GI Disorders PDF

Structure and Function of the Digestive System Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. Gastro- Intestinal Tract Copyright © 2019, Elsevier Canada, a division of Reed Elsevier...

Structure and Function of the Digestive System Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. Gastro- Intestinal Tract Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 2  Stomach Modified from Patton, K.T., & Thibodeau, G.A. (2014). The human body in health & disease (6th ed.). St Louis, MO: Mosby. Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 3 Gastro-Intestinal Tract Chemical digestion of food particles Absorption of digested food Elimination of waste products by defecation Immune and microbial protection against infection Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 4 GASTROINTESTINAL DISORDERS Peptic Ulcer Disease (Gastric & Duodenal) Intestinal Obstruction Cirrhosis of the Liver Acute Pancreatitis Intestinal Digestion and Absorption Initiated in stomach Actions of gastric hydrochloric acid and pepsin Continues in proximal portion of small intestine Action of pancreatic enzymes, intestinal enzymes, and bile salts Carbohydrate breakdown Proteins degraded Fats emulsified Nutrients absorbed by active transport, diffusion, or facilitated diffusion Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 6 Gastric Secretion Stomach secretes large volumes of gastric juices Mucus Acid Enzymes Hormones Intrinsic factor Gastroferrin Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 7 Gastric Secretion Mucus Stimulated by prostaglandins Mucosal barrier Gastric mucosal blood flow Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 8 Gastric Secretion Acid Secreted by parietal cells Dissolves food fibers, acts as a bactericide against swallowed micro- organisms, and converts pepsinogen to pepsin Pepsin Secreted by chief cells Proteolytic enzyme Breaks down protein and forms polypeptides in the stomach Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 9 Normal Protective Mechanisms of the Stomach Mucus secreted by the superficial mucosal cells forms a layer that can trap or slow the diffusion of H+ ions across the mucosal barrier in the stomach Presence of HCO3 helps neutralize HCl acid in the lumen of the GI tract. Peptic Ulcer Disease: Causes & predisposing factors Helicobacter pylori (H. pylori) Hyperacidity (not an increase in acid) Ulcerogenic drugs (aspirin, NSAIDs, alcohol, corticosteriods) Cigarette smoking Genetic / environmental Stress, low socioeconomic status (LSES) Peptic Ulcer Disease Ulceration with loss of tissue Includes both duodenal and gastric ulcers Develops when the mucosa cannot protect itself from corrosive substances and a back diffusion of acid results Gastritis Inflammatory disorder of the gastric mucosa Acute gastritis This Photo by Unknown Author is licensed under CC BY-SA Caused by injury of the protective mucosal barrier (NSAIDS), H pylori, chemicals Chronic gastritis (older adults) Chronic fundal gastritis (type A, immune) Chronic antral gastritis (type B, nonimmune) Symptoms vague This Photo by Unknown Author is licensed under CC BY Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 14 Peptic Ulcer Disease Break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum Acute and chronic ulcers Superficial Erosions Deep Zollinger-Ellison syndrome This Photo by Unknown Author is licensed under CC BY-SA Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 15 Lesions caused by peptic ulcer disease ) Duodenal Ulcers Most common of the peptic ulcers Developmental factors: Helicobacter pylori infection Hypersecretion of stomach acid and pepsin Use of NSAIDs Characterized by intermittent pain in the epigastric area Relieved rapidly by ingestion of food or antacids Management aimed at relieving the causes and effects of hyperacidity and preventing complications Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 17 Clinical Manifestations Pain is typically described as burning or cramp-like Chronic intermittent pain in the epigastric region Pain usually occurs 2-3 hours after eating, when the stomach is empty May report nocturnal pain Pain is relieved by food or antacids Some patients will have no pain, and the first manifestation may be a hemorrhage or perforation Duodenal ulcers can heal spontaneously, but will recur without treatment Gastric Ulcer Gastric ulcers tend to develop in the antral region of the stomach, adjacent to the acid- secreting mucosa of the body Pathophysiology Primary defect is an increased mucosal permeability to hydrogen ions Gastric secretion tends to be normal or less than normal Manifestations and treatment similar to duodenal ulcers except food causes pain Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 19 Clinical Manifestations Pain may be described as burning Pain occurs within 15-30 minutes of eating While duodenal ulcers have pattern of healing & recurring, gastric ulcers tend to be chronic Gastric ulcers are more associated with anorexia, vomiting & weight loss than duodenal ulcers 21 Diagnostic Tests Endoscopy & biopsy Endoscopy allows ulceration to be seen Biopsy of tissue can be obtained to identify h. pylori and to rule out gastric cancer Diagnostic tests for h. pylori (note: testing for h. pylori is recommended for all patients with PUD) In addition to biopsy, h. pylori can be detected by serum antibody tests and by urea breath test (this is because urea is a by-product of the metabolism of h. pylori) Barium swallow (if endoscopy is contraindicated) Management Protein pump inhibitors (PPIs) reduce acid secretion, which relieves symptoms & promotes healing H2-receptor antagonists (examples: famitodine, ranitidine) used less often, and protein pump inhibitors are usually used (examples: omeprazole, lansoprazole) Treatment of h. pylori Combination of antibiotics and protein pump inhibitors (typically 2 antibiotics and 1 PPI) Antacids Neutralize gastric contents & decrease pain Complications Hemorrhage Develops from erosion of granulation tissue at the base of the ulcer during healing, or from erosion of the ulcer through a major blood vessel Gastric artery with gastric ulcers Pancreoduodenal artery with duodenal ulcers More prevalent with duodenal ulcers Complications Perforation & peritonitis Perforation is considered the most deadly complication Duodenal ulcers occur more commonly, and have a higher rate of perforation, however perforation of gastric ulcers have a higher mortality rate Perforation of a peptic ulcer occurs when the ulcer penetrates the serosal surface (which is the outermost surface), and the gastric contents empty into the peritoneal cavity Large perforations require immediate surgical closure Complications Peritonitis the contents being spilled into the abdominal. cavity include air, saliva, food particles, HCl acid, pepsin, bacteria, bile & pancreatic fluid and enzymes Bacterial peritonitis can lead to septic shock if not treated Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 27 28  Pathophysiology Noxious stimuli (examples: H. pylori, NSAID use) ↓ Disrupts the mucosa (inner-most lining of the upper gastrointestinal tract) ↓ Exposure of gastric acid to the underlying area ↓ Inflammatory response initiated ↓ Histamine is released by damaged cells The release of histamine from the damaged mucosa results in Vasodilation & increased capillary permeability  Leads to mucosal edema and fluid shifting into the gastric lumen resulting in a loss of plasma proteins  Stimulation of gastric cells to secrete more acid  This increased acid leads to more damage  Gastric Ulcer Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 30 Stress-Related Mucosal Disease Acute form of peptic ulcer that is related to severe illness or major trauma Ischemic ulcers Within hours of trauma, burns, hemorrhage, heart failure, or sepsis Curling ulcers Develop as a result of burn injury Cushing ulcers Develop as a result of a brain injury or brain surgery Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 31 Surgical Treatment of Ulcer Most common indications are recurrent or uncontrolled bleeding and perforation of the stomach or duodenum. Objectives are to reduce stimuli for acid secretion, decrease the number of acid-secreting cells in the stomach, and correct complications of ulcer disease. Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 32 Disorders of Motility Intestinal obstruction and paralytic ileus Intestinal obstruction is any condition that prevents the flow of chyme through the intestinal lumen Simple obstruction Mechanical blockage of the lumen Functional obstruction (paralytic ileus) Failure of intestinal motility Often occurs after intestinal or abdominal surgery, pancreatitis, or hypokalemia Intestinal obstruction and paralytic ileus Signs of small intestinal obstruction Colicky pains Nausea and vomiting Signs of large intestinal obstruction Hypogastric pain and abdominal distension Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 34 Manifestations Abdominal pain Colicky (intermittent pain that eases, and then returns) Pain may be continuous with severe distension With ischemia, pain becomes more constant and severe Nausea & vomiting Projectile vomiting Vomiting will relieve pain Abdominal distention Mild distension in the proximal small intestine Greater distension in the lower part of the small intestine Manifestations Partial obstruction can cause diarrhea or constipation, and complete obstruction causes constipation only In complete obstruction, may have tinkly bowel sounds accompanied by crampy abdominal pain These bowel sounds are high-pitched and occur above the area of the obstruction Metabolic acidosis may result (as obstruction prevents bicarbonate from pancreatic secretions, and bile from being reabsorbed) If patient becomes hypotensive, will see sweating & tachycardia Manifestations of Large Bowel Obstruction Large bowel obstruction is less common than small bowel Hypogastric abdominal pain Pain can vary from mild to severe Severe pain with ischemia and development of peritonitis Distention Vomiting may be gradual, and occurs late Borborygmi are audible abdominal sounds that are produced by hyperactive intestinal motility (as the intestines are trying to move contents past the obstruction) Emergencies Peritonitis Perforation In both large and small bowel obstruction, perforation is associated with Acute, constant pain Nausea & vomiting Fever Leukocytosis (increased WBCs) Strangulation of bowel occurs when an obstruction cuts off blood supply, and it results in pain that is severe, constant & rapid in onset Diagnostic Tests Abdominal x-rays and CT scan Sigmoidoscopy or colonoscopy Can provide direct visualization of an obstruction Labs: CBC, electrolytes Leukocytosis may indicated strangulation or perforation Elevated hematocrit may indicate dehydration Decreased hemoglobin & hematocrit may indicate bleeding from a neoplasm or strangulation Decreased sodium, potassium & chloride in small bowel obstruction Treatment Decompression: NG & suction Decompression removes the intestinal contents (gas and fluid) Correct fluid, electrolyte and acid-base imbalances – will require IV fluids Relief or removal of obstruction (surgery) Resection Partial or total colectomy May require colostomy or ileostomy Mechanical bowel obstructions  Intestinal Obstruction Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 43 Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 44 This Photo by Unknown Author is licensed under CC BY-SA Accessory Organs of Digestion Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 45  Vascular and Hematological Liver Functions  Stores blood  Hemostatic functions  Synthesizes clotting factors Because bile salts are needed for reabsorption of fats, vitamin K absorption depends on adequate bile production in the liver Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 46 Metabolism of Bilirubin Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 47 Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 48  Liver Functions  Metabolism of nutrients  Fats  Proteins  Carbohydrates  Metabolic detoxification  Storage of minerals and vitamins Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 49 Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 50 Hepatic Portal Circulation From Herlihy, B. (2015). The human body in health and illness (5th ed.). St Louis, MO: Saunders Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 51  Liver Disorders  4th leading cause of death  Most common cause fatty liver disease  Hep B and Hep C also major causes  400 liver transplants annually Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 52 Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 53  Cirrhosis Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 54  Pathophysiology Cellular ischemia, followed by necrosis (liver cells are called hepatocytes) ↓ Destroyed hepatocytes are replaced by fibrous scar tissue ↓ Architecture (make-up) of the liver becomes nodular ↓ Irregular, disorganized regeneration, poor cellular nutrition and hypoxia secondary to reduced blood flow and scar tissue ↓ Reduced function of the liver  Manifestations Early clinical manifestations are mild and include fatigue, weight loss, anorexia, jaundice, constipation, diarrhea and dull pain As the disease worsens, manifestations include:  Portal hypertension  Esophageal varices  Ascites  Hematological disorders  Hypoalbuminemia  Hepatic encephalopathy  Hepatorenal syndrome  Hyperbilirubinemia  Hyperestrogenemia  Portal Hypertension  Fibrosis and changes to the blood vessels in the liver due to cirrhosis leads to resistance to blood flow within the portal venous system  Causes portal hypertension, which is abnormally high blood pressure in the portal venous system  The portal venous system refers to a system of veins that come from the stomach, bowel, spleen and pancreas to the portal vein  The portal vein then breaks off into smaller blood vessels and travels through the liver (see image on next slide)  Portal Hypertension This increased venous pressure in the portal circulation leads to  Esophageal varices  Ascites  Systemic hypertension  Splenomegaly  Large collateral veins  Esophageal varices  Esophageal Varices  Esophageal varices is the most common clinical manifestation of portal hypertension  Varices are groups of torturous veins that are enlarged & swollen due to portal hypertension  Varices develop slowly over years  Patient may have anemia and/or melena from chronic bleeding  Rupture of the varices is caused by increased venous pressure and be gastric acid  Rupture will lead to hemorrhage, and patient will have vomiting of large amounts of bright red blood  Portal hypertension may not be diagnosed until patient has had bleeding from esophageal varices  Ascites  Accumulation of serous fluid in the peritoneal cavity  Serous fluid fills the body’s cavities, it is typically a thin, watery, pale yellow, transparent fluid  Several factors that lead to ascites:  Portal hypertension  Hypoalbuminemia  Hyperaldosteronism  Pathophysiology of Ascites Portal hypertension  The increased pressure of portal hypertension pushes proteins from the blood vessels into the lymph space  The lymphatic system is unable to move the excess protein and water and these leak through the liver capsule into the peritoneal cavity  The osmotic pressure from the proteins causes additional fluid to be pulled into the peritoneal cavity Hypoalbuminemia  In advanced cirrhosis, there is decreased production of albumin, which results in decreased colloidal oncotic pressure  This decrease leads to fluid leaking out of the interstitial spaces and into the peritoneal cavity, contributing to ascites Mechanisms of Ascites Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 63  Complications  Varices Lower esophagus Stomach Abdominal wall Rectum  Splenomegaly Hepatopulmonary syndrome Portopulmonary syndrome  Vomiting of blood from bleeding esophageal varices is the most common clinical manifestation Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 64  Varices Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 65  This Photo by Unknown Author is licensed under CC BY This Photo by Unknown Author is licensed under CC BY-NC Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 66 This Photo by Unknown Author is licensed under CC BY-SA Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 67 Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 69 Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 70  Complications  Hepatic encephalopathy  Neurological syndrome of impaired behavioural, cognitive, and motor function  Develops rapidly during fulminant hepatitis or slowly during course of liver disease  Cells in the nervous system are vulnerable to neurotoxins absorbed from the GI tract that, because of liver dysfunction, circulate to the brain Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 71 Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 72  Hematological Problems Includes thrombocytopenia, leukopenia, anemia and coagulation disorders Thrombocytopenia, leukopenia & anemia are related to splenomegaly  Splenomegaly is a result of portal hypertension  The spleen becomes enlarged because of the back-up of blood  Normally the spleen filters and destroys damaged blood cells, and it stores RBCs and platelets  With splenomegaly, these functions are changed, and the spleen stores too many platelets, and it destroys healthy RBCs Anemia is also caused by inadequate RBC production, and bleeding from varices  Hematological Problems  Decreased clotting factors  In advanced cirrhosis, the liver is unable to produce prothrombin and other factors needed for blood clotting  Signs & symptoms include increased bleeding  Epistaxis  Purpura & petechiae  Easy bruising  Gingival bleeding  Hepatic Encephalopathy  This is a neuropsychiatric manifestation of liver damage from cirrhosis  Signs range from lethargy to coma  This is a terminal complication of advanced cirrhosis  Can occur with any advanced liver disease in which ammonia enters the systemic circulation without being detoxified by the liver  Hepatic Encephalopathy  Protein broken down (metabolized), ammonia is created  Ammonia usually goes to the liver via the portal circulation and is converted to urea which then is excreted by the kidneys  In advanced liver disease, such as cirrhosis, ammonia is not converted to urea and instead accumulates in the systemic circulation  Ammonia crosses the blood-brain barrier and causes toxic neurological effects  Hepatic encephalopathy is associated with increased levels of ammonia, but it is not well understood how ammonia causes the symptoms  Hepatorenal Syndrome  This is kidney failure with advancing azotemia, oliguria and intractable ascites  Results because of decreased blood volume to kidneys secondary to portal hypertension  In patients with cirrhosis, it is typically seen following diuretic therapy, gastrointestinal hemorrhage, or paracentesis  Creatinine will be elevated  Liver transplantation will reverse the kidney failure Hyperbilirubinemia This refers to increased levels of bilirubin, and it is responsible for the jaundice seen in cirrhosis Jaundice is the yellow or greenish appearance of the skin Patient may also have pruritus because of the accumulation of bile salts under the skin Bilirubin comes from breaking down old RBCs Normally, the bilirubin travels to the liver which helps to excrete In cirrhosis, the liver cannot excrete bilirubin, and bilirubin remains in the systemic circulation, resulting in hyperbilirubinemia  Hyperestrogenemia  One of the functions of the liver is to conjugate and excrete the gonadal and adrenal steroid hormones  If the liver function is impaired then the body will accumulate estrogen.  Increase in estrogen can cause gynecomastia (in males), palmar erythema, spider angiomas, amenorrhea in younger women and vaginal bleeding in older women  In addition, a decrease in testosterone (not enough protein to bind to) can cause impotence and testicular atrophy  Diagnostic Testing  LFTs (AST, ALT, GGT) are increased (release of these enzymes from the damaged liver)  Decreased albumin  PT, INR and PTT prolonged  Increased bilirubin  Liver biopsy (to identify liver cell changes, not necessary with clinical manifestations of cirrhosis)  Treatment  Rest  Vitamin supplements  Nutritious diet  Stopping alcohol use will slow progression of cirrhosis, will improve symptoms and lengthen life  Liver transplant in end-stage liver disease Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 83  Disorders of the Pancreas  Pancreatitis  Inflammation of the pancreas  Develops because of obstruction to the outflow of pancreatic digestive enzymes caused by bile and pancreatic duct obstruction Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 84  Disorders of the Pancreas  Acute pancreatitis  Chronic pancreatitis  Usually mild and resolves  Process of progressive spontaneously fibrotic destruction of the  May result from direct pancreas cellular injury from alcohol,  Related to chronic alcohol medications, or viral abuse infection  Continuous or intermittent  Cardinal manifestation is abdominal pain and weight constant epigastric or loss are common midabdominal pain  Risk factor for pancreatic cancer Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 85  Acute Pancreatitis  Acute pancreatitis mild-moderate, self-resolves (goes away by itself) within a week  20% of cases of acute pancreatitis are severe, requiring hospitalization  Acute inflammation of the pancreas develops because there is an obstruction to the outflow of pancreatic digestive enzymes caused by bile, and pancreatic duct obstruction  It can also develop from alcohol, medications and viral infection  Pancreatitis is more severe and has a worse prognosis when it is caused by alcohol, than by biliary tract disease  Pathophysiology  Back up of pancreatic secretions  Amylase, lipase & trypsin These enzymes cause autodigestion of the pancreas, and this results in inflammation of the pancreas  Binge drinking of alcohol increases the release of pancreatic enzymes, and plays a role in the activation of these enzymes  Chronic alcohol use is thought to lead to the formation of protein plugs that obstruct pancreatic ducts  Gallstones produced in the gallbladder can block the bile duct, which stops the pancreatic enzymes from travelling to the small intestine, and forces the enzymes back into the pancreas – which leads to autodigestion of the pancreas by those enzymes  Clinical Manifestations  Pain, which is epigastric or mid-abdominal, and ranges from mild to severe  Pain is caused by edema, by peritoneal irritation & inflammation, by obstruction of the biliary tract, and by inflammation of the nerves  Fever  Leukocytosis  Nausea and vomiting (if the pancreatitis leads to paralytic ileus)  Jaundice, if there is obstruction of the bile duct  Abdominal distension secondary to fluid accumulation  Diagnostic Tests Labs  Increased amylase  Increased lipase  While both amylase and lipase will be elevated, lipase is more sensitive for the diagnosis of pancreatitis  Decreased calcium  Tetany is a sign of severe hypocalcemia Imaging  Abdominal X ray  Abdominal U/S  Abdominal CT scan  Management  Pain medication  Electrolyte replacements if necessary (based on lab findings)  Bowel rest: NPO and NG tube with suctioning (may only be required initially)  Nutrition  If there is no ileus, can start nutrition within 24-48 hours  Can use enteral feeds  IV fluids to prevent hypotension and shock  Antibiotics in presence of infection  Gallbladder Saclike organ that lies on the inferior surface of the liver Function is to store and concentrate bile between meals Holds about 90 mL of bile Begins to contract 30 minutes after eating under the influence of the vagus nerve and cholecystokinin Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 91  Disorders of the Gallbladder  Obstruction or inflammation (cholecystitis) most common cause of gallbladder problems  Cholelithiasis—gallstone formation  Risks Obesity Middle age Female Oral contraceptive use Rapid weight loss First Nations ancestry Genetic predisposition Gallbladder, pancreas, or ileal disease Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 93  Disorders of the Gallbladder  Gallstones  Formed from impaired metabolism of cholesterol, bilirubin, and bile acids -3 types  Type depends on chemical composition Cholesterol  Formed from bile that is supersaturated with cholesterol produced by the liver Pigmented brown  Formed from calcium bilirubinate and fatty acid soaps that bind with calcium Black  Composed of calcium bilirubinate with mucin glycoproteins  Associated with chronic liver disease and hemolytic disease Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 94 Disorders of the Gallbladder Often asymptomatic or vague Epigastric and right hypochondrium pain Intolerance to fatty foods Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 95  Gallstones From Kissane, J.M. (Ed.). (1990). Anderson’s pathology (9th ed.). St Louis, MO: Mosby. Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 96 Disorders of the Gallbladder Cholecystitis Almost always caused by a gallstone lodged in the cystic duct Pain is similar to that caused by gallstones Fever, leukocytosis, rebound tenderness, and abdominal muscle guarding are common findings Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 97  Case Study  55-year-old man complains of pain and burning pressure around stomach 2 to 3 hours after eating.  He has a history of former alcohol abuse and smoking.  He has had 4.5-kg weight loss in 2 months accompanied by nausea, vomiting, and decreased appetite.  EGD reveals ulcers; biopsy sample positive for H. pylori. 98  Discussion Questions 1. He asks you how this happened. What are his risk factors? 2. What are his treatment options? 3. What are complications of peptic ulcer disease? 4. What lifestyle modifications are necessary to ensure healing? 99