NCSBN – Lesson 8D: Gastrointestinal System Study Guide,100% CORRECT

NCSBN – Lesson 8D: Gastrointestinal System Study Guide Confusion and irritability are signs of renal encephalopathy secondary to elevated levels of BUN and creatinine in the blood. The other options do not explain the client's behavior. Potassium levels are generally high in renal failure. Side effects of calcium depletion manifest as abdominal and muscle cramping and hyperactive reflexes. Metabolic acidosis, not alkalosis, is seen in renal failure. Eating before sleeping enhances regurgitation of stomach contents, which have increased acidity, into the esophagus. An upright posture should be maintained for about two hours after eating to allow for stomach emptying. Thickening agents and sitting upright for an hour after eating are interventions for clients with swallowing difficulties. Common dietary modifications in GERD include decreasing total fat intake; avoiding large meals, chocolate, caffeine or known irritants; a soft diet is not necessary. Expected findings in the client with inflammatory bowel disease include persistent diarrhea, abdominal pain and tenderness and even visible blood and mucus in the stools. Abdominal distention, along with chills and fever, can indicate possible intestinal obstruction (toxic megacolon) or fistula formation. Liver disease interferes with the production of prothrombin and other factors essential for blood clotting. In addition, hemorrhage, especially from esophageal varices, can be life-threatening. This takes priority over the other nursing diagnosis. Cloudy drainage is a sign of infection that may indicate peritonitis (inflammation of the peritoneum), a serious complication of peritoneal dialysis. Muscle weakness, slight pink-tinged drainage, and abdominal discomfort are expected during or after the procedure of catheter placement or peritoneal dialysis. Disorders of the Stomach During the cephalic phase of digestion, the stomach secretes hydrochloric acid and pepsin to help break down food. The primary purpose of the stomach is to hold food, mix food with gastric juices via peristaltic contractions and empty chyme into the small intestines. Gastric reflux and peptic ulcer disease are common disorders of the stomach. Pernicious anemia is also categorized in this section because of the role the parietal cells play. Pernicious Anemia – Disorders of the Stomach Pernicious anemia is a deficiency in the production of RBC through a lack of vitamin B12. • Etiology o Pernicious anemia is thought to possibly be an autoimmune disease. It is seen in clients following a gastric resection. ▪ Large RBC – macrocytic normochromic or large immature cells with normal hemoglobin (Hgb) concentrations ▪ Parietal cells of the stomach fail to excrete intrinsic factor, which is necessary for the absorption of vitamin B12 ▪ Hydrochloric acid secretion is also reduced, which also prevents adequate absorption of vitamin B12 • Assessment Findings o Anemia – findings depend on severity o Tissue hypoxia producing fatigue, weakness, dyspnea, pallor and palpitations o GI symptoms – sore tongue (beefy red), anorexia, N&V, diarrhea and abdominal pain o Neurological symptoms – paresthesia in hands and feet, weakness, impaired coordination and balance, and changes in the LOC • Diagnostic Studies o Complete blood count with differential o Bone-marrow biopsy (to differentiate the type of anemia) o Lack of free hydrochloric acid in stomach (nasogastric/endoscopic analysis) o Schilling test (a multi-step test to measure the absorption of vitamin B12 and/or intrinsic factor) • Management o Lifelong vitamin B12 therapy injected intramuscularly. o Initially needed weekly and then moved to monthly (if related to lack of intrinsic factor/absorption issue). o Adequate nutrition with dietary sources of vitamin B12 will need to be followed. Blood transfusions may also be needed in extreme cases. • Nursing Interventions o Monitor for impaired gas exchange o Manage fatigue o Decrease and monitor the risk of injury related to impaired level of consciousness and coordination o Educate clients and support their understanding of self-care needs due to their chronic illness ▪ Need for lifelong B12 replacement ▪ Helping clients cope with needed accommodations that impact their activities of daily living (ADL) Peptic Ulcer Disease (PUD) – Disorders of the Stomach Gastroscope (endoscope) view of a gastric ulcer (white, upper right) on the lining of the stomach. Gastric ulcers are an ulceration of the mucous membrane of the esophagus, stomach or duodenum, due to action of the gastric acid juice. • Etiology & Pathophysiology o The Helicobacter pylori (H. pylori) overgrowth is the cause of gastric ulcers. ▪ Risk factors include aspirin, NSAIDs, steroids, caffeine, alcohol intake, stress and family history. o These ulcers are a result of excess production of HCl acid and unusually rapid gastric emptying. Risk factors include a family history and increased stress. o Pathophysiology includes: ▪ The ulcer is located 0.5-2 cm below the pylorus ▪ Arteriosclerotic changes in adjacent blood vessels ▪ Vagus nerve stimulation causes tissues to release gastrin, which increases secretion of hydrochloric acid • Assessment Findings o Pain, burning or gas, worse with food o Pain in left upper epigastric area (located near xiphoid process o Nausea/vomiting (coffee ground emesis) o Bleeding and hematemesis o Pain and heartburn occur during night or when the stomach is empty. ▪ Pain is often relieved by eating. o Clients will report melena (tarry stool). o Complications of PUD include: ▪ Hemorrhage ▪ Perforation and peritonitis – results in severe abdominal pain and "board-like" abdomen ▪ Paralytic ileus (obstruction) – scarring may cause an obstruction • Diagnostics Studies o Endoscopy is an excellent visual way to see a PUD. In addition, stool for occult blood will be evaluated, as well as a complete blood count. • Management o NPO (nothing by mouth) if client has complications o Nasogastric tube (severe cases) o Pharmacologic Intervention: o Anti-infectives: clarithromycin; metronidazole o H2 receptor antagonists: cimetidine; ranitidine hydrochloride; famotidine; nizatidine ▪ Be aware that cimetidine can cause delirium in the elderly and increases the bioavailability of many drugs including beta blockers, morphine and famotidine. o Anticholinergics: dicyclomine hydrochloride o Antacids: aluminum hydroxide; aluminum-magnesium combinations; calcium carbonate o Cytoprotective: sucralfate o Proton pump inhibitors: omeprazole, lansoprazole o Prokinetics: metoclopramide • Managing Complications of PUD: o Administer intra-arterial vasopressin, IV fluids and blood replacement for hemorrhage o Surgical Intervention: ▪ Vagotomy – eliminates the stimulation of gastric cells ▪ Pyloroplasty – widening pylorus to improve gastric emptying ▪ Subtotal gastrectomy ▪ Billroth I (gastroduodenostomy) ▪ Billroth II (gastrojejunostomy) ▪ Total gastrectomy • Complementary & Integrative Health o Herbal remedies or dietary supplements such as licorice root, cat's claw or goldenseal have been used. Very little research has been done to support their use. o Mind and body practices such as acupuncture, therapeutic massage, guided imagery, progressive relaxation, meditation, yoga and aromatherapy can help with stress reduction. Figure 8-D.1 To help remember treatment for PUD, remember this phrase: "Please Make Tummy Better" • Nursing Interventions o Pain relief o Assess for bleeding o Assess for post-operative complications, e.g., infection, bleeding and respiratory complications o Observe drainage for signs of bleeding o Discuss lifestyle changes including stopping smoking and decreasing stress o Teaching – medications and diet o Maintain patency of nasogastric (NG) tube o Mouth care Gastroesophageal Reflux Disease (GERD) – Disorders of the Stomach GERD is a condition in which the gastric contents leak backwards from the stomach into the esophagus. • Etiology & Pathophysiology o When muscle fibers (called the lower esophageal sphincter or LES) don't close well, gastric contents leak back into the esophagus (reflux). Reflux causes symptoms and can damage the esophagus. Risk factors include hiatal hernia, obesity, pregnancy, smoking and scleroderma. • Assessment Findings o The client will complain of heartburn or burning pain in the chest, increased by bending, stooping, lying down or eating. ▪ This is usually relieved by antacids. o Nausea is common after eating. o Pediatric clients may present with vomiting or spitting up with meals, failure to thrive, irritability and pallor or cyanosis. • Diagnostics Studies o History and physical o Barium swallow o Esophagogastroduodenoscopy (EGD) o Esophageal pH o Esophageal manometry studies o Scintigraphy – assess gastric emptying • Management o Depends on severity of findings o More frequent feedings with frequent burping o Eat smaller meals and decrease caffeine intake, avoid acidic foods o Do not lie down two hours after eating and sleep with head of bed elevated o Stop smoking o Surgery (Nissen fundoplication) may be necessary o Pharmacologic Intervention: ▪ H2-receptor antagonists, including cimetidine or famotidine ▪ Proton pump inhibitors, including esomeprazole or pantoprazole ▪ Over-the-counter antacids • Nursing Interventions o The nurse will monitor nutritional status and electrolyte levels. Teaching points will include diet and medication. Disorders of the Intestines Nearly all digestion takes place in the small intestines. Once chyme passes through the small intestine, it enters the colon where absorption takes place. This section reviews common disorders that can occur within the small and/or large intestines. Ulcerative Colitis (UC) – Disorders of the Intestines Ulcerative colitis (UC) is an inflammatory bowel disease that causes swelling, ulcerations and loss of function of the large intestine. • Etiology o The etiology of UC is unknown. There is a peak incidence between age 15-35 years and a secondary peak between age 50-70 years. o Ulceration and inflammation of the entire length of the colon involves the mucosa and submucosa. UC begins in rectum and extends to the distal colon and extends proximally. The abscesses and ulcers lead to bleeding and diarrhea. o Scarring produces narrowing, thickening and shortening of the colon. The client will experience remissions and exacerbations. • Assessment Findings o Bloody diarrhea ▪ Mild • <4 stools/daily, with or without blood, no systemic signs of toxicity and normal ESR ▪ Moderate • >4 stools/daily, minimal signs of toxicity ▪ Severe • >6 stools/daily, toxicity (fever, tachycardia, anemia, elevated ESR) ▪ Fulminant • >10stools/daily, continuous bleeding, fever, abdominal tenderness/distension, need for blood transfusion, colon dilation o Stools may also contain pus and mucus o Left-sided abdominal pain (tenderness and cramping) o Fever, weight loss, anemia, tachycardia and dehydration o Impaired absorption of fat-soluble vitamins such as E and K o Systemic manifestations: ▪ Skin lesions – erythema nodosum ▪ Joint inflammation ▪ Inflammation of the eyes – uveitis ▪ Liver disease • Diagnostics Studies o A complete blood count (CBC), a stool for occult blood and a stool culture to rule out infectious process will be completed. o A sigmoidoscopy or a colonoscopy may also be performed. • Management o Rest o Fluid, electrolyte and blood replacement o Pharmacologic Intervention: ▪ Steroids as antiinflammatory drugs: prednisone; hydrocortisone ▪ Immunosuppressives: azathioprine; 6-mercaptopurine(6-MP); methotrexate; cyclosporine ▪ Monoclonal antibodies: infliximab ▪ Anti-infectives: sulfasalazine primary drug of choice ▪ Metronidazole for secondary infections ▪ Anticholinergics: dicyclomine ▪ Antidiarrheals: Loperamide; diphenoxylate o Dietary restrictions – a high-calorie and high-protein diet with low roughage and no milk products o Surgical management: ▪ Total proctocolectomy and ileostomy ▪ Ileorectal anastomosis ▪ Total proctocolectomy with continent ileostomy (Kock pouch) ▪ Total colectomy with ileal pouch (reservoir) • Complications o Complications from UC include increased risk of colon cancer, fluid and electrolyte imbalances, toxic megacolon, perforation and bleeding, and hemorrhage. o Loss of form to the haustra (bubbly shape of colon) • Nursing Interventions o Manage pain o Manage diarrhea o Maintain optimum fluid and nutritional intake o Enhance coping o Enhance knowledge of disease process and management o Reduce anxiety o Prevent skin breakdown o Monitor and manage potential complications Crohn's Disease – Disorders of the Intestines Don't confuse these three! Ileum = most distal part of the small intestine Ileus = an obstruction (often in the intestine) Ilium = part of the hipbone Crohn's disease is a type of inflammatory bowel disease resulting in swelling and dysfunction of the intestinal tract, especially the small intestine. • Etiology o The etiology of Crohn's disease is unknown. It is a slow progressive disease. Some suspect it may be caused by an autoimmune disorder. o Crohn's begins with inflammation of segments of the bowel, especially the ileum, jejunum and colon, with areas of normal bowel between inflamed bowel (cobblestone appearance). o The inflammation involves all layers of bowel wall (transmural). Ulcerations, fissures, fistulas and abscesses form. The bowel wall will then thicken and narrow, producing strictures. • Assessment Findings o Diarrhea with steatorrhea (unprocessed fats) with no obvious blood or mucous in stool. o RLQ abdominal pain ▪ colicky pain (sharp, localized GI pain that comes and goes like in spasm like waves o Fatigue, weight loss, dehydration and fever will also be reported. o Systemic manifestations include: ▪ Arthritis and clubbing of fingers ▪ Skin inflammations ▪ Nephrolithiasis • Diagnostics Studies o Stool for occult blood o Stool culture to rule out infectious process o Sigmoidoscopy o Colonoscopy o Barium enema • Complications o Complications from Crohn's disease can include obstructions from strictures, fistula formations (anal too) and bowel perforation and infection (peritonitis). • Management o Rest and remaining NPO is important during an exacerbation. TPN or eternal nutrition may be considered. o Implement a diet that is high in calories and protein and low in roughage and fat after the acute stage has passed. o Pharmacologic Intervention: ▪ Steroids as anti-inflammatory drugs: prednisone; hydrocortisone ▪ Immunosuppressives: azathioprine; 6-mercaptopurine (6-MP); methotrexate; cyclosporine ▪ Monoclonal antibodies: infliximab ▪ Anti-infectives: sulfasalazine primary drug of choice ▪ Metronidazole to prevent/treat secondary infections ▪ Anticholinergics: dicyclomine ▪ Antidiarrheals: loperamide - drug of choice o Balloon dilation of strictures may be an option as well as surgery. Surgery will not cure Crohn's disease but it may limit the damage. Surgical interventions may include colectomy with ileostomy or a subtotal colectomy with an ileostomy or ileorectal anastomosis. • Nursing Interventions o The nurse will monitor the client for diarrhea, fluid balance, skin integrity, coping and self-care needs. Administer medications as ordered and assess body image issues. During recovery, provide a nutrition assessment and appropriate referrals. Diverticular Disease – Disorders of the Intestines Diverticular disease is an outpouching of the intestinal mucosa. • Etiology o The etiology of diverticular disease is unknown, but contributing factors include constipation, low-fiber diet and obesity. o Diverticulus is most common in the sigmoid colon. o The colon wall thickens and increases the pressure in the bowel. o Stool and bacteria retained in the diverticulum become inflamed and small perforations begin to occur. The surrounding tissue becomes inflamed, which is known as diverticulitis. • Assessment Findings o Frequently asymptomatic o Crampy, LLQ abdominal pain o Alternating constipation and diarrhea o Bloating and flatulence o Low-grade fever, chills, anorexia and nausea o Leukocytosis (elevated WBC) • Diagnostic Studies o Barium enema o Complete blood count, urinalysis, stool for occult blood o Flexible sigmoidoscopy o Colonoscopy • Management o If diverticulosis (outpouching) is diagnosed, a high-fiber, high-residue diet is recommended. ▪ Pharmacologic interventions include bulk laxatives, stool softeners and anticholinergics. o If diverticulitis (inflammation) is diagnosed, the client will be NPO for 24-48 hours and a low-fiber diet will be implemented after 48 hours. ▪ Antibiotics will also be administered. ▪ A bowel resection with a temporary colostomy may be necessary. • Complications o Complications that may occur include abscess formation, perforation with peritonitis, fistula, bowel obstruction or hemorrhage. o Diverticular bleeding ▪ Arteries around herniated sacs expands, artery wall can break down and release blood • Painless bleeding, blood in rectum, bright blood in stool o Fistula ▪ Opening can be created that allow contents of intestines to flow into the bladder (most common) • Nursing Interventions o Teach the client about maintaining an appropriate diet, and avoiding straining coughing and lifting more than 10 pounds. Constipation – Disorders of the Intestines Constipation occurs when the client has had fewer than three bowel movements in a week. ▪ Etiology o The etiology of constipation consists of its risk factors which include: ▪ Insufficient dietary fiber ▪ Insufficient fluid intake ▪ Medications, especially opiates ▪ Lack of activity ▪ Ignoring the urge to defecate ▪ Chronic laxative abuse ▪ Lack of privacy and/or psychological factors ▪ Pregnancy ▪ Neuromuscular impairment ▪ Hypothyroidism ▪ Assessment Findings o Hard, dry stool o Abdominal distention o Decreased frequency of usual patterns o Straining o Nausea and anorexia o Palpable mass o Fecal impaction with frequent small liquid stools o Hemorrhoids ▪ Enlarged veins located within tissue of the lower portion of the rectum or anus ▪ Complications o Complications of constipation can include obstruction and/or perforation and cardiovascular alterations. ▪ Diagnostic Studies o A history and physical exam will be performed. ▪ Management o Pharmacologic Intervention: ▪ Cathartics • Saline or osmotic laxatives – Milk of Magnesia, magnesium citrate • Stimulant laxatives – bisacodyl • Bulk-forming laxatives – psyllium • Lubricant-emollient – mineral oil • Stool softeners – docusate sodium ▪ Enemas • Cleansing – saline, soap solution (volume ordered varies between 500-1000 mL) • Softening or retention – oil (usually around 100-120 mL, packaged in a plastic squeeze bottle fitted with a five centimeter, pre- lubricated rectal tube) • Stimulant – such as Fleet's (a pre-packaged plastic squeeze bottle with 100 mL solution containing 16 grams sodium biphosphate and six grams of sodium phosphate) ▪ Complementary & Integrative Health o Bran or other high fiber dietary substances can help prevent constipation. o Peppermint oil may help reduce bloating and gas symptoms of irritable bowel syndrome. o There's little research to support the use of flaxseed, aloe latex or other herbal remedies. o Studies support the use of biofeedback for obstructive constipation. Hypnotherapy may help symptoms of irritable bowel syndrome. ▪ Nursing Interventions o Teach the client to include changes in diet (increase fiber and fluids) and as well as being aware of and obeying the urge to defecate. Discuss normal bowel habits and encourage the client to increase activity. Diarrhea – Disorders of the Intestines Diarrhea is the increase in frequency, volume and fluid content of stool. ▪ Etiology & Pathophysiology o Acute diarrhea is usually caused by an infectious agent or a medication such as a laxative. o Chronic diarrhea is caused by inflammatory bowel disorders such as ulcerative colitis or malabsorption disorders and may also be caused by lactose intolerance. o Side effects of medications can also cause chronic diarrhea. Chronic diarrhea can also indicate a bowel impaction (where liquid stool leaks around impaction). ▪ Assessment Findings o The client will have several large, watery stools daily or frequent small stools that may contain blood and/or mucus. ▪ Diagnostic Studies o Evaluation and diagnostic studies will depend on cause, duration and severity. ▪ Acute ▪ Complications • Serum electrolytes • Serum osmolality • Stool specimen for analysis and culture ▪ Chronic • Stool specimen for analysis and culture • Sigmoidoscopy • Biopsy of bowel mucosa to identify inflammation o Two primary complications of diarrhea are dehydration and electrolyte imbalance. ▪ Management o For clients with mild diarrhea, use oral fluids to replace nutrients and electrolytes such as Gatorade or Pedialyte. o For clients with moderate diarrhea use medications that decrease motility, e.g., diphenoxylate/atropine or loperamide. o For clients with severe diarrhea, replace fluids, administer antimicrobials as ordered and withhold solid food for 24 hours. ▪ Complementary & Integrative health o Herbal remedies or dietary supplements (such as goldenseal) can be used, however very little research has been done to support their use. There is some evidence that probiotics may be helpful for acute diarrhea and antibiotic- associated diarrhea. ▪ Nursing Interventions o Monitor for fluid and electrolyte imbalance and prevent skin excoriation. o Teach the client about foods that may affect bowel elimination, e.g., fruits, vegetables, dairy products and products with caffeine. Intestinal Obstruction – Disorders of the Intestines Intestinal obstruction (paralytic ileus, bowel obstruction or ileus) is a partial or complete blockage of the bowel that prevents the contents of the intestine from passing through. ▪ Etiology & Pathophysiology o Mechanical ▪ adhesions, hernias, neoplasms, volvulus, intussusception o Functional ▪ paralytic ileus, occlusion of vascular supply, complication of other conditions (diabetes mellitus, amyloidosis, muscular dystrophy, Parkinson's disease, neurological disorders) o The abdomen becomes distended from the accumulation of fluid, gas and intestinal contents. o Venous pressure and low blood pressure (hypotension) can cause fluid shifts and lead to hypovolemic shock. o The bacteria then proliferate and can cause an infection. o Bowel obstructions are more common in the small bowel. o Large bowel obstructions are commonly caused by cancer of the bowel. ▪ Assessment Findings o Abdominal pain o Distention (more with large bowel obstruction) o Nausea/vomiting (more with small bowel obstruction) – vomitus will be bile- stained (yellowish brown) = fluid from the small intestine o Hypoxia o Metabolic acidosis o Bowel necrosis from impaired circulation o Low fluid volume increases white blood cells (WBC), hemoglobin (Hgb), hematocrit (HCT) and blood urea nitrogen (BUN) (called hemoconcentration or the dehydration effect) ▪ Diagnostic Studies o An upper-GI and lower-GI series, as well as an abdominal X-ray (to check for air in the bowel) will be performed. ▪ Management o The abdomen will need to be decompressed via a nasogastric (NG) tube. o A surgical bowel resection may also be necessary. ▪ Complications o Complications of an obstruction include perforation and peritonitis, shock and strangulation of the bowel. ▪ Nursing Interventions o Manage the client's pain, but avoid using morphine or codeine, which slow bowel motion. o Measure the abdominal girth (monitor for distention) per orders and provide good oral care if client has a NG tube. o Maintain fluid and electrolyte balance. Colorectal Cancer – Disorders of the Intestines Colorectal cancer occurs equally in both males and females and is the third most common cancer death in the United States. It makes up around 15% of all new cancer cases. Colorectal cancer typically develops slowly which makes early detection key for a positive prognosis. ▪ Etiology & Pathophysiology o A clear risk factor for colorectal cancer is age. Some disorders or other conditions can also increase the risk of colorectal cancer (UC, Crohn's, genetic abnormalities). Colorectal polyps, high fat/low fiber diet, smoking, alcohol consumption and sedentary lifestyle have also been linked to colorectal cancer. o As with all cancers, the cancer is classified by the tissues or blood cells in which it originates. Cancer begins with one single cell mutation. This cell will grow out of control and will fail to mature as normal cells do. Further, the cancers cells can spread from the site of origin through metastasis. ▪ Assessment Findings o Early stages of this cancer typically don't present with any symptoms. o Rectal bleeding, blood in the stool, changes in bowel habits and lower abdominal pain/cramping can be seen in advanced cases. ▪ Screening for early detection is critical for survival. ▪ Diagnostic Studies o The digital rectal exam (DRE), fecal occult blood test, proctoscopy/sigmoidoscopy, colonoscopy and CT scan can be used to screen for and diagnosis colorectal cancer. ▪ Management o Surgery to remove the tumor, finding out if the cancer has spread, removing lymph nodes that drain to the cancer invaded area, and restoring bowel continuity are goals of surgical interventions if applicable. o Chemotherapy and targeted therapy (radiation) often follow. ▪ Nursing Interventions o The nurse can promote health by encouraging all clients over the age of 50 to have regular screening. o Teaching about bowel cleansing will be necessary for clients to be screened properly. o Nursing care for a client after a colon resection will follow general postoperative care of a client. o Some clients may have an NG tube to suction to prevent gastric dilation. o Monitor for bright red blood indicating a hemorrhage or coffee-ground drainage. o Nausea and vomiting are common and antiemetics can be administered as ordered. o Monitor fluid and electrolyte status, BP, HR, RR. o Clients who have had an abdominal resection (ARP) may have an open wound, drains and a colostomy. ▪ Packed wounds require reinforced, frequent and aseptic dressing changes. ▪ The nurse will assess and document the drainage regularly. ▪ Be aware that some clients may experience phantom rectal pain which is normal and typically subsides soon after. o If the wound is closed, assess the incision for suture integrity and signs of inflammation and infection. ▪ Additionally, monitor for edema, erythema and drainage around the incision. o When the client is ready for discharge, the nurse will educate the client and family on incision care, diet, medications, pain management, and ostomy care (if applicable). ▪ The client will progress to a regular diet as tolerated. ▪ It is important to note that clients may experience sexual dysfunction after an ARP. ▪ They will also need to understand how to manage bowel changes (no ostomy). Disorders of the Liver The liver is a highly vascular organ and performs multiple complex functions related to the digestive system. The liver performs important functions including filtering and detoxifying blood, removing ammonia, storing essential nutrients and converting glucose to glycogen. This section reviews some common disorders of the liver. Hepatitis – Disorders of the Liver Hepatitis is an acute inflammatory disease of the liver. • Etiology & Pathophysiology o Hepatitis is caused by a virus. After infected, the liver becomes inflamed and the Kupffer cells become enlarged. As a result, bile stasis, jaundice and potential damage and loss of function of the liver cells occurs. o The liver may regenerate its cells with no residual damage, or severe liver damage can occur, which is permanent. • Hepatitis is an inflammation of the liver, which can lead to: o Swelling o Scarring (cirrhosis) o Cancer • Hepatitis develops in three stages: o Pre-icteric (pre-jaundice) or prodromal stage • when general flu-like symptoms occur o Icteric stage • jaundice occurs (although not all patients with hepatitis develop jaundice) o Post-icteric (post-jaundice) or recovery stage • patient continues to have fatigue and malaise • Non-viral hepatitis o Drug-induced hepatitis is an idiosyncratic reaction to a drug (such as sulfonamides, isoniazid, and halothane) due to hypersensitivity o Toxic hepatitis (acute liver cell necrosis) is caused by ingestion, inhalation, or injection of certain chemicals (such as carbon tetrachloride, chloroform, poisonous mushrooms) that have a poisonous effect on the liver (hepatotoxins) • Viral hepatitis overview o There are at least five different viruses known to cause viral hepatitis, including hepatitis A, B, C, D and E 1. Hepatitis A: sometimes called "infectious hepatitis" 2. Hepatitis B: sometimes called "serum hepatitis" 3. Hepatitis C: formerly known as "non-A, non-B hepatitis"; it is the most common form of viral hepatitis 4. Hepatitis D: most commonly found in intravenous (IV) drug users, who are also carriers of the hepatitis B virus 5. Hepatitis E: like viral hepatitis A and most often found in people who live in countries with poor sanitation o Viral hepatitis is diagnosed as either acute or chronic: • Acute: the initial infection, which may be mild or severe • Chronic: if the infection lasts longer than six months o Hepatitis B, C, and D can produce both an acute and chronic infection o Hepatitis A and E do not cause chronic hepatitis • Nursing implications associated with viral hepatitis: o Rest • clients with viral hepatitis experience fatigue and malaise during all phases of the infection o Provide a restful environment o Bed rest during acute phase o Encourage alternating between periods of rest with periods of activity during convalescence o Diet • Symptoms include anorexia, nausea and abdominal pain • Modify diet to client's needs and tolerances and encourage client to eat • Alternate form of nutrition therapy may be needed if client is unable to tolerate prescribed diet • Administer antacids after meals • Do not give antacids @ same time as H2 receptor antagonists (histamine blockers) • Maintain gastric pH greater than 3.5 o Circulation • may exhibit bradycardia (related to severe hyperbilirubinemia) o Sensory • smokers may report distaste for/aversion to cigarettes o Medications • avoid OTC medications that contain aspirin or NSAIDs • Diagnostic studies o Blood work • (Serum) albumin: decreased • Alkaline phosphatase (ALP): slight elevation (unless severe cholestasis present) • Alanine aminotransferease (ALT) and aspartate aminotransferease (AST) liver enzymes: initially elevated; may rise 1-2 weeks before jaundice is apparent and then decline • (Serum) bilirubin: above 2.5 mg/100 mL; if above 200 mg/100 mL, probable poor prognosis due to increased cellular necrosis • Bromsulphalein (BSP) excretion test: blood level elevated • (Blood) glucose: transient hyperglycemia/hypoglycemia (due to altered liver function) • Complete blood count (CBC): red blood cells decreased because of shortened lifespan (liver enzyme alterations) or hemorrhage. • Hepatitis A, B, C, D, E panels (antibody/antigen tests): specify type and stage of disease and determine possible carriers • Liver enzymes/isoenzymes: abnormal (4-10 times normal values); of limited value in differentiating between viral and nonviral hepatitis • Prothrombin time: may be prolonged (liver dysfunction) • White blood cell (WBC) count and differential: leukopenia, leukocytosis, monocytosis, atypical lymphocytes, and plasma cells may be present o Stools: clay-colored, steatorrhea due to decreased hepatic function o Urinalysis: elevated bilirubin levels; protein/hematuria may occur o Other • Liver biopsy: usually not needed, but should be considered if diagnosis is uncertain or if clinical course is atypical • Liver scan: aids in estimation of severity of parenchymal damage • Emotional support o enhance self-concept and acceptance of situation • Infection control • Discharge goals: o Meet basic self-care needs o Prevent or minimize complications o Educate clients about disease process, prognosis and therapeutic regimen • Referrals: o Community health nurse to provide follow-up visits • A health investigation in the community may be warranted (particularly with hepatitis A) Type A Hepatitis Virus (HAV) Fecal-oral contamination Person-to-person (infected food preparers) Water-borne Food-borne Eating raw or partially cooked shellfish contaminated with HAV Type B Hepatitis Virus (HBV) Body secretions of infected persons Contaminated needles, syringes Mothers to babies Hepatitis C Virus (HCV) Body secretions of infected persons Transfusions; transfusion products Personnel and clients in renal and dialysis units Individuals getting tattoo/body piercing done with unsterile instruments Mode of Transmission Type A Hepatitis Virus (HAV) 2-6 weeks Type B Hepatitis Virus (HBV) 4-24 weeks Hepatitis C Virus (HCV) 2-15 weeks Incubation Type A Hepatitis Virus (HAV) Children with hepatitis A usually have no symptoms Adult symptoms: usually asymptomatic at first with abrupt onset of flu-like symptoms (headache, malaise, fever, lassitude) and non- specific GI symptoms (anorexia, nausea, upper abdominal discomfort, vomiting) Type B Hepatitis Virus (HBV) Many people with newly acquired HBV have no symptoms or very mild flu-like symptoms Insidious onset of variable symptoms; includes same symptoms as Type A plus the following: arthralgias and uticarial skin rashes Hepatitis C Virus (HCV) Insidious onset of symptoms; most people do not have symptoms Similar to Type B but less severe Prodromal Phase (Pre- icteric) Type A Hepatitis Virus (HAV) Jaundice Dark urine Pale stools Tender and enlarged liver Pruritis Type B Hepatitis Virus (HBV) Prolonged acute phase with anorexia, malaise and abdominal pain Jaundice may or may not occur Hepatitis C Virus (HCV) Similar to Type B, but less severe Most cases are without jaundice Icteric Phase Note: symptoms tend to subside when jaundice reaches its peak (usually within 2 weeks) Type A Hepatitis Virus (HAV) 2-6 weeks Type B Hepatitis Virus (HBV) Prolonged Hepatitis C Virus (HCV) Prolonged Post-icteric Phase Type A Hepatitis Virus (HAV) No specific treatment is necessary for hepatitis A Type B Hepatitis Virus (HBV) Two medications are available to treat chronic HBV: Interferon (IFN) and Lamivudine Hepatitis C Virus (HCV) Three types of interferon, plus a combination of interferon and Ribavirin for adults: Primary clinical toxicity of Ribavirin is hemolytic anemia Pregnancy Category X: female clients taking Ribavirin must take at least 2 other reliable forms of effective contraception to avoid pregnancy Many HCV victims will eventually need a liver transplant Treatment Type A Hepatitis Virus (HAV) Hepatitis A will clear up on its own, usually with no serious after-effects Type B Hepatitis Virus (HBV) Vast majority of adults recover spontaneously: develop immunity to the virus and are not infectious to others Small percentage become Hepatitis C Virus (HCV) Vast majority of HVC infections are classified as chronic Many of those with chronic HCV develop cirrhosis Outcome chronically infected and are considered "carriers" and, eventually, liver failure Type A Hepatitis Virus (HAV) Immune globulin (IG): provides temporary immunity after exposure HAV vaccine Type B Hepatitis Virus (HBV) HBV vaccine: all newborns start the first of three vaccinations within 12 hours after birth; the second is given at 1-2 months and the third is scheduled for six months of age Hepatitis C Virus (HCV) No vaccine for HCV is currently available Don't share drug needles Practice safer sex Avoid handling anything that may have the blood of an infected person on it Prevention Overview of Viral Hepatitis Hepatitis B – Disorders of the Liver Hepatitis B (HBV) is a form of liver inflammation due to infection by the hepatitis B virus (HBV). It may be acute or chronic. • Etiology & Pathophysiology o Hepatitis B is caused by HBV and can be transmitted through contact with infected blood (often via needle sticks). o It can also be spread through sexual contact with a person infected by HBV or during childbirth (passed from mother to child). o Once infected, damage to the hepatocytes causes inflammation and necrosis. Risk factors include male homosexual (and bisexual) activity, intravenous (IV) drug use and proximity to infected blood for health care professionals. • Assessment Findings o Jaundice if liver fails to conjugate or excrete bilirubin o Clay-colored stools from lack of urobilin o Urine is dark from urobilin excreted in urine rather than stool o Urine foams when shaken o Pruritus from bile salts excreted through skin o RUQ pain from edema and inflammation of liver o Anorexia, N&V, malaise and weight loss o Prolonged bleeding from impaired absorption of vitamin K o Anemia from decreased RBC lifespan o Liver cancer – most serious complication of chronic HBV infection • Diagnostic Studies o These tests search for serologic markers of HBV: • HBsAg – hepatitis B surface antigen indicates acute or chronic hepatitis B or carrier state • Anti-Hbc – antibodies to B core antigens • HBeAg – indicates a highly infectious stage of hepatitis B • Elevated alanine aminotransferase (ALT), formerly known as SGPT • Elevated bilirubin • Elevated aspartate aminotransferase (AST), formerly known as SGOT • Elevated alkaline phosphatase • Prolonged PT • Management o Symptomatic treatment of pain o Antiemetics as needed o Prevention: • Hepatitis B vaccine provides active immunity (Engerix-B, Recombivax HB) • Hepatitis B immune globulin provides passive immunity • Observe standard and enteric precautions • Good hand washing • Nursing Interventions o Fatigue – provide rest periods; the client may require bed rest initially o Maintain skin integrity o The client will tolerate less activity o Nutritional needs: • Increase carbohydrates and proteins; decrease fat • Avoid alcohol • Eat frequent, small meals o Remedy any knowledge deficits o Arrange for home care needs o Teach infection control: • Use disposable utensils and dishes or keep separate from dishes used by others • Good hand washing • Do not share razors, toothbrush, etc. Hepatitis C – Disorders of the Liver Hepatitis C is a viral disease caused by the hepatitis C virus (HCV) that leads to inflammation of the liver. • Etiology & Pathophysiology o Hepatitis C is caused by HCV, which is transmitted parenterally through dialysis, blood transfusion before July 1992, shared needles or razors, unprotected sexual contact with someone who has HCV or tattoo or acupuncture with contaminated instruments. o The pathology is the same with all hepatitis infections. • Assessment Findings o Prodromal Stage • In the prodromal stage, the following findings may be caused by circulating immune complexes. During this phase, the infection is HIGHLY transmissible. o Fatigue o Anorexia o Mild weight loss o Generalized malaise and depression o Headache, weakness, joint and muscle pain o Intolerance to light o Nausea and vomiting o Fever o RUQ tenderness o Dark-colored urine and clay-colored stools o Clinical Stage (Icteric) • The clinical stage begins 1-2 weeks after the prodromal stage. • It is the actual phase of the illness. • Findings will include: o Itching o abdominal pain or tenderness o indigestion o appetite loss o jaundice. Jaundice can last for up to two weeks. o Recovery Stage • Recovery begins with the resolution of jaundice and lasts up to six weeks in uncomplicated cases. • The prognosis is poor if edema and hepatic encephalopathy develop. • Diagnostic Studies o Liver enzyme testing (ALT, AST, ALP, GGT and serum bilirubin) – to identify and monitor liver damage o EIA assay – to detect hepatitis C antibodies o Hepatitis C RNA assay – to measure viral load o Liver biopsy – to evaluate for chronic hepatitis • Management o Currently there is no vaccine available for hepatitis C. However, there are many new medications being developed that are curing clients of the disease. Interferon alpha and antiviral medication such as ribavirin are common medication choices. • Nursing Interventions o It is important to promote rest, provide adequate nutrition, manage itching and maintain skin integrity. Teach the client to avoid alcohol and other hepatotoxic agents. Cirrhosis – Disorders of the Liver Cirrhosis is an irreversible, chronic, progressive degeneration of the liver, with fibrosis and areas of nodular regeneration. • Etiology & Pathophysiology o Types of cirrhosis: • Laennec's (alcoholic) cirrhosis – related to alcohol abuse • Post-necrotic cirrhosis – associated with viral hepatitis or exposure to hepatotoxin • Biliary cirrhosis – associated with inflammation or obstruction of the gallbladder or bile duct • Cardiac cirrhosis – associated with heart failure o The liver becomes nodular with fibrosis and scar tissue. The hepatocytes are destroyed and the tissue dies (necrosis). Necrosis, nodules and scar tissue obstruct flow of blood, lymph and bile. • Assessment Findings o Weakness, fatigue, weight loss and hepatomegaly (enlargement of the liver) o RUQ pain o Jaundice, pruritus and steatorrhea (decreased absorption of fat and fat-soluble vitamins) o Clay-colored stools o Increased bilirubin in urine, producing dark colored urine o Impaired aldosterone metabolism resulting in edema o The liver fails to convert glycogen to glucose, resulting in hypoglycemia o Impaired estrogen metabolism: gynecomastia, menstrual changes, changes in distribution of body hair and vascular changes (i.e., spider angiomas and palmar erythema) o Impaired metabolism of protein, carbohydrate and fat: • Produces less plasma protein, resulting in edema and ascites • Produces less of proteins needed for clotting (fibrinogen and prothrombin) • Absorbs less vitamin K, resulting in prolonged bleeding • Diagnostic Studies o Laboratory: • Liver enzyme tests (formerly called liver function tests) — elevated ALT, AST, alkaline phosphatase • Prothrombin time • Complete blood count • Cholesterol — decreased due to impaired liver synthesis • Serum bilirubin and urine bilirubin - elevated o Endoscopic retrograde cholangiopancreatography (ERCP) — to examine bile ducts o CT scan of liver o Liver biopsy • Management o Steroids for post-necrotic cirrhosis o Replace B vitamins and fat-soluble vitamins o Diet: • Increased carbohydrates • Protein may be restricted, depending on the amount of damage and symptoms (especially with elevated ammonia levels) • Possible sodium restrictions with complications (ascites, hepatic encephalopathy) • calories daily • No alcohol • Complications o Complications can include portal hypertension, ascites and hepatomegaly (enlargement of the liver) • Nursing Interventions o Monitor for bleeding o Promote adequate or optimal nutrition o Instruct to avoid alcohol and other hepatotoxic agents o Manage itching and maintain skin integrity o Provide rest periods – the client will not tolerate strenuous activities o Remedy any knowledge deficit about cirrhosis and its therapies o Assess for changes in (LOC) such as confusion o Manage itching and maintain skin integrity o Monitor fluid balance: • Measure abdominal girth daily • Weigh the client daily • Measure intake and output (I/O) Portal Hypertension – Disorders of the Liver Portal hypertension is an increased pressure in portal circulation due to scar tissue in the liver, which restricts the flow of blood to the liver. • Etiology & Pathophysiology o Normal blood flow is altered, producing an increased resistance to flow through the liver. Congestion in the portal system dilates veins, especially in the esophagus and rectum. • Assessment Findings o Prominent abdominal-wall veins (caput medusa) o Hemorrhoids o Enlarged spleen o Anemia from increased destruction of RBC o Esophageal varices and GI bleeding • Diagnostic Studies o Endoscopy is the best diagnostic tool. • Management o Sclerotherapy – the injection of a sclerosing agent into varices o Balloon tamponade: • Sengstaken-Blakemore tube is inserted into the stomach • Gastric balloon is inflated and presses on the lower esophagus while allowing suctioning • Esophageal balloon places pressure on varices o Pressure is released as ordered to prevent necrosis • Traction for increased pressure is added by attaching a tube to a football helmet • Assess for bleeding and signs of shock • Assess for respiratory distress – aspiration or displacement of tube; suction PRN • Keep the head of bed elevated • Aspiration is a risk since the client cannot swallow saliva when the esophageal balloon is inflated • Complications o Esophageal varices (overload) are dilated sub-mucosal veins in the lower part of the esophagus. o They are often a consequence of portal hypertension, commonly due to cirrhosis. o Clients with esophageal varices have a strong tendency to develop bleeding. o Splenomegaly – enlarged spleen o Ascites • Pharmacologic Intervention o Vasopressin o Nitroglycerin – decreases myocardial effects o Beta-adrenergic neuron-blocking agents – decreases risk of recurrent bleeding by decreasing pressure in the portal system o Cathartics – removes blood from the GI tract and decreases absorption of ammonia • Surgical Intervention o A shunt will be placed to decrease blood flow to liver and therefore pressure. A transjugular intrahepatic portosystemic shunt (TIPS) is a shunt placed between the hepatic and portal veins. • Nursing Interventions o Prevent bleeding o Avoid intake of alcohol or irritating or rough food o Avoid increased pressure in abdomen o If bleeding occurs, administer transfusions, fresh frozen plasma and vitamin K o Monitor for infection Ascites – Disorders of the Liver A collection of fluid in the peritoneal cavity between the organs and the abdominal wall. • Etiology & Pathophysiology o Portal hypertension causes increased plasma and lymphatic hydrostatic pressure in the portal system. o Hypoalbuminemia causes decreased colloid osmotic pressure. Hyperadldosteronism, due to the liver's inability to metabolize aldosterone, causes the body to retain sodium and water. • Fluid then leaks from the intravascular space into the abdomen. • Assessment Findings o Abdominal distention o protruding umbilicus o dull sound on percussion of the abdomen o fluid wave o Bulging flank o Dyspnea • Diagnostic Studies o Abdominal X-ray o CT scan o Ultrasound • Management o Pharmacologic Intervention: o Diuretics: spironolactone – aldosterone antagonist, spares potassium o IV albumin o Paracentesis to remove fluid o Low-sodium diet o Peritoneal venous shunt – allows the drainage of fluid from the peritoneum to superior vena cava • Nursing Interventions o Monitor fluid balance: measure I/O, daily weight, abdominal girth and skin turgor o Restrict fluids o Monitor for ineffective breathing patterns o Position client in a semi-Fowler's position o Monitor for impaired skin integrity o Remedy the client's knowledge deficits Hepatic Encephalopathy – Disorders of the Liver Hepatic encephalopathy is impaired ammonia metabolism that results in neurotoxins in the blood and cerebral edema. • Etiology & Pathophysiology o Ammonia is produced in the bowel by the action of bacteria on protein. As a result, nitrogenous waste and neurotoxins increase. • Assessment Findings o Changes in the client's LOC from confusion to coma o Changes in sleep pattern o Memory loss o Asterixis – flapping tremor o Impaired handwriting o Hyperventilation with respiratory alkalosis o Fetor hepaticus – musty, sweet odor to the client's breath • Diagnostic Studies o A test of the serum ammonia level will indicate hepatic encephalopathy. • Management o Neomycin sulfate – inhibits the action of intestinal bacteria o Lactulose – converts ammonia into ammonium (not absorbable and is excreted) and reduces the number of ammonia-forming organisms in the bowel o Low-protein diet • Nursing Interventions o Maintain safety: tremor, confusion can lead to injury o Provide uninterrupted rest periods o Assess fluid and electrolyte balances and body weight –ascites and low intake decrease fluid volume o Monitor changes in bowel movements (medications can cause diarrhea) Liver Cancer - Disorders of the Liver Liver cancer is the most common cause of death in clients with liver cirrhosis (cirrhosis caused by Hepatitis C). The most common type of liver cancer is hepatocellular carcinoma (HCC). • Etiology & Pathophysiology o In primary liver cancer, singular or nodular lesions can spread throughout the liver. o Tumors can infiltrate other organs such as the gallbladder. o The most common site of primary liver cancer metastasis is to the lung. o Metastatic carcinoma of the liver is more common than primary liver cancer due to the vascular nature of the liver. • Assessment Findings o Symptoms of early liver cancer can be non-existent or very difficult to decipher. o The symptoms typically manifest as the underlying cirrhosis. o They can present with hepatomegaly, splenomegaly, fatigue, edema or ascites. o In the late stages, clients can present with fever, jaundice, anorexia, weight loss, palpable mass and RUQ pain. • Diagnostic Studies o Diagnostic studies include an ultrasound, CT scan and MRI. o If a diagnosis cannot be made a biopsy may be done, although risks of a biopsy include bleeding and tumor cell seeding. • Management o The key to avoiding liver cancer is identifying and treating chronic hepatitis B and C infections. o Treatment of alcohol abuse can also lower the risk. o Frequent liver cancer screening is important for the high risk population. o The treatment of liver cancer depends on the stage of the cancer and other system involvement. o Many clients are not surgical candidates because their cancer is too advanced. o Non-surgical interventions may include percutaneous ablation, chemoembolization, radioembolization and sorafenib oral therapy. • Nursing Interventions o The primary nursing intervention is keeping the client comfortable. o Similar nursing intervention for the care of the cirrhosis clients is applicable for liver cancer clients as well. Key preparation for the nurse/family is understanding the possibility of hepatic encephalopathy or massive blood loss from GI bleeding. Disorders of the Pancreas & Gallbladder The gallbladder's job is to store and concentrate bile produced by the liver. The pancreas is considered part of the digestive system because enzymes, or digestive juices, are secreted by the pancreas into the small intestine. This section reviews disorders associated with the pancreas and gallbladder. Acute Pancreatitis – Disorders of the Pancreas & Gallbladder Acute pancreatitis is an inflammation of the pancreas. • Etiology & Pathophysiology o Acute pancreatitis can be caused by multiple factors, such as heavy alcohol use, gallstones, drug ingestion, viral infections or trauma. o Pancreatic enzymes (trypsin, phospholipase A2 and elastase) become activated in the gland and damage the pancreatic tissue. o Activation of the complement system and the inflammatory cascade produces cytokines. Activated enzymes and cytokines that enter the peritoneal cavity cause a chemical burn and third-spacing (a condition when too much fluid moves from the blood vessels into the interstitial or "third" space – the nonfunctional areas between the cells). o Further, the activated enzymes and cytokines that enter the systemic circulation cause a systemic inflammatory response, leading to respiratory distress syndrome and renal failure. • Assessment Findings o Upper abdominal pain that sometimes radiates to the back • Mid-epigastric/epigastric/peri-umbilical region • LUQ for Chronic Pancreatitis  LT alcohol abuse o Nausea and vomiting o Tachycardia o Slow and shallow respirations o Swollen and tender abdomen o Fever o Complications o Atelectasis, limited diaphragmatic excursion o Hypovolemia and shock o Abscess or pseudocyst o Hemorrhage into retroperitoneal space (produces bluish discoloration around umbilicus) • Diagnostic Studies o Laboratory o Serum amylase, serum lipase and urinary amylase – elevated enzymes o Complete blood count – elevated WBC, decreased Hgb and HCT o LDH and AST (SGOT) – elevated o Blood sugar – hyperglycemia o Hypocalcemia o Chest X-ray o CT scan o Ultrasound o Endoscopic retrograde cholangiopancreatography (ERCP) • Management o The goal is to be able to identify and treat the cause of the pancreatitis. o Pharmacologic Intervention: • Pain relief – meperidine reduces smooth muscle spasms; morphine may also be used • Hyperglycemia – insulin • Calcium replacement • Anticholinergics • H2-receptor antagonists o Further management includes fluid maintenance to prevent shock, calcium replacement and decreasing stimulation to the pancreas. o A NG tube may need to be placed. o The client will probably be NPO. o However, if eating is allowed, be sure that the client's food is high in protein and carbohydrates, and low in fat. • Nursing Interventions o Manage pain o Monitor fluid and electrolyte balances o Alcohol is strictly prohibited o Monitor alteration in breathing patterns o Monitor nutritional status o Oral care when NPO Cholecystitis – Disorders of the Pancreas & Gallbladder Cholecystitis is an inflammation of the gallbladder. • Etiology & Pathophysiology o Cholecystitis is usually due to gallstones (cholelithiasis). o There are two types: • cholesterol (most common) • pigment (unconjugated bilirubin). Fair (skin and o Risk factors include being age 40 or older, using birth control pills and being 6-9 months post-partum (due to elevated progesterone levels). o The common bile duct is obstructed by a gallstone and bile cannot be excreted. o The remaining bile distends and inflames the gallbladder. o The gallbladder may scar, causing it to store less bile from the liver. The gallbladder can also perorate. • Assessment Findings o Colicky pain in URQ with possible radiation to right shoulder and back o Indigestion after eating fatty foods • Clay stools + fatty stools o Tea coloured frothy urine o Nausea and vomiting o Yellowing/Jaundice (if the liver is involved or inflamed or the common duct obstructed) o Low-grade fever • Diagnostic Studies o Endoscopic retrograde cholangiopancreatography (ERCP) o Endoscopic retrograde catheterization of the gallbladder (ERCG) o Complete blood count, amylase, lipase and serum bilirubin o Ultrasound • Management o Rest o Low-fat diet o Removal of stone in the common duct by endoscopy o Pharmacologic Intervention: • Chenodiol – side effects are diarrhea and hepatotoxicity • Ursodiol • Control pain – meperidine is drug of choice • Replace vitamin K if bleeding time is prolonged • Extracorporeal shock wave lithotripsy – may have hematuria after procedure, but not longer than 24 hours • Choledocholithotomy: to remove or break up stones and place T-tube in the common bile duct • Laparoscopic laser cholecystectomy • Cholecystectomy • Nursing Interventions o Monitor vital signs and pain. Teach clients about the need to restrict fatty foods in their diet.