Gastrointestinal System
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| Pathophysiologic concepts | |
| Anorexia | |
| Constipation | |
| Diarrhea | |
| Dysphagia | |
| Jaundice | |
| Nausea | |
| Vomiting | |
| Disorders | |
| Appendicitis | |
| Cholecystitis | |
| Cirrhosis | |
| Crohn's disease | |
| Diverticular disease | |
| Gastroesophageal reflux disease | |
| Hemorrhoids | |
| Hepatitis, nonviral | |
| Hepatitis, viral | |
| Hirschsprung's disease | |
| Hyperbilirubinemia | |
| Irritable bowel syndrome | |
| Liver failure | |
| Malabsorption | |
| Pancreatitis | |
| Peptic ulcer | |
| Ulcerative colitis |
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.
| AGE ALERT The elderly typically experience a decrease in intestinal motility in addition to a slowing and dulling of neural impulses in the GI tract. Many older persons restrict fluid intake to prevent waking at night to use the bathroom or because of a fear of incontinence. This places them at risk for dehydration and 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.
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WHAT HAPPENS IN SWALLOWING
Before peristalsis can begin, the neural pattern to initiate swallowing, illustrated here, must occur:
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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.
| CULTURAL DIVERSITY Jaundice in dark-skinned persons may appear as yellow staining in the sclera, hard palate, and palmar or plantar surfaces. |
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.
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JAUNDICE: IMPAIRED BILIRUBIN METABOLISM
Jaundice occurs in three forms: prehepatic, hepatic, and posthepatic. In all three, bilirubin levels in the blood increase.
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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.
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UNDERSTANDING GALLSTONE FORMATION
Abnormal metabolism of cholesterol and bile salts plays an important role in gallstone formation. The liver makes bile continuously. The gall bladder concentrates and stores it until the duodenum signals it needs it to help digest fat. Changes in the composition of bile may allow gallstones to form. Changes to the absorptive ability of the gallbladder lining may also contribute to gallstone formation. TOO MUCH CHOLESTEROL Certain conditions, such as age, obesity, and estrogen imbalance, cause the liver to secrete bile that's abnormally high in cholesterol or lacking the proper concentration of bile salts. The coronary arteries are made of three layers: intima (the innermost layer, media (the middle layer), and adventitia (the outermost layer). <center></center>INSIDE THE GALLBLADDER When the gallbladder concentrates this bile, inflammation may occur. Excessive reabsorption of water and bile salts makes the bile less soluble. Cholesterol, calcium, and bilirubin precipitate into gallstones. Fat entering the duodenum causes the intestinal mucosa to secrete the hormone cholecystokinin, which stimulates the gallbladder to contract and empty. If a stone lodges in the cystic duct, the gallbladder contracts but can't empty. <center></center>JAUNDICE, IRRITATION, INFLAMMATION If a stone lodges in the common bile duct, the bile can't flow into the duodenum. Bilirubin is absorbed into the blood and causes jaundice. Biliary narrowing and swelling of the tissue around the stone can also cause irritation and inflammation of the common bile duct. <center></center>UP THE BILIARY TREE Inflammation can progress up the biliary tree into any of the bile ducts. This causes scar tissue, fluid accumulation, cirrhosis, portal hypertension, and bleeding. <center></center> |
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
Cirrhosis begins with hepatic scarring or fibrosis. The scar begins as an increase in extracellular matrix components ― fibril-forming collagens, proteoglycans, fibronectin, and hyaluronic acid. The site of collagen deposition varies with the cause. Hepatocyte function is eventually impaired as the matrix changes. Fat-storing cells are believed to be the source of the new matrix components. Contraction of these cells may also contribute to disruption of the lobular architecture and obstruction of the flow of blood or bile. Cellular changes producing bands of scar tissue also disrupt the lobular structure.
Signs and symptoms
The following are signs and symptoms of the early stages:
- anorexia from distaste for certain foods
- nausea and vomiting from inflammatory response and systemic effects of liver inflammation
- diarrhea from malabsorption
- dull abdominal ache from liver inflammation.
The following are signs and symptoms of the late stages:
- respiratory ― pleural effusion, limited thoracic expansion due to abdominal ascites; interferes with efficient gas exchange and causes hypoxia
- central nervous system ― progressive signs or symptoms of hepatic encephalopathy, including lethargy, mental changes, slurred speech, asterixis, peripheral neuritis, paranoia, hallucinations, extreme obtundation, and coma ― secondary to loss of ammonia to urea conversion and consequent delivery of toxic ammonia to the brain
- hematologic ― bleeding tendencies (nosebleeds, easy bruising, bleeding gums), anemia resulting from thrombocytopenia (secondary to splenomegaly and decreased vitamin K absorption), splenomegaly, and portal hypertension
- endocrine ― testicular atrophy, menstrual irregularities, gynecomastia, and loss of chest and axillary hair from decreased hormone metabolism
- skin ― severe pruritus secondary to jaundice from bilirubinemia; extreme dryness and poor tissue turgor related to malnutrition; abnormal pigmentation, spider angiomas, palmar erythema, and jaundice related to impaired hepatic function
- hepatic ― jaundice from decreased bilirubin metabolism; hepatomegaly secondary to liver scarring and portal hypertension; ascites and edema of the legs from portal hypertension and decreased plasma proteins; hepatic encephalopathy from ammonia toxicity; and hepatorenal syndrome from advanced liver disease and subsequent renal failure
- miscellaneous ― musty breath secondary to ammonia build up; enlarged superficial abdominal veins due to portal hypertension; pain in the right upper abdominal quadrant that worsens when patient sits up or leans forward, due to inflammation and irritation of area nerve fibers; palpable liver or spleen due to organomegaly; temperature of 101° to 103° F (38° to 39° C) due to inflammatory response; pain and increased temperature from liver inflammation
- hemorrhage from esophageal varices resulting from portal hypertension. (See What happens in portal hypertension .)
Complications
Complications may include:
- ascites
- portal hypertension
- jaundice
- coagulopathy
- hepatic encephalopathy
- bleeding esophageal varices; acute GI bleeding
- liver failure
- renal failure.
Diagnosis
- Liver biopsy reveals tissue destruction and fibrosis.
- Abdominal X-ray shows enlarged liver, cysts, or gas within the biliary tract or liver, liver calcification, and massive fluid accumulation (ascites).
- Computed tomography and liver scans show liver size, abnormal masses, and hepatic blood flow and obstruction.
- Esophagogastroduodenoscopy reveals bleeding esophageal varices, stomach irritation or ulceration, or duodenal bleeding and irritation.
- Blood studies reveal elevated liver enzymes, total serum bilirubin, and indirect bilirubin; decreased total serum albumin and protein; prolonged prothrombin time; decreased hemoglobin, hematocrit, and serum electrolytes; and deficiency of vitamins A, C, and K.
- Urine studies show increased bilirubin and urobilirubinogen.
- Fecal studies show decreased fecal urobilirubinogen.
Treatment
- Vitamins and nutritional supplements to help heal damaged liver cells and improve nutritional status
- Antacids to reduce gastric distress and decrease the potential for gastrointestinal bleeding
- Potassium-sparing diuretics to reduce fluid accumulation
- Vasopressin to treat esophageal varices
- Esophagogastric intubation with multilumen tubes to control bleeding from esophageal varices or other hemorrhage sites by using balloons to exert pressure on bleeding site.
- Gastric lavage until the contents are clear; with antacids and histamine antagonists if bleeding is secondary to a gastric ulcer
- Esophageal balloon tamponade to compress bleeding vessels and stop blood loss from esophageal varices
- Paracentesis to relieve abdominal pressure and remove ascitic fluid
- Surgical shunt placement to divert ascites into venous circulation, leading to weight loss, increased abdominal girth, increased sodium excretion from the kidneys, and improved urine output
- Sclerosing agents injected into oozing vessels to cause clotting and sclerosis
- Insertion of portosystemic shunts to control bleeding from esophageal varices and decrease portal hypertension (diverts a portion of the portal vein blood flow away from the liver; seldom performed).
Crohn's disease
Crohn's disease, also known as regional enteritis or granulomatous colitis, is inflammation of any part of the gastrointestinal tract (usually the proximal portion of the colon and less commonly the terminal ileum), extending through all layers of the intestinal wall. It may also involve regional lymph nodes and the mesentery. Crohn's disease is most prevalent in adults ages 20 to 40.
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WHAT HAPPENS IN PORTAL HYPERTENSION
Portal hypertension (elevated pressure in the portal vein) occurs when blood flow meets increased resistance. This common result of cirrhosis may also stem from mechanical obstruction and occlusion of the hepatic veins (Budd-Chiari syndrome). As the pressure in the portal vein rises, blood backs up into the spleen and flows through collateral channels to the venous system, bypassing the liver. Thus, portal hypertension causes:
In many patients, the first sign of portal hypertension is bleeding esophageal varices (dilated tortuous veins in the submucosa of the lower esophagus). Esophageal varices commonly cause massive hematemesis, requiring emergency care to control hemorrhage and prevent hypovolemic shock. <center></center> |
| CULTURAL DIVERSITY Crohn's disease is two to three times more common in Ashkenazic Jews and least common in African Americans. Up to 20% of patients have a positive family history for the disease. |
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BOWEL CHANGES IN CROHN'S DISEASE
As Crohn's disease progresses, fibrosis thickens the bowel wall and narrows the lumen. Narrowing ― or stenosis ― can occur in any part of the intestine and cause varying degrees of intestinal obstruction. At first, the mucosa may appear normal, but as the disease progresses it takes on a “cobblestone” appearance as shown. <center></center> |
The exact cause is unknown but the following conditions may contribute:
- steady, colicky pain in the right lower quadrant due to acute inflammation and nerve fiber irritation
- cramping due to acute inflammation
- tenderness due to acute inflammation
- weight loss secondary to diarrhea and malabsorption
- diarrhea due to bile salt malabsorption, loss of healthy intestinal surface area, and bacterial growth
- steatorrhea secondary to fat malabsorption
- bloody stools secondary to bleeding from inflammation and ulceration.
- anal fistula
- perineal abscess
- fistulas to the bladder or vagina or to the skin in an old scar area
- intestinal obstruction
- nutrient deficiencies from poor digestion and malabsorption of bile salts and vitamin B 12
- fluid imbalances.
- Fecal occult test reveals minute amounts of blood in stools.
- Small bowel X-ray shows irregular mucosa, ulceration, and stiffening.
- Barium enema reveals the string sign (segments of stricture separated by normal bowel) and possibly fissures and narrowing of the bowel.
- Sigmoidoscopy and colonoscopy reveal patchy areas of inflammation (helps to rule out ulcerative colitis), with cobblestone-like mucosal surface. With colon involvement, ulcers may be seen.
- Biopsy reveals granulomas in up to half of all specimens.
- Blood tests reveal increased white blood cell count and erythrocyte sedimentation rate, and decreased potassium, calcium, magnesium, and hemoglobin levels.
- Corticosteroids to reduce inflammation and, subsequently, diarrhea, pain, and bleeding
- Immunosuppressants to suppress the response to antigens
- Sulfasalazine to reduce inflammation
- Metronidazole to treat perianal complications
- Antidiarrheals to combat diarrhea (not used with patients with significant bowel obstruction)
- Narcotic analgesics to control pain and diarrhea
- Stress reduction and reduced physical activity to rest the bowel and allow it to heal
- Vitamin supplements to replace and compensate for the bowel's inability to absorb vitamins
- Dietary changes (elimination of fruits, vegetables, high fiber foods, dairy products, spicy and fatty foods, foods that irritate the mucosa, carbonated or caffeinated beverages, and other foods or liquids that stimulate excessive intestinal activity) to decrease bowel activity while still providing adequate nutrition
- Surgery, if necessary, to repair bowel perforation and correct massive hemorrhage, fistulas or acute intestinal obstruction; colectomy with ileostomy in patients with extensive disease of the large intestine and rectum.
Diverticular disease
| CULTURAL DIVERSITY Diverticular disease is common in Western countries, suggesting that a low-fiber diet reduces stool bulk and leads to excessive colonic motility. This consequent increased intraluminal pressure causes herniation of the mucosa. |
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PATHOGENESIS OF DIVERTICULAR DISEASE
The etiology of diverticular disease hasn't been determined. It's thought to arise from a disordered colonic motility pattern. These diagrams compare normal and abnormal patterns. <center></center> |
Diverticular disease has two clinical forms:
- diverticulosis, in which diverticula are present but don't cause symptoms
- diverticulitis, in which diverticula are inflamed and may cause potentially fatal obstruction, infection, or hemorrhage.
| AGE ALERT Diverticular disease is most prevalent in men over age 40 and persons who eat a low fiber diet. More than half of patients older than 50 years have colonic diverticula. |
- Diminished colonic motility and increased intraluminal pressure
- Low fiber diet
- Defects in colon wall strength.
Mild diverticulitis. In mild diverticulitis, signs and symptoms include:
- moderate left lower abdominal pain secondary to inflammation of diverticula
- low-grade fever from trapping of bacteria-rich stool in the diverticula
- leukocytosis from infection secondary to trapping of bacteria-rich stool in the diverticula.
Severe diverticulitis. In severe diverticulitis, signs and symptoms include:
- abdominal rigidity from rupture of the diverticula, abscesses, and peritonitis
- left lower quadrant pain secondary to rupture of the diverticula and subsequent inflammation and infection
- high fever, chills, hypotension from sepsis, and shock from the release of fecal material from the rupture site
- microscopic or massive hemorrhage from rupture of diverticulum near a vessel.
Chronic diverticulitis. In chronic diverticulitis, signs and symptoms include:
- constipation, ribbon-like stools, intermittent diarrhea, and abdominal distention resulting from intestinal obstruction (possible when fibrosis and adhesions narrow the bowel's lumen)
- abdominal rigidity and pain, diminishing or absent bowel sounds, nausea, and vomiting secondary to intestinal obstruction.
- Upper GI series confirms or rules out diverticulosis of the esophagus and upper bowel.
- Barium enema reveals filling of diverticula, which confirms diagnosis.
- Biopsy reveals evidence of benign disease, ruling out cancer.
- Blood studies show an elevated erythrocyte sedimentation rate in diverticulitis.
- Liquid or bland diet, stool softeners, and occasional doses of mineral oil for symptomatic diverticulosis to relieve symptoms, minimize irritation, and lessen the risk of progression to diverticulitis
- High-residue diet for treatment of diverticulosis after pain has subsided to help decrease intra-abdominal pressure during defecation
- Exercise to increase the rate of stool passage
- Antibiotics to treat infection of the diverticula
- Meperidine (Demerol) to control pain and to relax smooth muscle
- Antispasmodics to control muscle spasms
- Colon resection with removal of involved segment to correct cases refractory to medical treatment
- Temporary colostomy if necessary to drain abscesses and rest the colon in diverticulitis accompanied by perforation, peritonitis, obstruction, or fistula
- Blood transfusions if necessary to treat blood loss from hemorrhage.
Gastroesophageal reflux disease
- weakened esophageal sphincter
- increased abdominal pressure, such as with obesity or pregnancy
- hiatal hernia
- medications such as morphine, diazepam, calcium channel blockers, meperidine, and anticholinergic agents
- food, alcohol, or cigarettes that lower LES pressure
- nasogastric intubation for more than 4 days.
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HOW HEARTBURN OCCURS
Hormonal fluctuations, mechanical stress, and the effects of certain foods and drugs can lower esophageal sphincter (LES) pressure. When LES pressure falls and intraabdominal or intragastric pressure rises, the normally contracted LES relaxes inappropriately and allows reflux of gastric acid or bile secretions into the lower esophagus. There, the reflux irritates and inflames the esophageal mucosa, causing pyrosis. Persistent inflammation can cause LES pressure to decrease even more and may trigger a recurrent cycle of reflux and pyrosis. |
- Burning pain in the epigastric area, possibly radiating to the arms and chest, from the reflux of gastric contents into the esophagus causing irritation and also esophageal spasm
- Pain, usually after a meal or when lying down, secondary to increased abdominal pressure causing reflux
- Feeling of fluid accumulation in the throat without a sour or bitter taste due to hypersecretion of saliva.
- Reflux esophagitis
- Esophageal stricture
- Esophageal ulceration
- Chronic pulmonary disease from aspiration of gastric contents in throat.
Diagnostic tests are aimed at determining the underlying cause of GERD:
- Esophageal acidity test evaluates the competence of the lower esophageal sphincter and provides objective measure of reflux.
- Acid perfusion test confirms esophagitis and distinguishes it from cardiac disorders.
- Esophagoscopy allows visual examination of the lining of the esophagus to reveal extent of disease and confirm pathologic changes in mucosa.
- Barium swallow identifies hiatal hernia as the cause.
- Upper GI series detects hiatal hernia or motility problems.
- Esophageal manometry evaluates resting pressure of LES and determines sphincter competence.
- Diet therapy with frequent, small meals and avoidance of eating before going to bed to reduce abdominal pressure and reduce the incidence of reflux
- Positioning ― sitting up during and after meals and sleeping with head of bed elevated ― to reduce abdominal pressure and prevent reflux
- Increased fluid intake to wash gastric contents out of the esophagus
- Antacids to neutralize acidic content of the stomach and minimize irritation
- Histamine H 2 antagonists to inhibit gastric acid secretion
- Proton pump inhibitors to reduce gastric acidity
- Cholinergic agents to increase LES pressure
- Smoking cessation to improve LES pressure (nicotine lowers LES pressure)
- Surgery if hiatal hernia is the cause or patient has refractory symptoms.
Hemorrhoids
- Painless, intermittent bleeding during defecation from irritation and injury to the hemorrhoid mucosa
- Bright red blood on stool or toilet tissue due to injury to hemorrhoid mucosa
- Anal itching from poor anal hygiene
- Vague feeling of anal discomfort when bleeding occurs
- Prolapse of rectal mucosa from straining
- Pain from thrombosis of external hemorrhoids.
- Constipation
- Local infection
- Thrombosis of hemorrhoids
- Secondary anemia from severe or recurrent bleeding.
- Physical examination confirms external hemorrhoids.
- Anoscopy and flexible sigmoidoscopy visualizes internal hemorrhoids.
Treatment depends on the type and severity of the hemorrhoids:
- high fiber diet, increased fluid intake, and bulking agents to relieve constipation
- avoidance of prolonged sitting on the toilet to prevent venous congestion
- local anesthetic agents to decrease local swelling and pain
- hydrocortisone cream and suppositories to reduce edematous, prolapsed hemorrhoids, and itching
- warm sitz baths to relieve pain
- injection sclerotherapy or rubber band ligation to reduce prolapsed hemorrhoids
- hemorrhoidectomy by cauterization or excision.
Hepatitis, nonviral
- anorexia, nausea and vomiting due to systemic effects of liver inflammation
- jaundice from decreased bilirubin metabolism, leading to hyperbilirubinemia
- dark urine from elevated urobilinogen
- hepatomegaly due to inflammation
- possible abdominal pain from liver inflammation
- clay colored stool secondary to decreased bile in the gastrointestinal tract from liver necrosis
- pruritus secondary to jaundice and hyperbilirubinemia.
- Liver enzymes, such as serum aspartate aminotransferase and alanine aminotransferase levels, are elevated.
- Total and direct bilirubin levels are elevated.
- Alkaline phosphatase levels are elevated.
- White blood cell count and eosinophil count are elevated.
- Liver biopsy identifies underlying pathology, especially infiltration with white blood cells and eosinophils.
- lavage, catharsis, or hyperventilation, depending on the route of exposure, to remove the causative agent
- acetylcysteine as an antidote for acetaminophen poisoning
- corticosteroid to relieve symptoms of drug-induced nonviral hepatitis.
Hepatitis, viral
Five major forms of hepatitis are currently recognized:
- Type A (infectious or short-incubation hepatitis) is most common among male homosexuals and in people with human immunodeficiency virus (HIV) infection.
- Type B (serum or long-incubation hepatitis) also is most common among HIV-positive individuals. Routine screening of donor blood for the hepatitis B surface antigen has reduced the incidence of post-transfusion cases, but transmission by needles shared by drug abusers remains a major problem.
- Type C accounts for about 20% of all viral hepatitis cases and for most post-transfusion cases.
- Type D (delta hepatitis) is responsible for about 50% of all cases of fulminant hepatitis, which has a high mortality. Developing in 1% of patients with viral hepatitis, fulminant hepatitis causes unremitting liver failure with encephalopathy. It progresses to coma and commonly leads to death within 2 weeks. In the United States, type D occurs only in people who are frequently exposed to blood and blood products, such as I.V. drug users and hemophilia patients.
- Type E (formerly grouped with types C and D under the name non-A, non-B hepatitis) occurs primarily among patients who have recently returned from an endemic area (such as India, Africa, Asia, or Central America). It's more common in young adults and more severe in pregnant woman. (See Viral hepatitis from A to E .)
- Other types continue to be identified with growing patient population and sophisticated laboratory identification techniques.
- The five major forms of viral hepatitis result from infection with the causative viruses: A, B, C, D, or E.
Signs and symptoms reflect the stage of the disease.
Prodromal stage. Signs and symptoms of the prodromal stage include:
- easy fatigue and generalized malaise due to systemic effects of liver inflammation
- anorexia and mild weight loss due to systemic effects of liver inflammation
- arthralgia and myalgia due to systemic effects of liver inflammation
- nausea and vomiting from gastrointestinal effects of liver inflammation
- changes in the senses of taste and smell related to liver inflammation
- fever secondary to inflammatory process
- right upper quadrant tenderness from liver inflammation and irritation of area nerve fibers
- dark colored urine from urobilinogen
- clay colored stools from decreased bile in the gastrointestinal tract.
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VIRAL HEPATITIS FROM A TO E
This chart compares the features of each type of viral hepatitis that has been characterized. Other types are emerging.
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Clinical stage. Signs and symptoms of the clinical stage include:
- worsening of all symptoms of prodromal stage
- itching from increased bilirubin in the blood
- abdominal pain or tenderness from continued liver inflammation
- jaundice from elevated bilirubin in the blood.
Recovery stage. The patient's symptoms subside and appetite returns.
- Chronic persistent hepatitis, which may prolong recovery up to 8 months
- Chronic active hepatitis
- Cirrhosis
- Hepatic failure and death
- Primary hepatocellular carcinoma.
- Hepatitis profile study identifies antibodies specific to the causative virus, establishing the type of hepatitis.
- Serum aspartate aminotransferase and serum alanine aminotransferase levels are increased in the prodromal stage.
- Serum alkaline phosphatase is slightly increased.
- Serum bilirubin may remain high into late disease, especially in severe cases.
- Prothrombin time prolonged (greater than 3 seconds longer than normal indicates severe liver damage).
- White blood cell counts reveal transient neutropenia and lymphopenia followed by lymphocytosis.
- Liver biopsy to confirm suspicion of chronic hepatitis.
- Rest to minimize energy demands
- Avoidance of alcohol or other drugs to prevent further hepatic damage
- Diet therapy with small, high-calorie meals to combat anorexia
- Parental nutrition if patient can't eat due to persistent vomiting
- Vaccination against hepatitis A and B to provide immunity to these viruses before transmission occurs.
Hirschsprung's disease
In the newborn, signs and symptoms include:
- failure to pass meconium within 24 to 48 hours due to inability to propel intestinal contents forward
- bile stained or fecal vomiting as a result of bowel obstruction
- abdominal distention secondary to retention of intestinal contents and bowel obstruction
- irritability due to resultant abdominal distention
- feeding difficulties and failure to thrive related to retention of intestinal contents and abdominal distention
- dehydration related to subsequent feeding difficulties and inability to ingest adequate fluids
- overflow diarrhea secondary to increased water secretion into bowel with bowel obstruction.
In children, signs and symptoms include:
- intractable constipation due to decreased gastrointestinal motility
- abdominal distention from retention of stool
- easily palpated fecal masses from retention of stool
- wasted extremities (in severe cases) secondary to impaired intestinal motility and its effects on nutrition and intake
- loss of subcutaneous tissue (in severe cases) secondary to malnutrition
- large protuberant abdomen due to retention of stool and consequent changes in fluid and electrolyte homeostasis.
In adults, signs and symptoms (occurs rarely and is more prevalent in men) include:
- abdominal distention from decreased bowel motility and constipation
- chronic intermittent constipation secondary to impaired intestinal motility.
- Bowel perforation
- Electrolyte imbalances
- Nutritional deficiencies
- Enterocolitis
- Hypovolemic shock
- Sepsis.
- Rectal biopsy confirms diagnosis by showing absence of ganglion cells.
- Barium enema, used in older infants, reveals a narrowed segment of distal colon with a sawtoothed appearance and a funnel-shaped segment above it. This confirms the diagnosis and assesses the extent of intestinal involvement.
- Rectal manometry detects failure of the internal anal sphincter to relax and contract.
- Upright plain abdominal X-rays show marked colonic distention.
- corrective surgery to pull the normal ganglionic segment through to the anus (usually delayed until the infant is at least 10 months old)
- daily colonic lavage to empty the bowel of the infant until the time of surgery
- temporary colostomy or ileostomy to compress the colon in instances of total bowel obstruction.
Hyperbilirubinemia
| CULTURAL DIVERSITY Hyperbilirubinia tends to be more common and more severe in Chinese, Japanese, Koreans, and Native Americans, whose mean peak of unconjugated bilirubin is approximately twice that of the rest of the population. |
- blood type incompatibility
- intrauterine infection (rubella, cytomegalic inclusion body disease, toxoplasmosis, syphilis and, occasionally, bacteria such as Escherichia coli , Staphylococcus, Pseudomonas, Klebsiella, Proteus, and Streptococcus)
- infection (gram-negative bacteria)
- polycythemia
- enclosed hemorrhages (bruises, subdural hematoma)
- respiratory distress syndrome (hyaline membrane disease)
- heinz body anemia from drugs and toxins (vitamin K 3 , sodium nitrate)
- transient neonatal hyperbilirubinemia
- abnormal red blood cell morphology
- deficiencies of red blood cell enzymes (glucose 6-phosphate dehydrogenase, hexokinase)
- physiologic jaundice
- breast feeding
- maternal diabetes
- crigler-Najjar syndrome
- gilbert syndrome
- herpes simplex
- pyloric stenosis
- hypothyroidism
- neonatal giant cell hepatitis
- bile duct atresia
- galactosemia
- choledochal cyst.
- Jaundice from the escape of unconjugated bilirubin to extra vascular tissue (primary sign of hyperbilirubinemia).
- Kernicterus
- Cerebral palsy, epilepsy, or mental retardation
- Perceptual-motor handicaps and learning disorders.
- Phototherapy (treatment of choice for physiologic jaundice, and pathologic jaundice due to erythroblastosis fetalis, after the initial exchange transfusion) with fluorescent lights to decompose bilirubin in the skin by oxidation (usually discontinued after bilirubin levels fall below 10mg/dl and continue to decrease for 24 hours)
- Exchange transfusion to replace the infant's blood with fresh blood (less then 48 hours old), removing some of the unconjugated bilirubin in serum; indicated for conditions such as hydrops fetalis, polycythemia, erythroblastosis fetalis; marked reticulocytosis, drug toxicity, and jaundice that develops within the first 6 hours after birth
- Albumin administration to provide additional albumin for binding unconjugated bilirubin
- Phenobarbital administration (rare) to the mother before delivery and to the newborn several days after delivery to stimulate the hepatic glucuronide-conjugating system
Irritable bowel syndrome
- Psychological stress (most common)
- Ingestion of irritants (coffee, raw fruit, or vegetables)
- Lactose intolerance
- Abuse of laxatives
- Hormonal changes (menstruation).
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WHAT HAPPENS IN IRRITABLE BOWEL SYNDROME
Typically, the patient with irritable bowel syndrome has a normal-appearing GI tract. However, careful examination of the colon may reveal functional irritability ― an abnormality in colonic smooth-muscle function marked by excessive peristalsis and spasms, even during remission. INTESTINAL FUNCTION To understand what happens in irritable bowel syndrome, consider how smooth muscle controls bowel function. Normally, segmental muscle contractions mix intestinal contents while peristalsis propels the contents through the GI tract. Motor activity is most propulsive in the proximal (stomach) and the distal (sigmoid) portions of the intestine. Activity in the rest of the intestines is slower, permitting nutrient and water absorption. In irritable bowel syndrome, the autonomic nervous system, which innervates the large intestine, doesn't cause the alternating contractions and relaxations that propel stools smoothly toward the rectum. The result is constipation or diarrhea or both. CONSTIPATION Some patients have spasmodic intestinal contractions that set up a partial obstruction by trapping gas and stools. This causes distention, bloating, gas pain, and constipation. DIARRHEA Other patients have dramatically increased intestinal motility. Usually eating or cholinergic stimulation triggers the small intestine's contents to rush into the large intestine, dumping watery stools and irritating the mucosa. The result is diarrhea. MIXED SYMPTOMS If further spasms trap liquid stools, the intestinal mucosa absorbs water from the stools, leaving them dry, hard, and difficult to pass. The result: a pattern of alternating diarrhea and constipation. |
- Crampy lower abdominal pain secondary to muscle contraction; usually occurring during the day and relieved by defecation or passage of flatus
- Pain that intensifies 1 to 2 hours after a meal from irritation of nerve fibers by causative stimulus
- Constipation alternating with diarrhea, with one dominant; secondary to motor disturbances from causative stimulus
- Mucus passed through the rectum from altered secretion in intestinal lumen due to motor abnormalities
- Abdominal distention and bloating caused by flatus and constipation.
- Physical examination reveals contributing psychological factors, such as a recent stressful life change.
- Stool samples for ova, parasites, bacteria, and blood rule out infection.
- Lactose intolerance test rules out lactose intolerance.
- Barium enema may reveal colon spasm and tubular appearance of descending colon without evidence of cancers and diverticulosis.
- Sigmoidoscopy or colonoscopy may reveal spastic contractions without evidence of colon cancer or inflammatory bowel disease.
- Rectal biopsy rules out malignancy.
- stress relief measures, including counseling or mild anti-anxiety agents
- investigation and avoidance of food irritants
- application of heat to abdomen
- bulking agents to reduce episodes of diarrhea and minimize effect of nonpropulsive colonic contractions
- antispasmodics (dicyclomine, hycomine sulfate) for pain
- loperamide possibly to reduce urgency and fecal soiling in patients with persistent diarrhea
- bowel training (if the cause of IBS is chronic laxative abuse) to regain muscle control.
Liver failure
Manifestations of liver failure include hepatic encephalopathy and hepatorenal syndrome.
- Jaundice from the failure of liver to conjugate bilirubin
- Abdominal pain or tenderness from liver inflammation
- Nausea and anorexia from systemic effects of inflammation
- Fatigue and weight loss from failure of hepatic metabolism
- Pruritus due to the accumulation of bilirubin in the skin
- Oliguria from intrarenal vasoconstriction
- Splenomegaly secondary to portal hypertension
- Ascites due to portal hypertension and decreased plasma proteins
- Peripheral edema from accumulation of fluid retained because of decreased plasma protein production and loss of albumin with ascites
- Varices of the esophagus, rectum, and abdominal wall secondary to portal hypertension
- Bleeding tendencies from thrombocytopenia (secondary to blood accumulation in the spleen) and prolonged prothrombin time (from the impaired production of coagulation factors)
- Petechia resulting from thrombocytopenia
- Amenorrhea secondary to altered steroid hormone production and metabolism
- Gynecomastia in males from estrogen buildup due to failure of hepatic biotransformation functions.
- Liver function tests reveal elevated levels of aspartate aminotransferase (AST), alanine aminotrasferase (ALT), alkaline phosphatase, and bilirubin.
- Blood studies reveal anemia, impaired red blood cell production, elevated bleeding and clotting times, low blood glucose levels, and increased serum ammonia levels.
- Urine osmolarity is increased.
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FUNCTIONS OF THE LIVER
The liver is one of the most essential organs of the body. To understand how liver disease affects the body, it is best to understand its main functions:
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- liver transplantation
- low protein, high carbohydrate diet to correct nutritional deficiences and prevent overtaxing liver
- lactulose to reduce ammonia blood levels and help alleviate some symptoms of hepatic encephalopathy.
For ascites , treatment includes:
- salt restriction and potassium-sparing diuretics to increase water excretion
- potassium supplements to reverse the effects of high aldosterone
- paracentesis to remove ascitic fluid and alleviate abdominal discomfort
- shunt placement to aid in removal of ascitic fluid and alleviate abdominal discomfort.
For portal hypertension , treament includes:
- shunt placement between the portal vein and another systemic vein to divert blood flow and relieve pressure.
For variceal bleeding , treatment includes:
- vasoconstrictor drugs to decrease blood flow
- balloon tamponade to control bleeding by exerting pressure on the varices with the use of a balloon catheter
- surgery to tie off bleeding collaterals sprouting from the portal vein
- vitamin K to control bleeding by decreasing prothrombin time.
Malabsorption
A wide variety of disorders result in malabsorption. (See Causes of malabsorption .)
- prior gastric surgery
- pancreatic disorders
- hepatobiliary disease
- disease of the small intestine, such as celiac disease
- hereditary disorder
- drug toxicity.
- weight loss and generalized malnutrition from impaired absorption of carbohydrate, fat, and protein
- diarrhea from decreased absorption of fluids, electrolytes, bile acids and fatty acids in colon
- steatorrhea from excess fat in stool
- flatulence and abdominal distention secondary to fermentation of undigested lactose
- nocturia from delayed absorption of water
- weakness and fatigue from anemia and electrolyte depletion from diarrhea
- edema from impaired absorption of amino acids, resulting in protein depletion and hypoproteinemia
- amenorrhea from protein depletion leading to hypopituitarism
- anemia from the impaired absorption of iron, folic acid, and vitamin B 12
- glossitis, cheilosis secondary to a deficiency of iron, folic acid, vitamin B 12 , and other vitamins
- peripheral neuropathy from a deficiency of vitamin B 12 and thiamine
- bruising, bleeding tendency from vitamin K malabsorption and hypoprothrombinemia
- bone pain, skeletal deformities, fractures from calcium malabsorption that leads to hypocalcemia; protein depletion leading to osteoporosis and vitamin D malabsorption causing impaired calcium absorption
- tetany, paresthesias resulting from calcium malabsorption leading to hypocalcemia and magnesium malabsorption, leading to hypomagnesemia and hypokalemia.
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CAUSES OF MALABSORPTION
Many disorders ― from systemic to organ-specific diseases ― may give rise to malabsorption. DISEASES OF THE SMALL INTESTINE Primary small bowel disease
Ischemic small bowel disease
Small bowel infections and infestations
Systemic disease involving small bowel
DRUG-INDUCED MALABSORPTION
HEREDITARY DISORDER
PANCREATIC DISORDERS
PREVIOUS GASTRIC SURGERY
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- Stool specimen for fat reveals excretion of greater than 6 g of fat per day.
- D-Xylose absorption test shows less than 20% of 25 g of D-Xylose in the urine after 5 hours, reflects disorders of proximal bowel.
- Schilling test reveals deficiency of vitamin B 12 absorption.
- Culture of duodenal and jejunal contents confirms bacterial overgrowth in the proximal bowel.
- Gastrointestinal barium studies show characteristic features of the small intestine.
- Small intestine biopsy reveals the atrophy of mucosal villi.
- Identification of cause and appropriate correction
- Gluten-free diet to stop progression of celiac disease and malabsorption
- Lactose-free diet to treat lactase deficiency
- Dietary supplementation to replace nutrient deficiencies
- Vitamin B 12 injections to treat vitamin B 12 deficiency.
Pancreatitis
- Biliary tract disease
- Alcoholism
- Abnormal organ structure
- Metabolic or endocrine disorders, such as high cholesterol levels or overactive thyroid
- Pancreatic cysts or tumors
- Penetrating peptic ulcers
- Blunt trauma or surgical trauma
- Drugs, such as glucocorticoids, sulfonamides, thiazides, and oral contraceptives, and NSAIDS
- Kidney failure or transplantation
- Endoscopic examination of the bile ducts and pancreas.
- Pain caused by the escape of inflammatory exudate and enzymes into the back of the peritoneum, edema and distention of the pancreatic capsule, and obstruction of the biliary tract
- Persistent vomiting (in a severe attack) from hypermotility or paralytic ileus secondary to pancreatitis or peritonitis
- Abdominal distention (in a severe attack) from bowel hypermotility and the accumulation of fluids in the abdominal cavity
- Diminished bowel activity (in severe attack) suggesting altered motility secondary to peritonitis
- Crackles at lung bases (in a severe attack) secondary to heart failure
- Left pleural effusion (in a severe attack) from circulating pancreatic enzymes
- Mottled skin from hemorrhagic necrosis of the pancreas
- Tachycardia secondary to dehydration and possible hypovolemia
- Low-grade fever resulting from the inflammatory response
- Cold, sweaty extremities secondary to cardiovascular collapse
- Restlessness related to pain associated with acute pancreatitis
- Extreme malaise (in chronic pancreatitis) related to malabsorption or diabetes.
- Massive hemorrhage/shock
- Pseudocysts
- Biliary and duodenal obstruction
- Portal and splenic vein thrombosis
- Diabetes mellitus
- Respiratory failure.
- Elevated serum amylase and lipase confirm diagnosis.
- Blood and urine glucose tests reveal transient glucose in urine and hyperglycemia. In chronic pancreatitis, serum glucose levels may be transiently elevated.
- White blood cell count is elevated.
- Serum bilirubin levels are elevated in both acute and chronic pancreatitis.
- Blood calcium levels may be decreased.
- Stool analysis shows elevated lipid and trypsin levels in chronic pancreatitis.
- Abdominal and chest X-rays detect pleural effusions and differentiate pancreatitis from diseases that cause similar symptoms; may detect pancreatic calculi.
- Computed tomography and ultrasonography show enlarged pancreas with cysts and pseudocysts.
- Endoscopic retrograde cholangiopancreatography identifies ductal system abnormalities, such as calcification or strictures; helps differentiate pancreatitis from other disorders such as pancreatic cancer.
- intravenous replacement of fluids, protein, and electrolytes to treat shock
- fluid volume replacement to help correct metabolic acidosis
- blood transfusions to replace blood loss from hemorrhage
- withholding of food and fluids to rest the pancreas and reduce pancreatic enzyme secretion
- nasogastric tube suctioning to decrease stomach distention and suppress pancreatic secretions
- meperidine to relieve abdominal pain
- antacids to neutralize gastric secretions
- histamine antagonists to decrease hydrochloric acid production
- antibiotics to fight bacterial infections
- anticholinergics to reduce vagal stimulation, decrease gastrointestinal motility, and inhibit pancreatic enzyme secretion
- insulin to correct hyperglycemia
- surgical drainage for a pancreatic abscess or a pseudocyst
- laparotomy (if biliary tract obstruction causes acute pancreatitis) to remove obstruction.
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A CLOSER LOOK AT PEPTIC ULCERS
A gastrointestinal lesion is not necessarily an ulcer. Lesions that don't extend below the mucosal lining (epithelium) are called erosions. Lesions of both acute and chronic ulcers can extend through the epithelium and perforate the stomach wall. Chronic ulcers also have scar tissue at the base. <center></center> |
Peptic ulcer
- Infection with Helicobacter pylori
- Use of nonsteroidal anti-inflammatory drugs (NSAIDs)
- Pathologic hypersecretory disorders.
Symptoms vary by the type of ulcer.
A gastric ulcer produces the following signs and symptoms:
- pain that worsens with eating due to stretching of the mucosa by food
- nausea and anorexia secondary to mucosal stretching.
A duodenal ulcer produces the following signs and symptoms:
- epigastric pain that is gnawing, dull, aching, or “hunger like” due to excessive acid production
- pain relieved by food or antacids, but usually recurring 2 to 4 hours later secondary to food acting as a buffer for acid.
- Barium swallow or upper GI and small bowel series may reveal the presence of the ulcer. This is the first test performed on a patient when symptoms aren't severe.
- Endenoscopy confirms the presence of an ulcer and permits cytologic studies and biopsy to rule out H. pylori or cancer.
- Upper GI tract X-rays reveal mucosal abnormalities.
- Stool analysis may reveal occult blood.
- Serologic testing may disclose clinical signs of infection, such as elevated white blood cell count.
- Gastric secretory studies show hyperchlorhydria.
- Carbon 13 urea breath test results reflect activity of H. pylori .
- Antimicrobial agents (tetracycline, bismuth subsalicylate, and metronidazole) to eradicate H. pylori infection (See Treating peptic ulcer .)
- Misoprostol (a prostaglandin analog) to inhibit gastric acid secretion and increase carbonate and mucus production, to protect the stomach lining
- Antacids to neutralize acid gastric contents by elevating the gastric pH, thus protecting the mucosa and relieving pain
- Avoidance of caffeine and alcohol to avoid stimulation of gastric acid secretion
- Anticholinergic drugs to inhibit the effect of the vagal nerve on acid-secreting cells
- H 2 blockers to reduce acid secretion
- Sucralfate, mucosal protectant to form an acid-impermeable membrane that adheres to the mucous membrane and also accelerates mucus production
- Dietary therapy with small infrequent meals and avoidance of eating before bedtime to neutralize gastric contents
- Insertion of a nasogastric tube (in instances of gastrointestinal bleeding) for gastric decompression and rest, and also to permit iced saline lavage that may also contain norepinephrine
- Gastroscopy to allow visualization of the bleeding site and coagulation by laser or cautery to control bleeding
- Surgery to repair perforation or treat unresponsiveness to conservative treatment, and suspected malignancy.
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Treating peptic ulcer
Peptic ulcers can result from factors that increase gastric acid production or from factors that impair mucosal barrier protection. This illustration highlights the actions of the major treatments used for peptic ulcer and where they interfere with the pathophysiologic chain of events. <center></center> |
Ulcerative colitis
Signs and symptoms may include:
- recurrent bloody diarrhea, often containing pus and mucus (hallmark sign), from accumulated blood and mucus in the bowel
- abdominal cramping and rectal urgency from accumulated blood and mucus
- weight loss secondary to malabsorption
- weakness related to possible malabsorption and subsequent anemia.
- Sigmoidoscopy confirms rectal involvement: specifically, mucosal friability and flattening and thick, inflammatory exudate.
- Colonoscopy reveals extent of the disease, stricture areas, and pseudopolyps (not performed when the patient has active signs and symptoms).
- Biopsy with colonoscopy confirms the diagnosis.
- Barium enema reveals the extent of the disease, detects complications, and identifies cancer (not performed when the patient has active signs and symptoms).
- Stool specimen analysis reveals blood, pus, and mucus but no disease-causing organisms.
- Serology shows decreased serum potassium, magnesium, and albumin levels; decreased WBC count; decreased hemoglobin; and prolonged prothrombin time. Elevated erythrocyte sedimentation rate correlates with severity of the attack.
- corticotropin and adrenal corticosteroids to control inflammation
- sulfasalazine for its anti-inflammatory and antimicrobial effects
- antidiarrheals to relieve frequent, troublesome diarrhea in patients whose ulcerative colitis is otherwise under control
- iron supplements to correct anemia
- total parental nutrition and nothing by mouth for patients with severe disease, to rest the intestinal tract, decrease stool volume, and restore nitrogen balance
- supplemental drinks to supplement nutrition in patients with moderate symptoms
- intravenous hydration to replace fluid loss from diarrhea
- surgery to correct massive dilation of the colon and to treat patients with symptoms that are unbearable or unresponsive to drugs and supportive measures
- proctocolectomy with ileostomy to divert stool and to allow rectal anastomosis to heal, removing all the potentially malignant epithelia of the rectum and colon.
