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ALTERATIONS OF DIGESTIVE FUNCTION
Clinical Manifestations of Gastro-Intestinal Dysfunction Anorexia Nonspecific symptom and is often associated with nausea, abdominal pain, diarrhea, and psychological stress Vomiting Tachycardic, tachypnea, diaphoresis, nausea Constipation Diarrhea Abdominal Pain GI Bleeding Upper GI bleeding is bleeding in the esophagus, stomach or duodenum and I characterized by frank, bright-red bleeding, or dark, grainy digested blood “coffee grounds” that has been affected by stomach acids Commonly caused by bleeding varices (varicose veins) in the esophagus, peptic ulcers, arteriovenous malformations, or a Mallory-Weiss tear at the esophageal gastric junction caused by severe retching Lower GI bleeding happens in the jejunum, ileum, colon, or rectum, can be caused by polyps, diverticulitis, inflammatory disease, cancer, or hemorrhoids Occult bleeding is caused by slow, chronic blood loss that is not obvious and results in iron deficiency anemia as iron stores in the bone marrow are slowly deplete Physiological response to GI bleeding depends on the amount and rate of the loss Changes in blood pressure (hypotension), heart rate (tachycardia) are the best indicators of massive blood loss in the GI Tract Signs of large-volume blood loss are postural hypotension, lightheadedness, and loss of vision Tachycardia develops as a compensatory response to maintain cardiac output and tissue perfusion If blood loss continues, hypovolemic shock develops Diminished blood flow to the kidneys causes decreased urine output and may lead to oliguria, tubular necrosis, and kidney failure Insufficient cerebral and coronary blood flow causes irreversible anoxia and death Accumulation of blood in the GI tract is irritating and increases peristalsis, causing vomiting, diarrhea, or both Bleeding from the lower GI tract, diarrhea is frankly bloody, and the upper GI tract is rapid enough to produce hematochezia (bright red stools), also producing melena (black-tarry stools) Upper GI bleeding is reflected by an increase in BUN levels Hematocrit and hemoglobin values are not the best indicators of acute GI bleeding because plasma volume and red cell volume are lost proportionately Dysphagia
Hiatal Hernia Diaphragmatic hernia with protrusion (herniation) of the upper part of the stomach through the diaphragm and into the thorax Sliding hiatal hernia is the most common o Proximal portion of the stomach moves into the thoracic cavity through the esophageal hiatus, and opening in the diaphragm for the esophagus and vagus nerves o GERD is associated with his hernia o Coughing, bending, tight clothing, ascites, obesity, and pregnancy accentuate the hernia Paraesophageal hiatal hernia o Herniation of the greater curvature of the stomach through a secondary opening in the diaphragm alongside the esophagus o Position of a portion of the stomach above the diaphragm causes congestions and mucosal blood flow leading to gastritis and ulcer formation o Strangulation of the hernia is a major complication o Presents with vomiting and epigastric and retrosternal epigastric pain is a surgical emergency o Treatment is to diminish reflux by eating small, frequent meals and avoiding the recumbent position after eating o Antacids to alleviate reflux esophagitis Mixed hiatal hernia o Less common and is a combination of sliding and paraesophageal hiatal hernias o Occurs in the conjunction with reflux esophagitis, peptic ulcer, cholecystitis, cholelithiasis, chronic pancreatitis, and diverticulosis Hiatal hernias are asymptomatic Diagnostic procedures include radiology with barium swallow, endoscopy, and high- resolution manometry o Chest x-ray will show the protrusion of the stomach into the thorax Pyloric Obstruction Narrowing or blocking of the opening between the stomach and the duodenum Can be congenital or acquired Acquired obstruction is caused by PUD or carcinoma near the pylorus Duodenal ulcers are more likely than gastric ulcers to obstruct the pylorus Ulceration causes obstruction resulting from inflammation, edema, spasm, fibrosis, or scarring Clinical Manifestations Vague epigastric fullness but becomes more distressing after eating and at the end of the day Nausea and epigastric pain may occur as the muscles of the stomach contract in attempts to force chyme past the obstruction Progression of the obstruction will lead to anorexia (weight loss), gastric distension and atony (lack of muscle tone and gastric motility) Succession splash = vomiting (Cardinal sign) Prolonged pyloric causes severe malnutrition, dehydration and extreme debilitation
Gastritis Inflammatory disorder of the gastric mucosa Acute gastritis is caused by injury of the protective mucosal barrier caused by medications, chemicals or H.pylori infection o NSAIDs inhibit the action of cyclooxygenase-1 (COX-1) and cause gastritis because they inhibit prostaglandin synthesis o H.pylori-associated acute gastritis causes inflammation, increased gastric secretion in antral gastritis, decreased gastric section in fundal gastritis, pain, nausea, and vomiting o Symptoms include vague abdominal discomfort, epigastric tenderness, and bleeding o Antacids or decreasing acid secretion with H2 receptor antagonists facilitates healing Chronic gastritis o Occurs in older adults and causes chronic inflammation, mucosal atrophy, and epithelial metaplasia o Type A immune fundal or type B nonimmune antral; if both occur as type AB or pangastritis, the antrum is more severely involved, type C is associated with reflux of bile and pancreatic secretions into the stomach causing chemical injury o Type A immune fundal is the rarest form of gastritis and is associated with loss of T lymphocyte tolerance and development of autoantibodies to gastric hydrogen- potassium-ATPase o Type B nonimmune antral gastritis involves the antrum only and is caused by H. pylori bacteria and is associated with the use of alcohol, tobacco, and NSAID High levels of hydrochloric acid secretion increase the risk of duodenal ulcers Can progress to autoimmune atrophic gastritis and involves the fundus becoming pangastritis o Signs and symptoms include anorexia, fullness, nausea, vomiting and epigastric pain; gastric bleeding o Gastroscopic examination and biopsy may show a longstanding inflammatory process and gastric atrophy in individual with no history of abdominal distress o Avoid alcohol and aspirin; manage by eating smaller email o H.pylori is treated with antibiotics and vitamin B12 is administered to correct pernicious anemia Peptic Ulcer Disease A break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum Ulcers develop when mucosal protective factors are overcome by erosive factor commonly caused by NSAIDs and H.pylori infection Superficial ulcerations are called erosions because they erode the mucosa but do not penetrate the muscularis mucosae True ulcers extend through the muscularis mucosae and damage blood vessels, causing hemorrhage, or perforate the GI wall
Zollinger-Ellison syndrome is a rare syndrome that also is associated with PUD caused by a gastrin-secreting neuroendocrine tumour or multiple tumours (Gastrinoma) of the pancreas or duodenum o Increased secretion of gastrin causes excess secretion of gastric acid, resulting in gastric and duodenal ulcers, GERD with abdominal pain and diarrhea Duodenal Ulcers Occur with greater frequency than other types of peptic ulcer and are commonly caused by H. pylori infection and NSAID use Idiopathic duodenal ulcers are rare and can be associate with altered mucosal defences, rapid gastric emptying, elevated serum gastrin levels, or acid production stimulated by smoking Pathophysiology H.pylori infection activates T and B lymphocytes with infiltration of neutrophils Release of inflammatory cytokines damages the gastric epithelium H.pylori virulence factor CagA (cytotoxin-associated gene A) produces vacuolating cytotoxin A (VacA), causing apoptosis of gastric epithelial cells and promoting inflammation Cause acid and pepsin concentrations in the duodenum to penetrate mucosal barrier causing ulceration Manifestations Chronic intermittent pain in the epigastric area Begins 2-3 hours AFTER eating when the stomach is empty Not unusual for the pain to occur in the middle of the night and disappear by morning Pain is relieved rapidly by ingestion of food or antacids Hemorrhage or perforation can be seen in a person with a history of NSAID or anticoagulant use Complication includes bleeding, perforation and obstruction of the duodenum or out of the stomach Heal spontaneous but recur within months without treatment Evaluation and Treatment Endoscopic evaluation allows visualization of lesions and biopsy Radioimmune assays of gastrin levels are evaluated to identify ulcers associated with gastric carcinomas H.pylori is detected using the urea breath test o Specific serum IgG and IgA antibodies, and measurement of H.Pylori stool antigen levels o Findings from gastric biopsy detect H.pylori infection and confirm eradiation after treatment o Treated with antibiotics and proton pump inhibitors Antacids to neutralize gastric contents and relieve pain; medications that block H receptor and inhibit secretion of acid (PPI) Gastric Ulcers Ulcers of the stomach and occur equally in males and females Pathophysiology Develops in the antral region Abnormality that increases the mucosal barrier’s permeability to hydrogen ions
Mild UC involves less mucosa o Resulting in less frequency of bowel movements, bleeding, and pain is minimal Severe UC involves the entire colon o Abdominal pain, fever, elevated pulse rate, frequent diarrhea (10-20 stools/day), urgency, bloody stools, cramp pain o Dehydration, weight loss, anemia, and fever result from fluid loss, bleeding, and inflammation Complication result in anal fissures, hemorrhoids, and perirectal abscess Evaluation and Treatment Diagnosis is based on clinical manifestations, medical history, laboratory, serological, radiological, endoscopic, and biopsy findings Infection causes are ruled out by stool culture Mild to moderate UC is treated with 5-aminosalicylate therapy followed by steroids For severe UC, thioprine and immunomodulatory agents or vedolizumab Crohn’s Disease Idiopathic inflammatory disorder that affects any part of the GI tract from mouth to anus Diarrhea is a common symptom with rectal bleeding if the colon is involved, weight loss and abdominal pain Imaging of the small intestine is used in the diagnosis of CD either a small bowel series or a capsule endoscopy (camera pill) Smoking cessation is a component of therapy Immunomodulators are effective for initial therapy or for resistance to other medications Irritable Bowel Syndrome A symptom-based disease characterized by recurrent abdominal pain with altered bowel habits Characterized by pain or discomfort and bloating o Women report more abdominal pain and constipation, men report more diarrhea o Gas, bloating, and nausea are usually relieved with defecation and do not interfere with sleep DISORDERS OF THE ACCESSORY ORGANS OF DIGESTION
Portal Hypertension Abnormally high blood pressure in the portal venous system caused by resistance to blood flow Normal pressure is 3 mmHg, in portal hypertension is 10 mmHg Pathophysiology Caused by disorder that obstruct or impede blood flow through any component of the portal venous system or vena cava Intrahepatic causes result from vascular remodelling with shunts, thrombosis, inflammation, or fibrosis of the sinusoids, as occurs in cirrhosis of the liver, biliary, cirrhosis, viral hepatitis, or schistosomiasis (a parasitic infection) Posthepatic causes occur from hepatic vein thrombosis or cardiac disorders that impair the pumping ability of the right side of the heart causes blood to collect and increases pressure in the veins of the portal system Most common cause is fibrosis and obstruction caused by cirrhosis of the liver Varices are distended, tortuous collateral veins o Prolonged elevation in the portal vein cause collateral veins to open between the portal vein and systemic veins and their transformation into varices, particularly in the lower esophagus and stomach, bit also over the abdominal wall (caput medusae) and rectum (hemorrhoidal varices) o Rupture of varices can cause life-threatening hemorrhage Splenomegaly is caused by increase pressure in the splenic vein which branches from the portal veins o Thrombocytopenia is the most common symptom o Can be palpated o Hepatopulmonary syndrome (vasodilation, intrapulmonary shunting, and hypoxia) and portopulmonary hypertension (pulmonary vasoconstriction and vascular remodelling) are complications of liver disease and portal hypertension o Dyspnea, cyanosis and clubbing may occur Clinical Manifestations Vomiting blood from bleeding esophageal varices (most common manifestation of portal hypertension) Rupture of esophageal varices causes hemorrhage and voluminous vomiting of dark- coloured blood; rupture is painless; caused by erosion by gastric acid and elevated venous pressure Evaluation and Treatment Diagnosed at the time of variceal bleeding confirmed by upper GI endoscopy and evaluation of portal venous pressure Individual has a history of jaundice, hepatitis, alcoholism, or cirrhosis Beta-blockers reduces pressure in the portal venous system and assist in prevent variceal bleeding Emergency management of bleeding varices include use of vasopressors and compression of the varices with inflatable tube or balloon, sclerotherapy, variceal ligation, or portocaval shunt Surgical construction of transjugular intrahepatic portosystemic shunts (TIPS) decompress the varices Ascites Accumulation of fluid in the peritoneal cavity
Syndrome may develop rapidly during acute fulminant hepatitis or slowly during the course of cirrhosis and the development of portal hypertension or after portosystemic bypass or shunting Pathophysiology Results from biochemical alterations that affect neurotransmission and brain function Liver dysfunction and the development of collateral vessels that shunt blood around the liver to the systemic circulation permit toxins from the GI tract and normally removed by the liver to accumulate and circulate freely to the brain Accumulation of toxins alters cerebral function Most hazardous substances are end products of intestinal protein digestion, AMMONIA, which cannot be converted to urea by the diseased liver Infection, hemorrhage, electrolyte imbalance (zinc deficiency included), constipation, and use of sedatives and analgesics can precipitate hepatic encephalopathy Clinical Manifestations Subtle changes in personality, memory loss, irritability, disinhibition, lethargy, and sleep disturbances are common initial manifestations Progression will result in confusion, disorientation to time and space, flapping tremor of the hands (asterixis), slow speech, bradykinesia, stupor, convulsions, and coma Evaluation and Treatment Diagnosis is based on a history of liver disease, clinical manifestations, psychometric tests, and exclusion of other causes of brain dysfunction o Electroencephalography and blood chemistry test o Tracking level of serum ammonia assess treatment effectiveness and liver function Correction of fluid and electrolyte imbalances and withdrawal of depressant medications metabolized by the liver are the first steps in treatment of hepatic encephalopathy Dietary protein is maintained to prevent malnutrition but at levels that reduce ammonia Lactulose prevents ammonia absorption in the colon Neomycin eliminates ammonia-producing intestinal bacteria but can be nephrotoxic Glutamase inhibitors reduce gut ammonia Rifaximin decreases intestinal production of ammonia and is used for lactulose nonresponders Jaundice Yellow or greenish pigmentation of the skin caused by hyperbilirubinemia Can result from extrahepatic (posthepatic) obstruction to bile flow, intrahepatic obstruction or prehepatic excessive production of unconjugated bilirubin Conjugated bilirubin is water soluble and appears in the urine; urine may darken several days before onset of jaundice Complete obstruction of bile flow from the liver to duodenum causes grey or light- coloured stools Partial obstruction, stools are normal in colour and bilirubin is present in urine Fever, chills, and pain accompany jaundice resulting from viral or bacterial inflammation of the liver Pruritis often accompanies jaundice as well because bilirubin accumulates in the skin Laboratory evaluation of serum establishes whether elevated plasma bilirubin is conjugated, unconjugated, or both
Hepatorenal Syndrome Functional kidney failure that develops as a complication of advanced liver disease Caused by portal hypertension, cardiac impairment, and other circulatory alterations associated with advanced liver disease (cirrhosis, fulminant hepatitis with portal hypertension) Manifestations include oliguria, sodium and water retention, hypotension, and peripheral vasodilation, ascites, GI bleeding o Systolic blood pressure is below 100mmHg Serum potassium levels do not become dangerously elevated until terminal stages of hepatorenal syndrome Blood urea level increases followed by increases in creatinine concentration Urine specific gravity is greater than 1. Prognosis is poor, treatments require albumin administration and vasopressin (Pressyn) Acute Liver Failure Rare clinical syndrome resulting in severe impairment or necrosis of liver cells without pre-existing liver disease or cirrhosis Can occur in viral hepatitis (hepatitis B) infection, compounded by infection with the delta virus, metabolic liver disorders Develops 6-8 weeks after the initial symptoms of viral hepatitis or metabolic liver disorders, or with 5-8 weeks of acetaminophen overdose Anorexia, vomiting, abdominal pain, and progressive jaundice are initial signs followed by ascites and GI bleeding Liver function test show elevation in direct and indirect serum bilirubin, serum transaminases, and blood ammonia INR/PTT is prolonged Cirrhosis Irreversible inflammatory and fibrotic liver disease Structural changes result from injury (viruses or toxicity from alcohol) and fibrosis, which is a consequence of infiltration of leukocytes, release of inflammatory mediators, and activation of hepatic stellate cells and myofibroblasts Chaotic fibrosis alters or obstructs biliary channels and blood flow, producing jaundice and portal hypertension New vascular channels form shunts and blood from the portal vein bypasses the liver, contributing to portal hypertension, metabolic alterations, and toxin accumulation Process of degeneration is disrupted by hypoxia, necrosis, atrophy, and liver failure Formation of fibrous bands and regenerating nodules distorts the architecture of the liver parenchyma and gives the liver a cobbly appearance o When palpating the liver, it feels firm or hard Alcoholic liver disease is related to the toxic effects of alcohol and coexisting liver disease Pathophysiology Alcoholic fatty liver (steatosis) o Mildest form of alcoholic liver disease o Caused by relatively small amounts of alcohol o May be asymptomatic
Most severe forms of this progresses to cirrhosis and end-stage liver disease Behavioural modification, dietary counselling, and regular exercise is the treatment Biliary cirrhosis Begin in bile canaliculi and bile ducts Primary Biliary cirrhosis Chronic, autoimmune, cholestatic liver disease Caused by autoimmune T cell and highly specific antimitochondrial antibody destruction of the small intrahepatic bile ducts, primary affects middle-aged women Detected by biochemical evidence of cholestatic liver disease Secondary Biliary cirrhosis Caused by prolonged partial or complete obstruction of the common bile duct or branches by gallstones, tumours, fibrotic strictures, or chronic pancreatitis Disorders of the Pancreas Pancreatitis or inflammation of the pancreas is a relatively rare and potentially serious disorder Risk factors include obstructive biliary tract disease (cholelithiasis), alcoholism, obesity, peptic ulcers, trauma, dyslipidemia, hypercalcemia, smoking, certain medications and genetic factors Acute Pancreatitis Mild and resolve spontaneously Requires hospitalization if it becomes severe Develops because of obstruction to the outflow of pancreatic digestive enzymes caused by bile and pancreatic duct obstruction Results from direct cellular injury from alcohol, medications, or viral infection Pathophysiology Backup of pancreatic secretions and activation and release of enzymes (activated typsin activated chymotrypsin, lipase, and elastase) within the pancreatic acinar cells Activated enzymes cause autodigestion of pancreatic cells and tissues resulting in inflammation Autodigestion causes vascular damage, coagulation necrosis, fat necrosis and formation of pseudocysts (walled-off collections of pancreatic secretions) Edema within the pancreatic capsule leads to ischemia and can contribute to necrosis In cases of alcohol abuse, the pancreatic acinar cell metabolizes ethanol with the generation of toxic metabolites that injure pancreatic acinar cells, causing release of activated enzyme Chronic alcohol use may also cause formation of protein plugs in pancreatic ducts and spasm of the sphincter of Oddi, resulting obstruction o Obstruction leads to intrapancreatic release of activated enzymes, autodigestion, inflammation, and pancreatitis Systemic effects of acute pancreatitis are related to release of proinflammatory cytokines (interleukin-6, tumor necrosis, factor-alpha, and platelet-activating factor) into the bloodstream Activation of leukocytes, injury to vessel walls, and coagulation abnormalities with development of vasodilation, hypotension and shock
o Complications can include acute respiratory distress syndrome (ARDS), heart failure, kidney failure, coagulopathies, intra-abdominal hypertension, and systemic inflammatory response syndrome (SIRS) Translocation of intestinal bacteria to the bloodstream my cause peritonitis or sepsis Manifestations Cardinal manifestations is epigastric or midabdominal constant pain ranging from mild abdominal discomfort to severe, incapacitating pain Pain may radiate to back Edema which distends the pancreatic ducts and capsule Chemical irritation and inflammation of the peritoneum Irritation or obstruction of the biliary tract Inflammation of the nerves Fever Nausea and vomiting caused by paralytic ileus secondary to pancreatitis or peritonitis Jaundice from obstruction of the bile duct Abdominal distention accompanies bowel hypomotility and accumulation of fluid in the peritoneal cavity Hypovolemia, hypotension, tachycardia, myocardial insufficiency, and shock occur because plasma volume is lost as inflammatory mediators released into the circulation increasing vascular permeability and dilate vessels Tachypnea and hypoxemia develop secondary to ascites Evaluation and Treatment Elevated serum amylase concentration is characteristic but is not diagnostic of severity or specificity of disease Elevated serum lipase level is the primary diagnostic marker for acute pancreatitis Goal of treatment is to stop the process of autodigestion and prevent systemic complications Narcotic medications to relieve pain To decrease pancreatic secretions (rest the gland) by administering nasogastric tube with continuous suction o Oral food and fluids will need to be withheld o Nasogastric suction may not be necessary with mild pancreatitis but helps to relieve pain and prevent paralytic ileus individuals who are nauseated and vomiting Feeding is initiated 24-48 hours if ileus is not present Parenteral fluids are essential to restore blood volume and prevent hypotension and shock Severe pancreatitis, enteral nutrition with use of jejunal tube feeding is well tolerated, decreases pancreatic enzyme secretion, prevent gut bacterial overgrowth and maintains gut barrier function H2 receptor antagonist decrease gastric acid production and decrease stimulation of the pancreas by secretin Antibiotics for infection Chronic Pancreatitis Process of progressive fibrotic destruction of the pancreas Chronic alcohol abuse is the most common cause
