce symptoms and/or complications; the most common condition affecting the esophagus Etiology ❏ LES relaxes inappropriately( most common) ❏ low basal LES tone ❏ hypersecretion of gastric acid ❏ delayed esophageal clearance ❏ delayed gastric emptying from any cause ❏ often associated with sliding hiatus hernia (see General Surgery Chapter) Signs and Symptoms acid regurgitation (bitter taste) waterbrash (sudden hypersalivation) heartburn (retrosternal burning radiating to mouth) non-specific chest pain dysphagia (abnormal motility or esophagitis, reflux-induced stricture) pharyngitis, laryngitis (with hoarseness) respiratory (chronic cough, asthma, aspiration pneumonia, wheezing) symptoms aggravated by • position (lying or bending) • increase in intra-abdominal pressure (pregnancy or lifting) • agents that decrease LES pressure (caffeine, fatty foods, alcohol, peppermint, cigarettes, nitrates, beta-adrenergic agonists, calcium channel blockers (CCB’s), theophylline, benzodiazepines, anticholinergics, morphine) • foods that delay gastric emptying (alcohol, coffee, chocolate) ❏ ❏ ❏ ❏ ❏ ❏ ❏ ❏ Investigations ❏ depends on questions being asked ❏ is reflux present? • 24-hour pH monitoring ❏ has relux damaged the esophagus? • endoscopy ❏ is relux causing the symptoms? • acid perfusion (Berstein) test ❏ is stricture present • barium swallow Management ❏ see Figure Complications ❏ acid regurgitation ––> esophageal inflammation, ulceration and bleeding ––> muscle spasm (DES) and/or stricture (scarring) ––> increased risk of Barrett's esophagus (columnar metaplasia) ––> increased risk of adenocarcinoma Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G5 ESOPHAGUS CONT GERD Symptoms Typical Atypical chest pain Red flag symptoms (e.g pharyngitis, laryngitis) Phase I Lifestyle modifications (LM) • elevate head of bed • partition meals into small portions • diet modification (avoid foods that aggravate symptoms) Over the counter products (OTC) • antacids, alginic acid (Gaviscon) Endoscopy and/or motility study Esophagitis No Response Response Phase II • continue LM, OTC • standard doses of H2 receptor antagonists or prokinetics (domperidone) • proton pump inhibitor (PPI) (omeprazole) if above therapy tried previously • continue LM, OTC No response in to weeks Response Normal • 24 hour pH monitoring • esophageal motility • look for other disease Endoscopy • contine LM, OTC • discontinue Phase II meds • restart as needed Erosive esophagitis with complications Normal Phase III • maintenance therapy with PPI for to months high dose PPI or H2 antagonist • if fail, then anti-reflux surgery (see General Surgery Chapter) • Nissen fundlopication (see General Surgery Chapter) • look for other conditions • establish symptoms due to GERD • continue LM, OTC and try PPI Figure The Three-Phase Management of GERD G6 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes ESOPHAGUS CONT ESOPHAGEAL MOTOR DISORDERS Symptoms ❏ dysphagia with solids and liquids ❏ chest pain Diagnosis ❏ esophageal motility study (see Figure 3) ACHALASIA Mechanism ❏ incomplete relaxation of LES with swallowing: most important ❏ high LES resting pressure (> 30 mm Hg) Pathogenesis ❏ unknown: thought to be abnormal inhibitory effect, possibly due to decreased release of nitric oxide Etiology ❏ idiopathic: most often ❏ secondary to cancer (esophagus, stomach, elsewhere) ❏ Chagas disease Diagnosis ❏ chest x-ray - absent air in the stomach, with a dilated fluid filled esophagus ❏ barium studies - prominent esophagus terminating in narrowing at the sphincter, giving a “bird’s beak” appearance ❏ endoscopic examination to exclude cancer, etc ❏ esophageal motility study required for definitive diagnosis Treatment ❏ dilatation of LES with balloon • > 50% good response and can repeat 1-3 times • 5% risk of perforation • may need lifelong GERD prophylaxis ❏ surgery (Heller myotomy) if refractive to above treatment Complications ❏ respiratory - aspiration pneumonia, bronchiectasis, lung abscesses ❏ gastrointestinal - malnutrition, increased risk of esophageal cancer DIFFUSE ESOPHAGEAL SPASM (DES) Definition ❏ normal peristalsis interspersed with frequent spontaneous abnormal waves which are high pressure, non peristaltic and repetitive Etiology ❏ unknown Diagnosis ❏ barium x-ray: corkscrew pattern, tertiary waves Treatment ❏ reassurance ❏ medical - nitrates, CCB’s, anticholinergics ❏ surgery (long esophageal myotomy) if unresponsive to above treatment SCLERODERMA Pathophysiology ❏ damage to small blood vessels ––> intramural neuronal dysfunction ––> progressive weakening of muscles in distal 2/3 of esophagus ––> aperistalsis and loss of LES tone ––> reflux ––> stricture ––> dysphagia Treatment ❏ aggressive GERD prophylaxis ❏ anti-reflux surgery (gastroplasty included) only as a last resort since it carries significant morbidity Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G7 ESOPHAGUS CONT Figure Manometry Tracings for Esophageal Motor Disorders ESOPHAGEAL STRUCTURAL DISORDERS DIVERTICULA Definition ❏ outpouchings of one or more layers of pharyngeal or esophageal wall ❏ commonly associated with motility disorders ❏ pulsion type: associated with high intraluminal pressures or mural muscular defect ❏ traction type: esophageal wall pulled outward by inflamed and peribronchial mediastinal lymph nodes - not clinically significant ❏ classified according to location Diagnosis ❏ barium swallow ❏ manometric studies (pulsion diverticulum) ❏ esophagoscopy - commonest cause of esophageal perforation Types ❏ pharyngoesophageal (Zenker's) diverticulum • most frequent • posterior pharyngeal outpouching most often on the left side, above cricopharyngeal muscle and below the inferior pharyngeal constrictor muscle • symptoms: dysphagia, regurgitation of undigested food, halitosis • treatment: myotomy of cricopharyngeal muscle +/– excise or suspend sac ❏ mid-esophageal diverticulum • secondary to mediastinal inflammation (traction type) or motor disorders • usually asymptomatic - no treatment required ❏ epiphrenic diverticulum • distal esophagus, large, associated with motility disturbances (pulsion type) • symptoms: asymptomatic or dysphagia, regurgitation, retrosternal pain, intermittent vomiting • complications: esophagitis, periesophagitis, hemorrhage secondary to ulceration • treatment • minor symptoms - no surgery • severe symptoms - diverticulotomy and anti-reflux operation (Nissen, Belsey) • 80-90% success rate BENIGN STRICTURE ❏ presents as progressive dysphagia in face of reflux symptoms ❏ diagnose with barium study or endoscopy ❏ treatment • dilation and reflux medication • anti-reflux surgery if above unsuccessful ESOPHAGEAL CANCER (see General Surgery Chapter) RINGS AND WEBS ❏ ring = circumferential narrowing (lower esophagus) vs web = partial occlusion (upper esophagus) Signs and Symptoms ❏ asymptomatic unless lumen diameter < 12 mm ❏ dysphagia occurs with large food bolus only ❏ Plummer-Vinson or Patterson-Kelly Syndrome • upper esophageal web with iron deficiency (+ cheilosis, koilonychia) • usually in middle aged females (> 40 years) • increased risk of hypopharyngeal carcinoma ❏ Schatzki Ring • mucosal ring at squamo-columnar junction above a hiatus hernia • causes intermittent dysphagia for solids • treatment involves shattering ring with bougie or use of peroral dilators G8 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes ESOPHAGUS CONT BARRETT'S ESOPHAGUS Definition ❏ metaplasia of normal squamous epithelium to columnar epithelium Etiology ❏ usually acquired (GERD, stricture) Pathophysiology ❏ endoscopy shows erythematous epithelium in distal esophagus Management ❏ aggressive anti-reflux regimen and if history shows intestinal metaplasia, endoscopic surveillance every 18-24 months for dysplasia/cancer Complications ❏ 50-fold increase in developing adenocarcinoma INFECTIOUS ESOPHAGITIS Definition ❏ severe mucosal inflammation and ulceration due to virus or fungus ❏ seen in diabetes, malignancy, and immunocompromised patients Symptoms ❏ odynophagia, dysphagia ❏ diagnosis: endoscopic visualization and biopsy Treatment ❏ Candida (see Colour Atlas G13) (most common): nystatin swish and swallow, ketoconazole, fluconazole ❏ Herpes (second most common): often self-limiting, acyclovir ❏ CMV: IV gancyclovir STOMACH AND DUODENUM Stomach Physiology ❏ parietal cells secrete hydrochloric acid (HCI) ❏ chief cells secrete pepsinogen ❏ acetylcholine (ACh), gastrin, and histamine modulate secretion of hydrochloric acid and pepsinogen • ACh - released by vagal nerve terminals in stomach in response to sensory stimuli and stretch reflexes in stomach • gastrin - released by G cells in gastric antrum in response to presence of food in stomach • histamine - released by mast cells in gastric wall ❏ superficial epithelial cells secrete mucus and bicarbonate (HCO3–, which protect underlying gastric mucosa from damage by HCl– and pepsin GASTRITIS Definition ❏ inflammation of the stomach diagnosed by histology ❏ acute gastritis - self-limiting syndrome caused by irritation of gastric mucosa by alcohol, corrosives, food poisoning, etc ❏ chronic gastritis - characterized by mononuclear and PMN cell infiltration of mucosa, glandular atrophy, and intestinal metaplasia; diagnosed on gastric biopsy Etiology ❏ the most common and important causes are: • infection with Helicobacter pylori • ingestion of NSAIDS • stress-related mucosal changes ❏ other causes of gastritis • atrophic gastritis • lymphocytic gastritis • eosinophilic gastritis ❏ other infections: TB, syphilis, CMV, fungal and parasitic infections ❏ systemic diseases: Sarcoid, Crohn's disease Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G9 STOMACH AND DUODENUM CONT Signs and Symptoms ❏ erosive: bleeding ❏ non-erosive: asymptomatic; rarely presents with upper GI symptoms PEPTIC ULCER DISEASE (PUD) Definition ❏ erosion - superficial to the muscularis mucosa, thus no scarring ❏ ulcer - penetrates the muscularis mucosa and can result in scarring Etiology (see Table 2) ❏ most common: Helicobacter pylori and NSAIDs ❏ others: Zollinger-Ellison (ZE), idiopathic, physiological stress, CMV, ischemic Clinical Pearl ❏ Must always biopsy gastric ulcer to rule our cancer, but duodenal ulcers are almost never malignant Table Etiology of Peptic Ulcer Disease Duodenal Gastric 90% 7% < 3% < 1% 60% 35% < 5% < 1% H pylori NSAIDs Stress-induced Zollinger-Ellison (ZE) syndrome HELICOBACTER PYLORI - INDUCED ULCERATION H Pylori ❏ common infection (20-40% of Canadians, prevalence increases with age) ❏ gram-negative rod ❏ lies on the mucus layer adjacent to epithelial cell surface; does not invade ❏ primarily resides in stomach, especially antrum ❏ present in • 90% of duodenal ulcers • 60% of gastric ulcers • 50% of non-ulcerative dyspepsia ❏ high prevalence in • developing countries (crowding) • low socioeconomic status (poor sanitation) ❏ infection most commonly acquired in childhood, presumably by fecal-oral route Table Diagnosis of H pylori Test Sensitivity Specificity Cost Non Invasive: Urea breath test 90-100% 89-100% $$ Serology 88-99% 89-95% $ -but remains positive for variable period (approximately 12 months) after treatment Invasive Endoscopy (OGD): Histology 93-99% 95-99% $$$ - gold standard Microbiology culture 80% 95% $$$ Rapid urease test 89-98% 93-98% $$ - rapid Pathogenesis of H Pylori-Induced PUD ❏ old rule: “no acid, no ulcer” still holds on most (but not all) occasions ❏ acid secreted by parietal cell (stimulated by vagal acetylcholine, gastrin, histamine) necessary for most ulcers ❏ mucosal defenses moderated by PGF2 and blood flow, mucus, etc ❏ two theories of how H pylori causes ulcer • H pylori produces toxins, which cause gastric mucosal inflammation and necrosis • H pylori blocks gastrin G cells in antrum from sensing luminal acid ––> increase serum gastrin ––> increase gastric acid ––> ulcer Clinical Associations of PUD ❏ cigarette smoking: increased risk of ulcer, risk of complications, chance of death from ulcer and impairs healing rate G10 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes LIVER CONT CIRRHOSIS Definition ❏ diffuse fibrosis plus hepatocellular nodular regeneration ❏ irreversible, although colchicine may be of some benefit Etiology ❏ alcohol (85%) ❏ viral (B, B+D, C but not A nor E) ❏ autoimmune ❏ genetic • Wilson’s disease • hemochromatosis • glycogen storage diseases • galactosemia • Gaucher’s disease • α-1-antitrypsin deficiency ❏ drugs and toxins • methyldopa, INH, MTX, OCP ❏ biliary cirrhosis • primary • secondary ❏ chronic hepatic congestion • cardiac cirrhosis (chronic right heart failure, constrictive pericarditis) • hepatic vein thrombosis (Budd-Chiari) ❏ idiopathic Management ❏ treat underlying disorder ❏ alcohol cessation ❏ follow patient for complications (see below) ❏ prognostic factors include • nutrition (EtOH consumption) • ascites • encephalopathy • labs: albumin, INR, bilirubin ❏ liver transplantation for end-stage disease Table 12 Clinical Features of Liver Disease Hepatocellular Dysfunction Portal Hypertension Constitutional Symptoms Anorexia Fatigue Fever / chills Muscle and Skin Jaundice Bruising (petechiae, ecchymosis) Muscle wasting Xanthomas and xanthelasmas Head and Neck Parotid hypertrophy Chest Spider nevi (distribution of superior vena clava (SVC)) Gynecomastia Pectoral alopecia Abdomen Hepatomegaly (RUQ pain) Ascites Genitals Testicular atrophy Altered hair distribution Extremities Palmar erythema Ankle edema Pale nails Clubbing Dupuytren’s contracture G38 – Gastroenterology Hepatic encephalopathy (fetor hepaticus) Splenomegaly Ascites Varices Caput medusae Asterixis Ankle edema Toronto Notes - MCCQE 2002 Review Notes LIVER CONT HEPATIC ENCEPHALOPATHY Definition ❏ acute neuropsychiatric syndrome secondary to liver disease • distinguish from non-liver-related neuropsychiatric disease in a patient with liver problems (e.g alcohol withdrawal or intoxication, sedatives, subdural hematoma, metabolic encephalopathy) Mechanism ❏ porto-systemic shunt around hepatocytes ––> toxins (believed to be ammonia from gut, mercaptans, fatty acids, amino acids) affect brain Table 13 Hepatic Failure vs Hepatic Encephalopathy Fulminant Hepatic Failure Portosystemic Encephalopathy Symptoms at Onset Agitation, delirium Somnolence Precipitating Factors Rarely found Commonly found Pathology Cerebral edema Astroglial cell proliferation Prognosis Usually death Usually responds to treatment Diagnosis ❏ chiefly clinical, supported by laboratory findings, exclusion of other neuropsychiatric diseases ❏ only pathognomonic finding is fetor hepaticus (musty odor of breath due to sulphur-containing comounds) ❏ asterixis (also seen in renal failure, respiratory failure, drug overdose, hypoglycemia) ❏ characteristic EEG findings: diffuse (non-focal), slow, high amplitude waves Precipitating Factors ❏ nitrogen load (GI bleed, protein load from food intake, renal failure, constipation) ❏ drugs (narcotics + CNS depressants) ❏ electrolyte imbalance (hypokalemia, alkalosis, hypoxia, hypovolemia) ❏ infection ❏ deterioration in hepatic function or superimposed liver disease Management ❏ treat underlying liver disease and precipitating factors ❏ decrease generation of nitrogenous compounds • decreased dietary protein to 50g/day; vegetable protein is better tolerated than animal protein • lactulose • prevents diffusion of NH3 (amononia) from the colon into blood by lowering pH and forming non-diffusible NH4+ (ammonium) • serves as a substrate for incorporation of ammonia by bacteria, promotes growth in bowel lumen of bacteria which produce minimal ammonia • also acts as a laxative • if inadequate response with lactulose, may try antibiotics • broad-spectrum antibiotics (tetracycline, metronidazole, neomycin) eliminate ammonia-producing bacteria from bowel lumen • neomycin is less effective than lactulose plus more side effects (ototoxicity, nephrotoxicity) • combination of the two may be more effective PORTAL HYPERTENSION Pathophysiology ❏ pressure = flow x resistance ❏ unlikely that increased flow alone can cause portal hypertension (can occur in AV-fistulae or massive splenomegaly) ❏ sites of increased resistance • pre-sinusoidal (e.g portal vein thrombosis, Schistosomiasis, sarcoidosis) • sinusoidal (e.g cirrhosis, alcoholic hepatitis) • post-sinusoidal (e.g right-sided heart failure, hepatic vein thrombosis, veno-occlusive disease, constrictive pericarditis) ❏ signs of portal hypertension - see Table 12 ❏ management (see General Surgery Chapter) • ß-blockers (propanolol, nadolol) and nitrates • decreased risk of bleeding from varices Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G39 LIVER CONT ASCITES Definition ❏ accumulation of excess free fluid in the peritoneal cavity Etiology ❏ see Table 14 Table 14 Serum-Ascites Albumin Ratio as an Indicator of the Causes of Ascites serum [alb] – ascitic [alb] > 11 g/L serum [alb] – ascitic [alb] < 11 g/L Cirrhosis/severe hepatitis Chronic hepatic congestion (right heart failure, Budd-Chiari) Nephrotic syndrome Massive liver metastases Myxedema Peritoneal carcinomatosis TB Pancreatic disease Pathogenesis of Ascites in Cirrhosis ❏ underfill theory • portal hypertension and hypoalbuminemia lead to transudation of Na+ and water into peritoneum • causes decreased intravascular volume and secondary renal Na+ and water retention ❏ overflow theory • liver disease primarily causes renal retention of Na+ and water which then "overflows" into peritoneal cavity ❏ combined theory • liver disease causes vasodilation • decreased effective intravascular volume (i.e volume to capacitance ratio low, but absolute volume is high) • secondary urinary Na+ and water retention Diagnosis ❏ ultrasound is gold standard ❏ clinically detectable when > 500 mL (bulging flanks, shifting dullness, fluid wave) ❏ diagnostic paracentesis - send ascitic fluid for: • • • • cells and differential chemistry (albumin, protein, amylase, triglycerides) culture and sensitivity and gram stain cytology for malignancy Treatment ❏ paracentesis safe (except large volumes) ❏ medical • Na+ restriction • diuretics (spironolactone, furosemide) • aim for 0.5 kg loss per day (rate of ascitic fluid absorption) ❏ surgical • peritoneal-systemic (LeVeen) shunts, TIPSS, liver transplantation • reserved for medically unresponsive cases Complication - Bacterial Peritonitis ❏ primary/spontaneous bacterial peritonitis (SBP) • complicates ascites, does not cause it (occurs in 10% of cirrhotic ascites) • 1/3 of patients are asymptomatic, thus not hesitate to a diagnostic paracentesis • fever, chills, abdominal pain, ileus, hypotension, worsening encephalopathy • gram negatives compose 70% of bugs - E coli (most common pathogen), Strep., Klebsiella ❏ secondary bacterial peritonitis • usually results from perforated viscus or surgical manipulation ❏ diagnosis: absolute neutrophil count in peritoneal fluid > 0.25x109 cells/L or WBC count > 0.5x109 cells/L + positive culture ❏ gram stain is positive in only 10-50% of patients ❏ treatment • IV antibiotics (cefotaxime is the treatment of choice until C&S is available) for 10-14 days • prophylaxis with daily Norfloxacin or TMP-SMX for 5/7 days may decrease the frequency of recurrent SBP G40 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes LIVER CONT RENAL FAILURE IN CIRRHOSIS ❏ classify as ❏ ❏ ❏ ❏ • pre-renal • acute tubular necrosis (ATN) • hepatorenal syndrome hepatorenal syndrome is secondary to • overaggressive diuresis or large volume paracentesis • GI bleeding • sepsis differentiate hepatorenal syndrome from pre-renal failure • clinical (very difficult) • intravenous fluid challenge (giving volume expanders improves prerenal failure) • pulmonary capillary wedge measurements (PCWP) (preferable) differentiate hepatorenal syndrome from ATN (see Table 15) treatment for hepatorenal syndrome is generally unsuccessful • vasopressin, octreotide, or norepinepherine may help (increased renal blood flow by increased systemic vascular resistance) • definitive treatment is liver transplant Table 15 Differential Diagnosis of Acute Azotemia in Liver Disease Laboratory Findings Prerenal Azotemia or Hepatorenal Syndrome Acute Renal Failure (ATN) Urine [Na+] (mEq/L) < 10 > 30 Urine:plasma creatinine ratio > 30:1 < 20:1 Urine Osmolality At least 100 mOsm greater than plasma osmolality Equal to plasma osmolality Urine Sediment Normal Casts and cellular debris HEPATOPULMONARY SYNDROME ❏ intrapulmonary vasodilation leading to hypoxia from ventilation/perfusion (V/Q) abnormalities ❏ improves with supplemental oxygen ❏ no proven medical therapy HAEMATOLOGIC CHANGES IN CIRRHOSIS ❏ pancytopenia from hypersplenism ❏ decreased clotting factors • fibrin, thrombin, I, II, V, VII, IX, X BILIARY TRACT JAUNDICE (see Table 16 and Figure 11) ❏ definition • yellow pigmentation of skin, sclerae and mucus membranes due to increased serum bilirubin ❏ history • dark urine, pale stools • pruritis • symptoms of biliary colic (obstructive jaundice) • history of drug and EtOH use, hepatitis • travel history • sexual history • family history ❏ physical exam • may be unremarkable ❏ investigations • bilirubin (conjugated and unconjugated) • AST, ALT, GGT, ALP • serologic tests for hepatitis • ultrasound for evidence of obstructive jaundice, CT • direct duct visualization (ERCP, PTC) (note: PTC only if obstruction is suspected to be periportal rather than near sphincter or if previous gastric surgery) • liver biopsy Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G41 BILIARY TRACT CONT Table 16 Classification of Jaundice I Predominantly Unconjugated Hyperbilirubinemia Overproduction • Hemolysis (spherocytosis, autoimmune disorders) • Ineffective erythropoiesis (megaloblastic anemias) Decreased hepatic uptake • Gilbert’s syndrome • Drugs (e.g rifampin, radiographic contrast agents) Decreased conjugation • Hepatocellular disease • Drug inhibition (e.g chloramphenicol) • Crigler-Najjar syndromes type I and II • Neonatal jaundice • Gilbert’s syndrome II Predominantly Conjugated Hyperbilirubinemia Impaired hepatic secretion • Familial disorders (e.g Rotor syndrome, Dubin-Johnson syndrome, cholestasis of pregnancy) • Hepatocellular disease • Drug-induced cholestasis (e.g oral contraceptives, chlorpromazine) • Primary biliary cirrhosis (PBC) • Sepsis • Post-operative Extrahepatic biliary obstruction • Intraductal obstruction • Gallstones • Biliary stricture • Infection • Malignancy (cholangiocarcinoma) • Sclerosing cholangitis • Extraductal obstruction • Malignancy (e.g pancreatic cancer, lymphoma) • Inflammation (e.g pancreatitis) Jaundice serum bilirubin incresed unconjugated bilirubin hemolytic anemia Gilbert’s syndrome drugs incresed conjugated bilirubin • history, physical exam, ALT, AST, ASP • ALT, AST, ALP suspect hepatocellular disease • incresed AST, ALT ultrasound normal suspect extra-hepatic (biliary) obstruction • age > 50 • previous biliary surgery • abdominal pain, mass, high fever • ALP incresed relatively > AST, ALT biliary obstruction ERCP • further investigations for incresed liver enzymes • consider D/C meds • consider liver biopsy Figure 11 Approach to Jaundice G42 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes BILIARY TRACT CONT GILBERT’S SYNDROME Defintion ❏ mild decrease in glucuronyl transferase activity leading to defective conjugation of bilirubin Etiology/Epidemiology ❏ some patients have decreased hepatobiliary uptake ❏ affects 7% of population, especially males ❏ autosomal dominant Signs and Symptoms ❏ presents in teens-20s, often as an incidental lab finding ❏ only manifestation is intermittent jaundice with increased serum unconjugated bilirubin developing most characteristically while fasting ❏ no treatment indicated (entirely benign) PRIMARY BILIARY CIRRHOSIS (PBC) Definition ❏ chronic inflammation and fibrous obliteration of intrahepatic bile ductules Etiology/Epidemiology ❏ probably autoimmune (associated with RA, thyroiditis, CREST syndrome, vasculitis) (see Rheumatology Chapter) ❏ affects mainly middle-aged women (male:female ratio of 1:9) Signs and Symptoms ❏ often asymptomatic ❏ earliest symptoms: pruritis, fatigue ❏ after several months-years: jaundice and melanosis (darkening skin) and other signs of cholestasis ❏ eventually: hepatocellular failure, portal hypertension, ascites ❏ physical examination • hepatomegaly with smooth surface in early stages, later on becomes nodular and cirrhotic • hypersplenism in late stages • xanthelasmas, xanthomas Investigations ❏ increased ALP, GGT ❏ + anti-mitochondrial antibodies (98% specificity) ❏ increased cholesterol ––> xanthelasmas, xanthomas (mild increase in LDL, larger increase in HDL) ❏ increased IgM ❏ diagnosis based on liver biopsy and normal ERCP (i.e rule out common bile duct (CBD) stones (see Colour Atlas G8) and sclerosing cholangitis) Clinical Course ❏ ultimately fatal although not all asymptomatic patients progress Management ❏ may treat with ursodiol, colchicine, methotrexate, cyclosporine, cholestyramine (for pruritis and hypercholesterolemia), parenteral fat soluble vitamins, Vitamin D/Ca2+ supplements ❏ only proven treatment is transplant Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G43 BILIARY TRACT CONT SECONDARY BILIARY CIRRHOSIS Definition ❏ results from prolonged partial or total obstruction of major bile ducts Etiology ❏ acquired: post-op strictures, gallstones, chronic pancreatitis, sclerosing cholangitis ❏ congenital: cystic fibrosis (CF), congenital biliary atresia, choledochal cysts Clinical Features ❏ like primary, ± fever (bouts of cholangitis), ± RUQ pain (biliary colic) ❏ portal hypertension only in advanced cases Diagnosis ❏ cholangiography Treatment ❏ release obstruction ❏ if contraindicated, give antibiotics for cholangitis prophylaxis SCLEROSING CHOLANGITIS Definition ❏ inflammation of entire biliary tree (intra and extrahepatic bile ducts) leading to scarring and obliteration Etiology ❏ primary/idiopathic • most common • associated with ulcerative colitis in up to 70% (usually male); associated with AIDS • one of the most common indications for transplant ❏ secondary • long-term choledocholithiasis • cholangiocarcinoma • surgical/traumatic injury (iatrogenic) • contiguous inflammatory process • post ERCP Signs and Symptoms ❏ often insidious, may present with fatigue and pruritis ❏ Charcot's Triad: RUQ pain, jaundice, fever/chills ❏ Reynold's Pentad: Charcot’s Triad plus hypotension and delirium (more severe) Diagnosis ❏ increased ALP, bilirubin ❏ minor increase in AST ❏ ERCP shows narrowing of bile ducts, both intrahepatic and extrahepatic bile ducts Treatment ❏ prophylactic antibiotics for bacterial cholangitis ❏ endoscopic sphincterotomy, biliary stent ❏ suppurative cholangitis requires emergency drainage of pus in CBD ❏ surgical stent or biliary-enteric anastomosis ❏ liver transplantation appears the best treatment for advanced sclerosing cholangitis (nearly 90% survive year; mean follow-up from time of diagnosis to need for transplant is years) Complications ❏ repeated bouts of cholangitis may lead to complete biliary obstruction with resultant secondary biliary cirrhosis and hepatic failure Prognosis ❏ unfavorable regardless of treatment ❏ mean survival after diagnosis remains 4-10 years ❏ 10-15% develop cholangiocarcinoma G44 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes PANCREAS ❏ physiology • acid in duodenum ––> secretin ––> water and bicarbonate from ductular cells • fat and protein in duodenum ––> CCK ––> enzymes from acinar cells (lipase, proteases) • secretin test • measure volume, HCO3 and enzymes in pancreatic juice in response to IV injection of secretin • gold standard to diagnose chronic pancreatic insufficiency, but rarely done as it is time-consuming ❏ causes of increased serum amylase • pancreatic disease • acute pancreatitis, chronic pancreatitis with ductal obstruction, pseudocyst, abscess, ascites, trauma, cancer • non-pancreatic abdominal disease • biliary tract disease, bowel obstruction/ischemia, perforated or penetrating ulcer, ruptured ectopic pregnancy, aneurysm, chronic liver disease, peritonitis • non-abdominal disease • cancer (lung, esophagus, etc.), salivary gland lesions, bulimia, renal transplant/insufficiency, burns, ketoacidosis • macroamylasemia • when serum amylase > times normal, the cause is almost always pancreatitis or renal disease ACUTE PANCREATITIS Etiology (mnemonic: GET MASHED) Gallstones (45%) Ethanol (35%) Tumours: pancreas, ampulla, choledochocele Microbiological • bacterial: mycoplasma, Campylobacter, TB, MAI, legionella, leptospirosis • viral: mumps, rubella, varicella, viral hepatitis, CMV, EBV, HIV, Coxsackievirus, echo virus, adenovirus • parasites: Ascariasis, Clonorchiasis, Echinococcosis Autoimmune: SLE, polyarteritis nodosa (PAN), Crohn’s Surgery/trauma • manipulation of sphincter of Oddi (e.g ERCP), post-cardiac surgery, blunt trauma to abdomen, penetrating peptic ulcer Hyperlipidemia (TG >11.3 mmol/L), hypercalcemia, hypothermia Emboli or ischemia Drugs/toxins: azathioprine, mercaptopurine, ddI, furosemide, estrogens, methyldopa, H2 blockers, valproic acid, antibiotics, acetaminophen, salicylates, ethanol, methanol, organophosphates Idiopathic: 3rd most common - thought to be hypertensive sphincter or microlithiasis Pathology ❏ mild • peripancreatic fat necrosis • interstitial edema ❏ severe • extensive peripancreatic and intrapancreatic fat necrosis • parenchymal necrosis and hemorrhage ––> infection in 60% • release of toxic factors into systemic circulation and peritoneal space ❏ severity of clinical features may not always correlate with pathology Signs and Symptoms ❏ clinical: patient can look well or pre-morbid • pain: epigastric, noncolicky, constant, can radiate to back, may improve when leaning forward (Inglefinger's sign); tender rigid abdomen; guarding • nausea and vomiting • abdominal distension from paralytic ileus • fever: chemical, not due to infection • jaundice: compression or obstruction of bile duct • tetany: transient hypocalcemia • hypovolemic shock: can lead to renal failure • adult respiratory distress syndrome • breakdown of phospholipase A2 • coma Investigations ❏ labs • increased pancreatic enzymes in blood • increased amylase: sensitive but not specific • increased lipase: higher sensitivity and specificity and stays elevated longer • increased WBC Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G45 PANCREAS CONT ❏ imaging (see Colour Atlas G7) • x-ray: “sentinel loop” (dilated proximal jejunem), calcification and “colon cut-off sign” (colonic spasm) • U/S: best for evaluating biliary tree (67% sensitivity, 100% specifity) • CT scan with IV contrast: useful prognostic indicator because contrast seen only in viable pancreatic tissue Non-viable areas can be biopsied percutaneously to diagnose infected pancreatic necrosis • ERCP + manometry: if no cause found Prognosis ❏ usually a benign, self-limiting course, single or recurrent ❏ occasionally severe leading to • shock • pulmonary edema • pancreatic abscess • coagulopathy • hyperglycemia and hypoglycemia • GI ulceration due to stress • death ❏ functional restitution to normal occurs if primary cause and complications are eliminated (exception: alcohol) ❏ occasional scarring and persistent pseudocysts ❏ rarely leads to chronic pancreatitis Severity ❏ not proportional to the level of amylase ❏ Ranson's Criteria - pancreatitis not due to gallstones (criteria slightly different for gallstone-induced pancreatitis) • at admission (mnemonic: GA LAW) • G - blood glucose > 11 mmol/L (with no history of hyperglycemia) • A - age > 55 • L - serum LDH > 350 IU/L • A - AST > 250 IU/L • W - WBC > 16 x 109/L • during first 48 hours (mnemonic: CHOBBS) • C - serum calcium < mmol/L • H - hematocrit drop > 10% • O - arterial PO2 < 60 mm Hg • B - base deficit > mmol/L • B - BUN rise > 1.8 mmol/L • S - estimated fluid sequestration > L ❏ difficult course if 2+ present ❏ high mortality if 3+ present ❏ after CT + contrast: % of pancreas not taking up dye is a valuable indicator of extent of necrosis and prognosis DDx ❏ perforated peptic ulcer ❏ biliary colic ❏ acute cholangitis, acute cholecystitis ❏ fatty infiltration of the liver (alcohol) ❏ small bowel obstruction (SBO) ❏ mesenteric infarction ❏ dissecting aneurysm ❏ nephrolithiasis ❏ acute coronary occlusion Management of Acute Pancreatitis ❏ goals: (1) hemodynamic stability (2) alleviate pain (3) stop progression of damage (4) treat local and systemic complications ❏ aspirate necrotic areas of pancreas to diagnose infection; drain if infected ❏ IV crystalloid and NG suction (rests pancreas) if stomach dilated or inflammation severe or patient vomiting ❏ analgesics to control pain ❏ nutritional support (IV), NPO ❏ no benefit: glucagon, atropine, trasylol, H2 blockers, peritoneal lavage ❏ follow clinically, and with CT/ultrasound to exclude complications ❏ debride abscesses ❏ drain pseudocysts if large or persisting or infected ❏ embolize hemorrhagic vessels G46 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes PANCREAS CONT Complications ❏ pseudocyst (cyst-like structure encapsulated with fibrous material, not epithelium) ❏ abscess ❏ lungs: pleural effusion, atelectasis, pneumonia, acute respiratory distress syndrome (ARDS) ❏ acute renal failure (ATN) ❏ CVS: pericardial effusion, pericarditis, shock ❏ antibiotics: especially quinolones (e.g ciprofloxacin), imipenen (other antibiotics not penetrate pancreas) may be useful as prophylaxis in severe pancreatitis CHRONIC PANCREATITIS Definition ❏ a continuing inflammatory disease of the pancreas characterized by • irreversible morphological changes • pain (typically) • permanent loss of function (e.g malabsorption syndrome, diabetes) Etiology ❏ nearly always alcoholic • alcohol increases viscosity of pancreatic juice • decreases pancreatic secretion of pancreatic stone protein (lithostatin) which normally solubilizes calcium salts ––> precipitation of calcium within pancreatic duct • result is duct obstruction and subsequent gland destruction ❏ cystic fibrosis (CF) ❏ severe protein-calorie malnutrition ❏ hereditary pancreatitis ❏ primary hyperparathyroidism ❏ hyperlipidemia ❏ idiopathic ❏ never gallstones Pathophysiology ❏ irregular sclerosis ❏ destruction of exocrine parenchyma ❏ varying degrees of ductular dilatation and associated ductal strictures ❏ protein plugs ❏ calcification ❏ edema ❏ focal necrosis ❏ inflammatory cells ❏ cysts and pseudocysts ❏ infection Signs and Symptoms ❏ early stages • recurrent attacks of severe abdominal pain (upper abdomen and back) • chronic painless pancreatitis - 10% ❏ late stages - occurs in 15% of patients • malabsorption syndrome when > 90% of function is lost • diabetes, calcification, jaundice, weight loss, pseudocyst, ascites, GI bleed ❏ laboratory • increase in serum glucose • increase in ALP (portion of common bile duct within pancreas is narrowed by pancreatic inflammation) Investigations ❏ flat plate (looking for pancreatic calcifications) ❏ ultrasound (calcification, dilated pancreatic ducts, pseudocyst) ❏ CT (calcification, dilated pancreatic ducts, pseudocyst) ❏ ERCP (abnormalities of pancreatic ducts-narrowing and dilatation) ❏ p-aminobenzoic acid (PABA) test (exocrine function-reflects duodenal chymotrypsin activity) ❏ 72-hour fecal fat test (exocrine function) ❏ secretin test, CCK test (exocrine function) ❏ fecal enzyme measurement Management ❏ general management • total abstinence from alcohol • enzyme replacement may help pain by resting pancreas via negative feedback • analgesics • celiac ganglion blocks • pain decreases with time as gland burns out ❏ steatorrhea • diet: restricted fat and protein (may also decrease pain) ❏ diabetes • insulin or oral hypoglycemic agents ❏ surgery • pancreatic resection if ductular obstruction (best seen on ERCP) • no surgical procedure can improve pancreatic function Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G47 CLINICAL NUTRITION RECOMMENDED NUTRIENT INTAKE (RNI) ❏ definition • RNI is the minimal intake of a nutrient that will be sufficient to meet the requirements of 97.5% of a healthy population • RNI will vary for different sub-populations, depending on: age, sex, pregnancy, lactation, etc ❏ setting the RNI • assume a normal distribution of nutrient requirements (usually from the experimental studies) • for calorie requirement, RNI = mean population requirement • for others, RNI = mean population requirement + x standard deviation • a correction factor for the average digestibility of the nutrient is also added into the final recommendation CARBOHYDRATES (CHO) Simple Sugars ❏ monosaccharides (glucose, fructose, galactose, etc.) ❏ disaccharides (sucrose, lactose, etc.) Complex Carbohydrates ❏ starch ❏ fiber (indigestible complex carbohydrates) • insoluble fiber acts mainly to increase stool bulk • soluble fiber "flattens" absorption curves for glucose and may reduce cholesterol absorption ❏ recommended intakes: 50+% as CHO (mostly complex CHO) and 32 g/day fiber LIPIDS ❏ note difference between saturated (S) and polyunsaturated (P) ❏ essential fatty acids = linoleic, linolenic, and arachidonic ❏ deficiency leads to abnormal cell membrane and capillary structure, eczematous skin lesions, thrombocytopenia, poor wound healing, and abnormal metabolism of prostaglandins, thromboxanes, and leukotrienes ❏ recommended intakes: < 30% of diet; P/S ratio about 2.0 PROTEIN ❏ essential amino acids: Arginine, Histidine, Isoleucine, Leucine, Threonine, Lysine, Methionine, Phenylalanine, Tryptophan, Valine ❏ mnemonic: Any Help In Learning These Little Molecules Proves Truly Valuable ❏ Arg and His are “semi-essential" amino acids (they can be synthesized by the body, but not fast enough to keep up with the demand) ❏ sources of protein must be mixed to ensure a balanced intake of the essential amino acids ❏ this can be done on a vegetarian diet ❏ recommended intake: about 15% but reduce red meats (high saturated fats and cholesterol) KWASHIORKOR AND MARASMUS ❏ kwashiorkor = syndrome produced by severe protein deficiency In face of adequate total calorie ingestion (usually complex carbohydrates) ❏ marasmus = severe protein and calories deficiency leading to wasting (low weight per height) ❏ response to starvation • first 24 hours: depletion of liver glycogen stores • after 24 hours: skeletal muscle breakdown (mobilize amino acids for gluconeogenesis and protein synthesis in liver) • in critical illness, serum tumour necrosis factor (TNF) is associated with movement of amino acids from periphery (muscle) to viscera (heart, etc.); nutrition is probably unable to prevent this process G48 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes CLINICAL NUTRITION CONT DETERMINATION OF NUTRITIONAL STATUS History ❏ weight gain or loss ❏ diet history; often unreliable, even when "food diaries" are kept ❏ GI functional inquiry (appetite, weight changes, nausea, vomiting, diarrhea, constipation) ❏ global clinical evaluation is shown to be useful Physical Examination ❏ hydration status ❏ weight and height (compare to standard tables) ❏ body mass index (BMI): weight (kg)/height2 (m2) ❏ muscle bulk, including forearm circumference ❏ subcutaneous fat (triceps skinfolds, etc.) ❏ cheilosis, glossitis, jaundice ❏ signs of specific nutrient deficiency Laboratory Investigations ❏ plasma proteins (albumin, pre-albumin, transferrin) • decrease may indicate decreased nutritional status (not very specific) ❏ thyroid-binding pre-albumin, retinol-binding protein • too sensitive ❏ small changes in nutritional status can result in large changes in the following indices • hemoglobin levels • total lymphocyte count • cell-mediated immunity • muscle strength (hand-grip dynanometer; electrical stimulation of adductor pollicis) • INR: a measure of vitamin K status • creatinine-height index, compare to standard tables • other methods are available but mainly for research (underwater weighing, total body water, total body potassium, total body nitrogen, etc.) ENTERAL NUTRITION Diets Taken by Mouth ❏ normal diet ("diet as tolerated" (DAT)) ❏ pureed diet ❏ soft diet: for difficulty chewing ❏ full fluids: inadequate in vitamins and minerals ❏ clear fluids: inadequate in most nutrients, for short-term use (e.g post-operative) Special Diets ❏ stricture diet (low fiber) ❏ post-gastrectomy (anti-dumping) diet • liquids separated from solids ❏ weight-reduction diet ❏ weight-gain diet ❏ diabetic diet: low fat, low simple sugars ❏ diet for IBS: high fiber ❏ low protein diet (renal disease) ❏ low sodium diet: HTN, CHF, liver disease ("healthy heart"), renal failure Approaches ❏ nasogastric (NG), nasoduodenal, or nasojejunal tube ❏ enterostomy feeding (e.g gastrostomy tube) ❏ jejunostomy feeding Indications ❏ oral consumption inadequate or contraindicated ❏ appropriate enteral feeding formula is available Relative Contraindications ❏ vomiting and aspiration ❏ intestinal obstruction ❏ small bowel ileus ❏ enteroenteral or enterocutaneous fistulae ❏ uncontrolled diarrhea ❏ UGI bleeding Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G49 CLINICAL NUTRITION CONT Feed Types for Enteral Nutrition ❏ blenderized ❏ milk-based ❏ semi-elemental (e.g Isocal, Ensure) ❏ elemental: simple sugars or oligosaccharides, amino acids or short peptides, etc (e.g Vital) Advantages ❏ avoids risks of parenteral nutrition ❏ no need for sterilized solutions or tubes ❏ relatively cheap Complications ❏ aspiration ❏ diarrhea Enteral Nutrition: Advantages Over Parenteral Nutrition ❏ fewer serious complications (especially sepsis) ❏ nutritional requirements for enterally administered nutrition better understood ❏ can supply gut-specific fuels such as glutamine and short chain fatty acids ❏ nutrients in the intestinal lumen prevent atrophy of the gut and pancreas ❏ prevents gallstones by stimulating gallbladder motility ❏ less expensive PARENTERAL NUTRITION Approaches ❏ parenteral nutrition to supplement enteral nutrition ❏ total parenteral nutrition (TPN) • when it is the only source of nutrition ❏ long-term TPN ("home TPN") Indications for TPN ❏ not well understood; only situations where TPN has been well shown to increase survival are after BMT and in short bowel syndrome ❏ preoperative: only useful in severely malnourished (i.e lost more than 15% of premorbid weight, serum albumin < 28 g/L) ❏ renal failure: TPN shown increase rate of recovery from acute renal failure, but not increased survival ❏ liver disease: branched chain amino acids may shorten duration of encephalopathy, but not increase survival ❏ IBD: TPN closes fistulae, and heals acute exacerbations of mucosal inflammation, but effect is transient ❏ some evidence for efficacy, but convincing data not available • radiation/chemotherapy-induced enteritis • AIDS • severe acute pancreatitis Indications for routine use of TPN ❏ patients with inability to absorb nutrients via the GI tract • small bowel resection (70% resected) • diseases of the small intestine (e.g scleroderma, SLE, Celiac, pseudo-obstruction, multiple enterocutaneous fistulae and Crohn's disease) not responding to other treatments • radiation enteritis • chronic severe diarrhea (e.g primary GI disease, viral or bacterial enteritis) • intractable and protracted vomiting ❏ patients undergoing high-dose chemotherapy, radiation and bone marrow transplantation with impaired gut function ❏ moderate to severe acute pancreatitis with GI symptoms associated with oral ingestion of food ❏ severe malnutrition in the face of a non-functioning GI tract ❏ severely catabolic patients with or without malnutrition when GI tract is not usable within days; examples include: • > 50% body surface area burn • multisystem trauma • extensive surgery • sepsis • severe inflammatory disease G50 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes CLINICAL NUTRITION CONT Relative Contraindications ❏ functional GI tract for enteral nutrition ❏ active infection; at least until appropriate antibiotic coverage ❏ inadequate venous access; triple-lumen central venous lines usually prevent this problem ❏ unreliable patient or clinical setting TPN Prescription ❏ energy 30 calories/kg ideal weight/day in nonstressed patient increased by 50% in severe illness ❏ optimal ratio of carbohydrate to fat unknown, but usually 30% of energy is given as fat ❏ protein: g/kg/day; increase by 50% in catabolic patients ❏ Na+: 150 mmol/day plus abnormal losses, less if edema, ascites, CHF ❏ K+: 60 mmol/day plus abnormal losses ❏ fluid: 35 ml/kg/day plus abnormal losses Complications of TPN ❏ sepsis: most serious of the common complications ❏ mechanical pneumothorax, etc from insertion of central line catheter migration and thrombosis, air embolus ❏ metabolic: CHF, hyperglycemia, gallstones, cholestasis ❏ TPN burn REFERENCES Esophageal and Gastric Disease Devault, K.R., Castell, D.O.: Guidelines fo the diagnoses and treatment of gastroesophageal reflux disease Arch Intern Med 115:2165-2173, 1995 DiPalma JA Management of severe gastroesophageal reflux disease Journal of Clinical Gastroenterology 32(1): 19 –26, 2001 Wilcox, C.M., Karowe, M.W.: Esophageal infections: etiology, diagnosis, and management Gastroenterology 2:188, 1994 Stomach and Duodenum American Gastroenterological Association Position statement: Evaluation of dyspepsia Gastroenterology 114:579-581, 1998 Howden, C.W., Hunt,R.H.: Guidelines for the management of Helicobacter Pylori infection Am J Gastroenterology 93:2330-2338, 1998 Laine, L., Peterson W.L.: Bleeding peptic ulcer NEJM 331:717-727, 1994 Lanza, F.L.: A guideline fo the treatment and prevention fo NSAID-induced ulcer Am J Gastroenterology 93:2037-2046, 1998 Peek, R.M., Blaser M.J.: Pathophysiology of Helicobacter Pylori-induced gastritis and peptic ulcer disease Am J Med 102:200-207, 1997 Soll AH Practice Parameters: committee of the American College of Gastroenterology:Medical treatment of peptic ulcer disease I 275: 622, 1996 Small and Large Bowel Aranda-Michel, J., Giannella, R Acute Diarrhea: A Practical Review American Journal of Medicine 10(6): 670 – 676, 1999 Donowitz M., Kokke FT., Saidi R Evaluation of Patients with Chronic Diarrhea NEJM 332 (11): 725 – 729, 1995 Ghosh, S., Shand A Ulcerative Colitis BMJ 320 (7242) 1119-1123, 2000 Hanauer SB Drug therapy: Inflammatory Bowel Disease NEJM 334(13): 841-848, 1996 Horwitz, BJ., Fisher RS Current Concepts: The Irritable Bowel Syndrome NEJM 344(24): 1846-1850, 2001 Jennings, JSR., Howdle, PD Celiac Disease Current Opinion in Gastroenterology 17(2): 118 – 126, 2001 Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G51 REFERENCES CONT Liver and Biliary Tract Angulo P Primary biliary cirrhosis and primary sclerosing cholangitis Clinics in Liver Disease 3(3): 529-70, 1999 Cecil Essentials of Medicine 5th edition Andreoli, T., Carpenter, C., Griggs, R and Loscalzo, J eds W.B Saunders Company, Philadelphia, 2001 Custis K Common biliary tract disorders Clin Fam Pract 2(1): 141-154, 2000 Diehl AM Alcoholic liver disease Clinics in Liver Disease 2(1): 103-118, 1998 Malik AH Acute and chronic viral hepatitis Clin Fam Pract 2(1): 35-57, 2000 Reynolds, T Ascites Clinics in Liver Disease 4(1): 151-168, 2000 Sandowski SA Cirrhosis Clin Fam Pract 2(1): 59-77, Mar 2000 Sherman, M Chronic viral hepatitis and chronic liver disease The Canadian Journal of Diagnosis 18(6):81-90, 2001 Sternlieb I Wilson’s disease Clinics in Liver Disease 4(1): 229-239, 2000 Yapp TR Hemochromatosis Clinics in Liver Disease 4(1): 211-228, 2000 Yu AS Management of ascites Clinics in Liver Disease 5(2): 541, 2001 Pancreas Steer, M.L Chronic pancreatitis NEJM 332:1482-1490, 1995 Steinberg, w Acute pancreatitis NEJM 330:1198-1210, 1994 Sternby B et al What is the best biochemical test to diagnose acute pancreatitis? A prospective clinical study Mayo Clin Proc 71: 1138, 1996 Rational Clinical Examination Grover SA, Barkun AN, Sackett DL Does this patient have splenomegaly? JAMA 270(18): 2218-21, 1993 Kitchens JM Does this patient have an alcohol problem? JAMA 272(22): 1782-1787, 1994 Naylor CD Physical exam of the liver JAMA 271 (23): 1859 – 1865, 1994 Williams JW, Simel DL Does this patient have ascites? How to divine fluid in the abdomen JAMA 267 (19): 2645-48, 1992 G52 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes [...]... ––> decrease portal pressure (high incidence of shunt occlusion and hepatic encephalopathy) Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G27 GASTROINTESTINAL BLEEDING CONT MALLORY WEISS TEAR Definition ❏ tear in gastric mucosa on lesser curvature near gastroesophageal junction (20% straddle junction, 5% in distal esophagus) Etiology ❏ due to rapid increases in gastric pressure (i.e... vessel, fibrin clot ❏ H2 antagonists have little impact on rebleeding rates and need for surgery ❏ esophageal varices have a high rebleeding rate (55%) and mortality (29%) G26 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes GASTROINTESTINAL BLEEDING CONT BLEEDING PEPTIC ULCER Signs and Symptoms ❏ see PUD section Approach to Treatment ❏ see Figure 7 judge risk of rebleeding or continuous bleeding... labelled red cell scan bleeding stops bleeding continues upper GI series angiogram bleeding continues at rate > 0.5 mL/min angiogram Figure 8 Approach to Hematochezia G28 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes GASTROINTESTINAL BLEEDING CONT COLON CANCER (see Colour Atlas G6, G11) Etiology/Epidemiology ❏ environmental influences (presumed) • high dietary fat consumption • low dietary... Metronidazole Sudan red stain for fat in stool Duodenal aspiration Rotavirus Fecal/oral Supportive Can cause severe dehydration Norwalk Agent Fecal/oral Supportive Often causes epidemics Viruses G14 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes SMALL AND LARGE BOWEL CONT Table 6 Approach to Acute Diarrhea A History 1 Search for Etiology Travel Homosexual contacts Outbreaks Seafood ingestion... immunodeficiency, hemolytic anemia, extremes of age, aneurysms, prosthetic valves grafts/joints Clinical Pearl ❏ Must rule out infection in all patients with bloody diarrhea Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G15 SMALL AND LARGE BOWEL CONT Common Clinical Syndromes ❏ Food Poisoning • brief explosive diarrhea following exposure to food contaminated with bacteria or bacterial toxins • 90% due... break down large molecules in the lumen of the intestine into their component small molecules ❏ malabsorption - inability to transport molecules across the intestinal mucosa to the body fluids G16 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes SMALL AND LARGE BOWEL CONT Investigations ❏ most definitively diagnosed by 72-hour stool collection (weight, fat content) but this is a cumbersome... (searching for Crohn's, lymphoma, etc.) ERCP: endoscopic retrograde pancreatography MRCP: magnetic retrograde pancreatography Figure 4 Approach to Malabsorption Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G17 SMALL AND LARGE BOWEL CONT Manifestations of Malabsorption ❏ fat soluble vitamin deficiency • vitamin A • night blindness • dry skin • keratomalacia • vitamin D • metabolic bone... lipolysis form micelles which solubilize fat and aid in absorption • fatty acids diffuse into cell cytoplasm • generalized malnutrition, weight loss, and diarrhea • measure fecal fat excretion G18 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes SMALL AND LARGE BOWEL CONT B12 Salivary Gland R B12 + R Pancreas Diagram of B12 Absorption Liver Stomach IF H+ R B12 + IF 1 B12 ingested and bound... pernicious anemia bacterial overgrowth normalizes with pancreatic enzymes (Stage IV) does not normalize pancreatic insufficiency ileal disease Figure 6 Schilling Test Toronto Notes - MCCQE 2002 Review Notes Gastroenterology – G19 SMALL AND LARGE BOWEL CONT CELIAC DISEASE (Gluten enteropathy / sprue) Definition ❏ abnormal jejunal mucosa which improves with gluten-free diet and deteriorates when gluten reintroduced... surgical damage to the ileocecal valve ❏ decreased motility • scleroderma • diabetes • intestinal pseudoobstruction ❏ achlorhydria ❏ described in elderly patients without any known etiologic factors G20 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes SMALL AND LARGE BOWEL CONT Signs and Symptoms ❏ steatorrhea: bacteria deconjugate bile salts impairing micellar lipid formation ❏ diarrhea: bowel ... Yersinia E coli (EHEC 0157:H7) C difficile Protozoal E histolytica (amebiasis) Strongyloides G2 – Gastroenterology RUQ Hepatitis Bilary colic Acute cholecystits PUD Pyelonephritis RLQ Appendicitis... Increased intracranial pressure (ICP) Cerebellar hemorrhage Hypercalcemia Autonomic dysfunction Gastroenterology – G3 ESOPHAGUS Anatomy and Physiology ❏ mucosa: stratified squamous epithelium... Symptoms Respiratory Symptoms Scleroderma Achalasia Figure Approach to Esophageal Dysphagia G4 – Gastroenterology Toronto Notes - MCCQE 2002 Review Notes ESOPHAGUS CONT HEARTBURN (Pyrosis) (see