Gastrointestinal Disorders: Etiology, Clinical Manifestations, and Pathophysiology, Study notes of Anatomy

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GI System Anatomy and Physiology Study Notes

Gastrointestinal Core Concepts and Objectives with Advanced Organizers

Examine the anatomy and physiology of the GI system:

1. Differentiate between the organs which make up the upper gastrointestinal track and the lower gastrointestinal track.

o The upper Gi track is made up of the mouth, esophagus, stomach, and the first part of the small intestine (duodenum) o The lower Gi track consist of the large intestine and the anus.

2. Explain the hepatoportal circulation anatomy and physiology.

o Metabolic function of the liver requires a large amount of blood. The liver receives blood from both arterial and venous sources. The hepatic artery is formed by the confluence of superior mesenteric artery and splenic veins and receives blood from the inferior mesenteric, gastric, and cystic veins. It provides oxygenated blood to the liver at the rate of 400 to 500mL/min (about 25% of the cardiac output. The hepatic portal vein receives deoxygenated blood from the inferior and superior mesenteric vein and the splenic vein, deliver 1000 to 1200mL/min of blood to the liver. Hepatic vein is rich in nutrients that have been absorbed from the intestinal track.

3. Discuss the effects of aging on the gastrointestinal tract.

o The changes in the GI system that are associated with aging are dependent upon a person’s health status, genetics, and environmental factors. Some changes can begin before the age of 50. As we age, we lose tooth enamel and dentin, which increases the risk for developing cavities. Periodontal disease, gum recession and osteoporosis can cause one to lose teeth. The sense of smell decreases as does the ability to taste secondary to a loss of taste buds. This leads to a reduced appetite in the elderly. Esophageal motility decreases with age and may lead to GERD. Gastric motility, gastric secretions and blood flow decreases with age which leads to an increased risk of injury to the mucosal lining. A decreased production in intrinsic factor is also noted as we age which may lead to B12 deficiency and pernicious anemia. Ileal villi become broader and shorter. Degeneration of the enteric nervous system neurons decreases intestinal absorption, motility, blood flow and impairs nutrient absorption. Nutrients are absorbed more slowly and in lesser amounts. The liver is not able to regenerate as fast in the elderly. Hepatic blood flow decreases with age as does the enzymatic activity both of which decreases drug metabolism. LFTs remain normal in the elderly and an elevation is a sign of a disorder and not a result of aging. The pancreas experiences some age-related fibrosis, fatty acid deposits and atrophy. The beta cells’ function declines as well as we age. Gastrointestinal Bleeds

4. Analyze the etiologies and pathophysiology of osmotic, secretory, and motility related diarrhea.

Type of Diarrhea Etiology Pathophysiology Osmotic Osmotic diarrhea is caused by the presence of a nonabsorbable substance in the intestines This is how the laxatives mag citrate, lactulose and MiraLAX work. Excessive ingestion of nonabsorbable sugars can cause this type of diarrhea. Other causes include tube feedings, dumping syndrome, malabsorption, pancreatic enzyme deficiency, bile salt deficiency, small intestine bacterial overgrowth, or celiac disease. This pulls water by osmosis into the intestinal lumen and results in large volume diarrhea Secretory These infections trigger enteroendocrine cells to secrete 5HT and the activation of afferent neurons that stimulate submucosal secretomotor neurons and alter sodium chloride transport resulting in decreased water absorption results in large volume losses secondary to infectious causes such as the rotavirus, bacterial enterotoxins, or C-diff

Motility is AKA as short bowel syndrome and results from the resection of the small intestine or a surgical bypass of the small intestine or a portion of it, IBS, diabetic neuropathy, hyperthyroidism, and laxative abuse. Complications of diarrhea may include dehydration, electrolyte imbalances, metabolic acidosis, weight loss, and malabsorption. Fatty stools are common in malabsorption syndromes as is bloating. Most infectious diarrhea usually lasts less than 2 weeks. Fever, cramping and bloody stools may be seen in chronic diarrhea and are caused by inflammatory bowel disease or dysentery.

5. Analyze the etiology, clinical manifestations, and pathophysiology of the upper and lower GI bleed. Disease Etiology Clinical Manifestations Pathophysiology Upper GI Bleed (^) by definition is any source of bleeding which occurs in the esophagus, stomach or the duodenum. It is characterized by frank, bright red or “coffee ground” (affected by the stomach) emesis. Hematemesis is bright red, bloody emesis and is an indicator of an upper GI bleed. Usually this type of bleed requires emergent intervention. Coffee ground emesis is emesis which looks like used coffee grounds. This is indicative of an upper GI bleed but unlike hematemesis, it is not necessarily an emergent issue. Melena is said to be present when a person’s stool is black and tarry. It is an indicator of an upper GI bleed. It is commonly caused by bleeding varices (varicose veins) in the esophagus or stomach, peptic ulcers, gastritis, or a Mallory-Weiss tear (tearing of the esophagus from the stomach). Lower GI Bleed (^) by any source of bleeding in the jejunum, ileum, colon, or rectum. It can be caused by inflammatory bowel disease, cancer, diverticula or hemorrhoids. In this case the person would experience clinical manifestations consistent with shock (decreased cardiac output, hypotension, acute renal failure, tachycardia, anemia). Hematochezia is the presence of bright red blood in the stools and the presence of hematochezia suggests that the bleed is in the lower GI tract, usually in the rectum, sigmoid colon or the descending colon. An upper or lower GI bleed, if left untreated or if it is severe, may result in a shock Peptic Ulcer Disease 6. Analyze the etiology, clinical manifestations, and pathophysiology of gastric and duodenal ulcers. Disease Etiology Clinical Manifestations Pathophysiology Gastric Ulcers (^) Ulcers occur between ages 55 and 65 and are typically caused by NSAIDS. NSAIDs block the production of the prostaglandins which protect the gastric mucosa. The epigastric pain associated with gastric ulcers is worse with eating and the pain is immediate. Again these individuals may also experience melena and hematemesis or coffee ground emesis. Complications include bleeding or perforation. If a perforation occurs luminal contents can escape into the peritoneum and cause a peritonitis They may be causes by duodenal reflux and H. pylori infection as well. Duodenal reflux causes of bile occurs after cholecystectomy, pyloroplasty or gastrojejunostomy. The reflex of pancreatitis enzymes and bile causes damage to the gastric mucosa which allows hydrogen ions to diffuse into the mucosa and damage the cells and alter cellular permeability.

Duodenal Ulcers (^) the most common and tend to develop in younger patients epigastric pain that is relieved by food. The pain will recur when the stomach is empty, which may be 30 minutes to two hours after eating. The individuals may have melena or hematemesis. Causative factors singly or in combination cause acid and pepsin concentration in the duodenum to penetrate the mucosal barrier and lead to ulceration Disorders of the Intestines

7. Differentiate between the etiology, clinical manifestations, and pathophysiology of disorders of the small and large intestines. a. Analyze the etiology, clinical manifestations, and pathophysiology of ulcerative colitis and crohn’s disease and describe the implications on nutritional status. Disease Etiology Clinical Manifestations Pathophysiology Nutrition Implications Ulcerative Colitis (^) is an inflammatory disease of the large intestine. It typically manifests in persons between the age of 20 to 40 years and is less common in persons who smoke. It is most commonly affecting the rectum and sigmoid colon chronic, recurrent, bloody diarrhea is severe inflammation and ulcerations of the large intestine which begins in the rectum and may involve the entire large intestine. It is different from Crohn’s in that it only affects the colon and does not affect the small intestine; A diet rich in fruit and vegetables, rich in n- fatty acids, and low in n- fatty acids Crohn’s Disease is a chronic inflammatory disorder of the GI tract which waxes and wanes. These individuals will have periods of remission and exacerbations. may affect any portion of the GI tract (from the mouth to the anus) but most often it causes issues in the ileum and proximal colon. It often affects persons in their 20s and 30s and those of Jewish decent. Risk factors include smoking, a family history of Crohn disease, Jewish decent, age less than 40, slight predominance in women and altered gut microbiome abdominal pain, diarrhea, dehydration, bloody stools, malabsorption, malnutrition, weight loss (most nutrients are absorbed in the small intestine), intestinal obstruction from chronic inflammation, fistulas (abnormal tracts/channels that develop in the presence of inflammation), and perforation of the intestine a transmural involvement of the affected area (which means the entire wall of the intestine is affected) and the presence of skip lesions. This means that there are areas of healthy, unaffected tissue surrounded by diseased tissue which are randomly present in the GI tract. Disease progression may lead to abscess formation in the GI tract. Possible causes include infectious agents (bacteria, viruses), autoimmune, psychosomatic, and impaired T- cell immunity. Due to malabsorption they may experience vitamin and mineral deficiencies such as B12, vitamin D, calcium, and folic acid. b. Compare the etiology, clinical manifestations, and pathophysiology of diverticulitis, diverticulosis, appendicitis, and bowel obstruction. Disease Etiology Clinical Manifestations Pathophysiology

Diverticulosis & Diverticulitis (^) is characterized as the presence of diverticula in the large intestine. Risk factors include older age, genetic predisposition, obesity, smoking, diet, lack of exercise, medication use such as aspirin and other NSAIDS, altered GI microbiome, and abnormal colonic peristalsis Diverticulosis is the presence of diverticula in an asymptomatic individual. Diverticulitis causes LLQ pain. This can result in abscess formation, rupture and peritonitis. Diverticula are outpouchings of mucosa from the muscle layer of the intestine that protrude into the intestinal lumen. They most commonly occur in the sigmoid colon Diverticulitis is an inflammation of the diverticula Appendicitis is an inflammation of the appendix. It usually occurs between the ages of 10-

The pain may initially be in the epigastric or periumbilical area then settle in the RLQ Symptoms include gastric or periumbilical pain, RLQ pain , N/V/D, anorexia Perforation, peritonitis and abscess formation are all potential complications Bowel Obstruction (^) A small bowl obstruction is caused most commonly by postoperative adhesions, but may be caused by colicky abdominal pain which may be continuous, nausea, vomiting, distention and if dehydration The pathological consequences of an intestinal obstruction are directly related to the location, the degree of the tumors, Crohn’s disease, hernias and intussusception. SBO causes distention secondary to impaired absorption and increased secretions which leads to fluid accumulation and gas proximal to the ileus. Distention in the intestines decreases their ability to absorb water and electrolytes and increases the secretion of these things into the lumen. is not as common as an SBO and typically occurs secondary to a tumor. This is a significant point to understand because people with SBO lose a lot of fluid and electrolytes hypotension and tachycardia may occur. Fever, leukocytosis, and rebound tenderness develop if ischemia is present and progresses. Obstruction of the pylorus results in profuse vomiting of clear gastric fluid. A partial SBO may cause diarrhea, but a complete SBO will cause constipation. A complete obstruction will also be accompanied by an increase in bowel sounds. Clinical manifestations include hypogastric pain, abdominal distention and vomiting which will occur late in the process. obstruction and the presence or absence of impaired perfusion., particularly potassium. One can lose up to 8L of fluid in 24 hours from an SBO. This means that their lytes have to be monitored and replaced as needed and you have to stay on top of their fluid output and replace all of the fluid lost and sometimes even more than what is lost. The distention will eventually lead to bacterial overgrowth and increase the distention and eventually this will lead to vomiting. The individuals must be closely monitored for dehydration and prevent the dehydration from occurring. Liver Disorders

8. Examine the etiology, clinical manifestations and pathophysiology of liver injury and failure. c. Analyze the risk factors, etiology, clinical manifestations, and pathophysiology of portal hypertension, ascites, hepatic encephalopathy, and jaundice. Disease Risk Factors Etiology Clinical Manifestations Pathophysiology Portal Hypertension Cirrhosis of the liver Abnormal high blood pressure in the portal venous system. Elevated venous pressure above 5mmHg Vomiting of blood from esophageal varices Caused by disorders that obstruct or impede blood flow through any component of the hepatic portal system Ascites (^) Cirrhosis Portal hypertension, decreased synthesis of albumin, Is the accumulation of fluid in the peritoneal cavity and is the complication of portal hypertension Increased abdominal girth This causes hydrostatic pressure to exceed oncotic pressure which leads to the formation of ascites. This is caused by low albumin and portal hypertension. It is the most common complication of cirrhosis. Hepatic (^) Is a complex neurologic

Encephalopath y use or abuse of ETOH, any infection a GI bleed, the syndrome characterized by mild and the only sign that the individual may The pathogenesis is not fully understood but the best explanation for it is the development of a portal impaired^ behavioral,^ have is difficulty with accumulation of ammonia. The liver vein thrombosis, sedatives cognitive,^ and^ motor^ doing simple tasks, i.e. normally detoxifies the blood it receives or any medication that has function^ working the remote from the GI tract of ammonia. Ammonia sedating effects volume control or the thermostat, is the byproduct of protein breakdown. depletion, constipation, or with recalling a In a cirrhotic, the liver is unable to electrolyte imbalances telephone number (their effectively detoxify ammonia and it and use of diuretics. home number). A hepatic accumulates. Ammonia is toxic to the encephalopathy can be so neurons and is therefore implicated in severe that the individual the development of hepatic becomes obtunded encephalopathy. The toxic effects that (coma), is unresponsive, ammonia has on neurons causes them unable to protect their to swell, which leads to cerebral edema airway and must be and increased intracranial pressure. intubated. They can be Persons who die from hepatic anywhere in between as encephalopathy typically die from the well. The consequence of results of increased intracranial pressure hepatic encephalopathy is and brain herniations. cerebral edema. If it goes untreated it can result in brain herniation and death. Jaundice (^) Can result from extrahepatic or intrahepatic obstruction is the yellowish or greenish pigmentation of the skin caused by hyperbilirubinemia Fever, chill pain , anorexia, malaise, fatigue, yellowing of skin Bilirubin conjugated by the hepatocytes cannot flow through the obstructed common duct into the duodenum d. Identify clinical manifestations of liver injury. The yellowing of skin and eyes, abdominal pain in the upper right quadrant and abdominal swelling. Jaundice AKA as icterus, is not a disorder but rather a manifestation, a sign of a disorder. It is the yellow discoloration of the skin or other tissues. It can be seen on the skin, in the sclera of the eyes or on the mucous membranes. It is usually visible when bilirubin levels reach 2.5-3mg/dL. Jaundice is classified into two broad categories: non-obstructive and obstructive. e. Analyze the etiology, clinical manifestations, and pathophysiology of alcoholic cirrhosis. Disease Etiology Clinical Manifestations Pathophysiology Alcoholic Cirrhosis Abuse of any type of alcoholic beverage Steatosis causes no specific symptoms or abnormal LFT results. Can be mild or severe, fatigue, weight loss and anorexia. Is caused by the toxic effects of alcohol metabolism on the liver, immunologic alteration, oxidative stress, from lipid peroxidation and malnutrition

9. Analyze the etiology, clinical manifestations and pathophysiology of viral hepatitis. f. Differentiate between the etiology, clinical manifestations, and pathophysiology of autoimmune hepatitis and viral hepatitis. Disease Etiology Clinical Manifestations Stages of Viral Hepatitis Pathophysiology Autoimmune Hepatitis Is a rare chronic progressive inflammatory liver disease that affects genetically susceptible individual. Cause is unknown There are NO symptoms of jaundice, fatigue, loss of appetite, amenorrhea or acute liver failure N/A T cells trigger the secretion of proinflammatory cytotoxic cytokines

Viral Hepatitis (^) Common systemic disease that affects the liver. abnormal liver function tests, jaundice, fatigue, anorexia, nausea, diarrhea, fever, cough, clay colored stool, and hepatomegaly. Prodromal phase- begins about 2 weeks after exposure and ends with the appearance of jaundice, fatigue, anorexia, nausea, headache, and low grade fever. Icteric Phase- begins about 1 to 2 weeks after and last 2 to 6 weeks. Is the acute phase of illness. the liver enlarged, smooth, tender and percussion over liver causes pain. recovery phase begins with the resolution of jaundice about 6 to 8 weeks after exposure. Liver may stay enlarged by symptoms diminish. cause inflammation and injury to the hepatocytes and some necrosis. This results in the formation of scar tissue and hepatocyte hyperplasia. The inflammation may obstruct the bile duct and cause obstructive jaundice. The damage is more severe in hepatitis B and C infections g. Analyze the differences in the characteristics of hepatitis A, B, C, D, E. Hepatitis Type A B C D E Incubation 30days 60-180days 35-72 days 30days -180days 15-60day Mode of Transmission (^) Fecal Oral Route Blood and body fluids (sex and kissing) Blood and body fluids: tattoos, IV drug us (sexual contact less likely) Blood and body fluids Fecal oral route Period of Communicability Up to 1 week after onset of jaundice As long as they are positive for HBsAg Indefinitely Indefinitely Not Known Chronic Carrier State (^) No Yes Yes Yes No Age Group Affected Children & young adults Any Any Any Children & young adults Vaccine Available Yes Yes No No No Prevention Hand washing Vaccine Vaccine No kissing, safe sex Safe sex Blood screened Protect from HBV. HBV coinfection required for HDV to be infective Yes Hand washing Immune Globulin Available Yes Yes No No No Miscellaneous Information Household contacts treated Household contacts treated Can exist without any s/s for years n/a n/a h. Determine immune status and infectious states based on lab interpretation. Type of Hepatitis Marker of Acute Infection Marker of Chronic Infection Marker of Immune Status Marker of infectiousness Hepatitis A N/A

IgM IgG A IgG means that the person has had a

previous infection or vaccination and is immune. Remember that the IgG antibody responds later in the infection, hence it is an indicator of immunity. Hepatitis B The presence of the hepatitis B surface antigen indicates that the patient has an acute infection and is infectious. The hepatitis B surface antibody is negative in acute infections. if it is positive and all other hepatitis B tests are negative, then this indicates that the person has acquired immunity from a vaccine. If there is a positive hepatitis B total core antibody and if all other hepatitis B serologies are negative, this means that the patient had a prior infection of hepatitis B The hepatitis B core antibody (IgM) is positive in acute infections. An acute infection is present when both the Hepatitis B Core antibody (IgM) and the Hepatitis B Surface antigen are positive. Chronic hepatitis B infections are present when the surface antigen and total core antibody are positive. Hepatitis C N/A positive hepatitis C antibody indicates a chronic hepatitis C infection.

N/A N/A

Gall Bladder Disorders

10. Differentiate between the risk factors, etiology, clinical manifestations, and pathophysiology of cholelithiasis and cholecystitis. Disease Risk Factors Etiology Clinical Manifestations Pathophysiology Cholelithiasi (^) Biliary colic is abrupt, sharp and is s (^) obesity, rapid weight Cholelithiasis is the located in the RUQ or epigastric area. (^) Gallstones may not cause signs loss, middle age, presence of stones in The^ pain^ increases^ steadily^ in^ intensity^ and symptoms if they are very female gender, oral the gallbladder. and then levels off in about 30-60 small. However, stones < 8mm contraceptives, native minutes.^ It^ lasts^ about^ two^ to^ eight^ can pass into the common bile American ancestry, hours^ or^ until^ there^ is^ no^ more^ food^ duct and cause an obstruction. ileal disease, low stimulating^ gallbladder^ contraction.^ If this happens the person will HDLs, and People^ with^ cholelithiasis^ are^ intolerant^ experience painful spasms and hypertriglyceridemia. to fatty foods. It is the presence of fat contractions of the bile duct. in the duodenum which stimulates (^) This is referred to as biliary gallbladder contraction to release bile. (^) colic. Bile is used in the digestion of fats. The pain associated with gallstones is typically present in the back, right shoulder or right scapula. It may also be located in the epigastric area. Usually these individuals have problems with nausea and vomiting. If the stone is large enough it will obstruct the common bile duct and cause obstructive jaundice. Being female. Cholecystitis is an inflammation of the gallbladder. It may be acute or chronic and results from an obstruction in the biliary tract. Acute cholecystitis is usually associated with cholelithiasis. The clinical manifestations of acute cholecystitis are similar to cholelithiasis and are precipitated by a fatty meal. Increased amounts of fat in the intestines increases the need for bile to emulsify fat. Secretion of bile puts a strain on the inflamed GB and causes pain. Chronic disease is more vague and may only be marked by GERD. A positive murphy’s sign is indicative of an acute cholecystitis. In order to test for a murphy’s sign, the examiner must palpate the right upper quadrant. While pushing up and in, the patient is instructed to take a deep breath in. If the patient stops inhaling while the clinician is palpating up and in, the murphy sign is then positive. Rebound tenderness may be present. Lab abnormalities may include a leukocytosis, and an increased Alkaline phosphatase and direct bilirubin levels. The gallstones are made of concentrated bile and this causes a chemical irritation of the inner wall of the gallbladder, mucosal swelling and ischemia. This causes venous congestion, lymphatic stasis, and inflammation. This is a prime condition for bacterial growth, especially staph or strep. Chronic cholecystitis can be caused by repeated episodes of acute or chronic irritation by the stones. Cholecystitis Pregnancy. Hormone therapy. Older age. Being Native American or Hispanic. Obesity. Losing or gaining weight rapidly. Diabetes.

Pancreatic Disorders

11. Describe the risk factors, etiology, clinical manifestations, and pathophysiology of acute pancreatitis. Disease Risk Factors Etiology Clinical Manifestations Pathophysiology Acute The most common Pancreatitis (^) obstructive biliary tract causes are ETOH use and (^) post prandial pain which is Acute pancreatitis is associated disease, alcoholism, PUD, gallstones. ETOH abrupt in onset, epigastric with the escape of pancreatic abdominal trauma, stimulates^ pancreatic^ pain that radiates to the back enzymes into the surrounding hyperlipidemia, smoking, secretions^ and^ obstructs^ and is worse lying down and area and into the pancreas. The some drugs, and genetic the^ sphincter^ of^ Oddi.^ better sitting up, and nausea enzymes begin the digestive factors Gallstones^ obstruct^ the^ and vomiting. If hemorrhaging process of the tissues which they biliary duct. Other occurs the patient will have touch. causes include (^) signs of hypovolemic shock medications, high (^) (low BP, tachycardia, cool triglycerides, viral (^) clammy skin). Individuals may infections, autoimmune, (^) also experience a fever, ischemia, post ERCP, hypocalcemia, jaundice, and genetic, abdominal tend to have a lot of fluid loss. trauma, and a scorpion (^) Diagnosis of acute pancreatitis bite (^) requires the presence of 1 out of 3 manifestations: symptoms consistent with acute pancreatitis, elevated lipase, or findings consistent with acute pancreatitis on CT. Gastrointestinal Malignancies 12. Explain the risk factors, etiology, clinical manifestations, and pathophysiology of esophageal, colon and pancreatic cancers. Disease Risk Factors Etiology Clinical Manifestations Pathophysiology Esophageal Cancer (^) smoking, abdominal obesity, reflux esophagitis, and sliding hiatal hernia Esophageal Cancer is not very common. Squamous cell carcinoma is most prevalent in China, Iran, South America and South Africa. It is found in the upper portion of the esophagus and Adenocarcinoma is the main form which occurs in the US. It is found in the lower portion of the esophagus. chest pain and dysphagia. chronic inflammation and metaplastic changes in the esophagus, which is what happens with Barrett’s esophagus or from chronic exposure to irritants. Individuals do not begin to show signs until later in the disease Colon Cancer (^) advancing age, high fat and low fiber diets, smoking, obesity, family history, low levels of physical activity, inflammatory bowel disease, and gastrectomy in any portion of the colon or rectum. It occurs typically in individuals over age 50 but we are seeing more cases in younger persons. Familiar tendencies are common. Symptoms include pain, abdominal mass, anemia, occult bleeding, obstruction, distention. Colon cancer screening should start at age 50 and include yearly tests for occult blood, colonoscopy every five-ten Most tumors are adenocarcinomas and typically grow slowly. CRC most commonly arise from polyps. Polyps may be benign or malignant. Polyps which are larger than 2cm, associated with many polyps (more than 20),

have a villous

years, sigmoidoscopy every five years with occult blood testing. The genetic association which contribute to CRC are complete and you do not need to know these. Just know that there is a genetic component. architecture have the most malignant potential. When the tumor becomes large enough it will alter bowel elimination patterns and potentially cause an intestinal obstruction. Pancreatic Cancer (^) It is more common in males and African Americans. Risk factors include ETOH use, family history, smoking, non O blood type, DM type 2, and chronic pancreatitis. jaundice, dull back pain, protein and fat malabsorption due to lack of enzymes when ductal obstruction occurs. Other manifestations include lethargy, weight loss, nausea, vomiting, new onset diabetes, changes in bowel patterns, and pruritis. tumors can arise from exocrine or endocrine cells; however, most arise from the exocrine cells of the ducts and are called ductal adenocarcinomas. Tumors of the head of the pancreas grow quickly and can obstruct the portal vein and common bile duct. The K-ras mutation a proto- oncogene is the most common genetic alteration associated with pancreatic cancer. It may metastasize to the liver. Pediatric Gastrointestinal Disorders

13. Differentiate between the risk factors, etiology, clinical manifestations, and pathophysiology of select pediatric gastrointestinal diseases. Disease Risk Factors Etiology Clinical Manifestations Pathophysiology Cleft Lip/ Palate The anomalies may be caused by vitamin B6, folic acid and B deficiencies, smoking and ETOH ingestion during pregnancy, steroid or statin use, maternal hyperhomocysteinemi a, maternal diabetes and from genetic mutations. caused by a combination of genes and other factors, such as things the mother comes in contact with in her environment, or what the mother eats or drinks, or certain medications she uses during pregnancy .As a result, the face and mouth develop with a cleft. The cleft may affect the lip or the external nose, the nasal cartilages, and the nasal septum. It typically is just beneath the center of one nostril. The defect may be unilateral or bilateral, symmetrical or asymmetrical. The greater the cleft lip is the more likely there will be missing teeth. They tend to have difficulty with feeding and some A cleft lip results from the incomplete fusion of the nasomedial and intermaxillary processes, which begins to fuse during the th 4 week of gestation A cleft palate is typically associated with a cleft lip but it may occur without it. It results from the failure of the primary palatal shelves or processes to fuse during the 3 rd month of gestation. This may affect only the uvula and soft palate or it may extend anterior to

may have

difficulty with swallowing. involve^ the^ nostril^ and^ hard^ palate.^ It^ too may be unilateral or bilateral. Pyloric Stenosis Caucasians are more commonly affect as are full term infants. Increase gastrin secretion by mom in the 3 rd trimester has been linked to the development of pyloric stenosis. Infantile hypertrophic pyloric stenosis is the most common cause of intestinal obstruction in infancy. In pyloric stenosis the pylorus is narrowed which slows the flow of food from the stomach to the duodenum. vomiting after eating These infants tend to begin to display symptoms 2-3 weeks after birth at which time they begin having nonbilious vomiting immediately after feeding. Often they want more food immediately after they vomit. They tend to be constipated because little food reaches the intestines. In severe cases this may lead to fluid and electrolyte imbalances, malnutrition, weight loss and can be fatal in 4-6 weeks. Infants tend to be irritable because they are hungry. The emesis may be blood streaked due to rupture of gastric and esophageal vessels. The causes are multifactorial and include a deficiency in nitric oxide synthase containing neurons, abnormal innervation of the myenteric plexus, the presence of infantile hypergastrinemia, and exposure to macrolide antibiotics. Neonatal Jaundice

• Physiologic
• Pathologic fetal mother ABO or Rh incompatibility, prematurity, exclusive breast feeding, maternal age greater than 25, male infant, delayed meconium passage, and birth trauma. Jaundice is said to be present in an infant when the total serum bilirubin level is greater than the 95 th percentile for the infant’s age in hours or a bilirubin level greater than 20mg/dL. When the bilirubin level has reach 2mg/dL jaundice is usually visible. There are two types of jaundice in the neonate: physiologic and pathologic. include yellow skin, dark urine, light colored stools and weight loss. Premature infants with respiratory distress, acidosis or sepsis are at an increased risk for kernicterus and neurologic dysfunction. Physiologic jaundice of the newborn is normally a transient condition which beings during the first week of life in otherwise healthy, full term infants. It is caused by mild unconjugated hyperbilirubinemia. Physiologic jaundice manifests during the second or third day of life and subsides after 1- 2 weeks of life in full term infants and 2-4 weeks in premature infants. After this time frame a persistent and/or rising bilirubin may be indicative of a pathologic jaundice. Pathologic jaundice tends to manifest within 24 hours of birth. These infants tend to have bilirubin levels > 20mg/dL or an indirect bilirubin level > 15mg/dL. Pathologic jaundice results from increased bilirubin production, impaired hepatic uptake or excretion of unconjugated bilirubin or a delayed maturation of liver conjugating mechanisms. The most common cause is hemolytic disease of the newborn. Unconjugated bilirubin is lipid soluble and may cross the blood brain barrier in infants. This can cause a bilirubin encephalopathy called kernicterus from the bilirubin being deposited in the brain cells.