Exam 5 Blueprint

Paracentesis

-A paracentesis is a sterile procedure in which a catheter is used to withdraw fluid from the abdominal cavity. This procedure can diagnose a medical condition or relieve pain, pressure, or difficulty breathing. In the patient with cirrhosis, this procedure is done for the person with impaired respiration or abdominal discomfort caused by severe ascites who does not respond to diuretic therapy. It is only a temporary measure of palliation because the fluid tends to reaccumulate rapidly. -Immediately before a paracentesis, have the patient void to prevent puncturing of the bladder during the procedure. Preprocedure: -Have the patient void or insert an indwelling catheter. -Obtain baseline vital signs and pulse oximetry. Weigh patient, inspect and palpate abdomen, and assess abdominal girth. Assess bladder for distention and determine last voiding. -Assess baseline laboratory values (e.g., CBC, electrolytes, coagulation studies). -Give any sedation or analgesia, if ordered. -Teach patient to remain immobile during the procedure. -Help the patient to a high-Fowler (sitting) position with feet on the floor. Postprocedure: -Perform assessment and compare to baseline: vital signs, pulse oximetry, abdominal girth, abdominal pain. Note any signs of hypovolemia. -Have the patient sit on the side of the bed or place in high-Fowler's position. -Label and send the fluid for laboratory analysis. -Check the dressing for bleeding and/or leakage of ascitic fluid. -Give IV fluid and/or albumin as ordered. -Measure any drainage and describe the collected fluid. -Reweigh the patient and monitor intake and output. -Maintain bedrest per agency protocol.

Laparoscopic cholecystectomy

Laparoscopic cholecystectomy: -Treatment of choice for symptomatic gallstones. - 90% of cholecystectomy cases. -Have patient lay in the left lateral sim's position. -In this procedure, the gallbladder is removed through 1 to 4 small punctures in the abdomen. The HCP makes a small cut below the umbilicus and inserts a needle into the area. CO2 gas is passed into the abdomen to expand the area, which allows the HCP to see the organs more clearly and gives more room to work. A laparoscope, which has a camera attached, and grasping forceps are inserted into the abdomen through the punctures. Using closed-circuit monitors to view the abdominal cavity, the HCP retracts and dissects the gallbladder and removes it with grasping forceps. This is a safe and routine procedure with minimal morbidity and quick recovery time. -Most patients have minimal postoperative pain and are discharged the day of surgery or the day after. They can usually resume normal activities and return to work within 1 week. The main complication is injury to the common bile duct. The few contraindications to laparoscopic cholecystectomy include peritonitis, cholangitis, gangrene or perforation of the gallbladder, portal hypertension, and serious bleeding disorders. -After a laparoscopic cholecystectomy, teach the patient to have liquids for the rest of the day and eat light meals for a few days. -Postoperative nursing care after a laparoscopic cholecystectomy includes monitoring for complications, such as bleeding, making the patient comfortable, and preparing the patient for discharge. Patients may report referred pain to the shoulder because of the CO2 that the HCP uses to inflate the abdominal cavity during surgery. It may not be released or absorbed by the body. The CO2 can irritate the phrenic nerve and diaphragm, causing some difficulty in breathing. Placing the patient in the Sims' position (on left side with right knee flexed) helps move the gas pocket away from the diaphragm. Encourage deep breathing along with movement and ambulation. NSAIDs or codeine can usually relieve pain. The patient is allowed clear liquids and can walk to the bathroom to void. Most patients go home the same day. -The patient who undergoes a laparoscopic cholecystectomy is discharged soon after the surgery, so home care and teaching are important. Postoperative teaching should include: 1.) Remove the bandages on the puncture sites the day after surgery and you can shower. 2.) Notify your HCP if any of the following signs and symptoms occurs: -Redness, swelling, bile-colored drainage or pus from any incision. -Severe abdominal pain, nausea, vomiting, fever, chills. 3.) You can gradually resume normal activities. 4.) Return to work within 1 week of surgery. 5.) You can resume your usual diet, but a low-fat diet is usually better tolerated for several weeks after surgery.

Progression of liver disease

1.) Normal liver. 2.) Fatty liver (hepatic steatosis). 3.) Hepatitis. 4.) Cirrhosis.

Acute Pancreatitis

-Acute pancreatitis is an acute inflammation of the pancreas. Spillage of pancreatic enzymes into surrounding pancreatic tissue causes autodigestion and severe pain. The degree of inflammation varies from mild edema to severe hemorrhagic necrosis. Pathophysiology: -Many factors can cause injury to the pancreas. In the United States, the most common cause is gallbladder disease (gallstones), which is more common in women. The second most common cause is chronic alcohol use. This is more common in men. -Other less common causes include drug reactions, pancreatic cancer, and hypertriglyceridemia (serum levels over 1000 mg/dL). Biliary sludge and microlithiasis, which is a mix of cholesterol crystals and calcium salts, can be present in patients with acute pancreatitis. -The most common pathogenic mechanism in acute pancreatitis is autodigestion of the pancreas. The causative factors injure pancreatic cells or activate the pancreatic enzymes in the pancreas rather than in the intestine. This may be due to reflux of bile acids into the pancreatic ducts through an open or distended sphincter of Oddi. This reflux may be caused by blockage created by gallstones. Obstruction of pancreatic ducts results in pancreatic ischemia. -The exact mechanism by which chronic alcohol use predisposes a person to pancreatitis is not known. We think that alcohol increases the production of digestive enzymes in the pancreas. -The pathophysiologic involvement of acute pancreatitis is classified as either mild pancreatitis (also known as edematous or interstitial pancreatitis) or severe pancreatitis (also called necrotizing pancreatitis). In severe pancreatitis, about half the patients have permanent decreases in pancreatic endocrine and exocrine function. Patients with severe pancreatitis are at high risk for developing pancreatic necrosis, organ failure, and septic complications, resulting in an overall fatality rate of 5%. Complications: -The severity of acute pancreatitis depends on the extent of pancreatic destruction. Acute pancreatitis can be life threatening. Some patients recover completely, others have recurring attacks, and others develop chronic pancreatitis. -Two significant local complications of acute pancreatitis are pseudocyst and abscess. A pancreatic pseudocyst is an accumulation of fluid, pancreatic enzymes, tissue debris, and inflammatory exudates surrounded by a wall next to the pancreas. Manifestations are abdominal pain, palpable epigastric mass, nausea, vomiting, and anorexia. The serum amylase level is often high. CT, MRI, and endoscopic ultrasound (EUS) may detect a pseudocyst. The cysts usually resolve spontaneously within a few weeks but may perforate, causing peritonitis or rupture into the stomach or the duodenum. Treatment options include surgical drainage, percutaneous catheter placement and drainage, and endoscopic drainage. -When a pseudocyst gets infected, a pancreatic abscess results from extensive necrosis in the pancreas. It may rupture or perforation into adjacent organs. Manifestations of an abscess include upper abdominal pain, abdominal mass, high fever, and leukocytosis. Pancreatic abscesses need prompt surgical drainage to prevent sepsis. -The main systemic complications of acute pancreatitis are cardiovascular and pulmonary (pleural effusion, atelectasis, pneumonia, and acute respiratory distress syndrome [ARDS]). The pulmonary complications are due to the passage of exudate containing pancreatic enzymes from the peritoneal cavity through transdiaphragmatic lymph channels. Enzyme-induced inflammation of the diaphragm occurs, with the result being atelectasis caused by reduced diaphragm movement. Trypsin can activate prothrombin and plasminogen, increasing the patient's risk for intravascular thrombi, pulmonary emboli, and DIC. Hypotension can occur from fluid shifts and sepsis. -Tetany, which can be caused by hypocalcemia, is a sign of severe disease. It is due in part to the combining of calcium and fatty acids during fat necrosis. We do not understand the exact mechanisms of how or why hypocalcemia occurs. Patients with severe acute pancreatitis are at risk for abdominal compartment syndrome from intraabdominal hypertension and edema. Diagnostics: -The primary diagnostic tests for acute pancreatitis are serum amylase and lipase. The serum amylase level is usually high early and stays high for 24 to 72 hours. Serum lipase level, which is high in acute pancreatitis, is an important test because other disorders (e.g., mumps, cerebral trauma, renal transplantation) may increase serum amylase levels. Other serum findings include an increase in liver enzymes, triglycerides, glucose, and bilirubin and a decrease in calcium. -Diagnostic evaluation of acute pancreatitis is directed at determining the cause. An abdominal ultrasound, x-ray, or contrast- enhanced CT scan may identify pancreatic problems. CT scan is the best imaging test for pancreatitis and related complications, such as pseudocysts and abscesses. ERCP is an option (although ERCP can cause acute pancreatitis), along with EUS, magnetic resonance cholangiopancreatography (MRCP), and angiography. Chest x-rays may show atelectasis and pleural effusions. Treatments: Surgical Therapy: -When the acute pancreatitis is related to gallstones, an urgent ERCP plus endoscopic sphincterotomy (severing of the muscle layers of the sphincter of Oddi) may be done. Laparoscopic cholecystectomy may follow ERCP to reduce the potential for recurrence. Surgical intervention may be needed when the diagnosis is uncertain and for patients who do not respond to conservative therapy. -Those with severe acute pancreatitis may need drainage of necrotic fluid collections. This is done surgically, under CT guidance, or endoscopically. Percutaneous drainage of a pseudocyst can be done, and a drainage tube left in place. Drug Therapy: -Several different drugs are used to prevent and treat problems associated with pancreatitis. Currently, there are no drugs that cure pancreatitis. Nutritional Therapy: -Initially, the patient with acute pancreatitis is on NPO status to reduce pancreatic secretion. Depending on the severity of the pancreatitis, EN is started. Because of infection risk, parenteral nutrition is reserved for patients who cannot tolerate EN. If IV lipids are given, monitor blood triglyceride levels. In cases of moderate to severe pancreatitis, the patient may need enteral feeding via a jejunal feeding tube. -When food is allowed, small, frequent feedings are given. The diet is high in carbohydrate content because that is the least stimulating to the exocrine part of the pancreas. Suspect intolerance to oral foods when the patient reports pain, has increasing abdominal girth, or has increased serum amylase and lipase levels. Supplemental fat-soluble vitamins may be given.

Chronic Pancreatitis

-Chronic pancreatitis is a continuous, prolonged, inflammatory, and fibrosing process of the pancreas. The pancreas is progressively destroyed as it is replaced by fibrotic tissue. Strictures and calcifications may occur in the pancreas. Pathophysiology: -Chronic pancreatitis can be due to chronic alcohol use; obstruction caused by gallstones, tumor, pseudocysts, or trauma; and systemic diseases (e.g., systemic lupus erythematosus), autoimmune pancreatitis, and cystic fibrosis. Some patients may not have an identifiable risk factor (idiopathic pancreatitis). Chronic pancreatitis may follow acute pancreatitis, but it may also occur in the absence of any history of an acute condition. -The most common cause of obstructive pancreatitis is inflammation of the sphincter of Oddi associated with gallstones. Cancer of the ampulla of Vater, duodenum, or pancreas can also cause this type of chronic pancreatitis. -The most common cause of nonobstructive pancreatitis (the most common type of chronic pancreatitis) is chronic alcohol use. There is inflammation and sclerosis, mainly in the head of the pancreas and around the pancreatic duct. In some people who drink alcohol, a genetic factor may predispose them to the direct toxic effect of the alcohol on the pancreas. Complications: -As with acute pancreatitis, a major manifestation of chronic pancreatitis is abdominal pain. The patient may have episodes of acute pain, but it usually is chronic (recurrent attacks at intervals of months or years). The attacks may become more frequent until they are almost constant, or they may decrease as pancreatic fibrosis develops. The pain is found in the same areas as in acute pancreatitis, but is usually described as a heavy, gnawing feeling or sometimes as burning and cramp-like. Food or antacids do not relieve the pain. -Other manifestations include symptoms of pancreatic insufficiency, including malabsorption with weight loss, constipation, mild jaundice with dark urine, steatorrhea, and diabetes. The steatorrhea may become severe, with voluminous, foul-smelling, fatty stools. Some abdominal tenderness may be present. -Chronic pancreatitis is associated with a variety of complications. These include pseudocyst formation, bile duct or duodenal obstruction, pancreatic ascites or pleural effusion, splenic vein thrombosis, pseudoaneurysms, and pancreatic cancer. Diagnostics: -Confirming the diagnosis of chronic pancreatitis can be hard. The diagnosis is based on the patient's signs and symptoms, laboratory studies, and imaging. In chronic pancreatitis, serum amylase and lipase levels may be increased slightly or not at all, depending on the degree of pancreatic fibrosis. Serum bilirubin and alkaline phosphatase levels may be increased. There is usually mild leukocytosis and a high sedimentation rate. -ERCP can visualize the pancreatic and common bile ducts. Imaging studies, such as CT, MRI, MRCP, abdominal ultrasound, and EUS, can show a variety of changes, including calcifications, ductal dilation, pseudocysts, and enlargement of the pancreas. -Stool samples are examined for fecal fat content. Deficiencies of fat-soluble vitamins and cobalamin, glucose intolerance, and diabetes may occur in those with chronic pancreatitis. A secretin stimulation test can assess the degree of pancreatic dysfunction. Treatments: -When the patient with chronic pancreatitis has an acute attack, the therapy is identical to that for acute pancreatitis. At other times, the focus is on prevention of further attacks, relief of pain, and control of pancreatic exocrine and endocrine insufficiency. It sometimes takes frequent doses of analgesics (morphine, fentanyl patch [Duragesic]) to relieve the pain if dietary measures and enzyme replacement are not effective. -Diet, pancreatic enzyme replacement, and control of diabetes are ways to control the pancreatic insufficiency. Small, bland, frequent meals that are low in fat content are recommended to decrease pancreatic stimulation. Smoking is associated with accelerated progression of chronic pancreatitis. Teach the patient not to consume alcohol and caffeinated beverages. If the patient is dependent on alcohol, refer the patient to other resources as needed. -Pancreatic enzyme products, such as pancrelipase (Pancrease, Zenpep, Creon, Viokace), contain amylase, lipase, and trypsin. They are used to replace the deficient pancreatic enzymes. The enzymes are usually enteric coated to prevent their breakdown or inactivation by gastric acid. They are usually taken with meals and snacks. Teach the patient and caregiver to monitor stools for steatorrhea to help determine the effectiveness of the enzymes. Bile salts may be given to help with fat-soluble vitamin (A, D, E, and K) absorption and prevent further fat loss. -If diabetes develops, it is controlled with insulin (most often) or oral hypoglycemic agents. Teach the patient about testing blood glucose levels and drug therapy. While acid-neutralizing drugs (e.g., antacids) and acid-inhibiting drugs (e.g., H2 receptor blockers, PPIs) may be given to control gastric acidity, they have little overall effect on patient outcomes. Antidepressants can reduce any neuropathic pain associated with chronic pancreatitis. -Treatment of chronic pancreatitis sometimes requires endoscopic therapy or surgery. When biliary disease is present or obstruction or pseudocyst develops, surgery may be needed. Surgical procedures can divert bile flow or relieve ductal obstruction. A choledochojejunostomy diverts bile around the ampulla of Vater, where there may be spasm or hypertrophy of the sphincter. In this procedure, the common bile duct is anastomosed into the jejunum. Another type of surgical diverting procedure is the Roux-en-Y pancreato-jejunostomy, in which the pancreatic duct is opened and an anastomosis made with the jejunum. Pancreatic drainage procedures can relieve ductal obstruction and are often done with ERCP. Some patients may have an ERCP with sphincterotomy and/or stent placement at the site of obstruction. These patients need follow-up procedures, such as ERCP, to either exchange or remove the stent.

Later signs of cirrhosis

-Late manifestations result from liver failure and portal hypertension. Jaundice, peripheral edema, and ascites develop gradually. Other late manifestations include skin lesions, hematologic problems, endocrine problems, and peripheral neuropathies. In the advanced stages, the liver becomes small and nodular. Liver function is dramatically impaired. Jaundice: -Jaundice results from decreased ability to conjugate and excrete bilirubin into the small intestines. There is an overgrowth of connective tissue in the liver, which compresses the bile ducts and leads to an obstruction. This results in an increase in the bilirubin in the vascular system, and jaundice occurs. The jaundice may be minimal or severe, depending on the degree of liver damage. Skin Lesions: -Various skin manifestations often occur with cirrhosis. Spider angiomas (telangiectasia or spider nevi) are small, dilated blood vessels with a bright red center point and spider-like branches. They occur on the nose, cheeks, upper trunk, neck, and shoulders. Palmar erythema (a red area that blanches with pressure) occurs on the palms of the hands. Both lesions are due to an increase in circulating estrogen due to the damaged liver's inability to metabolize steroid hormones. Hematologic Problems: -Hematologic problems include thrombocytopenia, leukopenia, anemia, and coagulation disorders. We think thrombocytopenia, leukopenia, and anemia are caused by the splenomegaly that results from backup of blood from the portal vein into the spleen (portal hypertension). Overactivity of the enlarged spleen results in increased removal of blood cells from circulation. Anemia can result from inadequate red blood cell (RBC) production and survival, poor diet, poor absorption of folic acid, and bleeding from varices. -The coagulation problems result from the liver's inability to make prothrombin and other factors essential for blood clotting. Manifestations of coagulation problems (bleeding tendencies) include epistaxis, purpura, petechiae, easy bruising, gingival bleeding, and heavy menstrual bleeding. Endocrine Problems: -The liver plays a vital role in the metabolism of hormones, such as estrogen and testosterone. In men with cirrhosis, gynecomastia (benign growth of the glandular tissue of the male breast), loss of axillary and pubic hair, testicular atrophy, and impotence with loss of libido may occur because of increased estrogen levels. Younger women with cirrhosis may develop amenorrhea, and older women may have vaginal bleeding. If the liver does not metabolize aldosterone properly, it can lead to hyperaldosteronism with sodium and water retention and potassium loss. Peripheral Neuropathy: -Peripheral neuropathy is a common finding in alcoholic cirrhosis. It is probably due to a dietary deficiency of thiamine, folic acid, and cobalamin. The neuropathy usually results in sensory and motor symptoms, but sensory symptoms may predominate.

Complications of cirrhosis

-Major complications of cirrhosis are portal hypertension, esophageal and gastric varices, peripheral edema, abdominal ascites, hepatic encephalopathy (mental status changes, including coma), and hepatorenal syndrome. Patients who are cirrhotic but who have no obvious complications have compensated cirrhosis. Those who have 1 or more complications of their liver disease have decompensated cirrhosis. Portal Hypertension and Esophageal and Gastric Varices: -In patients with cirrhosis, the liver undergoes structural changes. These changes lead to obstruction of blood flow in and out of the liver. This results in increased pressure within the liver's circulatory system (portal hypertension). Portal hypertension is characterized by increased venous pressure in the portal circulation, splenomegaly, large collateral veins, ascites, and gastric and esophageal varices. -As a way of reducing pressure, the body develops alternate circulatory pathways, referred to as collateral circulation. The collateral channels often form in the lower esophagus, anterior abdominal wall, parietal peritoneum, and rectum. Varicosities (distended veins) develop in areas where the collateral and systemic circulations communicate, resulting in esophageal and gastric varices, caput medusae (ring of varices around the umbilicus), and hemorrhoids. -Esophageal varices are a complex of tortuous, enlarged veins at the lower end of the esophagus. Gastric varices are found in the upper part of the stomach. These varices are fragile and do not tolerate high pressure, so they can bleed easily. Large varices are more likely to bleed. Esophageal varices can cause variceal hemorrhages with a 5-year mortality of 20%. The patient may present with melena or hematemesis. Ruptured esophageal varices are the most life-threatening complication of cirrhosis and considered a medical emergency. Peripheral Edema and Ascites: -Peripheral edema occurs in the lower extremities and presacral area. Peripheral edema can occur before, concurrently with, or after ascites development. Edema results from decreased colloidal oncotic pressure from impaired liver synthesis of albumin and increased portacaval pressure from portal hypertension. -Ascites is the accumulation of serous fluid in the peritoneal or abdominal cavity. It is a common manifestation of cirrhosis. Several mechanisms lead to ascites. One mechanism of ascites occurs with portal hypertension, which causes proteins to shift from the blood vessels into the lymph space. When the lymphatic system is unable to carry off the excess proteins and water, they leak into the peritoneal cavity. The osmotic pressure of the proteins pulls more fluid into the peritoneal cavity. -A second mechanism of ascites formation is hypoalbuminemia resulting from the liver's decreased ability to synthesize albumin. The hypoalbuminemia results in decreased colloidal oncotic pressure. -A third mechanism of ascites is hyperaldosteronism, which occurs when the damaged hepatocytes metabolize aldosterone. The increased aldosterone level causes increased sodium reabsorption by the renal tubules. Sodium retention, combined with an increase in antidiuretic hormone in blood, leads to further water retention and edema. Edema decreases intravascular volume with decreased renal blood flow and glomerular filtration. -Ascites is manifested by abdominal distention with weight gain. If the ascites is severe, the increase in abdominal pressure from the fluid accumulation may cause eversion of the umbilicus. Abdominal striae with distended abdominal wall veins may be present. Patients may have signs of dehydration (e.g., dry tongue and skin, sunken eyeballs, muscle weakness) and a decrease in urine output. Hypokalemia is common. It is due to an excessive loss of potassium caused by hyperaldosteronism. Low potassium levels can also result from diuretic therapy used to treat the ascites. -Because of decreased immune function associated with cirrhosis, patients with ascites are at risk for spontaneous bacterial peritonitis (SBP). SBP is a bacterial infection of the ascitic fluid. In SBP, bacteria normally found in the intestines move into the peritoneal space. The bacteria most often responsible for the infection are a gram-negative enteric pathogen, such as Escherichia coli. SBP is a common complication of hospitalized patients with cirrhosis and ascites. Worsening vasodilation contributes to the development of SBP. Hepatic Encephalopathy: -Hepatic encephalopathy is a neuropsychiatric manifestation of liver disease. The pathogenesis is multifactorial. It includes the neurotoxic effects of ammonia, abnormal neurotransmission, astrocyte swelling, and inflammatory cytokines. A major source of ammonia is the bacterial and enzymatic deamination of amino acids in the intestines. The ammonia that results from deamination normally goes to the liver via the portal circulation and is converted to urea. The kidneys then excrete urea. When blood is shunted past the liver via the collateral vessels or the liver is so damaged that it is unable to convert ammonia to urea, the levels of ammonia in the systemic circulation increase. The ammonia crosses the blood-brain barrier and produces neurologic toxic manifestations. -Factors that increase ammonia in the circulation may precipitate hepatic encephalopathy. Hepatic encephalopathy can occur after placement of a transjugular intrahepatic portosystemic shunt (TIPS). TIPS reduces portal hypertension by diverting blood flow around the liver. -Manifestations include changes in neurologic and mental responsiveness; impaired consciousness; and inappropriate behavior, ranging from sleep problems to trouble concentrating to deep coma. Changes may occur (1) suddenly from an increase in ammonia in response to bleeding varices or infection or (2) gradually as blood ammonia levels slowly increase. We often use a grading system to classify the stages of hepatic encephalopathy. -A characteristic manifestation is asterixis (flapping tremors). This may take several forms, with the most common involving the arms and hands. When asked to hold the arms and hands stretched out, the patient is unable to hold this position and performs a series of rapid flexion and extension movements of the hands. -Impairments in writing involve difficulty in moving the pen or pencil from left to right and apraxia (inability to construct simple figures). Other signs include hyperventilation, hypothermia, tongue fasciculations, and grimacing and grasping reflexes. Fetor hepaticus (musty, sweet odor of the patient's breath) occurs in some patients. This odor is from the accumulation of digestive by-products that the liver is unable to degrade. Hepatorenal Syndrome: -Hepatorenal syndrome is a type of renal failure with azotemia, oliguria, and intractable ascites. In this syndrome, the kidneys have no structural abnormality. The cause is complex. The final common pathway is likely to be portal hypertension along with liver decompensation, resulting in splanchnic and systemic vasodilation and decreased arterial blood volume. As a result, renal vasoconstriction occurs, and renal failure follows. Liver transplantation can reverse renal failure. In the patient with cirrhosis, hepatorenal syndrome can follow diuretic therapy, GI hemorrhage, or paracentesis.

Examination techniques for abdominal assessment

-We use 2 systems to anatomically describe the surface of the abdomen. One system divides the abdomen into 4 quadrants by a perpendicular line from the sternum to the pubic bone and a horizontal line across the abdomen at the umbilicus. The other system divides the abdomen into 9 regions. Only the epigastric, umbilical, and suprapubic or hypogastric regions are commonly assessed. -For the abdominal examination, good lighting should shine across the abdomen. The patient should be in the supine position and as relaxed as possible. To help relax the abdominal muscles, have the patient slightly flex the knees and raise the head of the bed slightly. The patient should have an empty bladder. Use warm hands when doing the abdominal examination to avoid eliciting muscle guarding. Ask the patient to breathe slowly through the mouth. -The standard approach for examining the abdomen is appropriate for an older adult. The abdomen may be thinner and laxer unless the patient is obese. Order of examination process: 1.) Inspection. 2.) Auscultation. 3.) Percussion. 4.) Palpation.

Hemorrhage: (Complication of PUD)

Hemorrhage: -Hemorrhage is the most common complication of PUD. Duodenal ulcers cause more upper GI bleeding episodes than gastric ulcers. Care: -Changes in vital signs and an increase in the amount and redness of aspirate often signal massive upper GI bleeding. With bleeding, the patient's pain often decreases because the blood helps neutralize the acidic gastric contents. It is important to maintain the patency of the NG tube so that blood clots do not obstruct the tube. If the tube becomes blocked, the patient can develop abdominal distention.

Nausea and Vomiting

Causes: -Pregnancy. -Infection. -Central nervous system (CNS) problems (e.g., meningitis, tumor). -Cardiovascular disease (CVD) (e.g., myocardial infarction, heart failure). -Metabolic disorders. -Psychologic factors (e.g., stress, fear). -When the GI tract becomes overly irritated, excited, or distended. -After surgery with general anesthesia or as a drug side effect (e.g., chemotherapy, opioids). Key Assessment Questions: Past health history: -GI disorders, chronic indigestion, food allergies, pregnancy, infection, CNS problems, recent travel, eating disorders, metabolic disorders, cancer, CVD, renal disease. Medications: -Antiemetics, digitalis, opioids, ferrous sulfate, aspirin, aminophylline, alcohol, antibiotics, chemotherapy. General anesthesia. Surgery or other treatments: -Recent surgery. Nutritional-metabolic: -Amount, frequency, character, and color of vomitus. Dry heaves. Anorexia, weight loss. Activity-exercise: -Weakness, fatigue. Cognitive-perceptual: -Abdominal tenderness or pain. Coping-stress tolerance: -Stress, fear. Treatment: Drugs (Antiemetics): -Promethazine (Phenergan) acts at chemoreceptor trigger zone to decrease N&V. Give deep IM. -Metoclopramide (Reglan) increases gastric motility and emptying. -Ondansetron and Dexamethasone block serotonin to decrease N&V. Used with chemotherapy induced N&V. Nutritional: - IV electrolytes and glucose. -Water initial fluid of choice for oral rehydration. Room temperature, flat soda pop and warm teas. -Sip 5 to 15 mL every 15 to 20 minutes. -GI rest (NPO) then progress as tolerated. Other: -Acupressure/acupuncture. -Relaxation. -Ginger or peppermint. -Alternative therapies. -Herbs/oils. -Position changes.

Gastric ulcers

Lesion: -Superficial, smooth margins. Round, oval, or cone shaped. Location of Lesion: -Predominantly antrum, also in body and fundus of stomach. Gastric Secretion: -Normal to decreased. Incidence: -Greater in women. -Peak age 50 to 60 years. -Increased cancer risk. -H. pylori infection in 80%. -Increased with incompetent pyloric sphincter and bile reflux. Clinical Manifestations: -Burning or gaseous pressure in epigastrium. -Pain 1 to 2 hours after meals. If penetrating ulcer, aggravation and discomfort with food Recurrence Rate: -High.

Total Bilirubin

Normal Range: - 0.2 to 1.2 mg/dL. -Increases with disease.

Aspartate aminotransferase (AST)

Normal Range: - 10 to 30 u/L. -Increases with liver injury.

Alanine aminotransferase (ALT)

Normal Range: - 10 to 40 u/L. -Increases with liver injury.

Acute Gastritis

Causes: Drugs: -Aspirin. -Bisphosphonates. -Corticosteroids. -Digitalis. -Iron supplements. -Nonsteroidal antiinflammatory drugs (NSAIDs). Diet: -Alcohol. -Large amounts of spicy, irritating foods. Microorganisms: -H. pylori. -Cytomegalovirus. -Mycobacterium species. -Salmonella organisms. -Staphylococcus organisms. -Treponema pallidum (syphilis). Environmental Factors: -Radiation. -Smoking. Diseases/Disorders: -Burns. -Crohn's disease. -Large hiatal hernia. -Physiologic stress. -Reflux of bile and pancreatic secretions. -Renal failure. -Sepsis. -Shock. Other Factors -Endoscopy procedures. -Nasogastric tube. -Psychologic stress. Key Assessment Questions: -How long have you had abdominal pain? -Do you smoke or drink? -What have you eaten in the past 24 hours? -Past medical history? -Current list of medications? Treatment: -Eliminating the cause and preventing or avoiding it in the future are generally all that is needed to treat acute gastritis. The plan of care is supportive and similar to that described for nausea and vomiting. If vomiting is present, rest, NPO status, and IV fluids may be prescribed. Antiemetics are given. Monitor for dehydration. It can occur rapidly in acute gastritis with vomiting. -In severe cases of acute gastritis, an NG tube may be used to (1) monitor for bleeding, (2) lavage the precipitating agent from the stomach, or (3) keep the stomach empty and free of noxious stimuli. Clear liquids are resumed when symptoms have subsided. Reintroduce solids gradually. -If the patient is at risk for hemorrhage, frequently check vital signs and test the vomitus for blood. All the management strategies discussed in the section on upper GI bleeding apply to the patient with severe gastritis. -Drug therapy focuses on reducing irritation of the gastric mucosa and providing symptomatic relief. H2 receptor blockers (e.g., ranitidine, cimetidine) or PPIs (e.g., omeprazole) reduce gastric HCl acid secretion. Teach the patient about the therapeutic effects of PPIs and H2 receptor blockers.

Perforation: (Complication of PUD)

Perforation: -Perforation is considered the most lethal complication of PUD. Perforation risk is highest with large penetrating duodenal ulcers. However, the mortality rate associated with perforation of gastric ulcers is higher. The patient with gastric ulcers is older and often has concurrent medical problems, which accounts for the higher mortality rate. -With perforation, the ulcer penetrates the serosal surface with spillage of either gastric or duodenal contents into the peritoneal cavity. The contents entering the peritoneal cavity may contain air, saliva, food particles, HCl acid, pepsin, bacteria, bile, and pancreatic fluid and enzymes. -The manifestations of perforation are sudden and dramatic in onset. During the initial phase (0 to 2 hours after perforation), the patient has sudden, severe upper abdominal pain that quickly spreads throughout the abdomen. The pain radiates to the back and shoulders. Food or antacids do not relieve the pain. The abdomen appears rigid and boardlike as the abdominal muscles try to protect from further injury. The patient's respirations become shallow and rapid. The heart rate is elevated, and the pulse is weak. Bowel sounds are usually absent. Nausea and vomiting may occur. -If the condition is untreated, bacterial peritonitis may occur within 6 to 12 hours. The intensity of peritonitis is proportional to the amount and duration of the spillage through the perforation. It is hard to determine from symptoms alone whether a gastric or duodenal ulcer has perforated, because the manifestations of peritonitis are the same. -The immediate focus of managing a patient with a perforation is to stop the spillage of gastric or duodenal contents into the peritoneal cavity and restore blood volume. An NG tube can provide continuous aspiration and gastric decompression to stop spillage through the perforation. For duodenal aspiration, the tube is placed as near to the perforation site as possible to facilitate decompression. -Circulating blood volume is replaced with lactated Ringer's and albumin solutions. These solutions substitute for the fluids lost from the vascular and interstitial space as peritonitis develops. Blood replacement in the form of packed RBCs may be needed. A central venous pressure line and an indwelling urinary catheter may be inserted and monitored hourly. The patient with a history of heart disease needs ECG monitor- ing or placement of a pulmonary artery catheter for accurate assessment of left ventricular function. Broad-spectrum antibiotic therapy is started immediately to treat bacterial peritonitis. -Small perforations may spontaneously seal themselves and symptoms cease. Spontaneous sealing occurs because of fibrin production in response to the perforation. This can lead to fibrinous fusion of the duodenum or gastric curvature to adjacent tissue (mainly the liver) and strictures that can obstruct the flow of intestinal contents and the passage of stool. -Larger perforations need immediate surgical closure. Whether the patient has an open or laparoscopic repair depends on the location of the ulcer and HCP preference. The procedure involving the least risk to the patient is simple oversewing of the perforation and reinforcement of the area with a graft of omentum. Excess gastric contents are suctioned from the peritoneal cavity during the surgical procedure. Care: -If the patient with an ulcer develops manifestations of a perforation, notify the HCP immediately. Take vital signs promptly and record them every 15 to 30 minutes. Temporarily stop all oral or NG drugs and feedings. If perforation exists, anything taken orally can add to the spillage into the peritoneal cavity and increase discomfort. Give IV fluid as ordered to replace the depleted plasma volume. Giving pain medications provides comfort. -Those with confirmed perforation will start on antibiotic therapy. If the perforation does not seal spontaneously, surgical closure is needed. Since surgery is done as soon as possible, there may not be time to prepare the patient and family.

Esophageal carcinoma

Risk Factors: -Cause is unknown. -BE. -Smoking. -Excess alcohol use. -Obesity. Symptoms: -Dysphagia. -Weight loss. -Pain (occurs later). -Narrow obstruction. Assessment Findings: -Highest incidence is in non-Hispanic white men. -Lowest incidence occurs in Asian Americans, Pacific Islanders, and Hispanics. Diagnosis: -Endoscopic biopsy is required to diagnose esophageal cancer. Endoscopic ultrasonography (EUS) is important in staging esophageal cancer. Esophagram (barium swallow) may show narrowing of the esophagus at the tumor site. Treatment: Surgical therapy: -Removal of part or all of the esophagus (esophagectomy) with use of a Dacron graft to replace the resected part. -Resection of a portion of the esophagus and anastomosis of the remaining portion to the stomach (esophagogastrostomy). -Resection of a portion of the esophagus and anastomosis of a segment of colon to the remaining portion (esophagoenterostomy). -Minimally invasive esophagectomy (e.g., laparoscopic vagal nerve-sparing surgery) is being done more often. It has the advantage of using smaller incisions, decreasing intensive care unit (ICU) and hospital stays, and producing fewer pulmonary complications. Endoscopic Therapy: -Endoscopic therapy includes photodynamic therapy, EMR, and radiofrequency ablation. In photodynamic therapy, the patient receives an IV injection of porfimer sodium (Photofrin), a photosensitizer. -The HCP directs light towards the cancerous area using a fiber passed through an endoscope. The light reacts with porfimer, starting a reaction that destroys the cancer cells. Patients must avoid direct sunlight for up to 6 weeks after the procedure. Radiation Therapy: -Depending on the type and stage of esophageal cancer, the patient may receive chemotherapy with or without radiation therapy. Concurrent therapy is given for palliation of symptoms, especially dysphagia, and to increase survival. Some patients receive radiation therapy before surgery. Chemotherapy: -Many different chemotherapy drugs can be used to treat esophageal cancer. The preferred regimens are carboplatin and paclitaxel, cisplatin with capecitabine (Xeloda), cisplatin and fluorouracil, and oxaliplatin with either fluorouracil or capecitabine. DCF (docetaxel, cisplatin, fluorouracil) is an option for metastatic disease. Other treatments include ECF (epirubicin [Ellence], cisplatin, fluorouracil) and irinotecan (Camptosar). Targeted Therapy: -Some esophageal cancers have too much HER-2 protein on their cell surfaces, which helps cancer cells to grow. Trastuzumab (Herceptin) is a drug that targets the HER-2 protein and kills the cancer cells. This drug can cause heart damage, so it is not given with other chemotherapy drugs that also cause heart damage, such as epirubicin. -Ramucirumab (Cyramza), an angiogenesis inhibitor, binds to the receptor for vascular endothelial growth factor (VEGF), a compound that stimulates blood vessel growth. Thus it prevents VEGF from binding to the receptor and signaling the body to make more blood vessels. This can help slow or stop the growth and spread of cancer. Ramucirumab treats advanced cancers that start at the gastroesophageal junction. Prognosis: -Esophageal cancer is not common. However, the rates are increasing. In the United States, around 17,280 new cases are diagnosed and 15,850 deaths occur from esophageal cancer each year. The overall 5-year survival rate is 19%. Common Nursing Care: -Ask the patient about a history of GERD, hiatal hernia, achalasia, BE, and tobacco and alcohol use. Assess the patient for progressive dysphagia and odynophagia (burning, squeezing pain while swallowing). Ask about the type of substances (e.g., meats, soft foods, liquids) that cause dysphagia. Assess the patient for pain (substernal, epigastric, or back areas), choking, heartburn, hoarseness, cough, anorexia, weight loss, and regurgitation. Health Promotion: -Counsel the patient with GERD, BE, or hiatal hernia about the importance of regular follow-up evaluation. Health counseling should focus on smoking cessation and reducing risk factors for GERD. Maintaining good oral hygiene and dietary habits (e.g., intake of fresh fruits and vegetables) is important. Encourage patients to seek medical attention for any esophageal problems, especially dysphagia. Preoperative care: -The patient and caregiver usually react with shock, disbelief, and depression when given the diagnosis of esophageal cancer. Provide emotional and physical support, provide information, clarify test results, and maintain a positive attitude with respect to the patient's immediate recovery and long-term survival. -In addition to general preoperative teaching and preparation, pay attention to the patient's nutritional needs. Many are poorly nourished because of the inability to ingest adequate amounts of food and fluids. A high-calorie, high-protein diet is recom- mended. Some patients need a liquid form of this diet. Others may need IV fluid replacement or parenteral nutrition (PN). Teach the patient and caregiver how to keep an intake and output record and assess for signs of fluid and electrolyte imbalance. Some treatment protocols include preoperative radiation and chemotherapy. -Meticulous oral care is essential. Cleanse the mouth thoroughly, including the tongue, gingivae, and teeth or dentures. It may be necessary to use swabs or a gauze pad and to scrub the mouth, including the tongue. Milk of Magnesia with mineral oil helps remove crust formation. -Teaching should include information about chest tubes (with a planned open thoracic approach), IV lines, NG tubes, pain management, gastrostomy or jejunostomy feeding, turning, coughing, and deep breathing. Postoperative Care: -During the immediate postoperative period, the patient usually receives care in the ICU for 1 to 2 days. In addition to usual postoperative complications, dysrhythmias may result from the proximity of the pericardium to the surgical site. Other complications include anastomotic leaks, fistula formation, interstitial pulmonary edema, and acute respiratory distress related to the disruption of the mediastinal lymph nodes. -The patient usually has an NG tube in place for 5 to 7 days. The drainage may be bloody for 8 to 12 hours. The drainage gradually changes to greenish yellow. Assessing the drainage, maintaining the tube, and providing oral and nasal care are key nursing responsibilities. Do not irrigate the NG tube, reposition it, or reinsert it without consulting the HCP. -If the chest cavity is entered, postoperative drainage is achieved with chest tube insertion. Assess the amount and type of drainage. Notify the HCP of excess drainage (e.g., over 400 to 600 mL in 8 hours). -Because of the location of the surgery and the patient' general condition, implement measures to prevent respiratory complications. Have the patient turn, cough and deep breathe, and use an incentive spirometer every 2 hours. Follow VTE prophylaxis measures and provide effective pain management. Position the patient in a semi-Fowler's or Fowler's position to prevent reflux and aspiration of gastric secretions. When the patient can drink fluids or eat, maintain the upright position for at least 2 hours after eating to assist with gastric emptying.

Acute Hepatitis

-Many patients with acute hepatitis have no symptoms and may not even know they have been infected. However, others may have intermittent or ongoing anorexia, lethargy, nausea, vomiting, skin rashes, diarrhea or constipation, malaise, fatigue, myalgias, arthralgias, other flu-like symptoms, and right upper quadrant tenderness (caused by liver inflammation). -Although the acute phase of viral hepatitis varies depending on the type of hepatitis, it usually lasts from 1 to 6 months. During this time, the patient may have a decreased sense of smell and find food repugnant. Smokers may have distaste for cigarettes. Physical examination often reveals hepatomegaly, lymphadenopathy, abdominal tenderness, and sometimes splenomegaly. The acute phase is the period of maximal infectivity. -A patient in the acute phase of hepatitis may be icteric (jaundiced) or anicteric. Jaundice, a yellowish discoloration of body tissues, results from a change in normal bilirubin metabolism or disruption of the flow of bile into the hepatic or biliary duct systems. The urine may appear darker due to excess bilirubin being excreted by the kidneys. If conjugated bilirubin cannot pass into the intestines from the liver because of obstruction or inflammation of the bile ducts, the stools will be clay colored. -Pruritus (intense generalized itching) sometimes accompanies jaundice. It occurs from the accumulation of bile salts beneath the skin. Itching can be intolerable to the patient. -As jaundice fades, the convalescent phase begins. The convalescent phase can last for weeks to months, with an average of 2 to 4 months. During this period, patients typically have malaise and easy fatigability. Hepatomegaly remains for several weeks. Splenomegaly (if present) subsides during this period. -Most patients with acute viral hepatitis recover completely. Almost all cases of acute hepatitis A resolve. However, some patients may have a relapse in the first 2 to 3 months after the infection. The disappearance of jaundice does not mean the patient has totally recovered. Some HBV infections and most HCV infections result in chronic hepatitis. -The overall mortality rate for acute hepatitis is less than 1%. The mortality rate is higher in older adults and those with underlying debilitating illnesses (including chronic liver disease). -Complications that can result from acute hepatitis are acute liver failure, chronic hepatitis, cirrhosis of the liver, portal hypertension, and liver cancer. Acute Liver Failure: -Sometimes, acute liver failure (fulminant hepatic failure) may occur, which is a serious condition with a poor prognosis. Manifestations include encephalopathy, GI bleeding, disseminated intravascular coagulation (DIC), fever with leukocytosis, renal manifestations (oliguria, azotemia), ascites, edema, hypotension, respiratory failure, hypoglycemia, bacterial infections, thrombocytopenia, and coagulopathies. Liver transplantation is usually the cure for these patients. - 1 to 6 months. Highest infectivity. Hepatocytes can regenerate. Anorexia. Distaste for food. Fatigue. Hepatomegaly. Jaundice: itchy, dark urine, clay stools. RUQ tenderness. Weight loss.

GI cancers

Includes: -Oral carcinoma. -Esophageal carcinoma. -Stomach cancer.

PT

Normal Range: - 11 to 16 seconds. -Time prolonged with disease.

Oral carcinoma

Risk Factors: -Poor oral hygiene. -Tobacco usage (pipe and cigar smoking, snuff, chewing tobacco). -Sun exposure. -Chronic alcohol intake. -Chronic irritation (jagged tooth, ill-fitting prosthesis, chemical or mechanical irritants). -HPV. Symptoms: -Indurated, painless ulcer. -Leukoplakia. -Erythroplakia. -Ulcerations. -Sore spot. -Rough area. -Pain. -Dysphagia. -A lump or thickening in the cheek. -A sore throat or a feeling that something is stuck. -Difficulty chewing and speaking (later signs). -Limited tongue movement. -Increased salivation. -Slurred speech. -Toothache. -Earache. Assessment Findings: -Incidence and mortality rates are higher in black men than in whites. -Death rates from oral cancer are decreasing in whites and increasing in nonwhites. Diagnosis: -Diagnostic tests are done to identify oral dysplasia, which is a precursor to oral cancer. Oral exfoliative cytologic study involves scraping the suspicious lesion and spreading the scraping on a slide for microscopic examination. The toluidine blue test is a screening test for oral cancer. When toluidine blue is applied topically to stain an area, cancer cells preferentially take up the dye. A negative cytologic smear or negative toluidine blue test does not necessarily rule out cancer. Once cancer is diagnosed, CT scan, MRI, and positron emission tomography (PET) are used for staging cancer. Treatment: -Surgical excision, radiation. -Surgery (mandibulectomy, radical neck dissection, resection of buccal mucosa), internal and external radiation. -Surgery (hemiglossectomy or glossectomy), radiation. Prognosis: -Oral cancer is more common after age 35. The average age at diagnosis is 65 years. It is 2 times more common in men than in women. The 5-year survival rate is 84% for localized cancer and 65% for all stages of oral cavity and pharynx cancer combined. Lip cancer has the most favorable prognosis of any of the oral tumors. The visibility of lip lesions usually leads to an earlier diagnosis. Common Nursing Care: -Many patients are malnourished before surgery. They may need placement of a percutaneous endoscopic gastrostomy (PEG) and enteral nutrition (EN) before radiation treatment or surgery. After radical neck surgery, the patient may be unable to ingest nutrients orally because of mucositis, swelling, location of sutures, or difficulty swallowing. PN is given for the first 24 to 48 hours. After that time, EN is given via NG, gastrostomy, or jejunostomy tube. Cervical esophagostomy and pharyngostomy are options for some patients. -Assess for feeding tolerance and adjust the amount, time, and formula if nausea, vomiting, diarrhea, or distention occurs. Give small amounts of water when the patient can swallow. Observe for choking. Suctioning may be needed to prevent aspiration. -You play a key role in the early detection and treatment of oral cancer. Identify patients at risk and provide information about predisposing factors. Review information about smoking cessation with the patient who smokes. Warn adolescents and teenagers about the danger of using snuff or chewing tobacco and electronic cigarettes. -Because early detection of oral cancer is important, teach the patient to report unexplained pain or soreness of the mouth, unusual bleeding, dysphagia, sore throat, voice changes, or swelling or lump in the neck. Refer any person with an ulcerative lesion that does not heal within 2 to 3 weeks to the HCP. -Preoperative care for the patient who will have a radical neck dissection must consider the patient's physical and psychosocial needs. Physical preparation is the same as that for any major surgery, with special emphasis on oral hygiene. Explanations and emotional support should include information on postoperative communication and feeding. Explain the surgical procedure and ensure that the patient understands the information.

Gastric outlet obstruction: (Complication of PUD)

Gastric Outlet Obstruction: -Both acute and chronic PUD can cause gastric outlet obstruction. Obstruction in the distal stomach and duodenum is the result of edema, inflammation, pylorospasm, or fibrous scar tissue formation. With obstruction the patient reports discomfort or pain that is worse toward the end of the day as the stomach fills and dilates. Belching or self-induced vomiting may provide some relief. Vomiting is common and often projectile. The vomitus may contain food particles that were ingested hours or days before. Constipation occurs because of dehydration and decreased diet intake from anorexia. Over time dilation of the stomach and visible swelling in the upper abdomen may occur. -The aim of therapy for obstruction is to decompress the stomach, correct any existing fluid and electrolyte imbalances, and improve the patient's general state of health. An NG tube is used as described previously. With continuous decompression for several days, the ulcer can begin healing and the inflammation and edema will subside. Pain relief results from the decompression. -IV fluids and electrolytes are replaced according to the degree of dehydration, vomiting, and electrolyte imbalance shown by laboratory studies. A PPI or H2 receptor blocker is used if the obstruction is due to an active ulcer. Balloon dilation can open a pyloric obstruction. Surgery may be needed to remove scar tissue. Care: -Gastric outlet obstruction can happen at any time. It is most likely to occur in the patient whose ulcer is close to the pylorus. The onset of symptoms is usually gradual. Constant NG aspiration of stomach contents can help relieve symptoms. This allows edema and inflammation to subside and permits normal flow of gastric contents through the pylorus. -Regularly irrigate the NG tube with a normal saline solution per agency policy to assist proper functioning. It may be helpful to reposition the patient from side to side so that the tube tip is not constantly lying against the mucosal surface. Maintain accurate intake and output records, especially of the gastric aspirate. -To check for ongoing obstruction, clamp the NG tube intermittently and measure the gastric residual volume. The frequency and amount of time the tube is clamped are related to the amount of aspirate obtained and the patient's comfort level. A common method is to clamp the tube overnight (usually 8 to 12 hours) and measure the gastric residual volume in the morning. When the aspirate falls below 200 mL, it is within a normal range and the patient can begin oral intake of clear liquids. Oral fluids begin at 30 mL/hr and then gradually increase in amount. As the amount of gastric residual decreases, solid foods are added, and the tube removed. -If the patient has resumed oral feedings and you note symptoms of obstruction, promptly inform the HCP. Generally, all that is needed to treat the problem is to resume gastric aspiration so that the edema and inflammation resulting from the acute episode resolve. IV fluids with electrolyte replacement keep the patient hydrated during this period. If conservative treatment is not successful, surgery is done after the acute phase has passed.

Stomach cancer

Risk Factors: -Probably begins with a nonspecific mucosal injury because of infection (H. pylori), autoimmune-related inflammation, repeated exposure to irritants such as bile or NSAIDs, and tobacco use. -Has been associated with diets high in smoked foods, salted fish and meat, and pickled vegetables. -Infection with H. pylori, especially at an early age, is a risk factor for stomach cancer. -People with lymphoma of the stomach (mucosa-associated lymphoid tissue [MALT]) are at higher risk of stomach cancer. -Other predisposing factors include atrophic gastritis, pernicious anemia, adenomatous polyps, hyperplastic polyps, and achlorhydria (absent or low production of gastric HCl). -Smoking and obesity both increase the risk for stomach cancer. Symptoms: -Stomach cancers often spread to adjacent organs before any distressing symptoms occur. Manifestations include unexplained weight loss, indigestion, abdominal discomfort or pain, and signs and symptoms of anemia. The patient may report early satiety, or a sense of being full sooner than usual. Anemia is common. It is caused by chronic blood loss as the lesion erodes through the mucosa or from pernicious anemia (caused by loss of intrinsic factor). The person appears pale and weak. They may report fatigue, weakness, dizziness, and, in extreme cases, shortness of breath. The stool may be positive for occult blood. Supraclavicular lymph nodes that are hard and enlarged suggest metastasis via the thoracic duct. The presence of ascites is a poor prognostic sign. Assessment Findings: -Asian Americans and Pacific Islanders, Hispanics, and blacks have higher rates of stomach cancer than non-Hispanic whites. -Asian Americans have higher survival rates than other ethnic groups. Diagnosis: -Upper GI endoscopy is the best diagnostic tool. The stomach can be distended with air during the procedure, stretching the mucosal folds. Tissue biopsy and histologic examination are important in diagnosing stomach cancer. -Endoscopic ultrasound, CT, MRI, and PET scanning can be used to stage the disease. Laparoscopy is done to determine peritoneal spread. -Blood studies detect anemia and determine its severity. Increased liver enzymes and serum amylase levels may mean liver and pancreatic involvement. Stool examination provides evidence of occult or gross bleeding. The presence of tumor markers can help diagnose cancer. Treatment: -The treatment of choice for stomach cancer is surgical removal of the tumor. Preoperative management focuses on correcting nutritional deficits and treating anemia. Transfusions of packed RBCs correct the anemia. If gastric outlet obstruction occurs, gastric decompression may be needed before surgery. Surgical Therapy: -The surgical aim is to remove as much of the stomach as required to remove the tumor and a margin of normal tissue. The location and extent of the lesion, the patient's physical condition, and the HCP's preference determine the specific surgery used (e.g., open versus laparoscopic). -Lesions in the antrum or pyloric region are generally treated by either a Billroth I or II procedure. When the lesion is in the fundus, a total gastrectomy with esophagojejunostomy is done. When metastasis has occurred to adjacent organs, such as the spleen, ovaries, or bowel, the surgical procedure is extended as needed. If the tumor extends into the transverse colon, partial colon resection is done. Chemotherapy and Radiation Therapy: -A number of chemotherapy drugs can be used to treat stomach cancer. These include fluorouracil, capecitabine (Xeloda), carboplatin, cisplatin, docetaxel (Taxotere), epirubicin (Ellence), irinotecan (Camptosar), oxaliplatin (Eloxatin), and paclitaxel. Combination therapies are preferred as the drugs affect different phases of the cell cycle. Examples of combination therapy include ECF (epirubicin, cisplatin, fluorouracil) and docetaxel, irinotecan, oxaliplatin, or cisplatin with fluorouracil or capecitabine. Intraperitoneal administration of chemotherapy agents may also be used to treat metastatic disease. -Radiation therapy may be used together with chemotherapy to reduce the recurrence or as a palliative measure to decrease tumor mass and provide temporary relief of obstruction. Targeted Therapy: -Trastuzumab (Herceptin) and ramucirumab (Cyramza) are targeted therapies used to treat stomach cancer. About 20% of patients with stomach cancer have too much HER-2 on the surface of the cancer cells. Trastuzumab targets the HER-2 protein and kills the cancer cells. Ramucirumab binds to the receptor for VEGF and prevents VEGF from binding to the receptor, thus preventing the growth and spread of cancer. Prognosis: -Stomach (gastric) cancer is an adenocarcinoma of the stomach wall. It accounts for more than 26,240 new cancer cases and 10,800 deaths annually. The rate of stomach (particularly distal) cancer has been steadily declining in the United States. However, cancer in the proximal gastric and gastroesophageal junction is increasing. -In the United States the incidence is higher in men than in women by a 2:1 ratio. Stomach cancer mostly affects older people. The average age of people at the time of diagnosis is 68. -At the time of diagnosis, only 10% to 20% of patients have disease confined to the stomach. The 5-year survival rate in this group is 71%. However, more than 50% have advanced metastatic disease. The overall 5-year survival rate of all people with stomach cancer is about 31%. Common Nursing Care: -The assessment of a person with stomach cancer is similar to that for PUD. Important data to obtain from the patient and caregiver include a nutritional assessment, a psychosocial history, the patient's perceptions of the health problem and need for care, and a physical examination. -The nutritional assessment obtains information about appetite and changes in eating patterns over the previous 6 months. Determine the patient's normal weight and any recent weight changes. Unexplained weight loss and anorexia are common. Evaluate the patient's nutritional status. Cachexia may be present if oral intake has been reduced for an extended period. A malnourished patient does not respond well to chemotherapy or radiation therapy and is a poor surgical risk. The patient may report a history of vague abdominal symptoms, including dyspepsia and intestinal gas discomfort or pain. If the patient reports pain, explore where and when it occurs and how it is relieved. -Determine the patient's personal perception of the health problem and method of coping with hospitalization, diagnostic tests, and procedures. A possible diagnosis of cancer and a treatment plan that may include surgery, chemotherapy, or radiation treatment is stressful. If surgery is planned, assess the patient's expectations about surgery (cure or palliation) and how the patient has responded to previous surgical procedures. Health Promotion: -Your role in the early detection of stomach cancer focuses on identifying the patient at risk because of specific disorders such as H. pylori infection, pernicious anemia, and achlorhydria. Be aware of symptoms associated with stomach cancer and the significant findings on physical examination. Symptoms often occur late and mimic other conditions, such as PUD. Poor appetite, weight loss, fatigue, and persistent stomach distress are symptoms of stomach cancer. Encourage patients with a positive family history of stomach cancer to undergo diagnostic evaluation if anemia, PUD, or vague epigastric distress are present. It is important that you recognize the possibility of stomach cancer in a patient who is treated for PUD and does not get relief with prescribed therapy. Acute Care: -When diagnostic tests confirm cancer, the patient and family generally react with shock, disbelief, and depression. Provide emotional and physical support, provide information, clarify test results, and maintain a positive attitude with respect to the patient's immediate recovery and long-term survival. -Because of changes in appetite and early satiety, the patient may be malnourished. Surgery may be delayed until the patient is more physically able to withstand it. A positive nutritional state enhances wound healing and the ability to deal with infection and other possible postoperative complications. The patient may better tolerate several small meals a day than 3 regular meals. It may be challenging to persuade the patient to eat when he or she has no appetite and is depressed. Getting the patient's caregiver to help with meals and encourage intake may be beneficial. Diet may be supplemented by commercial liquid supplements and vitamins. If the patient is unable to ingest oral feedings, the HCP may prescribe EN or PN. -If needed, packed RBCs and fluid volume restoration may be given during the preoperative period. The preoperative teaching plan and the postoperative care of the patient having stomach cancer surgery is described in the next section on gastric surgery. -Radiation therapy or chemotherapy is used as an adjuvant to surgery or for palliation. Your role is to provide detailed instructions, reassure the patient, and ensure completion of the designated number of treatments. Start by assessing the patient's knowledge of these therapies. Teach the patient about skin care, need for nutrition and fluid intake, and the use of antiemetic drugs. Ambulatory Care: -When chemotherapy or radiation treatment is continuing after discharge, a referral to home health care may be beneficial. The home health nurse can help with recovery, determine the degree of patient adherence, and provide support to the patient and caregiver. Provide the patient with a list of community agencies (e.g., American Cancer Society) that are available before the patient goes home. Encourage the patient to adhere to the prescribed therapies, keep appointments for chemotherapy administration or radiation treatments, and keep the HCP informed of changes in physical condition. Recurrence of cancer is common, and patients need regular follow-up examinations and imaging assessments.

Causes of cirrhosis

-Any chronic liver disease, including disease from excess alcohol use and NAFLD, can cause cirrhosis. The most common causes of cirrhosis in the United States are chronic hepatitis C infection and alcohol-induced liver disease. In patients with alcohol-induced liver disease, controversy exists as to the degree to which malnutrition adds to the damage caused by the alcohol itself. Some cases of nutrition-related cirrhosis have resulted from extreme dieting, malabsorption, and obesity. Environmental factors and genetic predisposition may lead to the development of cirrhosis, regardless of dietary or alcohol intake. -Around 20% of patients with chronic hepatitis C and 25% of those with chronic hepatitis B develop cirrhosis. Chronic inflammation and cell necrosis from viral hepatitis can result in progressive fibrosis and cirrhosis. Chronic hepatitis combined with alcohol use has a synergistic effect in accelerating liver damage. -Biliary causes of cirrhosis include primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC). -Cardiac cirrhosis includes a spectrum of hepatic problems that result from long-standing, severe, right-sided heart failure. It causes hepatic venous congestion, parenchymal damage, necrosis of liver cells, and fibrosis over time. Treatment is aimed at managing the patient's underlying heart failure.

Sengastaken-Blakemore Tube

-Balloon tamponade is an option when endoscopy does not control acute esophageal or gastric variceal hemorrhage. Balloon tamponade controls the hemorrhage by mechanical compression of the varices. Several types of tubes are available. The Sengstaken-Blakemore tube has 2 balloons, gastric and esophageal, with 3 lumens: 1 for the gastric balloon, 1 for the esophageal balloon, and 1 for gastric aspiration. Two other types of balloons are the Minnesota tube (a modified Sengstaken- Blakemore tube with an esophageal suction port above the esophageal balloon) and the Linton-Nachlas tube. Safety Alert: -Label each lumen to avoid confusion. -Secure the tube to prevent movement of the tube that could result in occlusion of the airway. -Deflate balloons for 5 minutes every 8 to 12 hours per agency policy to prevent tissue necrosis.

Chronic Hepatitis

-Chronic HBV is more likely to develop in infants born to infected mothers and in those who acquire the infection before age 5 than in those who acquire the virus after age 5. -Problems with the patient's cellular immune response may be important in the development of the chronic HBsAg carrier state and the progression of acute HBV to chronic HBV. More than 50% of immunocompromised adults who are acutely infected with HBV progress to chronic infection. -HCV infection is more likely than HBV to become chronic. As previously mentioned, many patients with chronic HCV infection develop chronic liver disease, cirrhosis, portal hypertension, and liver cancer. Risk factors for progression to cirrhosis include male gender, alcohol use, concomitant fatty liver disease, and excess iron deposition in the liver. In some patients, co-infection with HIV may cause complications or require treatment modification. Manifestations of chronic hepatitis include anemia and coagulation problems (easy bruising, bleeding). Since the liver produces clotting factors, clotting and bleeding times can be impaired or prolonged. -Skin manifestations may include spider angiomas, palmar erythema, and gynecomastia. Some patients have spleen, liver, or cervical lymph node enlargement. -In patients with severe liver damage, hepatic encephalopathy is a potentially life-threatening spectrum of neurologic, psychiatric, and motor disturbances. Hepatic encephalopathy results from the liver's inability to remove toxins (especially ammonia) from the blood. -Ascites, a common manifestation of hepatitis (especially chronic hepatitis), is the accumulation of excess fluid in the peritoneal cavity. Fluid accumulates due to reduced protein levels in the blood, which reduces the plasma oncotic pressure. - 6 months or longer. Hepatocytes repeatedly destroyed. Fibrosis (scar tissue) develops. Acute liver failure, transplant only cure. Cirrhosis, Portal HTN, Liver cancer. Coagulation problems. Hep C more chronic than Hep B.

Cirrhosis

-Cirrhosis is the end stage of liver disease. Cirrhosis is characterized by extensive degeneration and destruction of the liver cells. This results in the replacement of liver tissue by fibrosis (scar tissue) and regenerative nodules that occur from the liver's attempt to repair itself. The development of cirrhosis usually happens after decades of chronic liver disease. -In cirrhosis, the liver cells try to regenerate, but the regenerative process is disorganized. This results in abnormal blood vessel and bile duct architecture. The overgrowth of new and fibrous connective tissue distorts the liver's normal lobular structure, resulting in lobules of irregular size and shape with impeded blood flow. Eventually, irregular and disorganized liver regeneration, poor cellular nutrition, and hypoxia (from inadequate blood flow and scar tissue) result in decreased liver function.

Inspection of the abdomen

-First part of the abdomen assessment. -Assess the abdomen for skin changes (color, texture, scars, striae, dilated veins, rashes, lesions), umbilicus (location and contour), symmetry, contour (flat, rounded [convex], concave, protuberant, distended), observable hernias or masses, and movement (pulsations, peristalsis). A normal aortic pulsation may be seen in the epigastric area. Look across the abdomen tangentially (across the abdomen in a line) for peristalsis. Peristalsis is not normally visible in an adult but may be visible in a thin person.

Palpation of the abdomen

-Fourth part of the abdomen assessment. -Use palpation to assess the abdominal organs and detect any tenderness, distention, masses, or fluid. Palpation is important because it may reveal a tumor. Begin with light palpation. Palpate any areas in which the patient reports tenderness last. -Use light palpation to detect tenderness or cutaneous hypersensitivity, muscular resistance, masses, and swelling. Help the patient relax for deeper palpation. Keep your fingers together and press gently with the pads of the fingertips, depressing the abdominal wall about 0.4 in (1 cm). Use smooth movements and palpate all quadrants. -Use deep palpation to delineate abdominal organs and masses. Use the palmar surfaces of your fingers to press more deeply. Again, palpate all quadrants and note the location, size, and shape of masses, as well as the presence of tenderness. During these maneuvers, observe the patient's facial expression because it will provide nonverbal cues of discomfort or pain. -An alternative method for deep abdominal palpation is the two-hand method. Place 1 hand on top of the other and apply pressure to the bottom hand with the fingers of the top hand. With the fingers of the bottom hand, feel for organs and masses. Practice both methods of palpation to determine which is most effective. -Check a problem area on the abdomen for rebound tenderness by pressing in slowly and firmly over the painful site. Withdraw the palpating fingers quickly. Pain on withdrawal of the fingers indicates peritoneal inflammation. Because assessing for rebound tenderness may produce pain and severe muscle spasm, it should be done at the end of the examination and only by an experienced practitioner. -To palpate the liver, place your left hand behind the patient to support the right eleventh and twelfth ribs. The patient may relax on your hand. Press the left hand forward and place the right hand on the patient's right abdomen lateral to the rectus muscle. The fingertips should be below the lower border of liver dullness and pointed toward the right costal margin. Gently press in and up. The patient should take a deep breath with the abdomen so that the liver drops and is in a better position for palpation. Try to feel the liver edge as it comes down to the fingertips. During inspiration, the liver edge should feel firm, sharp, and smooth. Describe the surface and contour and any tenderness. If the patient has chronic obstructive pulmonary disease, large lungs, or a low diaphragm, the liver may be palpated 0.4 to 0.8 in (1 to 2 cm) below the right costal margin. -To palpate the spleen, move to the patient's left side. Place your right hand under the patient, and support and press the patient's left lower rib cage forward. Place your left hand below the left costal margin and press it in toward the spleen. Ask the patient to breathe deeply. The fingertips can feel the tip or edge of an enlarged spleen. The spleen is normally not palpable. If it is palpable, do not continue because manual compression of an enlarged spleen may cause it to rupture.

Bleeding varices

-If the patient has esophageal or gastric varices, observe for any signs of bleeding from the varices, such as hematemesis and melena. If hematemesis occurs, assess the patient for hemorrhage, call the HCP, and be ready to transfer the patient to the endoscopy suite and/or assist with equipment to control the bleeding. Maintain the patient's airway. Patients with bleeding varices are usually admitted to the intensive care unit (ICU). -Balloon tamponade is an option for patients who have bleeding that is unresponsive to band ligation or sclerotherapy. When balloon tamponade is used, explain to the patient and caregiver the use of the tube and how the balloon is inserted. Check the balloons for patency. It is usually the HCP's responsibility to insert the tube by either the nose or mouth. Then the gastric balloon is inflated with 250 mL of air, and the tube is retracted until resistance (lower esophageal sphincter) is felt. The tube is secured by placing a piece of sponge or foam rubber at the nostrils (nasal cuff). For continued bleeding, the esophageal balloon is then inflated. A sphygmomanometer is used to measure and maintain the desired pressure at 20 to 40 mm Hg. An x-ray verifies the balloon's position. -Nursing care includes monitoring for complications of rupture or erosion of the esophagus, regurgitation and aspiration of gastric contents, and occlusion of the airway by the balloon. If the gastric balloon breaks or is deflated, the esophageal balloon will slip upward, obstructing the airway and causing asphyxiation. If this happens, cut the tube or deflate the esophageal balloon. Keep scissors at the bedside. Minimize regurgitation by oral and pharyngeal suctioning and by keeping the patient in a semi-Fowler's position. -The patient is unable to swallow saliva because the inflated esophageal balloon occludes the esophagus. Encourage the patient to expectorate and provide an emesis basin and tissues. Frequent oral and nasal care offers relief from the taste of blood and irritation from mouth breathing.

Prevention of cirrhosis

-No known prevention unless alcohol is a contributing factor, then treatment for alcoholism may be necessary

Non-alcoholic fatty liver disease

-Nonalcoholic fatty liver disease (NAFLD) refers to a wide spectrum of liver diseases ranging from a fatty liver (steatosis) to nonalcoholic steatohepatitis (NASH) to cirrhosis. The term nonalcoholic is used because NAFLD and NASH occur in people who do not consume excess amounts of alcohol. -The fundamental characteristic of NAFLD is the accumulation of fatty infiltration in the hepatocytes. In NASH, the fat accumulation is associated with varying degrees of inflammation and fibrosis of the liver. If NASH is untreated, it can become a serious liver disease leading to cirrhosis, liver cancer, and liver failure. -Currently, NAFLD is increasing because of the growing number of people who are obese. NAFLD occurs in 90% to 95% of severely obese children and adults. NASH occurs in 8% to 20% of obese persons with NAFLD. NAFLD should be considered in patients with risk factors, including obesity, diabetes, hyperlipidemia, and hypertension (also known as metabolic syndrome). -Elevated liver function tests (ALT, AST) are often the first sign of NAFLD. Ultrasound and CT scans can be used to diagnose NAFLD. Definitive diagnosis is by a liver biopsy. -There is no currently approved medication for NAFLD. The goal of therapy is weight loss of at least 10% of body weight, if overweight or obese and exercise. Reducing risk factors, including hyperlipidemia, hypertension, and diabetes, is important.

Early signs of cirrhosis

-Patients may be unaware of their liver condition because there are few symptoms in early-stage disease. If a person does have symptoms, these may include fatigue or an enlarged liver. Blood tests may show normal liver function (compensated cirrhosis). The diagnosis of cirrhosis is often made later when a patient presents with symptoms of more advanced liver disease.

Drugs for GI diseases

-Proton Pump Inhibitors (PPIs). -Histamine (H2) Receptor Blockers. -Antacids. -Cholinergic. -Cytoprotective. -Prokinetic. -Prostaglandin (Synthetic).

Auscultation of the abdomen

-Second part of the abdominal assessment. -When you examine the abdomen, auscultate before percussion and palpation because these latter procedures may alter the bowel sounds. Use the diaphragm of the stethoscope to auscultate bowel sounds because they are relatively high pitched. Use the bell of the stethoscope to detect lower pitched sounds. Warm the stethoscope in your hands before auscultating to help prevent abdominal muscle contraction. Listen in the epigastrium and in all 4 quadrants. Start in the right lower quadrant because bowel sounds are normally present there. Listen for bowel sounds for at least 2 minutes. Do not count bowel sounds. Determine if they are normal, hypoactive, or hyperactive. -The frequency and intensity of bowel sounds vary depending on the phase of digestion. Normal sounds are relatively high pitched and gurgling. Stomach growling or loud gurgles (borborygmi) indicate hyperperistalsis. The bowel sounds are high pitched (rushes and tinkling) when the intestines are under tension, as in intestinal obstruction. Listen for decreased or absent bowel sounds. A perfectly "silent abdomen" is uncommon. If you are patient and listen for several minutes, you will often find the bowel sounds are not absent but are hypoactive. If you do not hear bowel sounds, note the amount of time you listened in each quadrant without hearing bowel sounds. -Listen for vascular sounds. A bruit, best heard with the bell of the stethoscope, is a swishing or buzzing sound and indicates turbulent blood flow. Normally you should not hear aortic bruits.

Post-op pancreatectomy metabolic changes

-Surgery is the most effective treatment for pancreatic cancer. Only 15% to 20% of patients have resectable tumors at the time of diagnosis. With the use of neoadjuvant chemotherapy (treatment before surgery), more patients can eventually become surgical candidates. The type of surgery depends on the size and location of the tumor. Pancreatic head tumors require the classic Whipple procedure or pancreaticoduodenectomy. In the Whipple surgery, the proximal pancreas (proximal pancreatectomy), along with duodenum (duodenectomy), distal segment of the common bile duct and distal part of the stomach (partial gastrectomy) are removed together followed by a surgical anastomosis of the pancreatic duct, common bile duct, and stomach to the jejunum. Pancreatic body and/or tail tumors require a distal pancreatectomy procedure. Sometimes, a total pancreatectomy is done. It causes diabetes and the patient is dependent on exogenous insulin and pancreatic enzyme supplementation for life. If the pancreatic tumor cannot be removed surgically, palliative measures, such as a cholecystojejunostomy, to relieve biliary obstruction and/or endoscopically placed biliary stents, can be done.

Complications of peptic ulcer disease (PUD)

-The 3 major complications of chronic PUD are hemorrhage, perforation, and gastric outlet obstruction. All these compli- cations are considered emergency situations and may need surgical intervention. Includes: -Hemorrhage. -Perforation. -Gastric Outlet Obstruction. Gastric surgeries: -Gastric surgeries are done to treat stomach cancer, as well as polyps, perforation, chronic gastritis, and PUD. Surgeries include partial gastrectomy, gastrectomy, vagotomy, and pyloroplasty. Partial gastrectomy with removal of the distal two thirds of the stomach and anastomosis of the gastric stump to the duodenum is a gastroduodenostomy or Billroth I operation. If the gastric stump is anastomosed to the jejunum, the surgery is a gastrojejunostomy or Billroth II operation. A total gastrectomy involves resection of the lower esophagus, removal of the entire stomach, and anastomosis of the esophagus to the jejunum. -Vagotomy is the severing of the vagus nerve, either totally (truncal) or selectively (highly selective vagotomy). These procedures decrease gastric acid secretion. Pyloroplasty consists of surgical enlargement of the pyloric sphincter to facilitate the easy passage of contents from the stomach. It is often done after vagotomy or to enlarge an opening that is constricted from scar tissue.

Treatment for cirrhosis

-The goal of treatment is to slow the progression of cirrhosis and to prevent and treat any complications. Conservative Therapy: -Rest. -B-complex vitamins. -Avoiding alcohol. -Minimizing or avoiding aspirin, acetaminophen, and NSAIDs. Ascites: -Management of ascites focuses on sodium restriction, diuretics, and fluid removal. Patients may need to limit sodium intake to 2 g/day. Very low sodium intake can result in reduced nutritional intake and malnutrition. The patient is usually not on restricted fluids unless severe ascites develops. When caring for patients with ascites, accurately monitor fluid and electrolyte balance. An albumin infusion may help maintain intravascular volume and adequate urine output by increasing plasma colloid oncotic pressure. -Diuretic therapy is an important part of management. Often a combination of drugs that work at multiple sites of the nephron is more effective than a single agent. Spironolactone (Aldactone) is an effective diuretic, even in patients with severe ascites. Spironolactone is also an antagonist of aldosterone and is potassium sparing. Other potassium-sparing diuretics include amiloride (Midamor) and triamterene (Dyrenium). A high-potency loop diuretic (e.g., furosemide [Lasix]), is often used in combination with a potassium-sparing drug. -Tolvaptan (Samsca), a vasopressin-receptor antagonist, can correct hyponatremia, a common problem in patients with cirrhosis. It causes an increase in water excretion, resulting in an increase in serum sodium concentration. -A paracentesis is a sterile procedure in which a catheter is used to withdraw fluid from the abdominal cavity. This procedure can diagnose a medical condition or relieve pain, pressure, or difficulty breathing. In the patient with cirrhosis, this procedure is done for the person with impaired respiration or abdominal discomfort caused by severe ascites who does not respond to diuretic therapy. It is only a temporary measure of palliation because the fluid tends to reaccumulate rapidly. -TIPS is used to treat ascites that does not respond to diuretics. A peritoneovenous shunt is a surgical procedure that provides continuous reinfusion of ascitic fluid into the venous system. It is rarely used due to the high rate of complications. Esophageal and Gastric Varices: -The main therapeutic goal for esophageal and gastric varices is to prevent bleeding and variceal rupture by reducing portal pressure. The patient who has esophageal and/or gastric varices should avoid alcohol, aspirin, and nonsteroidal antiinflammatory drugs (NSAIDs). -All patients with cirrhosis should have an upper endoscopy (esophagogastroduodenoscopy [EGD]) to screen for varices. Patients with varices at risk for bleeding are often started on a nonselective beta-blocker (nadolol [Corgard] or propranolol [Inderal]) to reduce the risk of hemorrhage. beta-Blockers decrease high portal pressure, which decreases the risk for rupture. -When variceal bleeding occurs, the first step is to stabilize the patient and manage the airway. IV therapy is started and may include giving blood products. Care then moves toward stopping the bleeding, identifying the source, and applying interventions to prevent further bleeding. Management that involves a combination of drug therapy and endoscopic therapy is more successful than either approach alone. -Drug therapy for bleeding varices may include the somatostatin analog octreotide (Sandostatin) or vasopressin. Both produce vasoconstriction of the splanchnic arterial bed, decrease portal blood flow, and decrease portal hypertension. Currently, octreotide is used more often because it has fewer side effects than vasopressin. -At the time of endoscopy, band ligation or sclerotherapy of varices may be used to prevent rebleeding. Endoscopic variceal ligation (EVL, or "banding") is done by placing a small rubber band (elastic O-ring) around the base of the varix (enlarged vein). Sclerotherapy involves injecting a sclerosing solution into the swollen veins through a needle placed through the endoscope. -Balloon tamponade is an option when endoscopy does not control acute esophageal or gastric variceal hemorrhage. Balloon tamponade controls the hemorrhage by mechanical compression of the varices. Several types of tubes are available. The Sengstaken-Blakemore tube has 2 balloons, gastric and esophageal, with 3 lumens: 1 for the gastric balloon, 1 for the esophageal balloon, and 1 for gastric aspiration. Two other types of balloons are the Minnesota tube (a modified Sengstaken- Blakemore tube with an esophageal suction port above the esophageal balloon) and the Linton-Nachlas tube. -Supportive measures during an acute variceal bleed include giving fresh frozen plasma and packed RBCs, vitamin K, and proton pump inhibitors (PPIs; e.g., pantoprazole). Lactulose and rifaximin (Xifaxan) may be given to prevent hepatic encephalopathy from breakdown of blood and the release of ammonia in the intestine. Antibiotics are given to prevent bacterial infection. -Because of the high incidence of recurrent bleeding with each bleeding episode, continued therapy is necessary. Long- term management of patients who have had an episode of bleeding includes nonselective beta-blockers, repeated band ligation of the varices, and portosystemic shunts in patients who develop recurrent bleeding. Shunting Procedures: -Nonsurgical and surgical methods of shunting blood away from the varices are available. Shunting procedures tend to be done more after a second major bleeding episode than during an initial bleeding episode. Transjugular intrahepatic portosystemic shunt (TIPS) is a nonsurgical procedure in which a tract (shunt) between the systemic and portal venous systems is created to redirect portal blood flow. A catheter is placed in the jugular vein and then threaded through the superior and inferior vena cava to the hepatic vein. The wall of the hepatic vein is punctured, and the catheter is directed to the portal vein. Stents are positioned along the passageway, overlapping in the liver tissue and extending into both veins. -This procedure reduces portal venous pressure and decompresses the varices, thus controlling bleeding. TIPS does not interfere with a future liver transplantation. Limitations of TIPS include the increased risk for hepatic encephalopathy (toxin-containing blood bypasses the liver) and stenosis of the stent. TIPS is contraindicated in patients with severe hepatic encephalopathy, liver cancer, severe hepatorenal syndrome, and portal vein thrombosis. -Various surgical shunting procedures can decrease portal hypertension by diverting some of the portal blood flow while allowing adequate liver perfusion. Currently, the surgical shunts most often used are the portacaval shunt and the distal splenorenal shunt. Hepatic Encephalopathy: -The goal of management of hepatic encephalopathy is to reduce ammonia formation. Lactulose, a drug that traps ammonia in the gut, reduces ammonia formation in the intestines. We can give it orally, as an enema, or through a nasogastric (NG) tube. The drug's laxative effect expels the ammonia from the colon. Antibiotics, such as rifaximin, also may be given, especially in patients who do not respond to lactulose. Regular and frequent bowel movements are necessary to minimize the ammonia buildup, so use measures to prevent constipation. -Control of hepatic encephalopathy also involves treatment of precipitating causes. This includes lowering dietary protein intake, preventing and controlling GI bleeds, and, in the case of a bleed, removing the blood promptly from the GI tract to decrease the protein accumulation in the gut. Drug Therapy: -There is no specific drug therapy for cirrhosis. However, several drugs are used to treat symptoms and complications of advanced liver disease. Nutritional Therapy: -The diet for the patient who has cirrhosis without complications is high in calories (3000 cal/day). It is high in carbohydrate content with moderate to low levels of fat. Protein restriction may be needed for some patients right after a severe flare of symptoms (i.e., episodic hepatic encephalopathy). However, protein restriction is rarely needed in patients with cirrhosis and persistent hepatic encephalopathy. For many, malnutrition is a more serious clinical problem than hepatic encephalopathy. -A patient with alcoholic cirrhosis often has protein-calorie malnutrition. Oral nutritional supplements containing protein from branched-chain amino acids that are metabolized by the muscles may be needed. These supplements provide protein that the liver can more easily metabolize. Parenteral nutrition or EN are used with severe cases of malnutrition. -The patient with ascites and edema is placed on a low-sodium diet. The degree of sodium restriction depends on the patient's condition. Teach the patient and caregiver about the degree of restriction. Table salt is a well-known source of sodium. Other foods high in sodium include canned soups and vegetables, many frozen foods, salted snacks (e.g., potato chips), nuts, smoked meats and fish, crackers, breads, baking soda, olives, pickles, ketchup, and beer. Teach the patient to read labels for sodium content. Offer suggestions about how to make the diet more palatable. Seasonings, like garlic, parsley, onion, lemon juice, and spices may make food more appetizing. Collaborate with a dietitian about dietary strategies.

Transhepatic Biliary Catheter (T-tube)

-The transhepatic biliary catheter can be used preoperatively in biliary obstruction and in hepatic dysfunction from obstructive jaundice. It also can be inserted for palliative care when inoperable liver, pancreatic, or bile duct cancer obstructs bile flow. The catheter is used when endoscopic drainage has been unsuccessful. The catheter is inserted percutaneously and allows for decompression of obstructed extrahepatic bile ducts so that bile can flow freely. After placement of the catheter into the obstructed duct internally, the external catheter is connected to a drainage bag. Encourage patients to replace fluids lost in the drainage bag with electrolyte-rich drinks. Cleanse the skin around the catheter insertion site daily with an antiseptic. Observe for bile leakage at the insertion site and any signs or symptoms of sudden abdominal pain, nausea, fever, or chills that may signal an occluded or malfunctioning drain. -If the patient has a T tube, maintain the system and monitor T-tube function and drainage. The T tube is usually connected to a closed gravity drainage system. If the Penrose or Jackson-Pratt drain or the T tube is draining large amounts of bile, it is helpful to use a sterile pouching system to protect the skin. Encourage the patient to replace any lost fluids and electrolytes.

Percussion of the abdomen

-Third part of the abdomen assessment. -The purpose of percussing the abdomen is to estimate the size of the liver and determine the presence of fluid, distention, and masses. Sound waves vary according to the density of underlying tissues. Air produces a higher pitched, hollow sound termed tympany. Fluid or masses produce a short, high-pitched sound with little resonance termed dullness. Lightly percuss all 4 quadrants of the abdomen and assess the distribution of tympany and dullness. Tympany is the predominant percussion sound of the abdomen. -To percuss the liver, start below the umbilicus in the right midclavicular line and percuss lightly upward until you hear dullness. This is the lower border of the liver. Next, start at the nipple line in the right midclavicular line and percuss downward between ribs to the area of dullness indicating the upper border of the liver. Measure the height or vertical space between the 2 borders to determine the size of the liver. The normal range of liver height in the right midclavicular line is 2.4 to 5 in (6 to 12.7 cm). -Technique for percussion of the abdomen. Moving clockwise, percuss lightly in all 4 quadrants.

Pain management with pancreatitis

-Treatment and control of pain are very important. IV opioid analgesics may be given. Pain medications may be combined with an antispasmodic agent. Atropine and other anticholinergic drugs are avoided when paralytic ileus is present because they can decrease GI mobility, making the problem worse. Other drugs that relax smooth muscles (spasmolytics), such as nitroglycerin or papaverine, may be used.

Cholecystitis

Cholecystitis: -Inflammation of the gallbladder wall, usually due to stones. Scar tissue can form with each attack, impairs function. Manifestations: -Acute pain, mod to severe. RUQ tenderness. May radiate to right shoulder or scapula. Indigestion, N/V. Diaphoresis. Chronic: fat intolerance, dyspepsia, heartburn, flatulence.

Chronic Gastritis

Causes: Drugs: -Aspirin. -Bisphosphonates. -Corticosteroids. -Digitalis. -Iron supplements. -Nonsteroidal antiinflammatory drugs (NSAIDs). Diet: -Alcohol. -Large amounts of spicy, irritating foods. Microorganisms: -H. pylori. -Cytomegalovirus. -Mycobacterium species. -Salmonella organisms. -Staphylococcus organisms. -Treponema pallidum (syphilis). Environmental Factors: -Radiation. -Smoking. Diseases/Disorders: -Burns. -Crohn's disease. -Large hiatal hernia. -Physiologic stress. -Reflux of bile and pancreatic secretions. -Renal failure. -Sepsis. -Shock. Other Factors -Endoscopy procedures. -Nasogastric tube. -Psychologic stress. Key Assessment Questions: -How long have you had abdominal pain? -Do you smoke or drink? -What have you eaten in the past 24 hours? -Past medical history? -Current list of medications? Treatment: -The treatment of chronic gastritis focuses on evaluating and eliminating the specific cause (e.g., cessation of alcohol use, abstinence from drugs, H. pylori eradication). Antibiotic combinations are used to eradicate H. pylori. The patient with pernicious anemia needs lifelong cobalamin therapy. -The patient undergoing treatment for chronic gastritis may have to adapt to lifestyle changes and strictly adhere to a drug regimen. Some patients find a non-irritating diet consisting of 6 small feedings a day helpful. Smoking is contraindicated in all forms of gastritis. An interprofessional team approach in which the HCP, nurse, dietitian, and pharmacist provide consistent information and support will increase the patient's success in making these changes.

Cholelithiasis

Cholecystitis: -Inflammation of the gallbladder wall, usually due to stones. Scar tissue can form with each attack, impairs function. Manifestations: -Biliary Colic" stones move, cause spasms. Steady pain, may progress to severe. Severe pain for 1 hour, RUQ tenderness persists. Pain may occur 3 to 6 hours after high-fat meal or when laying down. Pain can occur after a fatty meal.

Important teaching points for a client with GERD

Common Symptoms: -Pyrosis, (heartburn). -Dyspepsia. -Regurgitation. Food that can Aggravate GERD: -ETOH. -Chocolate (theobromine). -Fatty foods. -Nicotine. -Peppermint/spearmint. -Caffeine (coffee/tea). Meds that can Aggravate GERD: -Beta adrenergic blockers. -Calcium channel blockers. -Anticholinergics. -Diazepam (Valium). -Morphine sulfate. -Nitrates. -Theophylline. -Progesterone. -NSAIDs. Include the following instructions when teaching the patient and caregiver about managing GERD: 1.) Explain the reason for a low-fat diet. 2.) Have the patient to eat small, frequent meals to prevent gastric distention. 3.) Explain the reason for avoiding alcohol, smoking (causes an almost immediate, marked decrease in lower esophageal sphincter pressure), and beverages that contain caffeine. 4.) Tell the patient to not lie down for 2 to 3 hours after eating, wear tight clothing around the waist, or bend over (especially after eating). 5.) Have the patient avoid eating within 3 hours of bedtime. 6.)Have the patient to sleep with head of bed elevated on 4 to 6 inch blocks (gravity fosters esophageal emptying). 7.) Provide information about drugs, including reason for their use and common side effects. 8.) Discuss strategies for weight reduction if appropriate. 9.) Encourage patient and caregiver to share concerns about lifestyle changes and living with a chronic problem.

Hiatal hernia

Diagnosis: -Hiatal hernia is herniation of part of the stomach into the esophagus through an opening, or hiatus, in the diaphragm. We also call it a diaphragmatic hernia or esophageal hernia. Hiatal hernias are the most common abnormality found on x-ray examination of the upper GI tract. They are common in older adults and occur more often in women. There are 2 types of hiatal hernias: 1.) Sliding. 2.) Paraesophageal or rolling. Sliding: -The junction of the stomach and esophagus is above the diaphragm, and a part of the stomach slides through the hiatal opening in the diaphragm. This occurs when the patient is supine. The hernia usually goes back into the abdominal cavity when the patient is standing upright. This is the most common type. Paraesophageal or rolling: -The fundus and greater curvature of the stomach roll up through the diaphragm, forming a pocket alongside the esophagus. The esophagogastric junction stays in the normal position. Acute paraesophageal hernia is a medical emergency. Diagnostic Studies: -An esophagram (barium swallow) may show the protrusion of gastric mucosa through the esophageal hiatus. Endoscopic visualization of the lower esophagus gives information on the degree of mucosal inflammation or other abnormalities. Surgical treatment: -Surgical approaches to hiatal hernias can include reduction of the herniated stomach into the abdomen, herniotomy (excision of the hernia sac), herniorrhaphy (closure of the hiatal defect), fundoplication, and gastropexy (attachment of the stomach below the diaphragm to prevent reherniation). The goals are to reduce the hernia, provide an acceptable LES pressure, and prevent movement of the gastroesophageal junction. -Surgery to repair hiatal hernia is often done laparoscopically by either Nissen or Toupet techniques. The approach used (thoracic or abdominal) depends on the patient. Client education: -Teach the patient to reduce intraabdominal pressure by eliminating constricting garments and avoiding lifting and straining.

Cholinergic

Examples: -bethanechol (Urecholine). Mechanism of Action: -Increases lower esophageal sphincter pressure, improve esophageal emptying, increase gastric emptying.

Histamine (H2) Receptor Blockers

Examples: -cimetidine. -famotidine (Pepcid). -nizatidine (Axid). -ranitidine (Zantac). Mechanism of Action: -Blocks the action of histamine on the H2 receptors to decrease HCl acid secretion. -Decreases the conversion of pepsinogen to pepsin. -Decreases irritation of the esophageal and gastric mucosa.

Proton Pump Inhibitors (PPIs)

Examples: -dexlansoprazole (Dexilant). -esomeprazole (Nexium). -lansoprazole (Prevacid). -omeprazole (Prilosec). -omeprazole and sodium bicarbonate (Zegerid). -pantoprazole (Protonix). -rabeprazole (Aciphex). Mechanism of Action: -Decreases acid secretion by inhibiting the proton pump (H+-K+-ATPase) responsible for the secretion of H+. -Decreases irritation of the esophageal and gastric mucosa.

Prokinetic

Examples: -metoclopramide (Reglan). Mechanism of Action: -Block effect of dopamine. -Increases gastric motility and emptying. -Reduce reflux

Prostaglandin (Synthetic)

Examples: -misoprostol (Cytotec). Mechanism of Action: -Protects lining of stomach. -Increases production of gastric mucus and mucosal secretion of bicarbonate. -Decreases HCl acid secretion.

Cytoprotective

Examples: -sucralfate (Carafate). Mechanism of Action: -Act to form a protective layer and serve as a barrier against acid, bile salts, and enzymes in the stomach.

Antacids, Acid Neutralizers

Examples: Single Substance: -aluminum hydroxide (Amphojel). -calcium carbonate (Tums). -sodium bicarbonate (Alka-Seltzer). -sodium citrate (Bicitra). Aluminum and Magnesium: -Gelusil, Maalox, Mylanta aluminum/magnesium. -trisilicate (Gaviscon). Mechanism of Action: -Neutralize HCl acid. -Taken 1 to 3 hours after meals and at bedtime.

PUD teaching

Include the following instructions when teaching the patient and caregiver about management of PUD: 1.) Avoiding foods that cause epigastric distress, such as acidic foods. 2.) Avoid cigarettes. Smoking promoting ulcer development and delays ulcer healing. 3.) Reduce or eliminate alcohol use. 4.) Avoid OTC drugs unless approved by the HCP. Many preparations contain ingredients, such as aspirin, that should not be taken unless approved by the HCP. Check with the HCP about the use of NSAIDs. 5.) Do not interchange brands of PPIs, antacids, or H2 receptor blockers that you can buy OTC without checking with the HCP. This can lead to harmful side effects. 6.) Take all medications as prescribed. This includes both antisecretory and antibiotic drugs. Not taking medications as prescribed can cause a relapse. 7.) It is important to report any of the following: -Increased nausea or vomiting. -Increased epigastric pain. -Bloody emesis or tarry stools. 8.) Stress can be related to signs and symptoms of PUD. Learn and use stress management strategies. 9.) Share concerns about lifestyle changes and living with a chronic illness.

Chronic hepatitis symptoms

Includes: -ALT, AST elevations (may be normal in some people). -Ascites and lower extremity edema. -Asterixis ("liver flap"). -Bleeding abnormalities (thrombocytopenia, easy bruising, prolonged clotting time). -Fatigue, malaise. -Hepatic encephalopathy: confusion, difficulty concentrating, easy agitation. -Hepatomegaly. -Increased bilirubin. -Jaundice. -Myalgias and/or arthralgias. -Palmar erythema. -Spider angiomas.

Acute hepatitis symptoms

Includes: -Anorexia. -Clay-colored stools. -Dark urine. -Decreased sense of taste and smell. -Diarrhea or constipation. -Fatigue, lethargy, malaise. -Flu-like symptoms (e.g., headache). -Hepatomegaly. -Jaundice. -Low-grade fever. -Lymphadenopathy. -Myalgias and/or arthralgias. -Nausea, vomiting. -Pruritus. -Right upper quadrant tenderness. -Splenomegaly. -Weight loss.

Common diagnostic tests for GI function

Includes: -Endoscopy. -Upper gastrointestinal series. -Lower gastrointestinal series. -Abdominal ultrasound. -ERCP. -Liver biopsy.

Causes of liver disease

Includes: -Excessive alcohol use. -Hepatitis. -Chemical hepatotoxicity. -Drug-induced liver injury. Excessive alcohol use: -Alcohol use is the most frequent cause of both acute and chronic liver disease. It can cause injury and necrosis of liver tissue. Alcohol use can cause a spectrum of manifestations, ranging from mild elevation in liver enzymes to acute alcoholic hepatitis. It may also cause advanced fibrosis and cirrhosis, which usually occurs after decades of excess alcohol use. Patients may have serious liver disease caused by another chronic disease (e.g., chronic HCV infection) in combination with alcoholic liver disease, which can compound the problem. -Acute alcoholic hepatitis is a syndrome of hepatomegaly, jaundice, elevated liver enzymes (AST, ALT, alkaline phosphate), and low-grade fever with possible ascites and prolonged PT time. These manifestations may improve if alcohol intake ceases. -Even at the end-stage of cirrhosis, abstinence can result in significant reversal in some patients. If liver function does not recover after abstaining from alcohol for 6 months or longer, liver transplantation may be considered. Chemical hepatotoxicity: -Is liver injury caused by exposure to certain compounds (e.g., carbon tetrachloride, gold compounds). Some agents can cause hepatotoxicity, while others may induce cholestasis, necrosis, or liver cancer. Fortunately, because of the decreased use of these agents, the incidence of chemically induced liver toxicity has decreased since the 1980s. Drug-induced liver injury: -(DILI) can present similarly to other forms of liver disease. The main cause of DILI is antimicrobial agents, especially amoxicillin-clavulanate. Many drugs (prescription, OTC, diet and herbal supplements) can cause an increase in liver enzymes and, in severe cases, jaundice and acute liver failure. The pattern of injury depends on the drug causing the reaction. The most common cause of acute liver failure is acetaminophen. In patients with chemical hepatotoxicity or DILI, all drugs identified as the cause of liver injury should be stopped.

Hepatitis types

Includes: -Hepatitis A Virus (HAV). -Hepatitis B Virus (HBV). -Hepatitis C Virus (HCV). -Hepatitis D Virus (HDV). -Hepatitis E Virus (HEV).

Bold labs for liver, biliary and pancreatic function

Includes: -Total Bilirubin. -PT. -PTT. -Ammonia. -Serum Cholesterol. -Alkaline phosphate (ALP). -Aspartate aminotransferase (AST). -Alanine aminotransferase (ALT). -Serum lipase. -Serum amylase.

Duodenal ulcers

Lesion: -Penetrating (associated with deformity of duodenal bulb from healing of recurrent ulcers). Location of Lesion: -First 1 to 2 cm of duodenum. Gastric Secretion: -Normal to increase. Incidence: -Greater in men, but increasing in women (especially postmenopausal). -Peak age 35 to 45 years. -No increase in cancer risk. -H. pylori infection in 90%. -Associated with other diseases (e.g., COPD, pancreatic disease, hyperparathyroidism, ZES, chronic renal failure). Clinical Manifestations: -Burning, cramping, pressure-like pain across midepigastrium and upper abdomen. Back pain with posterior ulcers -Pain 2 to 5 hours after meals and mid-morning, mid-afternoon, middle of night. Periodic and episodic. Pain relief with antacids and food Recurrence Rate: -High.

Ammonia

Normal Range: - 15 to 45 ug/dL. -Increases with disease.

PTT

Normal Range: - 25 to 35 seconds. -Time prolonged with disease.

Serum amylase

Normal Range: - 30 to 122 u/L. -Increases with disease.

Serum lipase

Normal Range: - 31 to 186 u/L. -Increases with disease.

Alkaline phosphate (ALP)

Normal Range: - 38 to 126 u/L. -Increases with liver disease.

Serum Cholesterol

Normal Range: -Less than 200 mg/dL. -Increases with biliary obstruction. -Decreases with malnutrition and liver disease.

Open cholecystectomy

Open cholecystectomy: -TCDB (turn, cough, deep breathe). -May place T tube in common bile duct. -Maintain patency. -Some patients may need an incisional (open) cholecystectomy. This involves removing the gallbladder through a right subcostal incision. A T tube may be inserted into the common bile duct during surgery when a common bile duct exploration is part of the surgical procedure. This ensures patency of the duct until the edema from the trauma of exploring and probing the duct has subsided. It also allows excess bile to drain while the small intestine is adjusting to receiving a continuous flow of bile. -After an incisional cholecystectomy, the patient will progress from liquids to a regular diet once bowel sounds have returned. -Postoperative nursing care for incisional cholecystectomy focuses on adequate ventilation and prevention of respiratory complications. Other nursing care is the same as general postoperative nursing care. -After an incisional cholecystectomy, tell the patient to avoid heavy lifting for 4 to 6 weeks. Usual sexual activities, including intercourse, can be resumed as soon as the patient feels ready, unless otherwise instructed by the HCP.

Gallbladder Disease

Risk Factors for GB Disease: -Sedentary lifestyle, obesity, estrogen therapy, women older than 40. Common postpartum complication. Multiparous (several children) "FFF". Obesity causes bile to contain more cholesterol. Signs and Symptoms of Bile Obstruction: -Jaundice, dark amber urine, clay colored stools, pruritus, intolerance to fatty foods, bleeding tendencies, steatorrhea (fatty stools). Fever, chills. Amber urine. Steatorrhea. Complications: -Gangrene, ruptured gallbladder, pancreatitis, biliary cirrhosis.

Upper gastrointestinal series: barium swallow

Purpose: -Fluoroscopic x-ray study using contrast medium. Used to diagnose structural abnormalities of esophagus, stomach, and duodenum. Nursing Responsibilities: Before: -Explain procedure, including the need to drink contrast medium and assume various positions on x-ray table. Keep patient NPO for at least 8 hours. Tell patient to avoid smoking after midnight. After: -Take measures to prevent contrast medium impaction (fluids, laxatives). Tell patient that stool may be white for up to 72 hours.

Abdominal ultrasound

Purposes: -A conductive gel is applied to skin, and a transducer is placed on the area. Detects abdominal masses (tumors, cysts), gallstones, biliary and liver disease. Nursing Responsibilities: Before: -Teach patient to be NPO for 8 to 12 hours. Air or gas can reduce quality of images. Food intake can cause gallbladder contraction, resulting in suboptimal study.

ERCP

Purposes: -Fiberoptic endoscope (using fluoroscopy) is orally inserted into descending duodenum. Then common bile and pancreatic ducts are cannulated. Contrast medium is injected into ducts to allow for direct visualization of structures. Can be used to retrieve a gallstone from distal common bile duct, dilate strictures, biopsy, and diagnose pseudocysts. Nursing Responsibilities: Before: -Explain procedure. Keep patient NPO 8 hours before. Ensure consent form is signed. Give sedation immediately before and during procedure. Give antibiotics if ordered. After: Check vital signs. Assess for perforation or infection. Pancreatitis is most common complication. Check for return of gag reflex.

Lower gastrointestinal series: barium enema

Purposes: -Fluoroscopic x-ray examination of colon using contrast medium, which is given rectally (enema). Double-contrast or air-contrast barium enema is test of choice. Air is infused after the barium flows through transverse colon. Used to detect the presence of tumors, diverticula, and polyps. Nursing Responsibilities: Before: -Give laxatives and enemas until colon is clear of stool evening before procedure. Follow clear liquid diet evening before procedure. Keep patient NPO for 8 hours before test. Teach patient about the barium enema. Explain that cramping and urge to defecate may occur during procedure and patient may be placed in various positions on tilt table. After: -Give fluids, laxatives, or suppositories to help in expelling barium. Observe stool for passage of contrast medium. Tell patient that stool may be white for up to 72 hours.

Endoscopy

Purposes: -Patient swallows a vitamin-sized capsule with camera, which provides endoscopic visualization of GI tract. Camera takes >50,000 images during test, relaying them to monitoring device that patient wears on a belt. Images then downloaded to computer. Used to look at areas of GI tract not accessible by upper and lower endoscopy. Nursing Responsibilities: Before: -Keep patient NPO for 8 hours. May have bowel preparation similar to colonoscopy. After swallowing capsule, clear liquids resumed in 2 hours and food in 4 hours. After: - 8 hours after swallowing device, patient returns to have monitoring device removed. Tell patient that capsule is disposable and will be present in a bowel movement.

Liver biopsy

Purposes: -The purpose of a liver biopsy is to obtain hepatic tissue to use to establish a diagnosis of cancer or assess and stage fibrosis. It may be done to follow the progress of liver disease, such as chronic hepatitis. Nursing Responsibilities: -Monitor VS. -Monitor for signs of bleeding. -Ask about a history of a bleeding disorder. -Monitor LFTs.

Hepatitis A Virus (HAV)

Symptoms: -Can cause a mild flu-like illness and jaundice. In more severe cases, it can cause acute liver failure. Common Modes of Transmission: -Fecal-oral (primarily fecal contamination and oral ingestion). Risk Factors: -Contaminated food, milk, water, shellfish. -Crowded conditions (e.g., day care, nursing home). -Persons with subclinical infections, infected food handlers, sexual contact, IV drug users. -Poor personal hygiene. -Poor sanitation. Patient teaching: -HAV vaccination and thorough hand washing are the best measures to prevent outbreaks. -If chronic you cannot donate blood. -Screening.

Hepatitis E Virus (HEV)

Symptoms: -Can cause acute and chronic hepatitis symptoms. Common Modes of Transmission: -Fecal-oral route. -Outbreaks associated with contaminated water supply in developing countries. Risk Factors: -Contaminated water, poor sanitation -Found in Asia, Africa, and Mexico. -Not common in United States but is increasing in some areas. Patient teaching: -Safe water initiatives in endemic regions. -Practice good hygiene. -Screening.

Hepatitis D Virus (HDV)

Symptoms: -Can cause acute and chronic hepatitis symptoms. Common Modes of Transmission: -HBV must precede HDV. -Chronic carriers of HBV always at risk. -Blood/body fluids. Risk Factors: -Contaminated needles, syringes, and blood products. -HBV-infected mother (perinatal transmission). -Sexual activity with infected partners. Asymptomatic carriers. -Tattoos or body piercing with contaminated needles. Patient teaching: -Get HBV vaccine to help prevent HDV. -Can cause infection only when HBV is present.

Hepatitis B Virus (HBV)

Symptoms: -In those who develop chronic HBV infections, the liver may range from a normal-appearing liver to severe liver inflammation and scarring (fibrosis). Around 25% of those who become chronically HBV-infected in childhood die from complications of chronic liver disease, including liver cancer. -Can cause acute and chronic hepatitis symptoms. Common Modes of Transmission: -Percutaneous (parenteral) or mucosal exposure to blood or blood products. -Sexual contact. -Perinatal transmission. -Blood/body fluids. Risk Factors: -Contaminated needles, syringes, and blood products. -HBV-infected mother (perinatal transmission). -Sexual activity with infected partners. Asymptomatic carriers. -Tattoos or body piercing with contaminated needles. Patient teaching: -Vaccine. -Screening. -Safe sex. -Handwashing. -Needle exchange.

Hepatitis C Virus (HCV)

Symptoms: -Most common cause of liver disease and liver failure. -Can cause acute and chronic hepatitis symptoms. Common Modes of Transmission: -Percutaneous (parenteral) or mucosal exposure to blood or blood products. -High-risk sexual contact. -Perinatal contact. -Blood/body fluids. Risk Factors: -Blood and blood products. -Needles and syringes. -Sexual activity with infected partners, low risk. Patient teaching: -No vaccine available. -Safe sex. -Handwashing. -Needle exchange. -If chronic you cannot donate blood. -Screening