GI Patho PDF

GI Alterations Clinical Manifestations of GI Dysfunction Anorexia – a lack of a desire to eat despite physiologic stimuli that would normally produce hunger ○ Nonspecific symptom that is often associated with nausea, abd pain, diarrhea, and psychologic distress Vomiting Vomiting center: medulla oblo...

GI Alterations Clinical Manifestations of GI Dysfunction Anorexia – a lack of a desire to eat despite physiologic stimuli that would normally produce hunger ○ Nonspecific symptom that is often associated with nausea, abd pain, diarrhea, and psychologic distress Vomiting Vomiting center: medulla oblongata Several types of stimuli initiate the vomiting reflex ○ Brain stimulation of receptors in the chemoreceptor trigger zone of the area in the fourth ventricle leads to vomiting. ○ Vestibular system initiates vomiting via the eighth cranial nerve Metabolic consequences of vomiting are fluids electrolyte, and acid-balance disturbances ○ Hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis Nausea – subjective experience that is associated with a number of conditions ○ The common associated symptoms of nausea are hyper-salivation and tachycardia Retching – nonproductive vomiting Projectile vomiting is spontaneous vomiting that does not follow nausea or retching ○ Caused by direct stimulation of the vomiting center by neurologic lesions (increased ICP, tumors, or aneurysms involving the brain stem) Vomiting is usually associated with nausea and follows retching. Constipation is defined as infrequent or difficult defecation ○ Must be individually defined because bowel patterns vary between individuals ○ Pathophysiology Normal transit (functional) constipation: Normal rate of stool passage, but difficulty with stool evacuation from low-residue, low-fluid diet Slow-transit constipation: Impaired colonic motor activity with infrequent bowel movements and straining Pelvic floor dysfunction (pelvic floor dyssynergia or anismus): Failure of the pelvic floor muscles or anal sphincter to relax with defecation Secondary: From an actual disease process or condition ○ Clinical manifestations Two of the following for at least 3 months: Straining with defecation at least 25% of the time Lumpy or hard stools at least 25% of the time Sensation of incomplete emptying at least 25% of the time Manual maneuvers to facilitate stool evacuation for at least 25% of defecations Fewer than three bowel movements per week Fecal impaction – hard, dry stool retained in rectum Diarrhea – increased frequency of bowel movements & increased volume, fluidity, weight of the feces ○ Large-volume diarrhea – volume of feces in increased; caused by excessive amounts of water or secretions or both in intestines ○ Small-volume diarrhea – volume of feces is not increased; result of increased intestinal motility ○ Systemic effects of prolonged diarrhea are dehydration, electrolyte imbalance, metabolic acidosis, and weight loss ○ Steatorrhea (fat in stools) and diarrhea are common signs of malabsorption syndromes ○ Systemic manifestations of diarrhea Manifestations of acute bacterial or viral infection Fever, with or without cramping pain Manifestations of inflammatory bowel disease Fever, cramping pain, bloody stools Manifestations of malabsorption syndromes Steatorrhea (fat in the stools) and diarrhea Abdominal pain – symptom of a number of gastrointestinal (GI) disorders ○ From stretching, inflammation, or ischemia ○ Parietal (somatic) pain: In the peritoneum ○ Visceral pain: In the organs themselves ○ Referred pain: Felt in another area, usually the back ○ RUQ = liver, gall bladder, bile duct ○ RLQ = appendix, right ovary/fallopian tube ○ LUQ = stomach, gastroesophageal junction, spleen ○ LLQ = descending colon (common site of diverticula), left ovary/fallopian tube Fecal Characteristics Color normally brown and odor dependent of food intake, form is normally soft Problems ○ Shape – narrow or ribbon like stool may reflect an obstruction in lower GI tract ○ Bloody stool = lower GI Bleed, inflammatory bowel disease, bacterial infection ○ Black Tarry Stools = Upper GI bleed, pepto-bismol intake, increased iron intake ○ ○ ○ Red, Blood in stool = lower GI tract problem hemorrhoids, cancer, ruptured diverticulum Clay-colored stool = gallbladder or liver disease (decrease in conjugated bilirubin causes) Frothy, Fatty Stool (steatorrhea) = with problems with fat digestion, children with cystic fibrosis, or in adults with pancreatic disease cholecystitis Indicates loss of bile, which again is necessary for adequate fat digestion Disorders of Motility Dysphagia – difficulty swallowing ○ Intrinsic – obstructions that originate in the wall of the esophageal lumen (tumors, strictures, and diverticular herniations) ○ Extrinsic – originate outside the esophageal lumen and narrow the esophagus by pressing inward (tumor) ○ Neuromotor function loss = difficulty beginning with both solids and liquids Gastroesophageal reflux disease (GERD) Physiologic reflux does not cause symptoms ○ LES relaxes and regurg of gastric contents into esophagus; acid is neutralized and cleared by peristaltic action in esophagus in 1-3 minutes, and LES tone is restored Nonerosive reflux (NERD) – symptoms of reflux disease but no visible mucosal injury Reflux esophagitis – combination of factors cause injury and inflammation Risk factors of GERD = obesity and H. pylori Clinical manifestations: ○ Heartburn, regurgitation of acidic chyme, and upper abd pain within 1 hour of eating ○ s/s worsen if person lies down or if intra-abd pressure increases (vomiting, coughing) ○ Association with GERD and; laryngitis, asthma, and chronic cough Gastritis Acute gastritis – associated with Helicobacter pylori, non steroidal anti-inflammatory drugs (NSAIDs), drugs, chemicals ○ Clinical manifestations – vague abdominal discomfort, epigastric tenderness, and bleeding Chronic Fundal Gastritis ○ Immune ○ Type A ○ Associated with auto antibodies to parietal cells and intrinsic factor, resulting in gastric atrophy and pernicious anemia Chronic Antral Gastritis ○ Nonimmune ○ Type B ○ Associated with H. pylori and NSAIDs Peptic Ulcer Disease A break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum Exact mechanism of causation not known ○ 2 basic pathophysiological processes; decreased mucosal protection and increased acid production ○ Decreased mucosal protection - NSAID use, stress ulcers, tobacco and alcohol use ○ Increased acid secretion - Zollinger-Ellison syndrome -gastronoma Superficial – called erosions because they erode the mucosa but do not penetrate the muscularis mucosae Deep – true ulcers extend through the muscularis mucosae and damage blood vessels causing hemorrhage or perforate the GI wall Duodenal Ulcers – most common of the peptic ulcers Tend to develop in younger people Most important developmental factor: Helicobacter pylori infection Other developmental factors: toxins and enzymes that promote inflammation and ulceration All cause acid and pepsin concentrations in the duodenum to penetrate the mucosal barrier and lead to ulceration Pain begins 30 minutes to 2 hours after eating, when the stomach is empty; can occur in the middle of the night and disappear by morning Relived by ingestion of food or antacids, “pain-food-relief” pattern Gastric Ulcer Frequent cause: H. pylori The primary defect is an increased mucosal permeability to hydrogen ions Gastric secretion tends to be normal or less than normal Pattern of pain-food-relief is common, but pain of gastric ulcers also occurs immediately after eating Tend to be chronic rather than alternate between periods of remission and exacerbation Cause more anorexia, vomiting, and weight loss than duodenal ulcers Stress Ulcer A stress ulcer is a peptic ulcer that is related to severe illness, neural injury, or systemic trauma Ischemic ulcers – within hours of trauma, hemorrhage, sepsis ○ Curling ulcers with burn injury Cushing ulcers – ulcers that develop as a result of a head/brain injury ○ Result of decreased mucosal blood flow and hypersecretion of acid caused by overstimulation of the vagal nuclei Pyloric Obstruction Also known as gastric outlet obstruction (GOO) The blocking or narrowing of the opening between the stomach and the duodenum Succussion splash – sloshing sound in abdomen ○ At this stage vomiting is cardinal sign ○ Copious and occurs several hours after eating ○ Contains undigested food but no bile Postgastrectomy Syndromes Dumping syndrome – rapid emptying of chyme from a surgically created residual stomach into the small intestine Developmental factors of early dumping syndrome: ○ Loss of gastric capacity ○ Loss of emptying control ○ Loss of feedback control by the duodenum when it is removed Malabsorption Syndromes Maldigestion – failure of the chemical processes of digestion Malabsorption – failure of the intestinal mucosa to absorb (transport) the digested nutrients Pancreatic insufficiency – insufficient pancreatic enzyme production ○ Lipase, amylase, trypsin, or chymotrypsin ○ Causes: Pancreatitis, pancreatic carcinoma, pancreatic resection, and cystic fibrosis ○ Fat maldigestion: Primary problem ○ Most common signs: Fatty stools (steatorrhea); weight loss Lactase deficiency – congenital defect in the lactase gene ○ Inability to break down lactose into monosaccharides and thus prevent lactose digestion and monosaccharide absorption ○ Fermentation of lactose by bacteria, causing gas (cramping pain, flatulence) and osmotic diarrhea Bile salt deficiency – conjugated bile salts are needed to emulsify and absorb fats and are synthesized from cholesterol in the liver. ○ Is the result of liver disease and bile obstructions. ○ Poor intestinal absorption of lipids causes fatty stools, diarrhea, and loss of fat-soluble vitamins (A, D, E, K). Fat-soluble vitamin deficiencies ○ Vitamin A – night blindness ○ Vitamin D – decreased calcium absorption, bone pain, osteoporosis, fractures ○ Vitamin K – prolonged prothrombin time, purpura, and petechiae ○ Vitamin E – testicular atrophy & neurologic defects in children Intestinal Obstruction & Ileus Intestinal obstruction – any condition that prevents the flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstructing lesion An ileus is an obstruction of the intestines Small intestine is more commonly obstructed because of narrower lumen Chronic or partial obstructions are more often associated with tumors or inflammatory disorders, particularly of the large intestine Small intestine obstruction – colicky pains caused by intestinal distention, followed by nausea and vomiting Large intestine obstruction – hypogastric pain and abdominal distention ○ Consequences related to the competence of the ileocecal valve ○ Acute colonic pseudo-obstruction (Ogilvie syndrome) is massive dilation of large bowel that occurs in critically ill patient and immobilized older adults Pylorus – early, profuse vomiting of clear gastric fluid Proximal small intestine – mild distention and vomiting of bile-stained fluid Lower in small intestine – more pronounced distention because a greater length of intestine is proximal to the obstruction ○ Vomiting may not occur or may occur later and contain fecal material Inflammatory Bowel Disease Feature Ulcerative Colitis Crohn's Disease Location of lesions Colon and rectum; no “skip” lesions All of GI tract—mouth to anus; “skip” lesions common Area affected Mucosal layer Entire intestinal wall Granuloma Rare Common “cobblestone” appearance Abdominal pain Occasional Common Bloody stools Common Less common Steatorrhea Rare Common Antineutrophil cytoplasmic antibody Common Rare Anti-saccharomyces cerevisiae antibody Rare Common Diverticular Disease of the Colon Diverticula – herniations of mucosa through the muscle layers of the colon wall, especially the sigmoid colon (left colon most commonly) Diverticulosis – asymptomatic diverticular disease Diverticulitis – inflammatory stage of diverticulosis; inflammation of the diverticula Clinical manifestations: ○ Cramping pain of lower abd can accompany constriction of the hypertrophied colonic muscles; which is exacerbated by eating Often incomplete relief of pain after defecation ○ Diarrhea, constipation, distention, or flatulence may occur ○ Diverticula with an obstructed opening become inflamed or abscesses form, and then patient gets fever, leukocytosis, and tenderness of the lower left quadrant ○ Right lower quadrant pain and severe complications (hemorrhage, perforation with peritonitis, bowel obstruction and fistula) are RARE Irritable Bowel Syndrome – functional gastrointestinal disorder with no specific structural or biochemical alterations as a cause of disease Characterized by recurrent abdominal pain and discomfort associated with altered bowel habits that present as diarrhea or constipation or both Symptoms are usually relieved with defecation and do not interfere with sleep Intestinal Vascular Insufficiency Mesenteric venous thrombosis – related to malignancies, Right sided heart failure, and DVT Acute mesenteric ischemia – there is decreased mucosal blood flow from arteries which supply the large and small intestine; results from dissecting aortic aneurysms, thrombi, or emboli Chronic mesenteric insufficiency – related to decreased blood flow; colicky pain after eating GI Bleeding Upper gastrointestinal bleeding ○ Esophagus, stomach, or duodenum ○ Commonly caused by bleeding peptic ulcers ○ Frank, bright red blood in emesis (Hematemesis – blood in vomit) or digested blood (“coffee grounds”) ○ Melena – dark tarry stools Lower gastrointestinal bleeding ○ Below the ligament of Treitz or bleeding from the jejunum, ileum, colon, or rectum ○ Can be caused by polyps, diverticulosis, cancer, hemorrhoids Hematochezia – bright red or burgundy blood from rectum Occult bleeding – normally caused by slow, nonobvious blood loss that results in iron deficiency anemia as iron stores in the bone marrow are slowly depleted Obesity Molecules that stimulate eating: Orexins (hypocretins [from the hypothalamus], a peptide family that act as neurotransmitters for stimulating eating) Molecules that inhibit eating: Anorexins Visceral obesity/intraabdominal,central, or masculine obesity – distribution of body fat is localized around the abdomen and upper body, resulting in an apple shape Peripheral obesity/gluteal-femoral, feminine, or subcutaneous obesity – distribution of body fat is extraperitoneal and distributed around the thighs and buttocks and through the muscle, resulting in a pear shape Appendicitis Obstruction of the lumen leads to increased epigastric and RLQ pain Rebound tenderness in right lower quadrant Gallbladder Black pigmented stones – formed in a sterile environment and are primarily composed of calcium bilirubinate polymer from hyperbilirubinemia. Brown stones – associated with bacterial infection of the bile ducts with formation of stone that is composed of calcium soaps, unconjugated bilirubin, cholesterol, fatty acids, and mucin Epigastric and right upper quadrant pain Intolerance to fatty foods Biliary colic – lodging of stones in the cystic or common duct Jaundice – stone in the common bile duct Cholecystitis – inflammation of the gallbladder; abdominal tenderness and fever Pancreas Pancreatitis – inflammation of the pancreas Associated with several clinical disorders (alcohol intake and cholelithiasis) Is caused by injury or damage to pancreatic cells and ducts, causing a leakage of pancreatic enzymes into the pancreatic tissue. These enzymes cause autodigestion of pancreatic tissue and leak into the bloodstream to cause injury to blood vessels and other organs. Ranson criteria for pancreatitis: on admission (GA LAW) ○ Glucose >200 ○ AST >250 ○ LDH >350 ○ Age >55 y.o. ○ WBC >16000 Ranson criteria for pancreatitis: initial 48hr (C & HOBBS) ○ Calcium < 8 ○ Hct drop > 10% ○ Oxygen (room air PaO2) < 60 mmHg ○ Base deficit > 4 ○ BUN incr > 5 ○ Sequestration of fluid > 6L Chronic pancreatitis – associated with increased intra-ductal pressure, increased tissue pressure, ischemia, neuritis, ongoing injuring, and changes in central pain perception Acute Liver Function Hepatocytes become edematous. Patchy areas of necrosis and inflammatory cell infiltrates disrupt the parenchyma. Hepatic necrosis is irreversible. Cirrhosis – irreversible inflammatory fibrotic disease that disrupts liver function and even liver structure Alcoholic liver disease – oxidation of alcohol, causing damage to hepatocytes ○ Stages: Steatosis (alcoholic fatty liver) – the mildest form; reversible if drinking is stopped. Alcoholic hepatitis (steatohepatitis) – characterized by inflammation; degeneration and necrosis of the hepatocytes occur. Alcoholic cirrhosis (fibrosis) – toxic effects of alcohol metabolism on the liver, immunologic alterations, oxidative stress from lipid peroxidation, and malnutrition occur. ○ Impairs the hepatocytes’ ability to oxidize fatty acids, synthesize enzymes and proteins, degrade hormones, and clear portal blood of ammonia and toxins ○ Clinical manifestations – nausea, anorexia, fever, abdominal pain, and jaundice Nonalcoholic fatty liver disease – infiltration of hepatocytes with fat that occurs in the absence of alcohol intake; associated with obesity. Biliary (bile canaliculi) – cirrhosis begins in bile canaliculi and ducts. ○ Primary biliary cirrhosis (autoimmune) – T lymphocyte–mediated and antibody-mediated destruction of the small intrahepatic bile ducts Secondary biliary cirrhosis – obstruction of common bile duct Liver Disorders Portal hypertension – abnormally high blood pressure in the portal venous system caused by resistance to portal blood flow ○ There are 3 regions affected: Prehepatic (the portal vein) – mainly caused by thrombosis or narrowing of the portal vein Intrahepatic (within the liver itself) – result from vascular remodeling with intrahepatic shunts, thrombosis, inflammation, or fibrosis of the sinusoids Posthepatic (hepatic vein) – occur from hepatic vein thrombosis or cardiac disorders (right sided heart failure or constrictive pericarditis) that impair the pumping ability of the right heart; blood backs up and increases pressure in portal system ○ High pressure in the portal veins causes collateral vessels to open between the portal veins and systemic veins; blood bypasses the obstructed portal vessels because blood pressure is considerably lower ○ Consequences: Varices (distended, tortuous, collateral veins) Splenomegaly (enlargement of the spleen) Ascites (accumulation of fluid in the peritoneal cavity, which is the space between the visceral peritoneum and the parietal peritoneum) ○ Hepatic encephalopathy Jaundice Extrahepatic obstruction to bile flow (gallstones) Intrahepatic obstruction (hepatocellular disease such as cirrhosis or hepatitis) Prehepatic obstruction – excessive production of bilirubin (excessive hemolysis of red blood cells) Viral Hepatitis Prodromal (pre-icteric) phase – begins approximately 2 weeks after exposure; ends with the appearance of jaundice…highly transmittable Icteric phase – the actual phase of illness Recovery phase – begins with the resolution of jaundice Hepatitis A – RNA hepatovirus; usually transmitted by the fecal-oral route Hepatitis B – transmitted through contact with infected blood, body fluids, and contaminated needles; 42-nm hepadnavirus with partially double stranded DNA genome Hepatitis C – single stranded RNA virus Cancer of GI Tract Esophageal carcinoma – alcohol and tobacco use concurrently, reflux esophagitis radiation exposure, and nutritional deficiencies are associated Gastric carcinoma – associated with H. pylori (CagA), high salt intake, food preservative (nitrates and nitrites), and atrophic gastritis Colorectal cancer – cancer of colon and rectum; second most common cancer death in the US Rectal carcinoma – located up to 15cm from the opening of the anus Primary liver cancer – infection with hepatitis A, C, and D viruses, particularly in conjunction with cirrhosis are known risk factors Cancer of the gallbladder – rare yet lethal Pancreatic cancer – ranks fifth as a cause of cancer deaths; one known risk factor is heavy cigarette smoking