GERD also referred to as reflux

occurs when the hydrochloric acid that is maintained in the stomach gets pushed into the esophagus.

Causes include hiatal hernia, pregnancy, a malfunction of the esophageal sphincter, foods such as chocolate, fatty foods and smoking.

S/S: burning in epigastric region or throat

especially after meals and in the supine position

N/V with blood can occur

occurs when the lining of the stomach becomes inflamed. Gastritis can be caused by bacterial or viral infections, medicines, alcohol, stress and certain foods such as hot and spicy.

S/S: upset stomach, N/V, and heartburn

Erosions of the stomach lining. If they are severe enough, these ulcerations can bleed. These ulcers can be caused by a bacterial infection, Helicobacter pylori. Increased amounts of stomach hydrochloric acid, cigarette smoking, drinking alcoholic beverages, and chronic aspirin use can contribute to stomach ulcers.

S/S: severe abdominal pain and nausea associated with vomiting and loss of weight. The vomit can have coffee ground appearance representing digested blood or the blood can be red.

Cause is unknown, although stomach ulcers may be a factor.

S/S: Commonly presents with a bloating sensation, gas, abdominal pain and cramping, bloody stool, nausea, and vomiting.

Located in RUQ of the abdominopelvic cavity.  The stomach mixes in ingested food saliva and gastric juices to form chyme and holds food until the small intestine is ready to accept food.

Gastric juice hydrochloric acid, intrinsic factor, gastric lipase, and pepsinogen.

Surface mucous cells and mucous neck cells secrete mucus, which acts as a protective barrier that prevents damage to the stomach. 

 Parietal cells secrete 

• Hydrochloric acid, which kills most microorganisms and denatures proteins. 

• Intrinsic factor, which is needed to absorb vitamin B12. (Vitamin B12 is needed to make red blood cells.) 

Chief cells secrete: 

• Gastric lipase, which breaks down fats. 

• Pepsinogen, which is converted to pepsin (the active form) when it makes contact with the hydrochloric acid. Pepsin breaks down protein. 

a muscular tube that extends from the stomach to the cecum of the large intestine. Most of the digested food is absorbed into the blood through the small intestine. The small intestine has three sections: 1. Duodenum 2. Jejunum 3. Ileum

The cells that make up the endothelial lining of the small intestine contain microvilli that increase the surface area for the absorption of digested food. The small intestine contains glands that secrete an alkaline mucus that protects the lining from digestive enzymes and stomach acid, called Brunner’s glands, and glands that secrete digestive enzymes, called crypts of Licherkühn. 

Crohn’s disease, or CD, is also known as regional enteritis and is a chronic inflammatory disease that affects the mucosa layer, resulting in inflammation and ulceration.

Intestinal stenosis can occur as a result of fibrosis in the submucosa layer and the hypertrophic muscular layer.

affects both the small and large intestines, but it can occur anywhere in the gastrointestinal tract, from the mouth to the anus. 

 causes:  unknown,  familial pattern, autoimmune component.

Infectious agents, such as enteric bacteria, mycobacteria, viruses, and chlamydiae, have also been suspected. 

S/S: abdominal pain, cramping, fever, diarrhea, decreased weight, and decrease in red blood cell production (caused by malabsorption)

The large intestine begins as the cecum, which is attached to the ileum of the small intestine. Off the cecum is a wormlike projection called the vermiform appendix or appendix. The appendix has no purpose in humans. The ascending colon travels superiorly to the transverse colon, which travels transversely across the abdomen to hook up with the descending colon. The descending colon travels inferiorly to the sigmoid colon, an S-shaped structure connected to the rectum. The rectum stores feces. The feces empty along the anal canal and exit the body through a muscular opening called the anus.

Function: in the absorption of water, ions, and vitamins and the formation of feces. Water, inorganic salts, epithelial cells, undigested food (such as fiber), and bacteria are expelled from the body as feces. 

 Appendicitis can be caused by an obstruction of hard fecal matter in the lumen, resulting in bacterial growth. The fecal matter is called a fecalith and starts the inflammatory process. Inflammation can also be caused by the compression from a mass, such as a tumor, an abscess, or even a gallstone. Parasites can also cause blockages. An example of such a parasite would be pinworms.

S/S:present as mild epigastric or umbilical pain. As the appendix continues to swell, it pushes against the abdominal wall and parietal peritoneum, causing severe localized pain in the lower right quadrant.

McBurney Point

Positive psoas sign, Rovsing’s sign, and obturator sign are indicative of appendicitis, which can be elicited on physical examination. 

Abdominal trauma can initiate an inflammatory response that results in inflammation of the appendix. 

Alternatively, appendicitis can occur if the appendix becomes twisted or occluded by bowel adhesions.

Affects the mucosal lining of the rectum and colon. Most tumors that grow in the gastrointestinal tract tend to be carcinomas. These carcinomas can be found in the colon, stomach, esophagus, and small intestine. 

Colon cancer-most common

Cancer of the small intestine-least common.

Cause : unknown, although high-fat, low-fiber diets may contribute, and polyps in the colon and/or rectum can become cancerous. 

S/S: Abdominal pain especially at night, blood in feces, pencil thin feces, bowel obstruction, weight loss and anemia.

Condition of the colon (most common in the sigmoid colon) in which pouchlike sacs called diverticula protrude through the mucosa wall of the colon. When these sacs become inflamed or swell, the condition is called diverticulitis.

 Cause:unknown, although infections of the diverticula and a poor diet lacking fiber have been known to cause the condition. Eating peanuts and seeds has been known to exacerbate the condition. 

Most diverticula are found in the sigmoid and descending colon.

Diverticula often become inflamed, at which point the condition becomes diverticulitis. 

S/S: asymptomatic (having no symptoms). If the condition is becoming exacerbated, the individual may experience abdominal pain, constipation, diarrhea, blood in the feces, nausea, and fever. 

Varices in the veins of the rectum and anus are referred to as hemorrhoids. Hemorrhoids can be caused by an increased or elevated pressure in veins, pregnancy and labor, obesity, and chronic constipation that causes the individual to strain while moving his or her bowels. 

S/S: bulges in the anal region, BRB in feces, Pain during defecation and itching in the anal region.

Hemorrhoids can be likened to varicose veins in the perianal region.

They are caused by decreased venous return and venous pooling in the blood vessels of the rectum.  

High venous pressure in the rectal region is commonly caused by: 

Constipation and straining during defecation

High pressure within the portal vein of the liver

Anal intercourse

Pregnancy

Prolonged sitting

Aging of support structures in the recto-anal region

Lack of fiber in the diet causes chronic constipation, which leads to hemorrhoids. In pregnancy, the gravid uterus places high pressure on the inferior vena cava, leading to hemorrhoids.

Can be chronic or acute and is also an inflammatory and ulcerative process. This disease process is restricted to the large intestine, beginning at the rectosigmoid region and extending upward, until it eventually affects the entire colon. 

cause of ulcerative colitis is unknown.

S/S:watery diarrhea that contains blood and mucus diarrhea can be sudden and urgent.

 high fever, weight loss, anemia (decrease in red blood cells), malaise, and toxemia. There is also a risk of hemorrhage, which is a common complication of ulcerative colitis.

Liver 

Gallbladder

Pancreas

composed of a right and a left lobe and is located in the right upper quadrant of the abdominopelvic cavity. The lobes of the liver are connected to each other and to the common bile duct (coming off the gallbladder) by the common hepatic duct. 

 functions in the metabolism of carbohydrates, lipids, and proteins; processes hormones and drugs; stores vitamins; and excretes bilirubin. 

Hepatitis is the inflammation of the liver. Hepatitis can be caused by a bacterial infection; a viral infection, such as hepatitis B virus (HBV); a parasitic infection; alcohol abuse and drug abuse, including overuse of acetaminophen; and undercooked or contaminated food. 

S/S: enlarged liver, jaundice (yellow color to the skin and sclera of the eyes), abdominal pain, nausea and vomiting, weakness, and urine that is very dark. 

The gallbladder lies between the lobes of the liver in the right upper quadrant. 

 Function: gallbladder stores bile. Under the influence of the hormone cholecystokinin, the gallbladder contracts, ejecting bile through the cystic duct into the common bile duct and into the duodenum of the small intestine, where it emulsifies fats. 

Inflammation of the gallbladder as a result of the blockage of a cystic duct by a gallstone.

S/S: presents as recurring colicky pain in the right upper quadrant that refers pain to the inferior angle of the right scapula. 

Gallstones are made up of solidified bile salts, phospholipids, and cholesterol. 

The pancreas is located posterior to the stomach and is both an endocrine gland and an exocrine gland. About 99 percent of pancreatic cells are acini cells and function in exocrine secretion of pancreatic digestion. The other 1 percent are endocrine cells and are called the islets of Langerhans. 

acini cells secrete: 

• Pancreatic lipase. Pancreatic lipase breaks down fats (triglycerides). 

• Pancreatic amylase. Pancreatic amylase breaks down starches (polysaccharides). 

• Pancreatic nucleases. Pancreatic nucleases include ribonuclease and deoxyribonuclease, which break down nucleic acids. 

• Trypsinogen. Trypsinogen is converted to its active form trypsin (in the intestines by enterokinase), which breaks down protein

Pancreatitis is inflammation of the pancreas. 

There are two forms: 

1. Acute pancreatitis. This form of pancreatitis resolves and is commonly the result of a biliary obstruction, usually calculi (stone). 

2. Chronic pancreatitis. This form of pancreatitis involves tissue changes that are not reversible and that result in progressive loss of both endocrine and exocrine function. The most common cause of chronic pancreatitis is chronic alcohol consumption. Pancreatitis presents as severe abdominal pain that is referred to the midthoracic region of the back and is described as a steady, deep, boring pain accompanied by nausea and vomiting. 

 Pancreatic cancers that are exocrine tumors are called ductal adenocarcinomas. The majority of these tumors occur in the head of the pancreas and cause obstructions that result in jaundice. Pancreatic cancer is twice as com- mon in men at an average age of 55 years. The cause of pancreatic cancer is unknown, although alcohol consumption and smoking are risk factors. 

S/S: severe abdominal pain that radiates to the thoracic region of the vertebral column, accompanied by weight loss, jaundice, nausea, vomiting, and fatigue

Constipation is a common problem, especially in the elderly. Problems occur when severe constipation causes fecal impaction and obstipation. 

Fecal impaction occurs when hard stool that cannot be passed is lodged in the sigmoid colon and rectum. Commonly, a patient can develop liquid stools that pass around a fecal impaction.  

Obstipation is a sensation to defecate with no passage of stool, liquid, or gas from the colon.

Cathartic colon is the anatomical and physiological change in the colon that occurs with chronic use of stimulant laxatives. 

Excessive laxative use is defined as more than 3 times per week for at least 1 year. 

Signs and symptoms of cathartic colon include bloating, a feeling of fullness, abdominal pain, and incomplete fecal evacuation.  

Radiological studies show an atonic and redundant colon. 

Abdominal Pain

Waves of sharp constricting pain that take the breath away. Pain is worsened by movement.

Involuntary Guarding

The patient’s abdominal muscles contract with palpation.

Abdominal Rigidity

The abdomen is stiff to the touch.

Rebound Tenderness

When the examiner deeply palpates the abdomen, pain is felt by the patient as the examiner lifts his or her hand.

Percussion of tympany: gas-filled intestine.

Right lower quadrant tenderness: appendicitis.

A rectal examination may elicit pain in disorders such as appendicitis. A digital exam may also demonstrate hard stool in the rectum with fecal impaction.  

Left lower quadrant tenderness: diverticulitis.  

Upper right quadrant tenderness: Murphy’s sign, which is commonly caused by cholecystitis, which is inflammation of the gallbladder. 

A stool sample should be obtained for fecal occult blood testing (FOBT) if melena is suspected.  

In female patients, a pelvic examination is needed to rule out a gynecological source of pain. Ectopic pregnancy or ovarian cysts can cause abdominal pain that appears similar to GI pain. 

Evaluation of the inguinal and femoral regions should be an integral part of the examination in a patient with suspected large bowel obstruction. 

Incarcerated hernias represent a frequently missed cause of bowel obstruction

Women with an acute abdomen require a pelvic examination and pregnancy test to rule out ectopic pregnancy.

FOBT or stool guaiac tests can detect blood in the stool.  

Accuracy is highest after completion of three tests at three different times. 

A chest x-ray can show free air under the diaphragm when there is perforation of the bowel or abdominal organ. 

Air under the diaphragm from perforation of the bowel commonly causes shoulder pain.

An ileostomy or colostomy is a reversible or irreversible surgical procedure in which the healthy end of the intestine is brought out of the abdomen through an incision in the anterior abdominal wall.  

In ileostomy, the ileum of the small intestine is surgically brought out to the exterior abdominal wall. In colostomy, the colon is similarly brought out to the anterior abdomen.  

The opening, also called a stoma, allows for excretion of intestinal contents into an attached collection appliance.  

Alternatively, endoscopically placed expandable stents can be used to relieve large bowel obstructions

Crohn’s disease is a chronic, transmural inflammatory process of the bowel that often leads to fibrosis and obstructive symptoms and can affect any part of the gastrointestinal tract from the mouth to the anus.  

The most common location is the terminal ileum and ascending right colon. 

There are areas of disease separated by healthy areas, referred to as skip lesions. 

The bowel mucosa develops granulomas, which is exhibited as an effect called cobblestoning

Complication of Crohn’s disease

Extreme dilation of a segment of the diseased colon, commonly the transverse colon 

It causes complete obstruction and impaired absorption of fluids and electrolytes. 

In toxic megacolon, life-threatening perforation and peritonitis can result. 

Episodes of diarrhea and abdominal pain

Remissions and exacerbations

Malabsorption and nutritional deficiencies common 

Impaired absorption of fats, folic acid, iron, calcium, and vitamins A, B12, C, D, and K 

Electrolytes, trace elements, and minerals are lost through diarrhea, including sodium, potassium, magnesium, zinc, and copper.  

Anemia from loss of blood in the stool 

Dehydration 

Abdominal tenderness

Hyperactive bowel sounds (borborygmi)

Steady progressive weight loss

Anorexia

Nausea

Vomiting

Diarrhea

Pallor

Fever 

Severe bouts can cause intestinal obstruction with accompanying signs of borborygmi, abdominal distension, and tympany on percussion. 

Arthritis

Uveitis (can cause retinal detachment)

Chelitis

Aphthous ulcers

Dermatological problems (erythema nodosum)

Hepatic or bile duct inflammation

UC solely involves the large intestine, whereas Crohn’s disease can affect any area of the GI tract. 

UC can lead to cancer.

Peak age of onset occurs at age 15 to 25 years and another peak occurs at age 55 to 65 years.

Etiology is unclear; ?autoimmune

UC affects only the mucosal layer of the large bowel.

Continuous areas of inflammation in the large intestine are involved.  

Formation of inflammatory areas of protruding growths is termed pseudopolyps.

UC can lead to colon cancer.

S/S:Colicky abdominal pain, Blood in stool, Diarrhea, Dehydration, Malabsorption and weight loss, Abdominal distension, Abdominal guarding, Fever, Uveitis

Dermatological disorders pyoderma gangrenosum and erythema nodosum, Arthritis, Pleuritis

Inflammation of the liver and bile ducts

The inability of intestinal contents to move through the large intestine is referred to as an intestinal or large bowel obstruction (LBO). Obstructions may be:

Partial or complete

Acute or chronic

Reversible or irreversible

The majority of LBOs occur in the sigmoid section of the bowel. 

LBO has a high mortality rate if diagnosis and treatment are not commenced within the first 24 hours.

LBO

large bowel obstruction

mechanical or nonmechanical

 Mechanical obstruction physically blocks the movement of material through the intestines. 

Mechanical blockage may be caused by scar tissue from a prior surgery (adhesions), benign or malignant tumors, abdominal hernia, swallowed foreign body, gallstone that migrated into the intestine, bolus of undigested food, intussusception, volvulus, stricture, or diverticula. i

Nonmechanical causes stem from disruption of peristalsis because of weakness of muscles of the intestinal wall (dysmotility syndrome or pseudo-obstruction) or paralysis of the bowel wall (paralytic ileus).  

S/S: Abdominal pain

Abdominal distension

Abdominal tenderness

Abdominal rigidity  

Partial obstruction  high-pitched bowel sounds

Complete obstruction  no bowel sounds, no feces in rectum

IBS

irritable bowel syndrome

IBS is a GI disorder characterized by abdominal pain and altered bowel activity in the absence of specific pathology. 

No specific motility or structural disorders of the intestine or bowel have been shown. There is no known etiology.

Common findings related to IBS include abdominal

discomfort and alterations in elimination, such as diarrhea and constipation, or a combination of the two. 

IBS should not be confused with inflammatory bowel disease (IBD). 

Weakness of the bowel wall

Increased intraluminal pressure 

Diverticulitis occurs when intestinal contents block the diverticulum, thus cutting off the blood supply and providing an environment conducive to the formation of infection.

The most significant risk factor for diverticular formation is a diet low in fiber.

Classic diverticulitis pain: dull, episodic, or steady left quadrant or midabdominal pain, fever, and nausea; LLQ tenderness on palpation.

There are usually alterations in bowel habits, including constipation, diarrhea, increased flatulence, anorexia, and low-grade fever. 

Traces of occult blood may be found in the stool.  

Patients with right-sided diverticular disease can have RLQ tenderness of the abdomen similar to appendicitis.  

Pain of diverticular disease of the transverse colon can simulate pain of peptic ulcer or pancreatitis.

Lower esophageal sphincter (LES): separates gastric contents from the esophagus; gastric contents are acidic and can harm esophageal epithelium 

Upper esophageal sphincter: prevents aspiration of contents

Gastric parietal cells: secrete hydrochloric acid and intrinsic factor.  Intrinsic factor is necessary for the absorption of vitamin B12 in the small intestine. The proton pump of parietal cells regulates synthesis of acid.

Gastric goblet cells: secrete mucus and prostaglandin E2 (PGE2), a lipid-rich molecule, which exerts a strong protective effect. PGE2 stimulates gastric mucus production and bicarbonate secretion, which reduce the effects of HCL. 

Small intestine villi and microvilli: Villi are thousands of tiny fingerlike projections that contain goblet cells, whose functions are to release digestive enzymes, secrete mucus, and absorb nutrients. 

Microvilli are located on the epithelial cells of the villi. This double set of villi is known as the brush border. 

The combination of the villi and microvilli double the surface area, significantly increasing the absorptive capacity of the small intestine. 

Nutrients such as amino acids, glucose, iron, calcium, and the fat-soluble vitamins A, D, E, and K are absorbed in the jejunum.  

The ileum is the last—and longest—segment of the small intestine. The primary functions of the ileum are the reabsorption of vitamin B12 and the return of bile acids to the liver. 

The return of bile acids to the liver from the ileum is termed the enterohepatic circulation process. Bile acids are recycled by this process. 

Difficulty swallowing; associated with lack of gag reflex

Possible causes:

Degenerative neurological diseases

Stroke

Zenker’s diverticulum: weakening of the esophageal wall that forms a pouch that can collect food and cause obstruction 

Schatzki ring: constrictive muscular band of esophageal tissue. A congenital abnormality, it is often located in the distal esophagus.

Plummer-Vinson syndrome: esophageal membranous webs

Achalasia: esophageal motility disorder

Esophageal stricture

Increased risk of food or fluids to enter the trachea rather than the esophagus, known as aspiration  aspiration pneumonia

In a patient with absent gag reflex, the tongue and uvula may be deviated to one side, which indicates dysfunction of cranial nerves IX, X, and XII. 

Commonly called “heartburn”

Etiology: 

Loose lower esophageal sphincter (with age or hiatal hernia or GERD)

Infection; Candida (thrush)

Chemical ingestion

Medications: calcium blockers, anticholinergic drugs, NSAIDs, bisphosphonate

Excessive vomiting: Mallory-Weiss syndrome, Boerhaave syndrome

Gastroesophageal acid reflux (GERD)

Decreased closure of the lower esophageal sphincter, which allows acidic gastric contents to reflux up into the esophagus.

Acid of the stomach damages the esophageal epithelium.

Complication: metaplasia of cells at the gastroesophageal junction = Barrett’s esophagus = can lead to esophageal cancer.

Upper GI Bleed 

The presence of bleeding in the esophagus, stomach, or duodenum is classified as a UGIB. 

The bleeding can occur from a lesion, erosion, ulceration, varicosed vein, or tear to the GI lining.

Peptic ulcer disease; H. pylori infection or excessive NSAID use

Esophageal varices; caused by portal vein hypertension

Mallory-Weiss syndrome; excessive forceful vomiting

Boerhaave syndrome: rupture of esophagus caused by forceful vomiting

Esophageal cancer

Hemorrhagic gastritis 

S/S:Hematemesis

Melena

Slow chronic bleed  iron deficiency anemia, fatigue, lethargy 

Acute large GI bleed  anxiety, dizziness, weakness, shortness of breath, tachycardia, tachypnea, pallor 

“Coffee ground” emesis: Blood that has a coffee ground appearance indicates the blood has mixed with the acid of the stomach.  

If bright red blood is apparent, there is current bleeding occurring from a blood vessel. This is a medical emergency

Varicose veins at the lower end of the esophagus

Commonly caused by portal vein hypertension which occurs in liver cirrhosis--- most commonly caused by alcoholism or chronic hepatitis

S/S: Jaundice

Nausea

Vomiting

Weight loss

Dark urine

Abdominal distension

Slow esophageal bleed  hematemesis and melena 

Acute large esophageal bleed  bright red blood in the vomitus, hypotension, tachycardia, abdominal pain, and confusion. 

In squamous cell carcinoma, cancer cells invade the lining of the esophagus.  

Adenocarcinoma occurs in the glandular tissues in the distal esophagus near the junction of the esophagus and the stomach; this is the most common form of esophageal cancer.  

Chronic alcohol use

Tobacco use

Chronic GERD (Barrett’s esophagus)*

*The risk of adenocarcinoma among patients with Barrett’s esophagus has been estimated to be 30 to 60 times that of the general population

S/S: Dysphagia: Inability to swallow is initially noted with solids, eventually progressing to liquids and saliva. 

Weight loss

Change of eating pattern

Risk of aspiration pneumonia

Chest pain

Burning sensation behind the sternum

If nerve involvement: hiccups, hoarse voice, pain at the back of the throat, chronic cough, and odynophagia (painful swallowing). Difficulty breathing can arise if the pressure on nerves limits the rise and fall of the diaphragm. 

A hiatal hernia occurs as a result of part of the stomach pushing up through the opening in the diaphragm and protruding into the thoracic cavity. Many are undiagnosed, asymptomatic, and discovered incidentally.

Signs and Symptoms:

Esophagitis

Dysphagia

Substernal burning

Belching

Epigastric discomfort

Pyloric stenosis is a constriction of the pyloric sphincter, the muscular valve that connects the stomach to the duodenum. 

The narrowing of this region impairs the movement of gastric contents into the small intestine. 

In infants, this is a congenital abnormality (boys are more likely to have it than girls). 

Adults develop pyloric stenosis secondary to an ulceration or fibrosis of tissue surrounding the pyloric sphincter. 

Signs and symptoms: gastroparesis, projectile vomiting, firm abdomen over pylorus

Inflammation in the lining of the stomach

Caused by a number of medications (aspirin, NSAIDs, corticosteroids) and factors such as infection, allergy, acute stress, bile reflux, alcohol abuse, radiation, and direct trauma

Presence of the Helicobacter pylori (H. pylori) bacterium is the most common cause of chronic gastritis, which usually affects the fundus of the stomach. 

H. pylori undermines the gastric lining and causes irritation or ulceration; H. pylori destroys parietal cells  excessive gastrin production  oversecretion of gastrin  stimulates HCL production  lack of HCL eventually occurs  atrophy of stomach lining, no absorption of iron and vitamin B12 

It is different than acute gastritis because it causes atrophy of the glandular stomach lining, a condition called atrophic gastritis

S/S:Symptoms: burning or gnawing epigastric pain, nausea, weight loss, anorexia, and hematemesis 

Precursor for stomach cancer

Inflammatory erosion in the stomach or duodenal lining.  Ulceration occurs four times more often in the duodenum than in the stomach. 

Etiology:H. pylori , NSAIDs*, Stress, Alcohol abuse, Excessive caffeine, Smoking , Genetic susceptibility 

S/S:Epigastric, abdominal pain

Episodes of pain occur between meals, about 2 to 3 hours after eating

Pain is intense; a burning and gnawing sensation is present that can be slightly relieved by food and can be strong enough to awaken a person from sleep.  

Perforation of the stomach or intestinal wall  sudden, excruciating abdominal pain, abdominal rigidity, pale skin, hematemesis, and cold sweat

Gastric bypass (also called Roux-en-Y gastric bypass)

Gastric banding

Sleeve gastrectomy 

Biliopancreatic diversion with duodenal switch    

Dumping syndrome is caused by rapid gastric emptying. 

Poorly digested material enters the intestine before its breakdown in the stomach  material causes a shift of fluid out of the intestinal cells into the intestinal lumen  the fluid shift reduces blood volume, creates hypotension, and causes diarrhea

Irritation to the lining of the stomach, small intestine, or large intestine by a pathogen or toxin. 

Etiology: virus, bacteria, parasite, or chemical toxin

Infection transmitted from person to person or can be a water- or foodborne illness

Norovirus MOST COMMON in adults (highly contagious; fecal-oral route or through close contact)  

Rotavirus MOST COMMON in children (fecal-oral route)  

Other bacteria:

Enterotoxigenic Escherichia coli

Salmonella

Shigella

Clostridium difficile  

Parasites: 

Ameba; dysentery (severe diarrheal condition with dehydration)

Giardia; dysentery (severe diarrheal condition with dehydration

The epithelium of the microvilli = target of the infectious agent. 

The virus or bacteria attaches to the epithelium  impairs the ability of the small intestine to absorb carbohydrates, fats, fluids, or electrolytes.  

Alternatively, infectious agent  secretes a toxin that irritates the intestinal membrane. 

The villi are damaged  decreases the absorptive ability of the intestinal brush border.  

With lack of absorption  intestinal contents become hypertonic compared with the surrounding intestinal cells  water entry into the intestine diarrhea.

Nausea

Vomiting

Abdominal cramping

Diarrhea 

Dehydration 

Hyperactivity of the intestine produces high-pitched bowel sounds = borborygmi. 

Hyponatremia possible

Hypokalemia possible

Metabolic acidosis possible

Metabolic alkalosis possible

Condition usually persists for 48 to 72 hours.

Stool for ova and parasites is necessary.

Children and elderly individuals are at high risk of dehydration in gastroenteritis. 

Often hospitalization is needed to administer intravenous fluids to replace losses.

Also called sprue and gluten-sensitive enteropathy

Occurs from a hypersensitivity reaction to gluten, a by-product of wheat, barley, and rye 

Unknown cause; autoimmune disease

In celiac disease, a gluten-derived peptide called gliadin damages the intestinal mucosa in persons with genetic predisposition to this disease. 

Patho: Autoimmune destruction leads to a decreased surface area, causing atrophy of the intestinal wall  greatly reducing the absorptive and transport properties of the small intestine. The decreased surface area impairs the absorption of all nutrients, vitamins, minerals, electrolytes, and bile salts. 

The inability to digest carbohydrates  buildup of gases within the intestinal system  abdominal bloating and diarrhea. 

The inability to absorb proteins impairs the body’s ability to build and maintain muscle tone  muscle wasting. 

When fats are not absorbed, vitamins A, D, E, and K are not absorbed and fat is excreted in the stool.  

Steatorrhea is the loss of fat in the stool; with steatorrhea, stool is light colored and soft

Deficiency of vitamin A  night blindness. 

Deficiency of vitamin D  calcium absorption is diminished and hypocalcemia occurs.

Hypocalcemia  muscle spasms and tetany; also stimulates parathyroid hormone (PTH). 

PTH  breakdown of bone with resulting osteomalacia and susceptibility to fractures. 

Deficiency of vitamin E  red blood cells and platelet membranes become excessively fragile, leading to hemolysis, anemia, and thrombocytopenia. 

Deficiency of vitamin K  defective clotting mechanisms, leading to spontaneous bleeding and bruising.  

Iron is not absorbed  iron deficiency anemia.

A serology celiac panel can determine if an immune reaction to gluten is present. 

Affected individuals show a positive antibody titer of IgA antitissue transglutaminase (IgA TTG

The ileum is the largest segment of the small intestine; it is responsible for absorption of fluids, electrolytes, fats, carbohydrates, proteins, vitamin B12, and the return of bile to the liver.  

Removing any part of the ileum reduces the GI absorptive surface and can lead to nutritional deficiencies.

In short bowel syndrome, the remaining intestine gradually adapts to the changes. 

The remaining intestinal villi increase in number and enlarge to accommodate the need for increased absorption. 

It is necessary for individuals with short bowel syndrome to receive enteral nutrition during the postoperative period until the intestine adapts sufficiently to adjust to oral feedings

The acute phase lasts up to 3 months, followed by the adaptation phase, which may last 12 to 18 months. Fluid loss can be 6 to 8 liters per day. 

Malnutrition can rapidly develop, leading to muscle wasting, fatigue, skin irritations, and anemia.

During the adaptation phase, the body begins to adjust by lengthening the microvilli, which creates an increased surface area for reabsorption.  

During the maintenance phase, the patient accommodates diet to the changed intestine

Small Bowel Obstruction

SBO

An acute obstruction has a sudden onset that can occur with adhesions or a herniation of the bowel. 

A chronic obstruction is often seen with inflammatory disease or tumors. 

A partial obstruction decreases the flow of intestinal content through the bowel. 

A complete obstruction prevents passage of all contents and fluid through the bowel and is considered a surgical emergency. 

S/S:Abdominal distension

Pain; sharp, cramping, intermittent

Nausea

Vomiting

Hyperactive bowel sounds occur. 

Nausea and vomiting can cause fluid and electrolyte depletion, which could potentially lead to dehydration, hypotension, or hypovolemic shock. 

Diarrhea is present with a partial obstruction. 

The peritoneal membrane is the serous membrane that surrounds the abdominal cavity and covers the organs. 

Peritonitis is the inflammation of the peritoneal membrane caused by bacterial infection or leakage of intestinal contents into the peritoneal cavity. 

The condition most often occurs when organ rupture  bacteria, bile, acids, or enzymes into the sterile peritoneal environment  abdominal sepsis. 

A perforated gallbladder or a lacerated liver can cause bile to enter the peritoneal cavity. 

Gastric acid from a perforated ulcer can leak into the peritoneal cavity. Peritonitis can also result from traumatic injury.  

Women can endure peritonitis from an infected fallopian tube or a ruptured ovarian cyst

A paralytic ileus is the decrease or absence of intestinal motility that occurs during peritonitis

Classic triad of symptoms: 

Abdominal pain

Abdominal rigidity

Rebound tenderness 

Abdominal pain occurs with any movement of inflamed tissues. The patient wants to remain still. A cough will cause abdominal pain in the patient with peritonitis.  

The patient’s abdominal musculature is contracted in peritonitis. When palpated, the abdomen is rigid, a sign called involuntary guarding.  

Rebound tenderness occurs as the clinician palpates the abdomen. 

A paralytic ileus is the decrease or absence of intestinal motility that occurs during peritonitis

Classic triad of symptoms: 

Abdominal pain

Abdominal rigidity

Rebound tenderness 

Abdominal pain occurs with any movement of inflamed tissues. The patient wants to remain still. A cough will cause abdominal pain in the patient with peritonitis.  

The patient’s abdominal musculature is contracted in peritonitis. When palpated, the abdomen is rigid, a sign called involuntary guarding.  

Rebound tenderness occurs as the clinician palpates the abdomen. 

Liver  bile [(bile acids (80%), phospholipids (16%), and cholesterol (4%)].  

Bile has two major functions: digestion and elimination.  

Bile emulsifies fats and facilitates absorption of fat-soluble vitamins; it also carries waste products for elimination.  

One of the waste products contained in bile is bilirubin, Hgb  heme + globin  Fe++ + porphyrin  biliverdin  bilirubin

Some bile is released into the hepatic duct, which travels into the common bile duct. 

Some bile is stored in the gallbladder.

Cholelithiasis: stones in the gallbladder

Cholecystitis: inflammation of the gallbladder, which may be acute or chronic

Choledocholithiasis: stones in the common bile duct that can lead to backup of bile into the gallbladder and liver.  

Biliary sludge is the precursor to gallstones. It is a combination of calcium bilirubinate, cholesterol crystals, and mucin. Motility disturbances contribute to the formation of biliary sludge. 

Biliary stasis, or delayed emptying of the gallbladder, leads to stone formation. Biliary sludge, biliary stasis, or gallstones can form if the gallbladder does not empty completely.  

When gallstones enter the cystic duct, cholangitis, which is obstruction and ductal inflammation, occurs. Gallstones can also enter and obstruct flow in the common bile duct or can move into the pancreas and cause pancreatitis, a potentially fatal inflammatory disorder. 

Nausea and vomiting 

Feeling of fullness

Abdominal distension

Abdominal pain

Pain after eating fatty foods

Jaundice of the skin and sclera

Steatorrhea

Abdominal assessment:

RUQ guarding

RUQ tenderness

Inflammation of the gallbladder

Most commonly caused by gallstones (cholesterol-rich stones); acalculous cholecystitis can occur.

Episodic colicky pain after eating; may refer to the right scapula.

Anorexia and feeling of fullness

“Female, flatulent, fat, forty, fertile, family history, fasting, feeling full ”

Classic physical examination finding: +Murphy’s sign; tenderness and quick inspiration with palpation of the RUQ

Risk Factors: Genetic predisposition,Female gender, particularly those who have had multiple pregnancies

Age greater than 40 years, ObesityHigh-calorie, high-cholesterol diet, Estrogen, Use of oral contraceptives

Antihyperlipidemia medications, Rapid weight loss and yo-yo dieting

Obstruction of the cystic duct by gallstones causes distension of the gallbladder. 

As the gallbladder becomes distended, blood flow and lymphatic drainage are compromised, leading to mucosal ischemia and necrosis. 

The distension of the gallbladder irritates the nerves that innervate the wall, causing intense pain. 

As distension subsides, the pain dampens, leading to a pattern of spasmodic pain known as biliary colic.

This occurs when small gallstones pass from the gallbladder and cystic duct into the common bile duct. 

Stones remain in the common bile duct, causing obstruction, which causes backup of bile into the liver, resulting in backup of bilirubin and bile salts in the bloodstream.  

Accumulation of bilirubin in the bloodstream results in jaundice and backup of bile salts into the bloodstream, which causes pruritus (itching). 

Pancreatitis is inflammation of the pancreas that causes pancreatic insufficiency, malabsorption, and diabetes. 

Acute Pancreatitis Signs and  Symptoms

Severe abdominal pain, which is characteristically dull, penetrating, and steady. 

Pain is sudden in onset and gradually intensifies in severity.

Located in the epigastric region, pain can radiate to the back. 

Nausea, vomiting, and diarrhea

Anorexia

Fever

Tachycardia

Hypotension

Dyspnea

Tachypnea

Physical Assessement: Abdominal tenderness, Muscular guarding, Abdominal distension, Bowel sounds are often diminished or absent.

Some patients exhibit jaundice. pale, diaphoretic, and lethargic.

Cullen sign is a bluish discoloration around the umbilicus resulting from blood in the peritoneal cavity because of hemorrhagic pancreatitis.  

Grey-Turner sign is a reddish-brown discoloration along the flanks resulting from retroperitoneal blood dissecting along the tissue planes

This occurs when small gallstones pass from the gallbladder and cystic duct into the common bile duct. 

Stones remain in the common bile duct, causing obstruction, which causes backup of bile into the liver, resulting in backup of bilirubin and bile salts in the bloodstream.  

Accumulation of bilirubin in the bloodstream results in jaundice and backup of bile salts into the bloodstream, which causes pruritus (itching). 

On admission

Age greater than 55 years

White blood cell (WBC) count greater than 16,000

Liver enzyme: lactic dehydrogenase (LDH) greater than 600 U/l

Liver enzyme: aspartate aminotransferase (AST) greater than 120 U/l

Glucose greater than 10 mmol/l

Within 48 hours

Hematocrit fall greater than 10%

Blood urea nitrogen rise greater than 0.9 mmol/l

Calcium lower than 2 mmol

Po2 lower than 60 mm Hg

Base deficit greater than 4

Fluid sequestration greater than 6 L

The pancreas becomes vulnerable to its own digestive enzymes and undergoes autodigestion in inflammatory conditions.

The pancreas can undergo chronic inflammation, a slow process that gradually destroys the gland and leaves it nonfunctional, fibrotic, and atrophied.

Vague back pain is often the initial symptom.

As the disease worsens, there is constant epigastric pain with radiation to the back.  

Back pain worsens when the patient assumes the supine position; often this causes intense nighttime abdominal pain.  

Nausea, vomiting, and accompanying anorexia are common.

Jaundice eventually develops when the common bile duct is obstructed.  

Darkening of urine; hyperbilirubinemia

Pruritus; bile salt backup

Steatorrhea; lack of bile to digest fat

Weight loss occurs because of malabsorption of all nutrients when pancreatic enzymes are no longer produced. 

Depression

New onset of diabetes mellitus 

Migratory thrombophlebitis

Venous thrombosis