Gastrointestinal System

佚名

T he gastrointestinal (GI) system has the critical task of supplying essential nutrients to fuel all the physiologic and pathophysiologic activities of the body. Its functioning profoundly affects the quality of life through its impact on overall health. The GI system has two major components: the alimentary canal, or GI tract, and the accessory organs. A malfunction anywhere in the system can produce far-reaching metabolic effects, eventually threatening life itself.

The alimentary canal is a hollow muscular tube that begins in the mouth and ends at the anus. It includes the oral cavity, pharynx, esophagus, stomach, small intestine, and large intestine. Peristalsis propels the ingested material along the tract; sphincters prevent its reflux. Accessory glands and organs include the salivary glands, liver, biliary duct system (gallbladder and bile ducts), and pancreas.

Together, the GI tract and accessory organs serve two major functions: digestion (breaking down food and fluids into simple chemicals that can be absorbed into the bloodstream and transported throughout the body) and elimination of waste products from the body through defecation.

PATHOPHYSIOLOGIC CONCEPTS

Disorders of the GI system often manifest as vague, nonspecific complaints or problems that reflect disruption in one or more of the system's functions. For example, movement through the GI tract can be slowed, accelerated, or blocked, and secretion, absorption, or motility can be altered. As a result, one patient may present with several problems, the most common being anorexia, constipation, diarrhea, dysphagia, jaundice, nausea, and vomiting.

Anorexia

Anorexia is a loss of appetite or a lack of desire for food. Nausea, abdominal pain, and diarrhea may accompany it. Anorexia can result from dysfunction, such as cancer, heart disease, or renal disease, in the gastrointestinal system or other systems.

Normally, a physiologic stimulus is responsible for the sensation of hunger. Falling blood glucose levels stimulate the hunger center in the hypothalamus; rising blood fat and amino acid levels promote satiety. Hunger is also stimulated by contraction of an empty stomach and suppressed when the GI tract becomes distended, possibly as a result of stimulation of the vagus nerve. Sight, touch, and smell play subtle roles in controlling the appetite center.

In anorexia, the physiologic stimuli are present but the person has no appetite or desire to eat. Slow gastric emptying or gastric stasis can cause anorexia. High levels of neurotransmitters such as serotonin (may contribute satiety) and excess cortisol levels (may suppress hypothalamic control of hunger) have been implicated.

Constipation

Constipation is hard stools and difficult or infrequent defecation, as defined by a decrease in the number of stools per week. It is defined individually, because normal bowel habits range from 2 to 3 episodes of stool passage per day to one per week. Causes of constipation include dehydration, consumption of a low bulk diet, a sedentary lifestyle, lack of regular exercise, and frequent repression of the urge to defecate.

When a person is dehydrated or delays defecation, more fluid is absorbed from the intestine, the stool becomes harder, and constipation ensues. High fiber diets cause water to be drawn into the stool by osmosis, thereby keeping stool soft and encouraging movement through the intestine. High fiber diets also causes intestinal dilation, which stimulates peristalsis. Conversely, a low fiber diet would contribute to constipation.

A sedentary lifestyle or lack of exercise can cause constipation because exercise stimulates the gastrointestinal tract and promotes defecation. Antacids, opiates, and other drugs that inhibit bowel motility also lead to constipation.

Stress stimulates the sympathetic nervous system, and GI motility slows. Absence or degeneration in the neural pathways of the large intestine also contributes to constipation. And other conditions, such as spinal cord trauma, multiple sclerosis, intestinal neoplasms, and hypothyroidism, can cause constipation.

Diarrhea

Diarrhea is an increase in the fluidity or volume of feces and the frequency of defecation. Factors that affect stool volume and consistency include water content of the colon and the presence of unabsorbed food, unabsorbable material, and intestinal secretions. Large-volume diarrhea is usually the result of an excessive amount of water, secretions, or both in the intestines. Small-volume diarrhea is usually caused by excessive intestinal motility. Diarrhea may also be caused by a parasympathetic stimulation of the gut initiated by psychological factors such as fear or stress.

The three major mechanisms of diarrhea are osmosis, secretion, and motility:

• Osmotic diarrhea: The presence of nonabsorbable substance, such as synthetic sugar, or increased numbers of osmotic particles in the intestine, increases osmotic pressure and draws excess water into the intestine, thereby increasing the weight and volume of the stool.
• Secretory diarrhea: A pathogen or tumor irritates the muscle and mucosal layers of the intestine. The consequent increase in motility and secretions (water, electrolytes, and mucus) results in diarrhea.
• Motility diarrhea: Inflammation, neuropathy, or obstruction causes a reflex increase in intestinal motility that may expel the irritant or clear the obstruction.

Dysphagia

Dysphagia ― difficulty swallowing ― can be caused by a mechanical obstruction of the esophagus or by impaired esophageal motility secondary to another disorder. Mechanical obstruction is characterized as intrinsic or extrinsic.

Intrinsic obstructions originate in the esophagus itself. Causes of intrinsic tumors include tumors, strictures, and diverticular herniations. Extrinsic obstructions originate outside of the esophagus and narrow the lumen by exerting pressure on the esophageal wall. Most extrinsic obstruction results from a tumor.

Distention and spasm at the site of the obstruction during swallowing may cause pain. Upper esophageal obstruction causes pain 2 to 4 seconds after swallowing; lower esophageal obstructions, 10 to 15 seconds after swallowing. If a tumor is present, dysphagia begins with difficulty swallowing solids and eventually progresses to difficulty swallowing semi-solids and liquids. Impaired motor function makes both liquids and solids difficult to swallow.

Neural or muscular disorders can also interfere with voluntary swallowing or peristalsis. This is known as functional dysphagia. Causes of functional dysphagia include dermatomyositis, cerebrovascular accident, Parkinson's disease, or achalasia. (See What happens in swallowing .) Malfunction of the upper esophageal striated muscles interferes with the voluntary phase of swallowing.

In achalasia, the esophageal ganglionic cells are thought to have degenerated, and the cardiac sphincter of the stomach cannot relax. The lower end of the esophagus loses neuromuscular coordination and muscle tone, and food accumulates, causing hypertrophy and dilation. Eventually, accumulated food raises the hydrostatic pressure and forces the sphincter open, and small amounts of food slowly move into the stomach.

Jaundice

Jaundice ― yellow pigmentation of the skin and sclera ― is caused by an excess accumulation of bilirubin in the blood. Bilirubin, a product of red blood cell breakdown, accumulates when production exceeds metabolism and excretion. This imbalance can result from excessive release of bilirubin precursors into the bloodstream or from impairment of its hepatic uptake, metabolism, or excretion. (See Jaundice: Impaired bilirubin metabolism .) Jaundice occurs when bilirubin levels exceed 34 to 43 mmol/L (2.0 to 2.5 mg/dl), which is about twice the upper limit of the normal range. Lower levels of bilirubin may cause detectable jaundice in patients with fair skin, and jaundice may be difficult to detect in patients with dark skin.

The three main types of jaundice are hemolytic jaundice, hepatocellular jaundice, or obstructive jaundice:

• Hemolytic jaundice: When red blood cell lysis exceeds the liver's capacity to conjugate bilirubin (binding bilirubin to a polar group makes it water soluble and able to be excreted by the kidneys), hemolytic jaundice occurs. Causes include transfusion reactions, sickle cell anemia, thalassemia, and autoimmune disease.
• Hepatocellular jaundice: Hepatocyte dysfunction limits uptake and conjugation of bilirubin. Liver dysfunction can occur in hepatitis, cancer, cirrhosis, or congenital disorders, and some drugs can cause it.
• Obstructive jaundice: When the flow of bile out of the liver (through the hepatic duct) or through the bile duct is blocked, the liver can conjugate bilirubin, but the bilirubin can't reach the small intestine. Blockage of the hepatic duct by stones or a tumor is considered an intrahepatic cause of obstructive jaundice. A blocked bile duct is an extrahepatic cause. Gallstones or a tumor may obstruct the bile duct.

Nausea

Nausea is feeling the desire to vomit. It may occur independently of vomiting, or it may precede or accompany it. Specific neural pathways have not been identified, but increased salivation, diminished functional activities of the stomach, and altered small intestinal motility have been associated with nausea. Nausea may also be stimulated by high brain centers.

Vomiting

Vomiting is the forceful oral expulsion of gastric contents. The gastric musculature provides the ejection force. The gastric fundus and gastroesophageal sphincter relax, and forceful contractions of the diaphragm and abdominal wall muscles increase intraabdominal pressure. This, combined with the annular contraction of the gastric pylorus, forces gastric contents into the esophagus. Increased intrathoracic pressure then moves the gastric content from the esophagus to the mouth.

Vomiting is controlled by two centers in the medulla: the vomiting center and the chemoreceptor trigger zone. The vomiting center initiates the actual act of vomiting. It is stimulated by the gastrointestinal tract, from higher brainstem and cortical centers, and from the chemoreceptor trigger zone. The chemoreceptor trigger zone can't induce vomiting by itself. Various stimuli or drugs activate the zone, such as apomorphine, levodopa, digitalis, bacterial toxins, radiation, and metabolic abnormalities. The activated zone sends impulses to the medullary vomiting center, and the following sequence begins:

• The abdominal muscles and diaphragm contract.
• Reverse peristalsis begins, causing intestinal material to flow back into the stomach, distending it.
• The stomach pushes the diaphragm into the thoracic cavity, raising the intrathoracic pressure.
• The pressure forces the upper esophageal sphincter open, the glottis closes, and the soft palate blocks the nasopharynx.
• The pressure also forces the material up through the sphincter and out through the mouth.

Both nausea and vomiting are manifestations of other disorders, such as acute abdominal emergencies, infections of the intestinal tract, central nervous system disorders, myocardial infarction, congestive heart failure, metabolic and endocrinologic disorders, or as the side effect of many drugs. Vomiting may also be psychogenic, resulting from emotional or psychological disturbance.

DISORDERS Appendicitis

The most common major surgical disease, appendicitis is inflammation and obstruction of the vermiform appendix. Appendicitis may occur at any age and affects both sexes equally; however, between puberty and age 25, it's more prevalent in men. Since the advent of antibiotics, the incidence and the death rate of appendicitis have declined; if untreated, this disease is invariably fatal.

Causes

Causes may include:

• mucosal ulceration
• fecal mass
• stricture
• barium ingestion
• viral infection.

Pathophysiology

Mucosal ulceration triggers inflammation, which temporarily obstructs the appendix. The obstruction blocks mucus outflow. Pressure in the now distended appendix increases, and the appendix contracts. Bacteria multiply, and inflammation and pressure continue to increase, restricting blood flow to the organ and causing severe abdominal pain.

Signs and symptoms

Signs and symptoms may include:

• abdominal pain caused by inflammation of the appendix and bowel obstruction and distention
• anorexia after the onset of pain
• nausea or vomiting caused by the inflammation
• low-grade temperature from systemic manifestation of inflammation and leukocytosis
• tenderness from inflammation.

Complications

Complications may include:

• wound infection
• intraabdominal abscess
• fecal fistula
• intestinal obstruction
• incisional hernia
• peritonitis
• death.

Diagnosis

• White blood cell count is moderately high with an increased number of immature cells.
• X-ray with radiographic contrast agent reveals failure of the appendix to fill with contrast.

Treatment

Treatment may include:

• maintenance of NPO status until surgery
• high Fowler's position to aid in pain relief
• GI intubation for decompression
• appendectomy
• antibiotics to treat infection if peritonitis occurs
• parental replacement of fluid and electrolytes to reverse possible dehydration resulting from surgery or nausea and vomiting.

Cholecystitis

Cholecystitis ― acute or chronic inflammation causing painful distention of the gallbladder ― is usually associated with a gallstone impacted in the cystic duct. Cholecystitis accounts for 10% to 25% of all patients requiring gallbladder surgery. The acute form is most common among middle-aged women; the chronic form, among the elderly. The prognosis is good with treatment.

Causes

• Gallstones (the most common cause)
• Poor or absent blood flow to the gallbladder
• Abnormal metabolism of cholesterol and bile salts.

Pathophysiology

In acute cholecystitis, inflammation of the gallbladder wall usually develops after a gallstone lodges in the cystic duct. (See Understanding gallstone formation .) When bile flow is blocked, the gallbladder becomes inflamed and distended. Bacterial growth, usually Escherichia coli , may contribute to the inflammation. Edema of the gallbladder (and sometimes the cystic duct) obstructs bile flow, which chemically irritates the gallbladder. Cells in the gallbladder wall may become oxygen starved and die as the distended organ presses on vessels and impairs blood flow. The dead cells slough off, and an exudate covers ulcerated areas, causing the gallbladder to adhere to surrounding structures.

Signs and symptoms

• Acute abdominal pain in the right upper quadrant that may radiate to the back, between the shoulders, or to the front of the chest secondary to inflammation and irritation of nerve fibers
• Colic due to the passage of gallstones along the bile duct
• Nausea and vomiting triggered by to the inflammatory response
• Chills related to fever
• Low-grade fever secondary to inflammation
• Jaundice from obstruction of the common bile duct by stones.

Complications

• Perforation and abscess formation
• Fistula formation
• Gangrene
• Empyema
• Cholangitis
• Hepatitis
• Pancreatitis
• Gallstone ileus
• Carcinoma.

Diagnosis

• X-ray reveals gallstones if they contain enough calcium to be radiopaque; also helps disclose porcelain gallbladder (hard, brittle gall bladder due to calcium deposited in wall), limy bile, and gallstone ileus.
• Ultrasonography detects gallstones as small as 2 mm and distinguishes between obstructive and nonobstructive jaundice.
• Technetium-labeled scan indicates reveals cystic duct obstruction and acute or chronic cholecystitis if ultrasound doesn't visualize the gallbladder.
• Percutaneous transhepatic cholangiography or cholesystoscopy supports the diagnosis of obstructive jaundice and reveals calculi in the ducts.
• Levels of serum alkaline phosphate, lactate dehydrogenase, aspartate aminotransferase, and total bilirubin are high; serum amylase slightly elevated; and icteric index elevated.
• White blood cell counts are slightly elevated during cholecystitis attack.

Treatment

• Cholecystectomy to surgically remove the inflamed gallbladder
• Choledochostomy to surgically create an opening into the common bile duct for drainage
• Percutaneous transhepatic cholecytostomy
• Endoscopic retrograde cholangiopancreatography for removal of gallstones
• Lithotripsy to break up gallstones and relieve obstruction
• Oral chenodeoxycholic acid or ursodeoxycholic acid to dissolve stones
• Low fat diet to prevent attacks
• Vitamin K to relieve itching, jaundice, and bleeding tendencies due to vitamin K deficiencies
• Antibiotics for use during acute attack for treatment of infection
• Nasogastric tube insertion during acute attack for abdominal decompression.

Cirrhosis

Cirrhosis is a chronic disease characterized by diffuse destruction and fibrotic regeneration of hepatic cells. As necrotic tissue yields to fibrosis, this disease damages liver tissue and normal vasculature, impairs blood and lymph flow, and ultimately causes hepatic insufficiency. It's twice as common in men as in women, and is especially prevalent among malnourished persons over the age of 50 with chronic alcoholism. Mortality is high; many patients die within 5 years of onset.

Causes

Cirrhosis may be a result of a wide range of diseases. The following clinical types of cirrhosis reflect its diverse etiology.

Hepatocellular disease. This group includes the following disorders:

• Postnecrotic cirrhosis accounts for 10% to 30% of patients and stems from various types of hepatitis (such as Types A, B, C, D viral hepatitis) or toxic exposures.
• La?nnec's cirrhosis, also called portal, nutritional, or alcoholic cirrhosis, is the most common type and is primarily caused by hepatitis C. Liver damage results from malnutrition (especially dietary protein) and chronic alcohol ingestion. Fibrous tissue forms in portal areas and around central veins.
• Autoimmune disease such as sarcoidosis or chronic inflammatory bowel disease may cause cirrhosis.

Cholestatic diseases. This group includes diseases of the biliary tree (biliary cirrhosis resulting from bile duct diseases suppressing bile flow) and sclerosing cholangitis.

Metabolic diseases. This group includes disorders such as Wilson's disease, alpha 1 -antitrypsin, and hemochromatosis (pigment cirrhosis).

Other types of cirrhosis. Other types of cirrhosis include Budd-Chiari syndrome (epigastric pain, liver enlargement, and ascites due to hepatic vein obstruction), cardiac cirrhosis, and cryptogenic cirrhosis. Cardiac cirrhosis is rare; the liver damage results from right heart failure. Cryptogenic refers to cirrhosis of unknown etiology.

Pathophysiology