Gastrointestinal structure/function

Transcription

1 Pathophysiology JP Advis DVM, Ph.D. Bartlett Hall, Animal Sciences, Cook, , 21 Course website: rci.rutgers.edu/~advis Lectures, tests, grades, office hours, textbook, Material to be covered: About lecture slides: Lectures 1-2: Introduction to Pathophysiology (2) Lectures 3-4: Mechanisms of Self-Defense and Stress (2) Lectures 5-8: Endocrine and Nervous System Dysfunctions (4) Lecture 9: Alterations of Skeletal Muscle Function (1) REVIEW AND TEST #1 Lectures 12-18: Cardiovascular, Respiratory and Renal Dysfunctions (7) REVIEW AND TEST #2 Lectures 21-24: Alterations of Digestive Function and Intermediary Metabolism (4) Lectures 25-26: Alterations of the Reproductive System (2) REVIEW AND TEST #3 There are not intended to be the sole source for studying the course material!!!!!!!!!!!!!!!! Slides are good to review the course material after you have study your course textbook Slides are a good indicator of the relative importance of lecture topics (see slide # per topic Group slides by titles when using them to review course material. Match lectures and text. Gastrointestinal structure/function The GI tract is a tube formed by distinct layers mediating all GI functions. These are controlled by ANS and hormones (through intrinsic and extrinsic reflexes). Swallowing and defecation are the exceptions which are controlled voluntarily. Gastric-duodenal interaction is the best example of the complex neuro-endocrine interrelationships between adjacent GI sections. Gastric acid secretion has three phases. Most digestion occurs in the duodenum and is under neuronal and endocrine control. Carbohydrates, aminoacids, and fats are absorbed mainly by the duodenum and jejunum, bile salts and vitb12 are absorbed by the ileum. B12 absorption requires Intrinsic Factor. Minerals and water-soluble vitamins are absorbed throughout small intestine. I strongly suggest that students review the basic physiology of the gastro-intestinal system from both their physiology and endocrinolgy courses. A summary chapter is provided in the course textbook, prior to the gastro-intestinal pathophysiology section. Page 1

2 Gastrointestinal structure/function The digestive system and the wall of the GI tract Parotid gland Submandibular gland Pharinx Esophagus Diaphragm Transverse colon Tongue Sublingual gland Larinx Trachea Liver Stomach Spleen Ascending colon Small intestine Cecum Vermiform appendix Rectum Gallbladder Pancreas Descending colon Sigmoid colon Anal canal Page 2

3 Blood vessels Mesentery Nerve SEROSA connective tissue layer peritoneum myenteric plexus submucosal plexus ENTERIC PLEXUS SUBMUCOSA duct in submucosa duct from gland MUCOSA mucous epithelium lamina propia muscularis mucosea MUSCULARIS circular muscle layer lymph node longitudinal muscle layer Gastrointestinal structure/function The salivary glands, their secretion and flow rate Page 3

4 Gastrointestinal structure/function The stomach, gastric pits and gastric glands Page 4

5 Esophagus Gastro esophageal opening Lower esophageal sphincter Fundus Body Duodenal bulb Duodenum Pyloric sphincter Pylorus Serosa Longitudinal muscle Circular muscle Oblique muscle Mucosa Submucosa Muscularis Antrum Rugae Surface mucosal cells Gastric pit Lamina propria Mucosa Muscularis mucosae Submucosa Blood vessels Oblique muscle layer Muscularis Circular muscle layer Longitudinal muscle layer Serosa Connective tissue Viceral peritoneum Page 5

6 Gastrointestinal structure/function The stomach, gastric secretion and parietal cell Concentration in gastric fluid in meq/l Cl H Na K Secretory rate Page 6

7 Gastrointestinal structure/function The small intestine Villi mucosa Lamina propria Muscularis mucosae Duodenal gland extending into mucosa Circular muscle layer Longitudinal muscle layer Serosa Cecum Appendix Ileum Jejunum Page 7

8 Gastrointestinal structure/function Carbohydrates digestion and absorption Digestion and absorption of foodstuffs Carbohydrates digestion and absorption Starch Salivary amylase MOUTH Dextrin, oligosacharides Pancreatic amylase Lactose Maltose Sucrose Brush border enzymes (lactose, maltose, sucrose) SMALL INTESTINE Galactose Glucose Fructose Absorbed by capillaries in the villi and transported to the liver by portal vein Page 8

9 Gastrointestinal structure/function Protein digestion and absorption Digestion and absorption of foodstuffs Protein digestion and absorption Proteins Pepsine in presence of hydrochloric acid STOMACH Proteins, proteases, peptones Pancreatic enzymes (trypsin, chemotrypsin, carboxypeptidases) SMALL INTESTINE Small polypeptides, dipeptides Brush border enzymes (aminopeptidases, and dipeptidases) SMALL INTESTINE Amino acids Absorbed by capillaries in the villi and transported to the liver by hepatic portal vessels Page 9

10 Gastrointestinal structure/function Fat digestion and absorption Digestion and absorption of foodstuffs Fat digestion and absorption Unemulsified fats Emulsifying agents (bile acids, fatty acids, monoclycerides, lecithin, cholesterol, and protein) SMALL INTESTINE Pancreatic lipases SMALL INTESTINE Monoglycerides and fatty acids Glycerol and fatty acids Absorbed by lacteals in the villi and transported to the liver in the systemic circulation, which receives lymphatic flow from the thoracic duct or via the hepatic portal vein Glycerol and short chain fatty acids absorbed by capillaries in the villi and transported to the liver by the portal vein Page 10

11 Gastrointestinal dysfunctions Anorexia, is lack of desire to eat despite physiological stimuli that would normally produce hunger. Vomiting, is forceful emptying of the stomach effected by gastrointestinal contraction and reverse peristalsis. Constipation, is often caused by unhealthy habits combined with lack of exercise. It also might result from impair GI motility or obstruction of the intestinal lumen. Diarrhea, can be caused by excessive fluid drawn into the intestinal lumen by osmosis, excessive secretion of fluids by intestinal mucosa, or excessive intestinal motility. Abdominal pain is due to stretching, inflammation, or ischemia. It originates in the organ itself or in the peritoneum. It can be acute or chronic. Visceral pain is often referred to the back. Manifestations of GI bleeding are hematemesis, melena, and hematochezia. Occult bleeding can only be detected by testing stools or vomitus for the presence of blood. Dysphagia can be caused by a functional or a mechanical obstruction of the esophagus. Achalasia is a dysphagia due to loss of innervations. Gastrointestinal dysfunctions Pathopysiology of gastrointestinal bleeding Page 11

12 Upper GI bleeding (esophageal varices bleeding ulcers Mallory-Weiss tear) Lower GI bleeding (intestinal polyps inflammatory disease intestinal cancer hemorroids) Acute, massive GI bleeding (loss of 1L or 20% of BV in a few hours) BV depletion Accumulation of blood in GI tract Increase peristalsis and diarrhea Digestion of blood proteins Increased BUN Decreased CO and systolic BP, increased HR Compensatory constriction of peripheral arteries Decreased blood flow to skin (pallor) Death Metabolic acidosis Decreased blood flow to kidneys Tubular necrosis Renal failure (anuria / oliguria) Decreased blood flow to GI Lactic acidosis Anoxia Compensatory failure Mesenteric insufficiency (pain) Bowel infarction, liver necrosis GI bleeding Decreased blood flow to brain (anxiety, confusion, stupor, coma) Decreased coronary blood flow (MI, pulmonary edema, heart failure, dysrhythmias) Gastrointestinal dysfunctions Achalasia, hiatal hernia, intestinal obstructions Page 12

13 Achalasia Hiatal hernia Intestinal obstruction Gastrointestinal dysfunctions Pathophysiology of intestinal obstruction Page 13

14 Intestinal obstruction Sequestration of fluid and gas proximal to obstruction Distention Pressure on diaphragm Low respiratory volume Atelectasis Pneumonia Prolonged increase of intraluminal wall tension Decreased venous return Intestinal bowel wall edema Colicky abdominal pain Nausea & vomiting (low food intake, nutrient absorption, CH reserve, ketosis) Loss of water & electrolytes Dehydration Hypokalemia (atony) Hypochloremia Decreased arterial BF Ischemia Alkalosis (early or high obstruction), low Cl + high bicarbonate Acidosis (late or low obstruction), high H + low K, ketosis (starvation) lactic acidosis Decreased ECF volume Decreased plasma volume Hemoconcentration Decreased CVP Tachycardia Increased capillary permeability (fluid loss to peritoneum) Perforation Hypovolemia Bacterial translocation Release of toxins Fever Peritonitis Shock Intestinal obstruction Gastrointestinal dysfunctions Lesions caused by peptic ulcer disease Page 14

15 Erosion True ulcer True ulcer mucosa muscularis mucosae submucosa tunica muscularis serosa Peptic ulcer Gastrointestinal dysfunctions Duodenal ulcer Lesions caused by duodenal ulcer Page 15

16 ulcer crater mucosa submucosa circular muscle coat longitudinal muscle coat serosa (viceral peritoneum ULCER duodenum common bile duct pyloric sphincter duodenal papillae head of pancreas superior mesenteric artery and vein Duodenal ulcer Gastrointestinal dysfunctions Duodenal ulcer Lesions caused by duodenal ulcer Page 16

17 Gastrointestinal dysfunctions Gastric ulcer Pathophysiology of gastric ulcer formation H. pylori, Bile salts, NSAIDs, alcohol, ischemia Damaged mucosa barrier Decreased function of mucosal cells Decreased quality of mucus Loss of tight junctions between cells Gastric ulcer Back-diffusion of acid into gastric mucosa Conversion of pepsinogen to pepsin Formation and liberation of histamine Acid secretion Local vasodilation Helicobacter pilori Further mucosal erosion Destruction of blood vessels Bleeding Increased capillary permeability Loss of plasma proteins Mucosal edema Loss of plasma and gastric lumen Mucosal injury ulceration Stimulation of cholinergic intramural plexus causing muscle spasm Page 17

18 Gastrointestinal dysfunctions Diverticular disease in sigmoid colon (herniations) Diverticular disease Page 18

19 Gastrointestinal dysfunctions Portal hypertension, ascitis, hepatic encephalopathy, jaundice, and hepatorenal syndrome are complications of many liver. Portal hypertension is caused by high resistance to venous flow in portal vein and its tributaries, including sinusoids & hepatic vein. It is the most serious complication of liver disease causing bleeding varices, ascitis, and hepatic encephalopathy. Jaundice is an hyperbilirubinemia caused by an obstraction of bile canaliculi in the liver, or of bile ducts outside the liver. Bilirubin is accumulated proximal to obstructed sites, enters bloodstream, its carried to the skin and deposited. Hemolytic jaundice is caused by RBC destruction at a rate exceeding liver capacity to metabolize unconjugated bilirubin. Hepatorenal syndrome is a functional kidney failure caused by advanced liver disease, mainly cirrhosis with portal hypertension. Renal failure is caused by a sudden decrease in kidney blood flow, usually due to massive gastrointestinal hemorrhage or liver failure. Pathophysiology of accessory organ Gastrointestinal dysfunctions Varices related to portal hypertension Page 19

20 Varices related to portal hypertension Gastrointestinal dysfunctions Ascitis Page 20

21 Ascitis Gastrointestinal dysfunctions Jaundice Page 21

22 Jaundice Gastrointestinal dysfunctions Cirrhosis Page 22

23 Cirrhosis Gastrointestinal dysfunctions Resected gallbladder with mixed gallstones Page 23

24 Resected gallbladder with mixed gallstones Your tenth case study SUMMARY: A 43-year old woman presents to the emergency department with the acute onset of abdominal pain. Her pain is located in the upper right quadrant (RUQ) and radiates to the right shoulder. She reports nausea and vomiting but not fever or chills. The RUQ pain is worse after she eats fatty meals. On examination, the patient has severe RUQ tenderness. Her with blood cell count is elevated, as are her liver function tests and alkaline phosphatase levels. The amylase and lipase levels are normal. TENTATIVE DIAGNOSIS: LAB TESTS: FINAL DIAGNOSIS: TREATMENT: Page 24

25 SUMMARY: A 43-year old woman presents to the emergency department with the acute onset of abdominal pain. Her pain is located in the upper right quadrant (RUQ) and radiates to the right shoulder. She reports nausea and vomiting but not fever or chills. The RUQ pain is worse after she eats fatty meals. On examination, the patient has severe RUQ tenderness. Her with blood cell count is elevated, as are her liver function tests and alkaline phosphatase levels. The amylase and lipase levels are normal. TENTATIVE DIAGNOSIS: LAB TESTS: FINAL DIAGNOSIS: TREATMENT: Page 25