GI and Hepatobiliary lecture
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The document discusses the gastrointestinal and hepatobiliary systems. It begins by describing the structure and functions of the GI tract, which is divided into upper, middle and lower sections. It then discusses various disorders that can affect these systems such as GERD, peptic ulcers, hepatitis, pancreatitis and gastroenteritis. The document provides details on the causes, symptoms, diagnoses and treatments for some of these conditions in 1-2 paragraphs each.
GI and Hepatobiliary lecture
- 1. THE GASTROINTESTI NAL AND HEPATOBILIARY SYSTEMS Barry University NUR 313
- 2. Objectives At the completion of this lecture, the students will be able to: Describe the structure and function of the gastrointestinal system Verbalize the difference between the upper, middle and lower GI tract. Understand various disorders of the GI system such as GERD, peptic ulcer disease, hepatitis, pancreatitis, and gastroenteritis. Describe diagnostic tests and treatments related to various disorders of the GI system. 2
- 3. Structure and Function Major Physiological Functions of the GI system Digestion of food Absorption of nutrients into the blood stream Motility, Secretion, Digestion, absorption 3
- 4. Structure and Function GI tract is divided into 3 parts: Upper: mouth, esophagus and stomach Intake source Middle: duodenum, jejunum and ileum Digestion and absorption Lower: cecum, colon, rectum Storage and elimination 4
- 5. Structure and Function Esophagus: straight, tube about 10 inches in length Smooth muscle layers with peristaltic movements to move food Connects oropharynx to stomach Upper Pharyngoesophageal sphincter keeps air from entering esophagus and stomach during breathing Lower Gastroesophageal Sphincter prevents reflux of gastric contents 5
- 6. Stucture and Function Stomach Pouch-like structure on left side of abdomen serves as food storage Pyloric sphincter controls rate of stomach emptying and prevents regurgitation of intestinal contents back into stomach 6
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- 8. Structure and Function: Middle and Lower GI Tract 8
- 9. Structure and Function: Motility Rhythmic intermittent contractions – mixing and moving food Esophagus, upper stomach, small intestines Tonic movements is a constant contractions Lower esophagus, ileocecal valve, anal sphincter Autonomic nervous system SNS PNS 9
- 10. Structure and Function Hormones: Gastrin: stimulates gastric acid, blood flow Cholecystokinin (CCK): Contraction of gallbladder and secretion of pancreatic enzymes Secretin: inhibits gastric acid secretion; stimulates secretion of water from the pancreas Ghrelin: peptide hormone stimulates food intake and digestive function (appetite) 10
- 11. Digestion and Absorption Digestion: The process of dismantling food into parts Requires hydrolysis, enzyme cleavage, fat emulsification Absorption: moving nutrients from external intestinal lumen to internal environment. 11
- 12. Disorders of the GI and Hepatobiliary systems Gastroesophageal Reflux Disease (GERD) Peptic Ulcer Disease Gastroenteritis IBD – Crohn’s & Ulcerative Colitis Diverticular Disease Appendicitis Intestinal Colorectal CA Peritonitis Hepatitis Cirrhosis Liver Failure Cholecystitis Pancreatitis 12
- 13. Gastroesophageal Reflux Disease Reflux of gastric contents into esophagus as a result of Reduction in lower esophageal sphincter tone Delayed gastric emptying Increase gastric acid secretion Irritation of esophageal mucosa 13 GERD
- 14. GERD 14
- 15. Risk Factors Factors which reduce LES tone Aging Obesity Pregnancy High fat meals 15
- 16. Signs and Symptoms Pyrosis (heartburn) cardinal symptom Belching Atypical Symptoms Esophageal pain referred to the neck, mid-back, upper abdomen Chest pain Chronic cough, wheezing, Hoarseness Chronic sore throat, dysphagia 16
- 17. Diagnosis History and physical alone if symptoms are typical Endoscopy and biopsy if symptoms are atypical Complications Barrett’s esophagus Strictures 17
- 19. Treatment Medication Avoid recumbence after eating Elevate head of bed when sleeping Reduce size of meals Reduce fat, acid, spices, caffeine, sweets, peppermints, chocolate, and alcohol Avoid constrictive garments 19
- 20. Peptic Ulcer Disease A group of ulcerative disorders that occur in areas of the upper gastrointestinal tract that are exposed to acid-pepsin secretions Erosion of the gastric membrane Gastric ulcers Duodenal ulcers Stress ulcers- Curling’s ulcer 20
- 21. Gastric Ulcer 21
- 23. Risk Factors Helicobacter pylori (H-Pylori) infection 90-95% of patients with duodenal ulcers 60-70% of patients with gastric ulcers NSAIDs aspirin 23
- 24. Signs and Symptoms Pain Burning, gnawing, cramp-like Frequently when stomach empty Midline epigastric, near xiphoid…may radiate to back or right shoulder Relieved by foods or antacids Periodicity: daily for weeks, then remits until next occurrence 24
- 25. Complications Bleeding Hematemesis Coffee ground emesis Hematochezia Melena Occult bleeding Gastric Outlet Obstruction Caused by edema, spasm, scar tissue Perforation Peritonitis 25
- 26. TREATMENT Antibiotics for H-Pylori Proton pump inhibitors (protonix), H2 Blockers (pepcid) Bismuth (Maalox, pepto bismol) Avoid symptom triggers Alcohol High fat Tobacco Spicy food 26
- 27. Infectious Enterocolitis Acute infection causing inflammation of the intestinal linings resulting in vomiting, diarrhea, and fever. Etiology Infection is by fecal-oral route. Risk Factors Improper hand washing and food preparation Day care center attendance (children) Recent use of antibiotics 27
- 28. Infectious Agents Rotavirus Clostridium difficile (C-diff) pseudomembraneous colitis→ toxic megacolon! Staphylococcus aureus Escherichia coli (E-coli) Shigella Salmonella Campylobacter Giardia lamblia 28
- 29. Symptoms Diarrhea and abdominal pain Treatment Supportive for 48 hours Avoid anti-diarrheal agent Rehydrate! – especially in pediatric and geriatric population Stool for WBC, stool cultures, stool for ova, cysts, and parasites Monitor hydration with BUN, urine specific gravity, electrolytes. 29
- 30. INFLAMMATORY BOWEL DISEASE (IBD) Idiopathic chronic disorders of the GI tract distinguished by the recurrent inflammatory involvement of intestinal segments. Two main types Crohn’s disease Ulcerative colitis (UC) 30
- 31. Incidence Peak age of onset 20-30’s (Crohn’s), and 30’s(UC) Family history Genetic predisposition – triggered by dietary antigen or microbial agent 31
- 32. Crohn’s Disease Definition Granulomatous inflammatory lesions of the GI tract. Location Mouth to anus. Mostly small intestine & proximal colon. Pattern “cobblestone” inflammatory appearance of submucosal layer Skip lesions if multiple Manifestations Intermittent diarrhea, steatorrhea, colicky pain, weight loss, F/E imbalances, nutritional deficiencies, malaise, low-grade fever. Complications: anal & perianal fistulas, abscesses, intestinal obstruction 32
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- 35. Diagnosis H&P Sigmoidoscopy & Colonoscopy with biopsy: inflammation; biopsy often reveals granulomatous inflammation X-rays CT scan Sedimentation rate: elevated CBC: possible anemia Electrolytes: imbalances 35
- 36. TREATMENT Gastroenterologist referral Corticosteroids Immunosuppressants Antibiotics- Metronidazole (Flagyl) Nutritious diet; residue free/bulk free to allow bowel rest 36
- 38. Ulcerative Colitis Definition Inflammatory condition confined to the mucosal layer of the rectum and colon Location Starts in rectum and spreads proximally through colon Pattern Confluent inflammatory pattern (no “skip” lesions) Lead to pinpoint mucosal hemorrhages; may develop into crypt abscesses; may become necrotic & ulcerate Pseudopolyps of mucosal layer Manifestations Bloody diarrhea, nocturnal diarrhea, mild abdominal cramping Complications: Colon cancer risk; toxic megacolon in severe fulminant type 38
- 39. Ulcerative Colitis Diagnosis H&P Colonoscopy Treatment Diet modifications Fiber reduces diarrhea Avoid caffeine, lactose, spicy, and gas-producing foods Corticosteroids Immunosuppressants Surgery 39
- 40. DIVERTICULAR DISEASE Diverticulum – saclike protrusions of the mucous membrane that herniates outward through muscular layer. (outpouches or outpocketings) Diverticula – plural for diverticulum Diverticulosis – the presence of diverticula Diverticulitis – diverticula become inflamed and may perforate (undigested food, fecal matter, and bacteria become trapped forming fecalith) 40
- 42. DIVERTICULAR DISEASE Increases dramatically with age More common in North America, Australia, and Europe Affects men and women equally Risk Factors Low fiber diet ↓strength of colon musculature ↓physical activity Poor bowel habits 42
- 43. ACUTE DIVERTICULITIS LLQ ABDOMINAL PAIN (93-100%) Tender palpable mass in LLQ Fever Mild to moderate leukocytosis Nausea, vomiting, and anorexia Constipation/Diarrhea 43
- 44. DIAGNOSIS Diverticulosis Usually no symptoms – picked up on routine colonoscopy or plain X-ray Vague abd discomfort, change in bowel habits, bloating, flatulence Flat and Upright abdominal films CT scan** Colonoscopy Barium enema—not for acute diverticulitis! 44
- 45. TREATMENT Increase dietary fiber Bowel retraining/ regular defacation Complications – Hospitalization NPO Nasogastric tube TPN Broad spectrum antibiotics Surgery 45
- 46. APPENDICITIS 46
- 47. APPENDICITIS Inflammation of the vermiform appendix Can lead to gangrene and perforation Cause: Intraluminal obstruction w/ fecalith Signs and Symptoms Initially: vague epigastric or periumbilical pain Nausea, vomiting, anorexia Follow onset of pain RLQ McBurney’s point rebound tenderness 75% have leukocytosis 10-18,000/mm3 Fever Psoas sign/ Obturator test 47
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- 49. DIAGNOSIS/TREATMENT Emergency Department History & Physical CT scan** (or U/S) Appendectomy (surgical) IV Antibiotics Complications Peritonitis Abscess formation Septicemia 49
- 50. Intestinal Obstruction Mechanical vs. Paralytic Mechanical: Hernias, adhesions, strictures, tumors, foreign bodies, intussusception, volvulus Severe colicky pain Borborygmy Paralytic: “adynamic” Neurogenic or muscular impairment of peristalsis Paralytic ileus Absent bowel signs S/S: Abdominal distention, pain, constipation, vomiting, F&E disturbances. 50
- 52. Diagnosis Abdominal X-ray CT U/S 52
- 53. Treatment Nasogastric tube → Sxn for bowel decompression Correct F&E imbalances Surgery if complete bowel obstruction or strangulation 53
- 54. COLORECTAL CANCER Uncontrolled growth of malignant cells in the large intestine Risk Factors - >40, polyps, family history, DM, Tobacco, diets rich in fats and red meats, ethnicity S/S – Change in bowel habits, occult blood, bloating, anorexia, weight loss Pain is a LATE sign! Diagnosis – Colonoscopy, CEA Treatment – Surgery, chemo, radiation Screening recommendations 54
- 56. Peritonitis Inflammatory response of the peritoneal membrane Causes: Bacterial or chemical irritation Perforated ulcers, diverticulum, appendix Gangrenous bowel or gallbladder 56
- 57. Signs & Symptoms Pain & tenderness Rigid/board-like, distended, guarded abdomen Shallow respirations N/V Fluid losses; Dehydration Fever ↑WBC count Tachycardia Hypotension 57
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- 60. Complications Paralytic ileus Hypovolemia Sepsis Shock 60
- 61. Treatment Correction of underlying cause Correction of F&E imbalances Surgery if indicated NPO NGT for decompression Antibiotics Analgesics 61
- 62. VIRAL HEPATITIS Viral infection affecting the liver Five viral causative agents: A,B,C,D,E Hepatitis B,C, and D can cause chronic infections Risk Factors: HAV & HEV Transmitted via fecal-oral route Travel to endemic areas Ingestion of contaminated food, water, milk, or shellfish IgM anti-HAV, IgG anti-HAV Hep A vaccine available 62
- 63. RISK FACTORS B&C HBV, HCV –blood/body fluids Shared needles Multiple sexual partners Tattoo recipients; body piercings Health care workers Can cause chronic hepatitis & cirrhosis All adolescents are considered high-risk for HBV Risk for hepatocellular CA w/ HCV HBV vaccine available 63
- 64. SIGNS AND SYMPTOMS Many are asymptomatic Nausea, vomiting, anorexia, RUQ abdominal pain, liver enlargement Malaise, fever Sclera become yellow (icteric) Jaundice, dark urine, clay-colored stools Elevated ALT, AST, bilirubin levels 64
- 65. DIAGNOSIS Liver function tests ALT, AST – hepatic injury ALT – Think Hepatitis B AST – Alcohol, Statins, Tylenol PT/albumin – measure synthetic activity of liver Bilirubin – measure of excretory function of liver 65
- 66. HEPATITIS B Serologies HBsAg- detected in acute or chronic HepB-infectious Anti-HBs or HBsAb- indicates recovery, immunity HBeAg Anti-HBe HBcAg Anti-HBc – previous or ongoing infection IgM Anti-HBc – acute infection IgG Anti-HBc 66
- 67. TREATMENT Vaccination Administer HBIG Avoid medications metabolized by the liver Abstinence from alcohol Bleeding precautions Treat partners Treated by Gastroenterologist/ Hepatologist 67
- 68. CIRRHOSIS End stage chronic liver disease Irreversible inflammatory disease Disrupts liver structure and function Inflammation causes structural fibrotic changes Disruption of blood flow…portal HTN Obstruction of biliary system…jaundice 68
- 69. Signs & Symptoms Most common Weight loss (masked by ascites) Weakness Anorexia Ascites Diarrhea Jaundice Abdominal pain (epigastric or RUQ) If portal HTN & liver failure: esophageal varices, bleeding, encephalopathy, splenomegaly. 69
- 70. The Fate of Bilirubin Hemoglobin from old red blood cells becomes bilirubin The liver converts bilirubin into conjugated bilirubin Bilirubin passes on to the intestine Bacteria convert it to urobilinogen º Some is lost in feces º Most is reabsorbed into the blood via portal circulation Returned to the liver to be reused unconjugated bilirubin in blood bilirubinemia jaundice liver links it to gluconuride conjugated bilirubin bile 70
- 71. The Fate of Bilirubin… Why would a man with liver failure develop jaundice? 71
- 72. Liver Failure Leads To … Hematologic disorders Anemia, thrombocytopenia (low platelet), coagulation defects, leukopenia (WBC) Metabolic disorders Fluid retention, hypokalemia, disordered sexual functions Which hormones would cause these endocrine disorders? 72
- 73. Liver Failure Leads To …(cont.) Skin disorders Jaundice, red palms, spider nevi Hepatorenal syndrome Azotemia, increased plasma creatinine, oliguria Hepatic encephalopathy Asterixis, confusion, coma, convulsions Ammonia not converted to urea 73
- 74. Veins Draining into the Hepatic Portal System Portal hypertension causes pressure in these veins to increase Varicosities and shunts develop Organs engorge with blood 74
- 76. Biliary Tract Hepatic duct Pancreatic duct Gall bladder Cystic duct Common bile duct Ampulla of Vater Sphincter of Oddi 76
- 77. Disorders of the Gallbladder Cholelithiasis (gallstones) Cholesterol, calcium salts, or mixed Acute and chronic cholecystitis Inflammation caused by chemical irritation due to concentrated bile. Can result in ischemia from mucosal swelling Choledocholithiasis Stones in the common bile duct Cholangitis Inflammation of the common bile duct 77
- 78. Cholestasis and Intrahepatic Biliary Disorders 78
- 79. Gall Stones 79
- 80. Cholecystitis Gall bladder disease Acute – Complete or partial obstruction of the cystic or common bile ducts. Inflammation caused by chemical irritation from the concentrated bile, mucosal swelling and ischemia. Bacterial infection Mucosal necrosis gangrene perforation Risk Factors The Five F’s 80
- 81. SIGNS AND SYMPTOMS RUQ pain that radiates to the tip of the right scapula Murphy’s sign Excessive belching Flatus Nausea and vomiting Low-grade fever Elevated WBC count Worsening symptoms after ingesting fried foods. 81
- 82. DIAGNOSIS/ TREATMENT Ultrasound Gallbladder scan Treatment Bowel rest, intravenous hydration, analgesia, and intravenous antibiotics. For mild cases of acute cholecystitis, antibiotic therapy with a single broad-spectrum antibiotic is adequate Laparoscopic cholecystectomy (“Lap Chole”) 82
- 83. The Pancreas Pancreas Exocrine pancreas releases digestive juices through a duct to the duodenum Endocrine pancreas releases hormones into the blood 83
- 84. Exocrine Pancreas Acini produce: Inactive digestive enzymes Trypsin inactivator These are sent to the duodenum In the duodenum, the digestive enzymes are activated 84
- 85. Biliary Reflux 5. Bile in pancreas disrupts tissues; digestive enzymes activated 4. Bile goes up pancreatic duct 1. Gallbladder contracts 2. Bile is sent down common bile duct 85 3. Blockage forms in ampulla of Vater: bile cannot enter duodenum
- 86. Pancreatitis 86
- 87. ACUTE PANCREATITIS Rapidly developing, potentially fatal, inflammatory disease of the pancreas Escape of pancreatic enzymes cause autodigestion of the pancreas and fat necrosis Causes: Gall stones/Alcohol/GI surgery 87
- 88. Autodigestion of the Pancreas Activated enzymes begin to digest the pancreas cells Severe pain results Inflammation produces large volumes of serous exudate hypovolemia Elevated enzymes (amylase, lipase) appear in the blood Areas of dead cells undergo fat necrosis Calcium from the blood deposits in them º Hypocalcemia 88
- 89. Acute Pancreatitis Signs & Symptoms Severe abrupt abdominal pain that may radiate to the back. Pain worse in supine position N/V Hyperglycemia Hypotension & tachycardia Fever Elevated pancreatic enzymes – Amylase, Lipase, Tx – aggressive hydration, antibiotics, NPO, NGT, pain management, surgery 89
- 90. Chronic Pancreatitis and Pancreatic Cancer Have signs and symptoms similar to acute pancreatitis MOST common cause: ETOH Permanent destruction of exocrine function and later stages also endocrine fxn destruction Often have: Digestive problems because of inability to deliver enzymes to the duodenum Glucose control problems because of damage to islets of Langerhans Signs of biliary obstruction because of underlying bile tract disorders or duct compression by tumors 90
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