Unit 6: Alterations and Disorders of the Gastrointestinal System

Mesenteric vascular insufficiency

-Blood supply to the stomach and intestine is blocked *Celiac artery *Superior and inferior mesenteric arteries -Mesenteric venous thrombosis -Acute mesenteric artery insufficiency -Chronic mesenteric ischemia -Clinical manifestations Abdominal pain, fever, bloody diarrhea, hypovolemia, leukocytosis, shock

irritable bowel syndrome (IBS)

-Functional gastrointestinal disorder with no specific structural or biochemical alterations -symptom complex marked by abdominal pain and altered bowel function (typically constipation, diarrhea, or alternating constipation and diarrhea) for which no organic cause can be determined; also called spastic colon -Clinical manifestations Lower abdominal pain Diarrhea-predominant, constipation-predominant, or alternating diarrhea and constipation Gas, bloating Nausea -No cure

15. Compare and contrast hepatitis in children.

-Hep A-One-third to one-half of cases occur in children. particularly children of nursery school age. Vaccines should begin at 1 year. -Hep B- Newborns infected with hepatitis B from their mothers develop chronic hepatitis and become carriers. Aggressive vaccination programs have reduced the incidence rate. Treatment option: Maternal antiviral therapy during pregnancy and lactation -Hep C- most common. Antivirals: Are effective in the treatment of hepatitis C. Liver transplantation: Required for those with liver failure. Currently, no vaccination is available.

Pancreatic exocrine insufficiency

-Insufficient pancreatic enzyme production Lipase, amylase, trypsin, or chymotrypsin -Causes: -Pancreatitis -Pancreatic carcinoma -Pancreatic resection -Cystic fibrosis -Fat maldigestion is the main problem, so the patient will exhibit fatty stools and weight loss -Treatment: Lipase supplements

Zollinger-Ellison syndrome

-a rare syndrome also associated with peptic ulcers caused by a gastrin-secreting neuroendocrine tumor or multiple tumors (gastrinoma) of the pancreas or duodenum. -Clinical manifestations Gastroesophageal reflux with abdominal pain and diarrhea Treatment Proton pump inhibitors: To reduce gastric acid secretion Surgical removal of tumors: To limit metastasis

Visceral pain

-arises from a stimulus (distention, inflammation, ischemia) acting on mechanical and chemical nociceptors of abdominal organs. -a poorly localized, vague, dull, or diffuse pain that arises from the abdominal organs, or viscera -i.e early stages of appendicitis

Gastroparesis

-delayed gastric emptying in the absence of mechanical gastric outlet obstruction. It is most commonly associated with diabetes mellitus, surgical vagotomy, or fundoplication. It can be idiopathic. The pathophysiology is not well understood but involves abnormalities of the autonomic nervous system, smooth muscle cells, enteric neurons, and gastrointestinal hormones

Achalasia

-loss of inhibitory myenteric innervation, loss of esophageal peristalsis, and failure of lower esophageal sphincter (LES) relaxation, thus causing functional obstruction of the lower esophagus. Food accumulates above the obstruction, distends the esophagus, and causes dysphagia -Chronic inflammation from esophageal food retention can increase risk for esophageal cancer.

Referred pain

-visceral pain felt at some distance from a diseased or an affected organ. Referred pain is usually well localized -feeling of pain when sensory information from internal and external areas converges on the same nerve cells in the spinal cord -i.e myocardial infarction

1. Summarize the process of digestion, including the phases of swallowing, absorption and excretion.

1. Ingestion of food 2. Propulsion of food and wastes from the mouth to the anus 3. Secretion of mucus, water, and enzymes 4. Mechanical digestion of food particles 5. Chemical digestion of food particles 6. Absorption of digested food 7. Elimination of waste products by defecation 8. Immune and microbial protection against infection

9. Summarize the multisystem interaction that is thought to contribute to IBS.

6. 1. Visceral hypersensitivity or hyperalgesia, particularly with distention of the rectum but also other areas of the gut. 2. Abnormal gastrointestinal permeability, motility, secretion, and sensitivity are associated with IBS. 3. Postinflammatory IBS has been associated with intestinal infection (bacterial enteritis) and low-grade inflammation. 4. Alteration in gut microbiota (dysbiosis) influences the sensory, motor, and immune systems of the gut and interacts with higher brain centers and may contribute to symptoms of IBS. 5. Food allergy or food intolerance 6. Psychosocial factors (epigenetic factors), including early life trauma or abuse or chronic emotional stress

6. Compare the pathophysiology of duodenal ulcers vs. gastric ulcers.

A peptic ulcer is a sore on the lining of your stomach or the first part of your small intestine (duodenum). If the ulcer is in your stomach, it is called a gastric ulcer. If the ulcer is in your duodenum, it is called a duodenal ulcer. Ulcers are fairly common. Big difference is the location of the ulcers

ANS: 3 The spectrum of alcoholic liver disease includes steatosis, alcoholic hepatitis (steatohepatitis), and alcoholic cirrhosis (fibrosis). 1. The clinical course of hepatitis usually consists of four phases: incubation, prodromal, icteric, and recovery phases. 2. Obstructive jaundice can result from extrahepatic or intrahepatic obstruction. Excessive hemolysis (breakdown) of red blood cells or absorption of hematoma can cause hemolytic jaundice (prehepatic or nonobstructive jaundice). 4. Overflow, underfill and peripheral artery vasodilation or forward theory are all theories for ascites.

A person has alcoholic liver disease. What is the sequence for the development of this disease? Incubation, prodromal, icteric, and recovery Prehepatic, intrahepatic, and extrahepatic Steatosis, steatohepatitis, and fibrosis Overflow, underfill, and peripheral artery vasodilation

ANS: 2 Tumors of the left, or descending, colon are small, elevated, button-like masses. Obstruction is common but occurs slowly and stools become narrow and pencil shaped.

A person has cancer in the left descending colon. What will the nurse typically find upon assessment? Stools mixed with mahogany-colored blood Narrow and pencil shaped stools Stools bloody with purulent mucus Clay-colored stools and the presence of steatorrhea

Crohn disease

AKA Granulomatous colitis, ileocolitis, or regional enteritis Idiopathic inflammatory disorder; affects any part of the digestive tract, from mouth to anus Difficult to differentiate from ulcerative colitis Similar risk factors and theories of causation Strong association Nucleotide-binding oligomerization domains (CARD15/NOD2) gene mutations

Portal hypertension

Abnormally high blood pressure in the portal venous system primarily caused by resistance to portal blood flow Increase to above 5 mmHg (normal is 3-5 mmHg) -Causes: Prehepatic, Intrahepatic, Posthepatic Can cause fatal consequences. Consequences: Varices, Distended, tortuous, collateral veins Lower esophagus, stomach, rectum, abdominal wall, spleen If rupture: Life-threatening Splenomegaly: Enlargement of the spleen Thrombocytopenia: Increased risk for bleeding Hepatopulmonary syndrome

ANS: 4 Intussusception is the telescoping or invagination of one portion of the intestine into another. Children develop colicky abdominal pain, vomiting, currant-jelly stools, and a sausage-shaped mass in the abdomen.

An infant arrives in the emergency department with a diagnosis of intussusception. Which data will the nurse typically find during the assessment? Olive-sized mass in the right upper quadrant Meconium ileus Painless rectal bleeding Currant-jelly stools

Clinical manifestations of acute liver failure

Anorexia, vomiting, abdominal pain, and progressive jaundice Treatment N-acetylcysteine: For acetaminophen poisoning Antiviral therapy: To improve survival in cases of viral hepatitis Lowering blood ammonia levels Liver transplantation

Diverticulosis

Asymptomatic diverticular disease. Usually there are multiple diverticula present. -Predisposing factors Older age, genetics, obesity, smoking, diet, lack of physical activity, and medications -Clinical manifestations Low cramping abdominal pain, diarrhea, constipation, distension, flatulence Diverticulitis: Fever, leukocytosis

Cancer of the Stomach

Begins in the glands of the stomach mucosa. Clinical manifestations Symptoms do not usually occur until the tumor has metastasized: Weight loss, upper abdominal pain, vomiting, hematemesis, anemia, change in bowel habits.

Cleft Lip and Cleft Palate

Both defects are developmental anomalies of the first brachial arch. Both are caused by multiple gene - environmental interactions. Maternal deficiency of B vitamins (B6, folic acid, B12) Maternal: Alcohol, smoking, diabetes mellitus, steroid or statins, hyperhomocysteinemia, gene mutations These factors reduce the amount of neural crest mesenchyme that develops into the embryonic face. Clinical manifestations Feeding difficulties Treatment Surgical correction at 3-6 months Special bottle for feeding

Kwashiorkor and Marasmus

Both types of malnutrition are associated with long-term starvation. Are collectively known as severe acute malnutrition; protein-energy malnutrition.

Peptic ulcer

Break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum Acute vs. chronic ulcers Superficial (erosions) vs. deep

Pathophysiology of crohns disease

Causes "skip" lesions. Inflamed areas mixed with uninflamed areas, noncaseating granulomas, fistulas, deep penetrating ulcers -Clinical manifestations Rectal bleeding and diarrhea are the most common signs; abdominal tenderness, anemia. Anemia may develop as a result of malabsorption of vitamin B12 and folic acid. -Complication: Short bowel syndrome with malabsorption, diarrhea, and nutritional deficiencies

Inflammatory Bowel Diseases

Chronic, relapsing inflammatory bowel disorders of unknown origin -Genetics Environmental factors Alterations of epithelial barrier functions Immune reactions to intestinal flora Varying phenotypes -Examples Ulcerative colitis Crohn's disease

jaundice (icterus)

Conditions characterized by excessive concentrations of bilirubin in the skin and tissues and deposition of excessive bile pigment in the skin, cornea, body fluids, and mucous membranes with the resulting yellow appearance of the patient. -Clinical manifestations Dark urine Clay-colored stools Yellow discoloration possibly occurring first in the sclera of the eye and then progressing to the skin Skin xanthomas (cholesterol deposits) and pruritus Anorexia, malaise, fatigue

Lactase deficiency

Congenital defect in the lactase gene Inability to breakdown lactose into monosaccharides and thus prevent lactose digestion and monosaccharide absorption Fermentation of lactose by bacteria, causing gas (cramping pain, flatulence) and osmotic diarrhea Treatment Avoidance of milk products; adherence to a lactose-free diet Maintenance of adequate calcium intake to decrease risk of osteoporosis Lactase enzyme replacement

Bile salt deficiency

Conjugated bile salts needed to emulsify and absorb fats Bile salts are conjugated in the bile that is secreted from the liver Can result from liver disease and bile obstructions Poor intestinal absorption of lipids causes fatty stools (steatorrhea), diarrhea, and loss of fat-soluble vitamins (A, D, E, K) -Treatment Increase medium-chain triglycerides in the diet. Parenterally administer vitamins A, D, and K. Cholestyramine

2. Differentiate between the pathophysiology of constipation vs. diarrhea.

Constipation is difficult or infrequent defecation Diarrhea in which the volume of feces is increased is called large-volume diarrhea

Treatment for early and late dumping

Consuming frequent small meals high in protein and low in carbohydrates Drinking fluids between meals instead of at mealtime Reclining on the left side after eating Reconstructing the pylorus or a gastrojejunostomy Administering Octreotide: To inhibit insulin release and slow intestinal transit time

Clinical manifestations of celiacs disease

Diarrhea, meconium ileus: Early signs Stools: Pale, bulky, greasy, foul smelling Failure of child to grow and thrive Malabsorption symptoms: Rickets, bleeding, anemia, fat-soluble vitamin deficiencies Dehydration, malabsorption, protein loss Magnesium and calcium malabsorption: Irritability, tremor, convulsions, tetany, bone pain, dental abnormalities, osteomalacia

Treatment of ascites

Dietary salt restriction Potassium-sparing diuretics Strong diuretics, such as furosemide or ethacrynic acid Vasopressin receptor 2 antagonists: For dilutional hyponatremia Possible administration of albumin Monitor serum electrolytes, especially sodium and potassium -Paracentesis: Removal of 1 or 2 L of ascitic fluid and relief of respiratory distress Removing too much fluid too fast relieves pressure on the blood vessels, causing arteriolar vasodilation and carries the risk of hypotension, shock, or death. Ascitic fluid reaccumulates in individuals with irreversible disease. Is likely to cause peritonitis. Liver transplant: Best treatment option

Dysphagia

Difficulty swallowing: Types Mechanical obstructions of esophagus Intrinsic vs. extrinsic Functional obstructions of esophageal motility -Clinical manifestations Upper esophageal obstruction: Discomfort occurring 2-4 seconds after swallowing Lower esophageal obstruction: Discomfort occurring 10-15 seconds after swallowing All types: Retrosternal pain, regurgitation of undigested food, unpleasant taste, vomiting, and weight loss

7. Identify the diagnostic approaches used to differentiate between duodenal ulcers, gastric ulcers, and gastric carcinoma.

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, H. pylori-specific serum immunoglobulin G (IgG) and immunoglobulin A (IgA) antibodies, and measurement of H. pylori stool antigen levels

Cancer of the Esophagus

Facilitated by chronic inflammation and dysplasia caused by gastroesophageal reflux and long-term exposure to irritants (alcohol and tobacco) Clinical manifestations Chest pain and dysphagia Back pain Treatment Removal of primary lesion and local lymph nodes

Malabsorption Syndromes

Failure of the intestinal mucosa to absorb (transport) the digested nutrients -celiac disease -short bowel syndrome -diverticulitis

Clinical manifestations of Necrotizing enterocolitis

Feeding intolerance, abdominal distention and bloody stools after 8-10 days of age, septicemia with elevated white blood cell count, falling platelet levels, unstable temperature, bradycardia, apnea

process of digestion

Food breakdown begins in the mouth with chewing and continues in the stomach, where food is churned and mixed with acid, mucus, and enzymes. From the stomach, the fluid and partially digested food pass into the small intestine, where bile and enzymes secreted by the liver, enzymes from the exocrine pancreas, and small intestinal epithelium break it down into absorbable components of proteins, carbohydrates, and fats. These nutrients pass through the small intestinal epithelium into underlying blood vessels and lymphatics that carry them to the liver via the hepatic portal circulation for further processing and storage. Ingested substances and secretions that are not absorbed in the small intestine pass into the large intestine, where fluid continues to be absorbed. Solid wastes pass into the rectum and are eliminated from the body through the anus.

Cholelithiasis

Gallstone formation Cholesterol stone formation in bile that is supersaturated with cholesterol

Cancer of the liver

Hepatocellular carcinoma that has developed in the hepatocytes Cholangiocellular carcinoma (cholangiocarcinoma) that has developed in the bile ducts Clinical manifestations Vague abdominal symptoms Risk factors Infection with hepatitis A, C, and D viruses, particularly in conjunction with cirrhosis Chronic alcoholic liver disease and nonalcoholic liver disease that results in cirrhosis

Diverticula

Herniation of mucosa through the muscle layers of the colon wall

Failure to thrive

Inadequate nutrition for optima growth and development Deceleration in weight gain, a low weight/height ratio, a low weight/height/head circumference ratio, or a low BMI Biologic, psychosocial, and environmental causes -Evaluation Falls below the third percentile on the growth curve or shows stagnation in length or width

Cholecystitis

Inflammation of the gallbladder Acute vs. chronic Clinical manifestations Fever, leukocytosis, rebound tenderness, and abdominal muscle guarding

appendisitis

Inflammation of the vermiform appendix Possible causes- Obstruction, ischemia, increased intraluminal pressure, infection, inflammation -Clinical manifestations Epigastric and periumbilical pain, rebound tenderness Nausea, vomiting, fever, anorexia Complications: Perforation, peritonitis, abscess formation -Treatment Antibiotics and appendectomy

Marasmus

Is a deficiency of all nutrients. Is common in children younger than 1 year old and attributable to a lack of protein and carbohydrates. -Patho: Metabolic processes are preserved. Growth is severely retarded. Muscle/fat wasting; anemia Clinical manifestations: Fatty liver and hepatomegaly; muscle wasting; diarrhea; dermatosis; infection; low hemoglobin level

11. Discuss the pathophysiology of cystic fibrosis.

Is a genetically transmitted disease (dysfunction of the CFTR protein) that involves many organs and systems. Usually causes death in childhood or young adulthood. Deficiency of pancreatic enzymes in the digestive tract Result of overproduction of extremely viscous mucus and pancreatic enzyme deficiency Classic triad 1 Deficiency of pancreatic enzyme 2 Overproduction of mucus in the respiratory tract 3 Abnormally elevated sodium and chloride concentrations

Stress-related mucosal disease

Is a peptic ulcer related to a severe illness, multisystem organ failure, or major trauma. Ischemic ulcer: Develops within hours of an event. Curling ulcer Develops after a burn injury. Cushing ulcer Develops as a result of head trauma or brain surgery from hypersecretion of hydrochloric acid from the vagal nuclei. Clinical manifestations Bleeding: Most common Treatment: Prophylactic therapy

Kwashiorkor

Is a severe deficiency of protein. Usually occurs ininfants or children from1-4 years of age who have been weaned from breast milk to a high-starch, protein-deficient diet. -Pathophysiology; Inadequate dietary protein Leaky gut syndrome, Intestinal inflammation, Stored fat in liver, Pancreatic atrophy/fibrosis Clinical manifestations: Generalized edema, dermatoses, hypopigmented hair, distended abdomen, hepatomegaly, normal weight for age (due to edema)

Cirrhosis

Is an irreversible inflammatory fibrotic disease that disrupts liver function and even liver structure. Most common causes are alcohol abuse and HCV. Hepatic function from nodular and fibrotic tissue synthesis (fibrosis) decreases. Biliary channels become obstructed and cause portal hypertension. Because of the hypertension, blood is shunted away from the liver, and hypoxic necrosis develops.

Necrotizing enterocolitis

Is an ischemic, inflammatory condition that causes bowel necrosis and perforation. Causes infant death, if left untreated. Is the most common gastrointestinal emergency of the newborn. Is thought to be from reduced mucosal blood flow and immature mucosal barrier. Ischemia leads to inflammation and necrosis of the intestinal segments and possible perforation.

Cleft lip

Is caused by the incomplete fusion of the nasomedial or intermaxillary process during the fourth week of development. Commonly occurs under one nostril, but the defect can be bilateral and symmetric or asymmetric.

14. Describe the pathophysiology of neonatal jaundice.

Jaundice develops due to increase the level of bilirubin and deposition under the skin and cause the yellow discoloration of the skin. Pathogenesis of neonatal jaundice includes physiologic process of bilirubin accumulation or pathological mechanism. The pathological jaundice may be acquired or inherited.

pathophysiology of Ulcerative colitis

Lesions are continuous with no skipped lesions, are limited to the mucosa, and are not transmural. -Clinical manifestations Large volumes of watery diarrhea, bloody stools, cramps, pain, urge to defecate Remission and exacerbations

Crohn's disease

Location of lesions- All of GI tract—mouth to anus; "skip" lesions common Area affected- Entire intestinal wall Granuloma- Common "cobblestone" appearance Abdominal pain- Common Bloody stools- Less common Steatorrhea- Common Antineutrophil cytoplasmic antibody- Rare Antisaccharomyces cerevisiae antibody- Common

Ulcerative Colitis

Location of lesions- Colon and rectum; no "skip" lesions Area affected- Mucosal layer Granuloma- Rare Abdominal pain- Occasional Bloody stools- Common Steatorrhea- Rare Antineutrophil cytoplasmic antibody- Common Antisaccharomyces cerevisiae antibody- Rare

10. Identify the maternal risk factors associated with congenital malformations of the gastrointestinal tract.

Maternal deficiency of B vitamins (B6, folic acid, B12) Maternal: Alcohol, smoking, diabetes mellitus, steroid or statins, hyperhomocysteinemia, gene mutations -Increased gastrin secretion by the mother in the last trimester Overproduction of gastric secretions in the infant that may be caused by stress-related factors in the mother Exogenous administration of prostaglandin E Increased risk factors if a family member has had pyloric stenosis -maternal exposure to methimazole, exogenous sex hormones, -fetal-maternal blood type incompatibility (ABO and Rh incompatibility), -Hep B & C

Intestinal microbiome

Metabolic functions -vitamin synthesis -digestion and absorption Development Protective functions -competition with pathogens -good bacteria keep bad in line

Duodenal ulcer

Most common of the peptic ulcers -commonly caused by H. pylori infection and NSAID use -Developmental factors Altered mucosal defenses High gastrin levels Rapid gastric emptying Acid production caused by cigarette smoking -Clinical manifestations Chronic intermittent pain in the epigastric area. Pain begins 30 minutes to 2 hours after eating when the stomach is empty. Pain is relieved by food and antacids.

Hirschsprung disease

Obstruction of colon Most common cause of colon obstruction Failure of neural crest cells to migrate into GI tract Skipped segments Delayed passage of meconium, poor feeding, poor weight gain, abdominal distension Treatment is surgical.

Infantile hypertrophic pyloric stenosis

Obstruction of the pyloric sphincter is caused by hypertrophy of the sphincter muscle. -the most common cause of intestinal obstruction in infancy. It is an acquired narrowing and distal obstruction of the pylorus and a common cause of postprandial or projectile vomiting. Risk factors Increased gastrin secretion by the mother in the last trimester Overproduction of gastric secretions in the infant that may be caused by stress-related factors in the mother

theories for ascites

Overflow, underfill and peripheral artery vasodilation or forward theory

Hiatal hernia

Protrusion (herniation) of the upper part of the stomach through the diaphragm and into the thorax -often asymptomatic, associated with other gastrointestinal disorders, primarily GERD. -four types: sliding (type I); paraesophageal (type II); and mixed (type III), which include elements of types I and II. In type IV the entire stomach and other abdominal organs slide into the thorax.

ANS: 1 In pyloric stenosis, the circular muscle of the pylorus is grossly enlarged because of an increase in cell size (hypertrophy) and an increase in cell number (hyperplasia), which obstructs the pyloric opening.

Pyloric stenosis is associated with muscle hyperplasia. diarrhea. anorexia. increased maternal cholecystokinin.

Dumping syndrome

Rapid emptying of hypertonic chyme from the stomach into the small intestine Complication of partial gastrectomy, bariatric procedure, or pyloroplasty Developmental factors for early dumping Loss of gastric capacity, loss of emptying control, and loss of feedback control by the duodenum when it is removed -Clinical manifestations Diarrhea, cramping, feeling of epigastric fullness, pain, nausea, and vomiting -Late dumping syndrome (1-3 hours after eating) Clinical manifestations Weakness, diaphoresis, and confusion

Biliary atresia

Rare congenital malformation, characterized by the absence or obstruction of the extrahepatic bile duct Inflammation, fibrosis, loss of epithelial cells, and obstruction of the bile canaliculi Primary clinical manifestation: Jaundice

Autoimmune Hepatitis

Rare, chronic, and progressive autoimmune inflammatory liver disease Clinical manifestations No symptoms Jaundice, fatigue, loss of appetite, amenorrhea, acute liver failure

Hepatorenal Syndrome

Renal failure demonstrating oliguria, hypotension, and peripheral vasodilation as a result of advanced liver disease Usually associated with alcoholic cirrhosis -Treatment Manage fluid and electrolyte disorders, bleeding, infections, and encephalopathy. Administer systemic vasoconstrictors (α-adrenergic agonists and octreotide) and albumin. Liver transplantation

Hepatopulmonary syndrome (HPS)

Respiratory complications with portal hypertension Intrapulmonary vasodilation Intrapulmonary shunting and hypoxia Portopulmonary hypertension (pulmonary vasoconstriction and vascular remodeling)

4. Describe the pathophysiology of GERD.

Resting tone of the lower esophageal sphincter tends to be lower than normal from either transient relaxation or weakness of the sphincter. Conditions that increase abdominal pressure can contribute to GERD. Vomiting, coughing, lifting, bending, obesity, or pregnancy

Cleft palate

Results from the incomplete fusion of the primary palatal shelves during the third month of gestation. Is commonly associated with cleft lip but can occur without it.

Acute Liver Failure

Severe impairment or necrosis of liver cells without preexisting liver disease or cirrhosis Leading cause: Acetaminophen overdose Pathophysiology Hepatocytes become edematous. Patchy areas of necrosis and inflammatory cell infiltrates disrupt the parenchyma. Hepatic necrosis is irreversible.

5. Discuss the potential consequences of intestinal obstruction.

Simple obstruction is mechanical blockage of the lumen by a lesion, but blood flow is preserved. It is the most common type of intestinal obstruction. -In a strangulated obstruction, blood flow is compromised, leading to intestinal ischemia and, if left untreated, necrosis and perforation.

Symptoms to differentiate between duodenal ulcers, gastric ulcers, and gastric carcinoma.

Symptoms and signs of advanced stomach cancer include fatigue, weight loss, anemia, black tarry stools, and severe nausea and vomiting, sometimes with blood. Stomach ulcer symptoms and signs include mild digestion, stomach discomfort, hunger pain, or abdominal burning a couple of hours after eating.

gastric ulcer

Tends to develop in the antral region of the stomach, adjacent to the acid-secreting mucosa of the body. Pathophysiology Frequent cause: H. pylori Primary defect: Increased mucosal permeability to hydrogen ions Gastric secretion: Normal or less than normal -Clinical manifestations Pain occurs immediately after eating. Tends to be chronic. Anorexia, vomiting, and weight loss Treatment Same as the treatment for duodenal ulcers

13. Summarize the incidence, etiology, and evaluation of pediatric inflammatory bowel disease.

The incidence in children is 10 per 100,000 children in the United States and Canada, and appears to be rising across the world with approximately 25% of children diagnosed before the age of 20. -The etiology of IBD is unknown, but there are host genetic, epigenetic, microbial, and environmental factors that together result in a dysregulated mucosal immune response -Evaluation may include laboratory monitoring, such as inflammatory markers, stool cultures, endoscopy, colonoscopy, videocapsule endoscopy, magnetic resonance enterography (MRE), and computer tomography (CT) scan. Fecal calprotectin (FC) level is elevated in IBD and can be used as a marker for IBD identification and response to treatment in children.

Diverticulitis

The inflammatory stage of diverticulosis

8. Discuss the differing pathophysiology of ulcerative colitis vs. crohn disease.

Ulcerative colitis is limited to the colon while Crohn's disease can occur anywhere between the mouth and the anus. -In Crohn's disease, there are healthy parts of the intestine mixed in between inflamed areas. -Ulcerative colitis, on the other hand, is continuous inflammation of the colon -Ulcerative colitis only affects the inner most lining of the colon while Crohn's disease can occur in all the layers of the bowel walls

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

ANS: 1 The major pathophysiologic characteristic in gluten-sensitive enteropathy is T cell-mediated autoimmune injury to the intestinal epithelial cells.

What is the pathophysiologic process that occurs in a person with gluten-sensitive enteropathy? T cell-mediated autoimmune injury to the intestinal epithelial cells Deficiency of pancreatic enzyme, which causes maldigestion Atopic disease, involving immediate and delayed hypersensitivity reactions to food ingestion Return of stomach contents because of an incompetent lower esophageal sphincter

ANS: 2 The immature mucosal barrier delays digestion and motility is slower, allowing for the accumulation of noxious substances that damage the intestine and increase permeability and increase the risk for infection.

Which disease is correctly matched to its pathophysiologic process? Kwashiorkor—severe deficiency of all nutrients Necrotizing enteropathy—noxious substances damage the intestines Marasmus—severe protein deficiency Lactose intolerance—inadequate intake, absorption, or excessive expenditure of calories

ANS: 1 The typical chronic lesion is a noncaseating granuloma.

Which finding is typical for Crohn's disease? Noncaseating granulomas Continuous primary lesion with no skipped lesions Prone to the development of Cushing ulcer Intermittent epigastric pain when the stomach is emp

ANS: 4 The most common clinical manifestation of portal hypertension is vomiting of blood (hematemesis) from bleeding esophageal varices.

Which intervention is most appropriate for a person with portal hypertension? Increase dietary fiber intake. Administer N-acetylcysteine. Eat small high-protein meals. Monitor for hematemesis.

ANS: 2 Rolling or jarring of the abdomen produces a sloshing sound called the succussion splash in a person with pyloric obstruction.

Which statement is correct regarding disorders of motility? Dysphagia causes hematemesis from accumulation of blood in the GI tract. A succussion splash from jarring of the abdomen occurs in pyloric obstruction. Achalasia is a type of referred pain from the esophagus to the small intestine. Obstruction in the proximal small intestine causes vomiting with fecal material.

Ulcerative colitis

a chronic inflammatory disease that causes ulceration of the colonic mucosa. Sigmoid colon and rectum Is common in those 20-40 years of age

H. pylori

a gram-negative spiral bacterium with a flagellum and is a major cause of acute and chronic gastritis, peptic ulcer disease in the duodenum and stomach, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) in about 20% of infected individuals. - is transmitted through the fecal-oral route and is usually acquired in childhood. -asymptomatic in about 70% of cases. In other cases, inflammation and immune responses promote mucosal ulcerations or prevent healing of injured tissue.

Ascities

accumulation of fluid in peritoneum d/t portal htn, hypoalbuminemia, hyperaldosteronism, fluid leaks. Most common cause: Cirrhosis Clinical manifestations Abdominal distention, increased abdominal girth, and weight gain Evaluation Serum-ascites albumin gradient (SAAG): Most specific diagnostic indicator

Celiac disease

an inherited autoimmune disease of the small intestine characterized by a severe reaction to foods containing gluten -Gluten: Is the protein component in cereal grains (wheat, rye, barley, oats, malt). Person loses villous epithelium in the intestinal tract; gluten protein acts as a toxin. Appears to be caused by environmental, genetic, and immunologic factors.

Parietal pain

arises from the parietal peritoneum. This pain is more localized sharp and intense than visceral pain, which arises from the organs themselves. - i.e. late stages of appendicitis RLQ

Melena

black, tarry stools; feces containing digested blood

Hematochezia

bright red blood in stool

Hepatic Encephalopathy

central nervous system dysfunction resulting from liver disease; frequently associated with elevated ammonia levels that produce changes in mental status, altered level of consciousness, and coma

Esophageal atresia

congenital lack of the connection between esophagus and stomach; food cannot enter stomach -Esophagus ends in a blind pouch. Endodermal cells exhibit defective growth. Pathophysiology Postviral infectious, environmental, and genetic factors VACTERL CHARGE Swallowed amniotic fluid -Clinical manifestations Esophageal atresia: Drooling, choking, swallowing difficulties, respirator distress, inability to pass orogastric tube Fistula: Recurrent aspiration, pneumonia, atelectasis

12. Describe the pathophysiology which leads to the malabsorption associated with celiac disease.

eating gluten triggers an immune response in your small intestine. Over time, this reaction damages your small intestine's lining and prevents it from absorbing some nutrients (malabsorption).

The clinical course of hepatitis usually consists of four phases:

incubation, prodromal, icteric, and recovery phases.

Hepatitis A

inflammation of the liver caused by the hepatitis A virus (HAV), usually transmitted orally through fecal contamination of food or water -Risk factors Crowded, unsanitary conditions Food and water contamination

Hepatitis B

inflammation of the liver caused by the hepatitis B virus (HBV), Parenterally and sexually transmitted Maternal transmission occurs if the mother is infected during the third trimester. Hepatitis B vaccine prevents the transmission and development of hepatitis B.

Hepatitis C

inflammation of the liver caused by the hepatitis C virus (HCV), which is transmitted by exposure to infected blood; this strain is rarely contracted sexually -Is responsible for most cases of posttransfusion hepatitis. Is also implicated in infections related to IV drug use and human immunodeficiency viral (HIV) infection. Coinfection with hepatitis B is common. Approximately 80% of those with hepatitis C develop chronic liver disease. No vaccine is available.

Intussusception

is the telescoping of a proximal segment of intestine into a distal segment, causing an obstruction. It is the most common cause of small bowel obstruction in children. Common in kids with CF. -Clinical manifestations Abdominal pain. Infants: Irritable (colicky) and flexes the knees. Vomiting occurs soon after the pain begins. "Currant jelly" stools, which appear dark and gelatinous because of their blood and mucus content.

Meconium

the greenish material that collects in the intestine of a fetus and forms the first stools of a newborn

GERD (gastroesophageal reflux disease)

the reflux of acid and pepsin or bile salts from the stomach to the esophagus that causes esophagitis.

Hematemesis

vomiting blood

Clinical manifestations of portal hypertension

vomiting of blood from bleeding esophageal varices -no definite treatment