Exam 4 GI

Gastrointestinal System

The gastrointestinal system (GI tract) can be thought of as a tube (with necessary structures) extending from the mouth to the anus for a 25-foot length. The structure of this tube (shown enlarged) is basically the same throughout its length.

Hiatal Hernias know hiatal and inguinal know surgical care

A hernia is a weakness in the abdominal muscle wall through which a segment of the bowel or other abdominal structure protrudes. Hernias can also penetrate through any other defect in the abdominal wall, through the diaphragm, or through other structures in the abdominal cavity. The most significant factors contributing to increased intra-abdominal pressure are obesity, pregnancy, and lifting heavy objects. An indirect inguinal hernia is a sac formed from the peritoneum that contains a portion of the intestine or omentum. The hernia pushes downward at an angle into the inguinal canal. In males, indirect inguinal hernias can become large and often descend into the scrotum. • Direct inguinal hernias, in contrast, pass through a weak point in the abdominal wall. weakening in the wall when to worry? when the bowel is twisted, which is a volvulus, which is an EMERGENCY. NO BLOOD FLOW TO INTESTINES = DEATH Also called diaphragmatic hernias uProtrusion of the stomach through the esophageal hiatus of the diaphragm into the chest uMay be asymptomatic or have symptoms similar to those with GERD uSliding versus paraesophageal uSliding hiatal hernias, where the gastroesophageal junction (GEJ) and the gastric cardia migrate into the thorax, account for 95% of hiatal hernia In paraesophageal hernias (PEH), only the gastric fundus herniates into the thorax, whereas in mixed hiatal hernias, the GEJ as well as the gastric fundus herniate Comparison of the normal stomach and sliding and paraesophageal (rolling) hiatal hernias. Assessment: Noticing uAsk about heartburn, regurgitation, pain, dysphagia, eructation. uAssess nutrition status. uNote location, onset, duration, quality of pain, exacerbating and relieving factors. uBarium swallow study with fluoroscopy Interventions: Responding uNonsurgical management uInterventions for GERD uElevate head of the bed while sleeping, eating small meals, losing excess weight, stopping smoking, not lying down or exercising after meals, and not wearing tight-fitting clothes. Eliminating or limiting intake of beverages that contain acid (such as orange juice and colas), alcohol, coffee, and certain foods (such as onions, and spicy, acidic, and fatty foods) is recommended. uSurgical management uSymptomatic paraesophageal hiatal hernia uCorrected surgically to prevent strangulation. u Surgery may be done through a tiny incision in the chest or abdomen through which thin instruments and a small video camera are inserted (thoracoscopic or laparoscopic surgery) or may require a full open operation. Care Coordination and Transition Management uTeach about activity restrictions. uShower starting around 36 hours after surgery uNo baths, pools or hot tubs for two weeks. uYou will usually be able drive when you have not needed the narcotic (prescription) pain medications for two days uNutrition modifications (coordinate with dietician) uYou will need to stay on a liquid/soft diet for approximately 3 weeks after surgery. uRemind to contact health care provider if signs of infection are present after surgery. uFever to 100.4 or greater uShaking chills uPain that increases over time uRedness, warmth, or pus draining from incision sites uPersistent nausea or inability to take in liquids

Nutrition Concept Exemplar:Gastroesophageal Reflux Disease (GERD)

Acidic bubbling up the esophagus, causes pain and irritation Teach - take meds, don't lay down, don't drink caffeine and alcohol, decrease acidic food (greasy, orange juice, spicy foods) sleep with your head up, Most common upper GI disorder in the U.S. uOccurs as a result of backward flow of stomach contents into esophagus uHiatal hernias increase risk for GERD uDuring healing, Barrett's epithelium and esophageal stricture are concerns. Health Promotion and Maintenance uPatients may be initially asymptomatic. uHealthy eating habits uLimitation of fried, fatty, spicy foods, and caffeine uSit upright for one hour after eating. Assessment: Noticing uHistory of heartburn, chest pain, asthma, hoarseness, pneumonia, dyspepsia uSymptoms may include u"Indigestion" uRegurgitation uEructation (act of vomiting), flatulence uDysphagia, odynophagia (chronic GERD) uDiagnostic assessment uBarium swallow - contrast chalky liquid, take series of pictures. tracks whole GI system to see if anything is wrong. Kidneys and liver have to filter it, so they need to increase water intake after procedure!!!!!! The BM is going to look white for 1-3 days. uEndoscopy upH monitoring examination uEsophageal manometry uis a test that is used to measure the function of the lower esophageal sphincter (the valve that prevents reflux, or backward flow, of gastric acid into the esophagus) and the muscles of the esophagus. This test will tell your doctor if your esophagus is able to move food to your stomach normally. Analysis: Interpreting •Potential for compromised nutrition status due to dietary selection •Acute pain due to reflux of gastric contents Care Coordination and Transition Management uSelf-management education uMaintain a healthy weight. ... uStop smoking. ... uElevate the head of your bed. ... uDon't lie down after a meal. ... uEat food slowly and chew thoroughly. ... uAvoid foods and drinks that trigger reflux. ... uAvoid tight-fitting clothing. Evaluation: Reflecting uExhibit adherence to choosing appropriate dietary selections, taking drugs as prescribed, and making appropriate lifestyle modifications. uReport decrease of reflux signs and symptoms associated with GERD. uAvoid complications resulting from GERD. uAcid-suppressive agents have become the drugs of choice for GERD. uBoth proton pump inhibitors (PPIs) and histamine H2-receptor antagonists (H2-RA) are effective and can be safely used to treat GERD. Endoscopy is direct visualization of the GI tract using a flexible fiberoptic endoscope, a tube that allows viewing and manipulation of internal body areas. It is commonly prescribed to evaluate bleeding, ulceration, inflammation, tumors, and cancer of the esophagus, stomach, biliary system, or bowel. Specimens for biopsy and cell studies (e.g., Helicobacter pylori) can be obtained through the endoscope. Esophagogastroduodenoscopy (EGD) is a visual examination of the esophagus, stomach, and duodenum by means of a fiberoptic endoscope. If GI bleeding is found during an EGD, the health care provider can use clips, thermocoagulation, injection therapy, or a topical hemostatic agent The priority for care to promote patient safety after esophagogastroduodenoscopy is to prevent aspiration. Do not offer fluids or food by mouth until you are sure that the gag reflex is intact! Monitor for signs of perforation, such as pain, bleeding, or fever. Endoscopic retrograde cholangiopancreatography (ERCP) includes visual and radiographic examination of the liver, gallbladder, bile ducts, and pancreas to identify the cause and location of obstruction. It is commonly used today for therapeutic purposes rather than for diagnosis. After a cannula is inserted into the common bile duct, a radiopaque dye is instilled, and several x-ray images are obtained. The health care provider may perform a papillotomy (a small incision in the sphincter around the ampulla of Vater) to remove gallstones. If a biliary duct stricture is found, plastic or metal stents may be inserted to keep the ducts open. Biopsy samples of tissue are also frequently taken during this test. Colonoscopy is an endoscopic examination of the entire large bowel. Be sure to fully assess all patients who may need a colonoscopyfgas

Pancreatitis

Acute pancreatitis is a serious and at times life-threatening inflammation of the pancreas. This inflammatory process is caused by a premature activation of excessive pancreatic enzymes that destroy ductal tissue and pancreatic cells, resulting in autodigestion and fibrosis of the pancreas. The pathologic changes occur in different degrees. The severity of pancreatitis depends on the extent of inflammation and tissue damage. Pancreatitis can range from mild involvement evidenced by edema and inflammation to necrotizing hemorrhagic pancreatitis (NHP). NHP is diffuse bleeding pancreatic tissue with fibrosis and tissue death. NPO IVF NGT low intermittent wall suctioning treat: antibiotics and pain meds S/S sharp pain, upper left abdomen to shoulder area Typically, a patient is diagnosed after presenting with severe abdominal pain in the mid-epigastric area or left upper quadrant. Assess the intensity and quality of pain. The patient often states that the pain had a sudden onset and radiates to the back, left flank, or left shoulder. The pain is described as intense, boring (feeling that it is going through the body), and continuous, and is worsened by lying in the supine position. Often the patient finds relief by assuming the fetal position (with the knees drawn up to the chest and the spine flexed) or by sitting upright and bending forward. He or she may report weight loss resulting from nausea and vomiting. Obtain the patient's weight. When performing an abdominal assessment, inspect for: • Generalized jaundice • Gray-blue discoloration of the abdomen and periumbilical area • Gray-blue discoloration of the flanks, caused by pancreatic enzyme leakage to cutaneous tissue from the peritoneal cavity Listen for bowel sounds; absent or decreased bowel sounds usually indicate paralytic (adynamic) ileus. On light palpation, note abdominal tenderness, rigidity, and guarding as a result of peritonitis. Pancreatic ascites creates a dull sound on percussion. Monitor and record vital signs frequently to assess for elevated temperature, tachycardia, and decreased blood pressure, or assign and closely supervise this activity. Auscultate the lung fields for adventitious sounds or diminished breath sounds and observe for dyspnea or orthopnea. RISK FactorsSIGNS and SYMPTOMS uExcessive Alcohol consumption uCigarette Smoking uObesity uFamily History uUpper abdominal pain uAbdominal pain that radiates to your back uAbdominal pain that feels worse after eating uFever uRapid pulse uNausea uVomiting uTenderness when touching the abdomen Critical Rescue For the patient with acute pancreatitis, monitor for significant changes in vital signs that may indicate the life-threatening complication of shock. Hypotension and tachycardia may result from pancreatic hemorrhage, excessive fluid volume shifting, or the toxic effects of abdominal sepsis from enzyme damage. Observe for changes in behavior and level of consciousness (LOC) that may be related to alcohol withdrawal, hypoxia, or impending sepsis with shock Analysis LAB VALUES u10-15% Mortality Rate uacute pain due to pancreatic inflammation and enzyme leakage. uhigh amylase(23-85 U/L) and lipase levels (0-160 U/L)—digestive enzymes made in your pancreas amylase levels usually increase within 12 to 24 hours and remain elevated for 2 to 3 days. Persistent elevations may be an indicator of duct obstruction or pancreatic duct leak (Pagana & Pagana, 2018). Lipase also helps determine the presence of acute pancreatitis. Serum levels may rise later than amylase and remain elevated for up to 2 weeks. Because these levels stay elevated for such a long time, the primary health care provider may find this test useful in diagnosing patients who are not examined until several days after the initial onset of symptoms. An increase in lipase and amylase in the urine is also expected uhigh blood glucose (70-100 mg/dl) uhigh levels of blood lipids-Triglycerides (<150mg/dl) usigns of infection or inflammation of the bile ducts, pancreas, gallbladder, or liver -CBC (elevated WBC) uC-Reactive-measure of inflammation in the body uweight loss due to inability to ingest food and absorb nutrients. Physiologic Integrity A client was admitted to the hospital yesterday with a diagnosis of acute pancreatitis. What assessment findings will the nurse expect for this client? Select all that apply. A. Severe boring abdominal pain B. Jaundice C. Nausea and/or vomiting D. Decreased serum amylase level E. Leukocytosis F. Dyspnea Planning and Implementation: Responding uManage Pain- Severe continuous "boring" abdominal pain is the most common symptom of pancreatitis! The main focus of nursing care is aimed at controlling pain by interventions that decrease GI tract activity, thus decreasing pancreatic stimulation. Pain assessment to measure the effectiveness of these interventions is an essential part of nursing care. uNonsurgical Management uIV Fluids uNPO while acute uPrimary drug classes is opioids and NSAIDS - Pain management for acute pancreatitis typically begins with the administration of opioids by patient-controlled analgesia (PCA). Drugs such as morphine or hydromorphone are typically given. Other options that have been used successfully to manage acute pain include IV or transdermal fentanyl and epidural analgesia Mild pancreatitis requires hydration with IV fluids, pain control, and drug therapy. The interprofessional health care team initially attempts to relieve pain with nonsurgical interventions, which include fasting and rest, drug therapy, and comfort measures. If the patient has a life-threatening complication or requires frequent assessment, he or she is admitted to a critical care unit for invasive hemodynamic monitoring. To rest the pancreas and reduce pancreatic enzyme secretion, withhold food and fluids (NPO) during the acute period. The primary health care provider prescribes IV isotonic fluid administration to maintain hydration. IV replacement of calcium and magnesium may also be needed. Measure and document intake and output. Some patients have an indwelling urinary catheter to obtain accurate measurements. Nasogastric drainage and suction are reserved for more severely ill patients who have continuous vomiting or biliary obstruction. Gastric decompression using a nasogastric tube (NGT) prevents gastric juices from flowing into the duodenum. Nursing Safety Priority Action Alert Because paralytic (adynamic) ileus is a common complication of acute pancreatitis, prolonged nasogastric intubation may be necessary. Assess frequently for the return of peristalsis by asking the patient if he or she has passed flatus or had a stool. The return of bowel sounds is not reliable as an indicator of peristalsis return; passage of flatus or a bowel movement is the most reliable indicator uPromote Nutrition When food is tolerated during the healing phase, the primary health care provider prescribes small, frequent, moderate- to high-carbohydrate, high-protein, low-fat meals. Food should be bland with little spice. GI stimulants such as caffeine-containing food (tea, coffee, cola, and chocolate), as well as alcohol, should be avoided. Monitor the patient beginning to resume oral food intake for nausea, vomiting, and diarrhea. If any of these symptoms occur, notify the primary health care provider immediately. To boost caloric intake, commercial liquid nutritional preparations supplement the diet. uCare Coordination and Transition Management-treat as a potential chronic problem If the patient uses alcohol, instruct him or her to abstain from drinking to prevent further pain attacks and extension of inflammation and pancreatic insufficiency. Tell the patient that if alcohol is consumed, acute pain will return, and further autodigestion of the pancreas may lead to chronic pancreatitis. Teach the patient to notify the primary health care provider after discharge to home if acute abdominal pain or biliary tract disease (as evidenced by jaundice, clay-colored stools, or darkened urine) occurs. These signs and symptoms are possible indicators of complications or disease progression. uEvaluation: Responding Action Alert For the patient with acute pancreatitis, monitor his or her respiratory status every 4 to 8 hours or more often as needed and provide oxygen to promote comfort in breathing. Respiratory complications such as pleural effusions increase patient discomfort. Fluid overload can be detected by assessing for weight gain, listening for crackles, and observing for dyspnea. Carefully monitor for signs of respiratory failure. Chronic pancreatitis is a progressive, destructive disease of the pancreas that has remissions and exacerbations ("flare-ups"). Inflammation and fibrosis of the tissue contribute to pancreatic insufficiency and diminished function of the organ. Chronic pancreatitis can be classified into several categories. Alcoholism is the primary risk factor for chronic calcifying pancreatitis (CCP), the most common type. In the early stages of the disease, pancreatic secretions precipitate as insoluble proteins that plug the pancreatic ducts and flow of pancreatic juices. As the protein plugs become more widespread, the cellular lining of the ducts changes and ulcerates. This inflammatory process causes fibrosis of the pancreatic tissue. Intraductal calcification and marked pancreatic tissue destruction (necrosis) develop in the late stages. The organ becomes hard and firm as a result of cell atrophy and pancreatic insufficiency Chronic Pancreatitis • Intense abdominal pain , a major symptom, that is continuous and burning or gnawing • Abdominal tenderness • Ascites • Possible left upper quadrant mass (if pancreatic pseudocyst or abscess is present) • Respiratory compromise manifesting with adventitious or diminished breath sounds, dyspnea, or orthopnea • Steatorrhea; clay-colored stools • Weight loss • Jaundice • Dark urine • Polyuria, polydipsia, polyphagia (diabetes mellitus) Action Alert If the patient has diabetes, insulin or oral antidiabetic agents for glucose control are prescribed. Patients maintained on total parenteral nutrition (TPN) are particularly susceptible to elevated glucose levels and require regular insulin additives to the solution. Monitor blood glucose to control hyperglycemia. Check finger stick blood glucose (FSBG) or sugar (FSBS) levels every 2 to 4 hours. Chapter 55 describes in detail the care associated with TPN. Prevention of Exacerbations of Chronic Pancreatitis • Avoid things that make your symptoms worse, such as drinking caffeinated beverages. • Avoid alcohol ingestion; refer to self-help group for assistance. • Avoid nicotine. • Eat bland, low-fat, high-protein, and moderate-carbohydrate meals; avoid gastric stimulants such as spices. • Eat small meals and snacks high in calories. • Take the pancreatic enzymes that have been prescribed for you with meals. • Rest frequently; restrict your activity to one floor until you regain your strength.

Cellular Regulation Concept Exemplar: Cirrhosis

Common problems and complications associated with hepatic cirrhosis depend on the amount of damage sustained by the liver. In compensated cirrhosis, the liver is scarred and cellular regulation is impaired, but the organ can still perform essential functions without causing major symptoms. In decompensated cirrhosis, liver function is impaired with obvious signs and symptoms of liver failure. The loss of hepatic function contributes to the development of metabolic abnormalities. Hepatic cell damage may lead to these common complications: • Portal hypertension • Ascites and esophageal varices • Biliary obstruction • Hepatic encephalopathy Compensated versus decompensated uCompensated: When you don't have any symptoms of the disease, you're considered to have compensated cirrhosis. uDecompensated: When your cirrhosis has progressed to the point that the liver is having trouble functioning and you start having symptoms of the disease, you're considered to have decompensated cirrhosis. uComplications uPortal hypertension - portal vein feeding the liver, the liver isn't working. blood doesn't get filtered so it gets backed up Portal hypertension, a persistent increase in pressure within the portal vein greater than 5 mm Hg, is a major complication of cirrhosis. It results from increased resistance to or obstruction (blockage) of the flow of blood through the portal vein and its branches. The blood meets resistance to flow and seeks collateral (alternative) venous channels around the high-pressure area. Blood flow backs into the spleen, causing splenomegaly (spleen enlargement). Veins in the esophagus, stomach, intestines, abdomen, and rectum become dilated. Portal hypertension can result in ascites (excessive abdominal [peritoneal] fluid), esophageal varices (distended veins), prominent abdominal veins (caput medusae), and hemorrhoids. uAscites and esophageal varices Ascites is the collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension (McCance et al., 2019). The collection of plasma protein in the peritoneal fluid reduces the amount of circulating plasma protein in the blood. When this decrease is combined with the inability of the liver to produce albumin because of impaired liver cell functioning, the serum colloid osmotic pressure is decreased in the circulatory system. The result is a fluid shift from the vascular system into the abdomen, a form of "third spacing." As a result, the patient may have hypovolemia and edema at the same time. Massive ascites may cause renal vasoconstriction, triggering the renin-angiotensin system. This results in sodium and water retention, which increases hydrostatic pressure and the vascular volume and leads to more ascites. As a result of portal hypertension, the blood backs up from the liver and enters the esophageal and gastric veins. Esophageal varices occur when fragile, thin-walled esophageal veins become distended and tortuous from increased pressure. The potential for varices to bleed depends on their size; size is determined by direct endoscopic observation. Varices occur most often in the distal esophagus but can be present also in the stomach and rectum. uCoagulation defects uJaundice uPSE with hepatic coma uHepatorenal syndrome uSpontaneous bacterial peritonitis PSE, Portal-systemic encephalopathy. Assessment: Noticing •Assess •Assess for exposure to alcohol and drugs, herbs, chemicals. •Determine •Determine if there has ever been a needlestick injury, tattoo placement, imprisonment, or employment as a healthcare worker, firefighter, or police officer. •Assess •Assess sexual history and orientation. •Inquire about •Inquire about family history. •Collect •Collect previous medical history. Treatments uMedications to reverse poisoning. uAcute liver failure caused by acetaminophen overdose is treated with a medication called acetylcysteine. uThis medication may also help treat other causes of acute liver failure. Mushroom and other poisonings also may be treated with drugs that can reverse the effects of the toxin and may reduce liver damage. uRelieving pressure caused by excess fluid in the brain. uCerebral edema caused by acute liver failure can increase pressure on your brain. Medications can help reduce the fluid buildup in your brain. uLiver transplant. uWhen acute liver failure can't be reversed, the only treatment may be a liver transplant. During a liver transplant, a surgeon removes your damaged liver and replaces it with a healthy liver from a donor. uScreening for infections. uYour medical team will take samples of your blood and urine every now and then to be tested for infection. If your doctor suspects that you have an infection, you'll receive medications to treat the infection. uPreventing severe bleeding. u Your doctor can give you medications to reduce the risk of bleeding. If you lose a lot of blood, your doctor may perform tests to find the source of the blood loss. You may require blood transfusions. uProviding nutritional support Bleeding esophageal varices are a life-threatening medical emergency. Severe blood loss may occur, resulting in shock from hypovolemia. The bleeding may present as either hematemesis (vomiting blood) or melena (black, tarry stools). Loss of consciousness may occur before any observed bleeding. Variceal bleeding can occur spontaneously with no precipitating factors. However, any activity that increases abdominal pressure may increase the likelihood of a variceal bleed, including heavy lifting or vigorous physical exercise. In addition, chest trauma or dry, hard food in the esophagus can cause bleeding. Assessment: Noticing PhysicalAssessment—esophageal varices(complication) Assessment: Noticing Because cirrhosis has a slow onset, many of the early signs and symptoms are vague and nonspecific. Assess for: • Fatigue • Significant change in weight • GI symptoms, such as anorexia and vomiting • Pain in the abdominal area and liver tenderness (both of which may be ignored by the patient) •Laboratory assessment •AST, ALT, LDH Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) typically are elevated because these enzymes are released into the blood during hepatic inflammation. •Alkaline phosphatase Increased alkaline phosphatase and gamma-glutamyl transpeptidase (GGT) levels are caused by biliary obstruction and therefore may increase in patients with cirrhosis. Alkaline phosphatase is a nonspecific bone, intestinal, and liver enzyme. However, alkaline phosphatase also increases when bone disease, such as osteoporosis, is present. Total serum bilirubin levels also rise. Indirect bilirubin levels increase in patients with cirrhosis because of the inability of the failing liver to excrete bilirubin. Therefore bilirubin is present in the urine (urobilinogen) in increased amounts. •GGT •Serum protein, albumin Total serum albumin levels are decreased in patients with severe or chronic liver disease as a result of decreased synthesis by the liver (Pagana & Pagana, 2018). Loss of osmotic "pull" proteins such as albumin promotes the movement of intravascular fluid into the interstitial tissues (e.g., ascites). Prothrombin time/international normalized ratio (PT/INR) is prolonged because the liver decreases the production of prothrombin. Late-Stage Cirrhosis • Jaundice and icterus (yellow coloration of the eye sclerae) • Dry skin • Pruritus (itchy skin) • Rashes • Purpuric lesions, such as petechiae (round, pinpoint, red-purple hemorrhagic lesions) or ecchymoses (large purple, blue, or yellow bruises) • Warm and bright red palms of the hands (palmar erythema) • Vascular lesions with a red center and radiating branches, known as spider angiomas (also called telangiectases, spider nevi, or vascular spiders), on the nose, cheeks, upper thorax, and shoulders • Ascites Massive ascites can be detected as a distended abdomen with bulging flanks (Fig. 53.2). The umbilicus may protrude, and dilated abdominal veins (caput medusae) may radiate from the umbilicus. Ascites can cause physical problems. • Peripheral dependent edema of the extremities and sacrum • Vitamin deficiency (especially fat-soluble vitamins A, D, E, and K) •Imaging assessment •Abdominal x-rays •CT, MRI •MR elastography •Other diagnostic assessment •Liver US, arteriography, EGD, ERCP Planning and Implementation: Responding •Managing fluid volume •Preventing or managing hemorrhage (see next slide) •Preventing or managing hepatic encephalopathy Hepatic Encephalopathy Hepatic encephalopathy (also called portal-systemic encephalopathy [PSE] ) is a complex cognitive syndrome that results from liver failure and cirrhosis. Patients report sleep disturbance, mood disturbance, mental status changes, and speech problems early as this complication begins. Hepatic encephalopathy may be reversible with early intervention. Later neurologic symptoms include an altered level of consciousness, impaired thinking processes, and neuromuscular problems. The nurse is caring for a client who is diagnosed with cirrhosis. Which serum laboratory value(s) will the nurse expect to be abnormal? Select all that apply. A. Prothrombin time B. Serum bilirubin C. Albumin D. Aspartate aminotransferase (AST) E. Lactate dehydrogenase (LDH) F. Acid phosphatase Physiological Integrity The nurse is caring for a client in end-stage liver failure. Which interventions should be implemented when observing for hepatic encephalopathy? Select all that apply. A. Assess the client's neurologic status as prescribed. B. Monitor the client's hemoglobin and hematocrit levels. C. Monitor the client's serum ammonia level. D. Monitor the client's electrolyte values daily. E. Prepare to insert an esophageal balloon tamponade tube. F. Make sure the client's fingernails are short.

Pancreatic Cancer

Signs and symptoms depend on the site of origin or metastasis. The head of the pancreas is the most common site. The tumors are usually small lesions with poorly defined margins. Jaundice results from tumor compression and obstruction of the common bile duct and from gallbladder dilation, causing the organ to enlarge. Cancers of the body and tail of the pancreas are usually large and invade the entire tail and body. These tumors may be palpable abdominal masses, especially in the thin patient. Through metastatic spread via the splenic vein, metastasis to the liver may cause hepatomegaly (enlargement of the liver). Regardless of where it originates, it spreads rapidly through the lymphatic and venous systems to other organs. Venous thromboembolism is a common complication of pancreatic cancer. Necrotic products of the pancreatic tumor are believed to have thromboplastic properties resulting in the blood's hypercoagulable state. In addition, the patient is at high risk because of decreased mobility and extensive surgical manipulation. Pancreatic Cancer • Jaundice • Icterus • Clay-colored (light) stools • Dark urine • Abdominal pain, usually vague, dull, or nonspecific, that radiates into the back • Weight loss • Anorexia • Nausea or vomiting • Glucose intolerance • Splenomegaly (enlarged spleen) • Flatulence • Gastrointestinal bleeding • New-onset diabetes mellitus • Ascites (abdominal fluid) • Leg or calf pain (from thrombophlebitis) • Weakness and fatigue Difficult to diagnose uTreatment has limited results uLow survival rates uNonsurgical management As in other types of cancer, chemotherapy or radiation is used to relieve pain by shrinking the tumor. It may be used before, after, or instead of surgery. Chemotherapy has had limited success in increasing survival time. In most cases, combining agents has been more successful than single-agent chemotherapy. 5-Fluorouracil (5-FU), a commonly used drug, may be given alone or with gemcitabine for locally advanced, or unresectable, pancreatic cancers. Observe for adverse drug effects, such as fatigue, rash, anorexia, and diarrhea. Chapter 20 discusses nursing implications of chemotherapy in more detail. Other targeted therapies being investigated include growth factor inhibitors, antiangiogenesis factors, and kinase inhibitors. Kinase inhibitors are a newer group of drugs that focus on cancer cells with little or no effect on healthy cells. Chapter 20 describes general nursing interventions associated with chemotherapy. uDrug therapy To control pain, the patient takes high doses of opioid analgesics (usually morphine) as prescribed before the pain escalates and peaks. Because of the poor prognosis, drug dependency is not a consideration. Chapter 5 describes in detail the care of the patient with chronic cancer pain. uRadiation therapy Intensive external beam radiation therapy to the pancreas may offer pain relief by shrinking tumor cells, alleviating obstruction, and improving food absorption. It does not improve survival rates. The patient may experience discomfort during and after the radiation treatments. uBiliary stent insertion For patients experiencing biliary obstruction who are at high surgical risk, biliary stents placed percutaneously (through the skin) can ensure patency to relieve pain. These stents are devices made of plastic materials that keep the ducts of the biliary system open. Using another approach, self-expandable stents may be inserted endoscopically to relieve obstruction. Partial pancreatectomy is the preferred surgery for tumors smaller than 3 cm in diameter, depending on location and length of time since diagnosis. Recent technologic advances have expanded the role of minimally invasive surgery (MIS) via laparoscopy in the staging, palliation, and removal of pancreatic cancers. The procedure selected depends on the purpose of the surgery and stage of the disease. For example, if the patient has a biliary obstruction, a laparoscopic procedure to relieve it is performed. This procedure diverts bile drainage into the jejunum. For larger tumors, the surgeon may perform either a radical pancreatectomy or the Whipple procedure (pancreaticoduodenectomy). These procedures have traditionally been done using an open surgical approach. Because of new advances in laparoscopic technology using a hand-assist or robotic-assist device, this method is beginning to replace the conventional method. Some surgeons are not yet trained in how to perform this technique. •Carcinoma of the pancreas. A cross-section through the head of the pancreas and adjacent common bile duct showing both an ill-defined mass in the pancreatic substance (arrowheads) and the green discoloration of the duct resulting from total obstruction of bile flow.

One of the most common causes of pancreatitis

bile duct obstruction

Surgical Management

uPreoperative care For optimal nutrition, TPN may be necessary in addition to tube feedings or as a single measure. When central venous access is required, a peripherally inserted central catheter (PICC) or other type of IV catheter may be necessary. Meticulous IV line care is an important nursing measure to prevent catheter sepsis. Sterile dressing changes and site observation are extremely important. Additional nursing care measures for the patient receiving TPN are given in Chapter 55. Monitor nutrition indicators such as serum prealbumin and albumin. For the laparoscopic procedure, no bowel preparation is needed. However, either approach requires that the patient have nothing by mouth (NPO) for at least 6 to 8 hours before surgery. Surgeon preference and agency policy determine the preferred protocol for preoperative preparation. uNG tube may be inserted - nose to ear to sternum - If put in lung? They'll cough, turn blue. Pull it back til they stop coughing - Why do we put them in? for nutrition, hydrate, suction stomach contents, decompress air and relieve distention uTPN typically begun uOperative procedure may include Whipple procedure The Whipple procedure (radical pancreaticoduodenectomy) is an extensive surgical procedure used most often to treat cancer of the head of the pancreas. The procedure entails removal of the proximal head of the pancreas, the duodenum, a portion of the jejunum, the stomach (partial or total gastrectomy), and the gallbladder, with anastomosis of the pancreatic duct (pancreaticojejunostomy), the common bile duct (choledochojejunostomy), and the stomach (gastrojejunostomy) to the jejunum (Fig. 54.3). In addition, the surgeon may remove the spleen (splenectomy). uPostoperative care uObserve for complications uGI drainage monitoring uPositioning uFluid and electrolyte assessment uGlucose monitoring For patients having one of these procedures, observe for and implement preventive measures for these common surgical complications: • Diabetes (Check blood glucose often.) • Hemorrhage (Monitor pulse, blood pressure, skin color, and mental status [e.g., LOC].) • Wound infection (Monitor temperature and assess wounds for redness and induration [hardness].) • Bowel obstruction (Check bowel sounds and stools.) • Intra-abdominal abscess (Monitor temperature and patient's report of severe pain.) Immediately after surgery the patient is NPO and usually has a nasogastric tube (NGT) to decompress the stomach. Monitor GI drainage and tube patency. In open surgical approaches, biliary drainage tubes are placed during surgery to remove drainage and secretions from the area and prevent stress on the anastomosis sites. Assess the tubes and drainage devices for tension or kinking and maintain them in a dependent position. Monitor the drainage for color, consistency, and amount. The drainage should be serosanguineous. The appearance of clear, colorless, bile-tinged drainage or frank blood with an increase in output may indicate disruption or leakage of an anastomosis site The development of a fistula (an abnormal passageway) is the most common and most serious postoperative complication. Biliary, pancreatic, or gastric fistulas result from partial or total breakdown of an anastomosis site. The secretions that drain from the fistula contain bile, pancreatic enzymes, or gastric secretions, depending on which site is ruptured. These secretions, particularly pancreatic fluid, are corrosive and irritating to the skin; and internal leakage causes chemical peritonitis. Peritonitis (inflammation and infection of the peritoneum causing boardlike abdominal rigidity) requires treatment with multiple antibiotics. If you suspect any postoperative complications resulting from MIS or open surgical approaches, call the surgeon or Rapid Response Team immediately and provide assessment findings that support your concerns.. NG, Nasogastric; TPN, total parenteral nutrition. Whipple procedure or radical pancreaticoduodenectomy. This surgical procedure involves resection of the proximal pancreas, adjoining duodenum, distal portion of the stomach, and distal portion of the common bile duct. The pancreatic duct, common bile ducts, and stomach are anastomosed to the jejunum. The three anastomoses that constitute the Whipple procedure: choledochojejunostomy, pancreaticojejunostomy, and gastrojejunostomy. Action Alert To detect early signs of hypovolemia and prevent shock, closely monitor vital signs for decreased blood pressure and increased heart rate, decreased vascular pressures with a pulmonary artery catheter (Swan-Ganz catheter) (in ICU setting), and decreased urine output. Be alert for pitting edema of the extremities, dependent edema in the sacrum and back, and an intake that far exceeds output. Maintain sequential compression devices to prevent deep vein thrombosis.

Intestinal Obstruction KNOW THIS page 1112

uTypes uNonmechanical u'ileus' or 'paralytic ileus uthe natural movement of the bowel peristalsis fails to happen paralytic ileus - get it from abdominal surgery. anything you eat, you'll throw up. treatment- put in an NG tube. NPO. get abdominal xrays every day. Ins and outs every day. In mechanical obstruction, the bowel is physically blocked by problems outside the intestine (e.g., adhesions), in the bowel wall (e.g., Crohn's disease), or in the intestinal lumen (e.g., tumors). Nonmechanical obstruction (also known as paralytic ileus or functional obstruction) does not involve a physical obstruction in or outside the intestine. Instead, peristalsis is decreased or absent because of neuromuscular disturbance, resulting in a slowing of the movement or a backup of intestinal contents uCaused by bacteria or viruses uMechanical uPartial or complete blockage of the intestine uCan happen along any point of the intestinal tract uAdhesions or scar tissue that form after surgery uImpacted stool uHernias uIntrospection (one segment of bowel into another) uVolvulus (twisted intestine) uTumors Physical Assessment uObstipation-severe form of constipation - Obstipation (no passage of stool) and failure to pass flatus are associated with complete obstruction; diarrhea may be present in partial obstruction. uAbdominal distension uPeristaltic waves may be visible uBobborygmi -rumbling or gurgling noise made by movement of fluid and gas in the intestines Diagnostic Assessment abdominal x-ray, CT, US, Barium Enema (enhancing imaging of colon) Nursing Care of Patients Who Have an Intestinal Obstruction • Monitor vital signs, especially blood pressure and pulse, for indications of fluid balance. • Assess the patient's abdomen at least twice a day for bowel sounds, distention, and passage of flatus. • Monitor fluid and electrolyte balance status, including laboratory values. • Manage the patient who has a nasogastric tube (NGT): • Monitor drainage. • Ensure tube patency. • Check tube placement. • Irrigate tube as prescribed. • Maintain the patient on NPO status. • Provide frequent mouth and nares care. • Maintain the patient in a semi-Fowler position. • Give analgesics for pain as prescribed. • Maintain IV therapy for fluid and electrolyte replacement. • Give alvimopan as prescribed for patients with a postoperative ileus. • Maintain parenteral nutrition if prescribed. Priority Collaborative management problems for patients with intestinal obstruction include Potential for injury (e.g., peritonitis, acute kidney injury, etc.) due to obstruction Acute pain due to obstruction Potential Infection related to complications Interventions u uNonsurgical Management uNasogastric tubes (decompresses bowel) uIV Fluid replacement In addition to being NPO, patients typically have a nasogastric tube (NGT) inserted to decompress the bowel by draining fluid and air. The tube is attached to suction. Nasogastric tubes. Most patients with an obstruction have an NGT unless the obstruction is mild. A Salem sump tube is inserted through the nose and placed into the stomach. It is attached to low continuous suction. At least every 4 hours, assess the patient with an NGT for proper placement of the tube, tube patency, and output (quality and quantity). Monitor the nasal skin around the tube for irritation. Use an approved device that secures the tube to the nose to prevent accidental removal. Assess for peristalsis by auscultating for bowel sounds with the suction disconnected (suction masks peristaltic sounds). IV fluid replacement and maintenance are indicated for all patients with intestinal obstruction because the patient is NPO and fluid and electrolyte balance is altered (particularly potassium and sodium) as a result of vomiting and nasogastric suction. uSurgical Management uExploratory laparotomy uPartial (see if goes away on own-low fiber diet) versus Complete Obstruction (surgery to the obstruction) exploratory laparotomy (a surgical opening of the abdominal cavity) to investigate the cause of the obstruction is performed. In the conventional open surgical approach, the surgeon makes a large incision, enters the abdominal cavity, and explores for obstruction and its cause, if possible (exploratory laparotomy). If adhesions are found, they are lysed (cut and released). Obstruction caused by a tumor or diverticulitis requires a colon resection with primary anastomosis or a temporary or permanent colostomy. If obstruction is caused by intestinal infarction, an embolectomy, thrombectomy, or resection of the gangrenous small or large bowel may be necessary. In severe cases a colectomy (surgical removal of the entire colon) may be needed.

Appendicitis

Appendicitis is an acute inflammation of the vermiform appendix that occurs most often among young adults. It is the most common cause of right lower quadrant (RLQ) pain. The appendix usually extends off the proximal cecum of the colon just below the ileocecal valve. Inflammation occurs when the lumen (opening) of the appendix is obstructed (blocked), leading to infection as bacteria invade the wall of the appendix. Food/bacteria gets trapped and causes infection. If it ruptures, it can cause peritonitis a serious medical condition appendix becomes inflamed and painful. uMcBurney's point is located midway between the anterior iliac crest and the umbilicus in the right lower quadrant. uClassic area for localized tenderness during the later stages of appendicitis Abdominal pain that increases with cough or movement and is relieved by bending the right hip or the knees suggests perforation and peritonitis.

Pancreatic Abscess

Area filled with pus within the pancreas Most serious complication of pancreatitis Always fatal if untreated Symptoms High fever Diagnostics & Treatments Blood cultures Percutaneous drainage Laparoscopy Antibiotic treatment alone does not resolve abscess. A secondary bacterial invasion may lead to suppuration (pus formation) of the pancreatic tissue called a pancreatic abscess. Pancreatic abscesses must be drained promptly to prevent sepsis. Mild infected lesions may be absorbed. When infected lesions are severe, calcification and fibrosis occur.

Inflammatory Disorders Plan of Care .

Assessment: Noticing Cardinal Signs abdominal pain, tenderness, and distension Laboratory Assessment: WBC counts are often elevated to 20,000/mm^3 Analysis: Interpreting/Planning: Responding Potential for Infection Potential for fluid volume shift due to fluid moving into interstitial or peritoneal space. Restore Fluid Volume Balance Diarrhea Risk for Deficient Fluid Volume Anxiety Ineffective Coping Acute Pain and Manage pain Imbalanced Nutrition: Less Than Body Requirements Deficient Knowledge

Gastric Cancer

Most cancers of the stomach are adenocarcinomas. This type of cancer develops in the mucosal cells that form the innermost lining of any portion or all of the stomach. Gastric cancer usually begins in the glands of the stomach mucosa. Atrophic gastritis and intestinal metaplasia (abnormal tissue development) are precancerous conditions. Inadequate acid secretion in patients with atrophic gastritis creates an alkaline environment that allows bacteria (especially H. pylori) to multiply. This infection causes mucosa-associated lymphoid tissue (MALT) lymphoma, which starts in the stomach Infection with H. pylori is the largest risk factor for gastric cancer because it carries the cytotoxin-associated gene A (CagA) gene. Patients with pernicious anemia, gastric polyps, chronic atrophic gastritis, and achlorhydria (absence of secretion of hydrochloric acid) are two to three times more likely to develop gastric cancer. uMost stomach cancers are adenocarcinomas. uMay be asymptomatic until detected in advanced stage Etiology and Genetic Risk uInfection with H. pylori- Infection with H. pylori is the largest risk factor for gastric cancer because it carries the cytotoxin-associated gene A (CagA) gene. Patients with pernicious anemia, gastric polyps, chronic atrophic gastritis, and achlorhydria (absence of secretion of hydrochloric acid) are two to three times more likely to develop gastric cancer. Causes are gastritis, bad diet uHistory of pernicious anemia, gastric polyps, chronic atrophic gastritis, achlorhydria uEating pickled foods, nitrates from processed foods, and salt added to foods - The disease also seems to be positively correlated with eating excessive pickled foods, nitrates from processed foods, and salt added to food. The ingestion of these foods over a long period can lead to atrophic gastritis, a precancerous condition. uPrior gastric surgery -Gastric surgery seems to increase the risk for gastric cancer because of the possible development of atrophic gastritis, which results in changes to the mucosa. Incidence and Prevalence uMore common in males than females, and those over 50 uIn U.S., Hispanic Americans, African Americans, and Asian/Pacific Islanders have higher incidence. Health Promotion and Maintenance uFollow treatment regimen closely. uEat well-balanced diet; limit pickled, processed, and salted foods. Assessment: Noticing uAsk about dietary history; previous H. pylori infection; gastric surgery or polyps. uIndigestion and abdominal discomfort are most common early symptoms. uAnemia, progressive weight loss, nausea and vomiting may be present in advanced cancer. In patients with advanced disease, anemia is evidenced by low hematocrit and hemoglobin values. Patients may have macrocytic or microcytic anemia associated with decreased iron or vitamin B12 absorption. The stool may be positive for occult blood. Hypoalbuminemia and abnormal results of liver tests (e.g., bilirubin and alkaline phosphatase) occur with advanced disease and hepatic metastasis. Early Versus Advanced Gastric Cancer Early Gastric Cancer • Dyspepsia • Abdominal discomfort initially relieved with antacids • Feeling of fullness • Epigastric, back, or retrosternal pain Advanced Gastric Cancer • Nausea and vomiting • Iron deficiency anemia • Palpable epigastric mass • Enlarged lymph nodes • Weakness and fatigue • Progressive weight loss uEGD, EUS, CT, PET, and MRI are used for diagnosis. The primary health care provider uses esophagogastroduodenoscopy (EGD) with biopsy for definitive diagnosis of gastric cancer. (See Chapter 48 for a discussion of nursing care associated with this diagnostic test.) The lesion can be viewed directly, and biopsies of all visible lesions can be performed to determine the presence of cancer cells. During the endoscopy, an endoscopic (endoluminal) ultrasound (EUS) of the gastric mucosa can also be performed. This technology allows the primary health care provider to evaluate the depth of the tumor and the presence of lymph node involvement, which permits more accurate staging of the disease. CT, positron emission tomography (PET), and MRI scans of the chest, abdomen, and pelvis are used in determining the extent of the disease and planning therapy. Interventions: Responding uNonsurgical management uRadiation, chemotherapy Combination chemotherapy with multiple cycles of drugs such as cisplatin and epirubicin before and after surgery may be given. Bone marrow suppression, nausea, and vomiting are common adverse drug effects. uSurgical management uGastrectomy or subtotal (partial) gatrectomy - Total: all of stomach removed - Partial: part of stomach removed Surgical resection by removing the tumor is the preferred method for treating gastric cancer. The primary surgical procedures for the treatment of gastric cancer are total and subtotal (partial) gastrectomy. Dietary restriction - no sugar, they get dumping syndrome Dumping syndrome is a term that refers to a group of vasomotor symptoms that occur after eating in patients who have had a gastrectomy. This syndrome is believed to occur as a result of the rapid emptying of food contents into the small intestine, which shifts fluid into the gut, causing abdominal distention. Observe for early manifestations of this syndrome, which typically occur within 30 minutes of eating. Symptoms include vertigo, tachycardia, syncope, sweating, pallor, palpitations, and the desire to lie down Dumping syndrome is managed by nutrition changes that include decreasing the amount of food taken at one time and eliminating liquids ingested with meals. In collaboration with the registered dietitian nutritionist, teach the patient to eat a high-protein, high-fat, low- to moderate-carbohydrate diet uPreoperative care Before conventional open-approach surgery, a nasogastric tube (NGT) is often inserted and connected to suction to remove secretions and empty the stomach. This allows surgery to take place without contamination of the peritoneal cavity by gastric secretions. The NGT remains in place for a few days after surgery to prevent the accumulation of secretions, which may lead to vomiting or GI distention and pressure on the incision. Patients having laparoscopic surgery (minimally invasive surgery [MIS]) do not require an NGT. uOperative procedures The surgeon usually removes part or all of the stomach to take out the tumor. For the patient with a removable growth in the proximal (upper) third of the stomach, a total gastrectomy is typically performed (Fig. 50.3). In this procedure the surgeon removes the entire stomach along with the lymph nodes and omentum. The surgeon sutures the esophagus to the duodenum or jejunum to reestablish continuity of the GI tract. uPostoperative care Provide evidence-based postoperative care for patients who have had general anesthesia to prevent atelectasis, paralytic ileus, wound infection, and peritonitis

Cholecystectomy

Cholecystectomy is the surgical removal of the gallbladder. One of two procedures is performed: the laparoscopic cholecystectomy or, in rare cases, the traditional open-approach cholecystectomy. Laparoscopic cholecystectomy. Laparoscopic cholecystectomy, a minimally invasive surgery (MIS), is the "gold standard" and is performed far more often than the traditional open approach. The advantages of MIS when compared with the open approach include: • Complications are not common. • The death rate is very low. • Bile duct injuries are rare. • Patient recovery is quicker. • Postoperative pain is less severe. The laparoscopic procedure (often called a "lap chole") is commonly performed on an ambulatory care basis in a same-day surgery suite or agency Laparoscopic versus traditional uMinimally invasive uPerformed far more than the traditional open approach uComplications are not common. uPatient recovery is quicker. uPostoperative pain is less severe. uPreoperative uFasting uIVF uPost Operative uAntibiotics uPain Medications Action Alert After a laparoscopic cholecystectomy, assess the patient's oxygen saturation level using pulse oximetry frequently until the effects of the anesthesia have passed. Remind the patient to perform deep-breathing exercises every hour. Traditional cholecystectomy.Use of the open surgical approach (abdominal laparotomy) has greatly declined during the past several decades. The few patients who have this type of surgical approach usually have severe biliary obstruction, and the ducts need to be explored to ensure patency. The nurse provides the usual preoperative care and teaching in the operating suite on the day of surgery (see Chapter 9). The surgeon removes the gallbladder through a right upper quadrant incision and explores the biliary ducts for the presence of stones or other cause of obstruction. The surgeon usually inserts a drainage tube such as a Jackson-Pratt (JP) drain. This tube is placed in the gallbladder bed to prevent fluid accumulation. The drainage is usually serosanguineous (serous fluid mixed with blood) and is stained with bile in the first 24 hours after surgery. A one-dose IV antibiotic may be given to prevent infection before or during surgery.

Cholecystitis

Cholecystitis is an inflammation of the gallbladder that affects many adults, very commonly in affluent countries. Two types of acute cholecystitis can occur: calculous and acalculous cholecystitis. The most common type is calculous cholecystitis, in which chemical irritation and inflammation result from gallstones, or calculi (cholelithiasis), that obstruct the cystic duct (most often), gallbladder neck, or common bile duct (choledocholithiasis) (Fig. 54.1). When the gallbladder is inflamed, trapped bile is reabsorbed and acts as a chemical irritant to the gallbladder wall. Reabsorbed bile, in combination with impaired circulation, edema, and distention of the gallbladder, causes ischemia and infection. The result is tissue sloughing with necrosis and gangrene within the gallbladder itself. The gallbladder wall may eventually perforate (rupture). If the perforation is small and localized, an abscess may form. Peritonitis (infection of the peritoneum) may result if the perforation is large. The exact mechanism of gallstone formation is not clearly understood, but abnormal metabolism of cholesterol and bile salts plays an important role. Chronic cholecystitis most often results when repeated episodes of cystic duct obstruction cause chronic inflammation . Calculi are almost always present. The gallbladder becomes fibrotic and atrophied, which results in decreased motility and deficient absorption. Young thin women, especially those who are athletic (e.g., gymnasts), may experience chronic cholecystitis without calculi. In this case, the gallbladder atrophies and causes pain that is often misdiagnosed as gastritis. This problem is most likely to occur when consuming a diet low in fat, such as a vegetarian diet. Gallstones- causes abdominal pain, have a temp, and malaise. Need to be removed with surgery, cholecystectomy T-tube - keeps common bile duct open, and helps drain bile after surgery. What do you teach pt for when gallbladder is removed? Can't eat fatty foods, fast food, greasy foods. When you eat this, you can have a lot of stomach pain and immediately have to go to the bathroom. Gallstones within the gallbladder and obstructing the common bile and cystic ducts. Assessment questions uWhen did your symptoms begin? uHave you had pain like this before? uAre your symptoms constant or do they come and go? uHow severe are your symptoms? uWhat, if anything, seems to improve your symptoms? uWhat, if anything, appears to worsen your symptoms?

Cirrhosis

Cirrhosis is extensive, irreversible scarring of the liver, usually caused by a chronic reaction to hepatic inflammation and necrosis. This scarring process directly impairs cellular regulation . The disease typically develops slowly and has a progressive, prolonged, destructive course resulting in end-stage liver disease. Cirrhosis is characterized by widespread fibrotic (scarred) bands of connective tissue that change the liver's anatomy and physiology. Inflammation caused by either toxins or disease results in extensive degeneration and destruction of hepatocytes (liver cells). As cirrhosis develops, the tissue becomes nodular. These nodules can block bile ducts and normal blood flow throughout the liver. Impairments in blood and lymph flow result from compression caused by excessive fibrous tissue. In early disease, the liver is usually enlarged and firm. As the pathologic process continues, the liver shrinks in size and becomes harder, resulting in decreased liver function over weeks to years. Characterized by widespread fibrotic (scarred) bands of connective tissue •This changed the liver's normal makeup and its associated cellular regulation. •Inflammation destroys hepatocytes. •Liver become nodular; blood and lymph flow are impaired.

Overview of the GI Tract Chapter 48

Class notes - GI order inspect, auscultation, percussion, palpation Start in right lower quadrant because that is where the ileocecal valve is. Accessory organs: liver, gallbladder, pancreas Liver- filters everything. breaks down fat Gallbladder- helps digest fat Pancreas - makes insulin. helps with digestion. If you have liver problems, don't take Tylenol Why is it important to test for blood in stool? Colon cancer GI Bleed - can happen in the entire GI tract, polyps can occur anywhere - Upper GI bleed is BRIGHT RED causes- ulcers, esophageal varacies, cancer, polyps - Lower GI bleed has black, tarry dark stool. Coffee grounds. priority nursing interventions- monitor VS, start IV, H+H, give blood what can cause it? Ulcers, stress, trauma, esophageal varices, cancer HandH type and screen How long do we listen to each quadrant? 5 mins uStructure and function uOral cavity uEsophagus uStomach uPancreas uLiver and gallbladder uSmall and large intestine

Crohn's Disease

Crohn's disease (CD) is a chronic inflammatory disease of the small intestine (most often), the colon, or both. Inflammation of the digestive tract uCauses uImmune System-bacteria or virus uHeredity uRisk factors-age, ethnicity(Caucasian), family history, smoking, NSAIDS uSigns and symptoms uAbdominal pain, severe diarrhea, fatigue, weight loss fever, blood in stool, pain and/or drainage around the anus, malnutrition Most patients report diarrhea, abdominal pain, and low-grade fever. Fever is common with fistulas, abscesses, and severe inflammation. If the disease occurs in only the ileum, diarrhea occurs five or six times per day, often with a soft, loose stool. Steatorrhea (fatty diarrheal stools) is common. Stools may contain bright red blood (McCance et al., 2019). Abdominal pain from inflammation is usually constant and often located in the right lower quadrant Action Alert For the patient with Crohn's disease, be especially alert for signs and symptoms of peritonitis (discussed earlier in this chapter), small-bowel obstruction, and nutritional and fluid imbalances. Early detection of a change in the patient's status helps reduce these life-threatening complications. uDiagnostic tests uColonoscopy, CT, MRI X-rays show the narrowing, ulcerations, strictures, and fistulas common with Crohn's disease. Magnetic resonance enterography (MRE) is performed to determine bowel activity uTreatments uNo cure uReduce the symptoms uAntiinflmmatory Drugs uCorticosteroids uImmune System Supressors For mild-to-moderate disease, 5-ASA drugs may be effective, although research shows that their usage for CD has produced mixed results (see the Drug Therapy discussion in the Ulcerative Colitis section). Most patients have moderate-to-severe disease and need stronger drug therapy to control their symptoms. Two agents that may be prescribed for CD are azathioprine and mercaptopurine. These drugs suppress the immune system and can lead to serious infections. Methotrexate may also be given to suppress immune activity of the disease. A group of biologic response modifiers (BRMs), also known as monoclonal antibody drugs, have been approved for use in CD when other drugs have been ineffective. These drugs inhibit tumor necrosis factor (TNF)-alpha, which decreases the inflammatory response. Examples of commonly used drugs for patients with CD include infliximab, adalimumab, natalizumab, and certolizumab pegol. These agents are not given to patients with a history of cancer, heart disease, or multiple sclerosis

Liver Problems

DON'T TAKE TYLENOL OR HARD MEDS ON LIVER IF YOU HAVE LIVER PROBLEMS! NEED TO INCREASE PROTEIN. For pain, give opioids not tylenol ETOH Cirrhosis - scarring Liver failure Jaundice Ascites = fluid. need to remove fluid Paracentesis Need Is and Os, daily weights, decrease sodium in diet Tremors = alcohol withdrawal is different than liver problem shaking. Flapping is liver issues, only the hands and they flap like a bird Asteriks - tremoring what is gonna be elevated when we have liver failure? everything is gonna be UP!!! Protein is gonna be the only thing that's low Incidence and Prevalence u1 in 10 Americans have liver diseases Etiology and Genetic Risk uHepatitis C—second leading cause in the United States uHepatitis B and D—most common cause worldwide uNAFLD (Non-Alcoholic Fatty Liver Disease) uAlcohol use—excessive and prolonged

Diverticula, Diverticulitis, Diverticulosis

Diverticulosis is the presence of many abnormal pouchlike herniations (diverticula) in the wall of the intestine. Acute diverticulitis is the inflammation or infection of diverticula. diverticula - how do they occur? food gets stuck in pockets and it gets infected. s/s -pain, bloating What can't you eat? nuts, seeds (strawberries, cucumbers, blackberries) Diverticula can occur in any part of the small or large intestine, but they usually occur in the sigmoid colon (Fig. 52.6). The muscle of the colon hypertrophies, thickens, and becomes rigid, and herniation of the mucosa and submucosa through the colon wall is seen. Diverticula seem to occur at points of weakness in the intestinal wall, often at areas where blood vessels interrupt the muscle layer. Muscle weakness develops as part of the aging process or because of a lack of fiber in the diet. Diverticula without inflammation cause few problems. However, if undigested food or bacteria become trapped in a diverticulum, blood supply to that area is reduced. Bacteria invade the diverticulum, resulting in diverticulitis, which then can perforate and develop a local abscess. A perforated diverticulum can progress to an intra-abdominal perforation with peritonitis. Lower GI bleeding may also occur (see earlier discussion in this chapter under Ulcerative Colitis). High intraluminal pressure forces the formation of a pouch in the weakened area of the mucosa. Diets low in fiber that cause less bulky stool and constipation have been implicated in the formation of diverticula. Retained undigested food in diverticula is suggested to be one cause of diverticulitis. The retained food reduces blood flow to that area and makes bacterial invasion of the sac easier treatment? Antibiotics and fluids Diverticular Group Diverticulosis, diverticular bleeding, and diverticulitis Affecting the colon or large intestine. Causes herniation or out-pouching of the walls of colon, creating small pouches Caused by trapped food or bacteria Pain, which may be constant and persist for several days. LLQ of the abdomen is the usual site of the pain. RLQ side of the abdomen is more painful, especially in people of Asian descent. Nausea and vomiting. Fever. Abdominal tenderness. Constipation or, less commonly, diarrhea. The patient with diverticulitis may have abdominal pain, most often localized to the left lower quadrant. It is intermittent at first but becomes progressively steady. Occasionally, pain may be just above the pubic bone or may occur on one side. Abdominal pain is generalized if peritonitis has occurred. Nausea and vomiting are common. The patient's temperature is elevated, ranging from a low-grade fever to 101°F (38.3°C). Chills may be present. Often an increased heart rate (tachycardia) occurs with fever Several abnormal outpouchings, or herniations, in the wall of the intestine, which are diverticula. These can occur anywhere in the small or large intestine but are found most often in the sigmoid, as shown in this figure. Diverticulitis is the inflammation of a diverticulum that occurs when undigested food or bacteria become trapped in the diverticulum. Diverticulitis • Provide antibiotics and analgesics as prescribed. Observe older patients carefully for side effects of these drugs, especially confusion (or increased confusion), and orthostatic hypotension. • Do not give laxatives or enemas. Teach the patient and family about the importance of avoiding these measures. • Encourage the patient to rest and to avoid activities that may increase intra-abdominal pressure, such as straining and bending. • While diverticulitis is active, provide a low-fiber diet. When the inflammation resolves, provide a high-fiber diet. Teach the patient and family about these diets and when they are appropriate. • Because older patients do not always experience the typical pain or fever expected, observe carefully for other signs of active disease, such as a sudden change in mental status. • Perform frequent abdominal assessments to determine distention and tenderness on palpation. • Check stools for occult or frank bleeding. The nurse is teaching a client about nutrition and diverticulosis. Which food will the nurse teach the client to avoid? A. Cucumber B. Beans C. Carrot D. Radish

Care of Patients with Problems of the Biliary System and Pancreas

Organs of the biliary system and the pancreatic ducts.

Immunity Concept Exemplar:Peptic Ulcer Disease

Peptic ulcer disease (PUD) results when GI mucosal defenses become impaired and no longer protect the epithelium from the effects of acid and pepsin. Mucosal lesion of stomach or duodenum uOccurs when mucosal defenses become impaired; epithelium not protected from effects of acid and pepsin

Peritonitis WHAT DOES IT FEEL LIKE?

Peritonitis is a life-threatening, acute inflammation and infection of the visceral/parietal peritoneum and endothelial lining of the abdominal cavity. The peritoneal cavity normally contains about 50 mL of sterile fluid (transudate), which prevents friction in the abdominal cavity during peristalsis. When the peritoneal cavity is contaminated by bacteria, the body begins an inflammatory reaction, walling off a localized area to fight the infection. inflammation of the peritoneum, typically caused by bacterial infection either via the blood or after rupture of an abdominal organ s/s - pain, fever. Pt is in. lot of pain. KNOW THIS. BOARD-LIKE ABDOMEN, IT IS HARD BECAUSE ALL GASTRIC CONTENTS ARE GOING INTO A CAVITY WHERE IT SHOULDN'T BE. Peritonitis • Rigid, board-like abdomen (classic) • Abdominal pain (localized, poorly localized, or referred to the shoulder or chest) • Distended abdomen • Nausea, anorexia, vomiting • Diminishing bowel sounds • Inability to pass flatus or feces • Rebound tenderness in the abdomen • High fever • Tachycardia • Dehydration from high fever (poor skin turgor) • Decreased urine output • Hiccups • Possible compromise in respiratory status decreased bowel sounds, since it isn't working Fix it? surgery - need to be open for a day or two because of potential infection, things need a pathway out Action Alert Monitor the patient's level of consciousness, vital signs, respiratory status (respiratory rate and breath sounds), and intake and output at least hourly immediately after abdominal surgery. Maintain the patient in a semi-Fowler position to promote drainage of peritoneal contents into the lower region of the abdominal cavity. This position also helps increase lung expansion. If an open conventional surgical procedure is needed, the infection may slow healing of an incision or the incision may be partially open to heal by second or third intention. These wounds require special care involving manual irrigation or packing as prescribed by the surgeon. If the surgeon requests peritoneal irrigation through a drain, maintain sterile technique during manual irrigation to prevent further risk for infection. Peritonitis is most often caused by contamination of the peritoneal cavity by bacteria or chemicals. Bacteria gain entry into the peritoneum by perforation (from appendicitis, diverticulitis, peptic ulcer disease) or from an external penetrating wound, a gangrenous gallbladder or bowel segment, bowel obstruction, or ascending infection through the genital tract. A client had an exploratory laparotomy to treat the cause of peritonitis and has a large incision that is closed with staples and two abdominal drains. Which finding(s) would the nurse report immediately to the surgeon? Select all that apply. A. Serosanguineous drainage B. Increased abdominal distention C. Fever and chills D. Pain level 2 on a scale of 0 to 10 E. Passing flatus

Pancreatic Pseudocyst

Pseudocyst created by additional pancreatitis complications - Hemorrhage - Infection - Bowel obstruction - Abscess - Fistula formation - Pancreatic ascites May spontaneously resolve Surgical intervention after 6 weeks If the infected fluid becomes walled off by fibrous tissue, a pancreatic pseudocyst forms. Pseudocysts often rupture spontaneously but may require surgical removal.

Esophageal Varices Treatment

Sengstaken-Blakemore tube in place for the emergency treatment of hemorrhage from esophageal varices. The tube has three openings for (1) gastric aspiration, (2) inflating the esophageal balloon, and (3) inflating the gastric balloon. The esophageal balloon is inflated to a pressure of 20 to 40 mm Hg (monitored by attachment to a gauge or a sphygmomanometer) that compresses the esophageal veins. The gastric balloon, inflated with 250 cc of air, applies pressure to the fundal veins when slight traction is applied. Evaluation: Reflecting uDecrease or no ascites uElectrolytes WNL uNo hemorrhage or immediately managed uNo encephalopathy or immediately managed uHighest quality of life possible uSuccessfully abstain from alcohol or drugs (if disease caused by these substances)

Skin Barriers

Skin barriers, such as wafers (A), are cut to fit ⅛ inch around the fistula. A drainable pouch (B) is applied over the wafer and clamped (C) until the pouch is to be emptied. Effluent should drain into the bag and not contact the skin Action Alert Teach the patient and family to apply a skin sealant (preferably without alcohol) and allow it to dry before application of the appliance (colostomy pouch) to facilitate less painful removal of the tape or adhesive. If peristomal skin becomes raw (skin stripping), stoma powder or paste or a combination may also be applied. The paste or other filler cream is also used to fill in crevices and creases to create a flat surface for the flange of the colostomy bag. If the patient develops a fungal rash (candidiasis), an antifungal cream or powder should be used. Perineal Wound Care Wound Care • Place an absorbent dressing (e.g., abdominal pad) over the wound. • Instruct the patient that he or she may: • Use a feminine napkin as a dressing • Wear jockey-type shorts rather than boxers Comfort Measures • If prescribed, soak the wound area in a sitz bath for 10 to 20 minutes three or four times per day or use warm/hot compresses or packs. • Administer an analgesic as prescribed and assess its effectiveness. • Instruct the patient about permissible activities. The patient should: • Assume a side-lying position in bed; avoid sitting for long periods • Use foam pads or a soft pillow on which to sit whenever in a sitting position • Avoid the use of air rings or rubber donut devices Prevention of Complications • Maintain fluid and electrolyte balance by monitoring intake and output and output from the perineal wound. • Observe incision integrity and monitor wound drains; watch for erythema, edema, bleeding, drainage, unusual odor, and excessive or constant pain. A client had an open partial colectomy and colostomy placement 6 hours ago. Which assessment would concern the nurse? A. Purple, moist stoma B. Stoma edema C. Liquid stool collecting in the drainage bag D. Serosanguineous fluid draining from the drain(s)

Nutrition Concept Exemplar: Esophageal Tumors

Some can be benign; most are malignant uMore than half metastasize uPrimary risk factors are smoking and obesity. uBarrett's esophagus results from acid and pepsin exposure. Assessment: Noticing uAssess for risk factors. uAsk about consumption of smoked/pickled foods, appetite and/or taste changes, weight loss. uMay report dysphagia, odynophagia (painful swallowing) u"Silent tumor" in early stages Psychosocial Assessment uHigh anxiety due to terminal nature of this cancer uFear of choking uSocial impact uCoping strengths, support systems, and resources Analysis: Interpreting uPotential for compromised nutrition due to impaired swallowing and possible metastasis Planning and Implementation:Responding uPromoting nutrition uNonsurgical management uNutrition and swallowing therapy uChemotherapy and radiation uOther therapies uSurgical management uPreoperative care uOperative procedures Postoperative care Care Coordination and Transition Management uHome care management uOngoing respiratory care uSelf-management education uInfection control uNutrition support uHealth care resources uReferrals to community or home care organizations uHospice services Evaluation: Reflecting uAble to consume adequate nutrition and maintain stable weight

TPN vs PPN

TPN - CENTRAL line - NO ORAL - ALL NUTRIENTS - LONG TERM vs PPN - PERIPHERAL line - CAN HAVE WITH ORAL - JUST BASIC NUTRITIONAL BLOCKS - TEMPORARY Central lines goes into the superior vena cava

Pancreatitis

There are multiple gallstones in the gallbladder, which were the cause of this patient's pancreatitis.

Gastrectomy

Total gastrectomy, with anastomosis of the esophagus to the jejunum (esophagojejunostomy), is the principal surgical intervention for extensive gastric cancer. - Total: all of stomach removed - Partial: part of stomach removed Which client statement regarding diet and nutrition after a total gastrectomy requires further teaching by the nurse? A. "I should stay sitting up for an hour after I eat." B. "I will avoid liquids with my meals." C. "I need to eat small frequent meals." D. "I need to stay away from concentrated sweets."

Ulcerative Colitis

Ulcerative colitis (UC) is a disease that creates widespread chronic inflammation of the rectum and rectosigmoid colon but can extend to the entire colon when the disease is extensive. Distribution of the disease can remain constant for years. UC is a disease that is associated with periodic remissions and exacerbations (flare-ups) and is often confused with Crohn's disease. Severe mucosal edema and inflammation with ulcerations and bleedingin digestive tract. Patients report tenesmus (an unpleasant and urgent sensation to defecate) and lower abdominal colicky pain relieved with defecation. Malaise, anorexia, anemia, dehydration, fever, and weight loss are common. Extraintestinal manifestations such as migratory polyarthritis, ankylosing spondylitis, and erythema nodosum are present in a large number of patients. Etiology and Risk Factors uImmune System Malfunction uExample -Fighting off virus or bacteria and causes the immune system to attack the cell in the digestive tract. uAge, ethnicity, and family history Analysis: Interpreting uThe priority collaborative problems for patients with ulcerative colitis include diarrhea due to inflammation of the bowel mucosa. acute pain or chronic noncancer pain due to inflammation and ulceration of the bowel mucosa and skin irritation. potential for lower GI bleeding and resulting anemia due to UC. Physiological Integrity The nurse is caring for an older adult client who experiences an exacerbation of ulcerative colitis with severe diarrhea and rectal bleeding that have lasted a week. For which complication(s) will the nurse assess? Select all that apply. A. Increased BUN B. Hypokalemia C. Leukocytosis D. Anemia E. Hyponatremia Planning and Implementation: Responding uDecrease diarrhea - The major concern for a patient with ulcerative colitis is the occurrence of frequent, bloody diarrhea and fecal incontinence from tenesmus. Therefore the expected outcome of treatment is for the patient to have decreased diarrhea, formed stools, and control of bowel movements, which allow for mucosal healing. uDrug Therapy- Drug therapy. Common drug therapy for UC includes aminosalicylates, glucocorticoids, antidiarrheal drugs, and immunomodulators. Teach patients about side effects and adverse drug events (ADEs) and when to call their primary health care provider. The aminosalicylates are drugs commonly used to treat mild-to-moderate UC and/or maintain remission. Several aminosalicylic acid compounds are available. These drugs, also called 5-ASAs, are thought to have an anti-inflammatory effect on the lining of the intestine by inhibiting prostaglandins and are usually effective in 2 to 4 weeks. Sulfasalazine, the first aminosalicylate approved for UC, is metabolized by the intestinal bacteria into 5-ASA, which delivers the beneficial effects of the drug, and sulfapyridine, which is responsible for unwanted side effects. Teach patients to take a folic acid supplement because sulfasalazine decreases its absorption uAnti inflammatory Drugs (5-Aminosalicylates) uCorticosteroids uImmune system suppressant agents uAntidiarrheals To provide symptomatic management of diarrhea, antidiarrheal drugs may be prescribed. However, these drugs are given very cautiously because they can cause colon dilation and toxic megacolon (massive dilation of the colon and subsequent colonic ileus that can lead to gangrene and peritonitis). Common antidiarrheal drugs include diphenoxylate hydrochloride and atropine sulfate and loperamide. Drug Alert Teach patients taking sulfasalazine to report nausea, vomiting, anorexia, rash, and headache to the health care provider. With higher doses, hemolytic anemia, hepatitis, male infertility, or agranulocytosis can occur. This drug is in the same family as sulfonamide antibiotics. Therefore, assess the patient for an allergy to sulfonamide or other drugs that contain sulfa before the patient takes the drug. The use of a thiazide diuretic may be a contraindication for sulfasalazine uNutrition Therapy Nutrition therapy and rest.Patients with severe symptoms who are hospitalized are kept NPO to ensure bowel rest. The primary health care provider may prescribe total parenteral nutrition (TPN) for severely ill and malnourished patients during severe exacerbations uSurgical Management- colostomy An ileostomy is a procedure in which a loop of the ileum is placed through an opening in the abdominal wall (stoma) for drainage of fecal material into a pouching system worn on the abdomen. This external pouching system consists of a solid skin barrier (wafer) to protect the skin and a fecal collection device (pouch), similar to the system used for patients with colostomies The ileostomy stoma (Fig. 52.3B) is usually placed in the right lower quadrant of the abdomen below the belt line. It should not be prolapsed or retract into the abdominal wall. Assess the stoma frequently after stoma placement. Recognize that it should be pinkish to cherry red to ensure an adequate blood supply. If the stoma looks pale, bluish, or dark, respond by reporting these findings to the surgeon immediately ( Stelton, 2019 )! uMinimize Pain uantidepressants, antispasmodics uMonitor for Lower GI Bleeding uComplications uSevere Bleeding uSevere Dehydration uBone loss (osteoporosis) uIncreased risk of colon cancer

ch 51 key terms

abdominoperineal (AP) resection Surgical removal of the sigmoid colon, rectum, and anus through combined abdominal and perineal incisions. borborygmi High-pitched bowel sounds that are proximal (above) an obstruction. colectomy Surgical removal of the entire colon. colon resection Surgical removal of part of the colon and regional lymph nodes. colostomy The surgical creation of an opening of the colon (stoma) onto the surface of the abdomen to allow passage of stool. exploratory laparotomy A surgical opening of the abdominal cavity. fecal occult blood test [FOBT] A laboratory test to determine the presence of occult (microscopic) blood in the stool. flatulence Excessive gas (flatus) in the intestines. hemorrhoidectomy Surgical removal of hemorrhoids. hemorrhoids Unnaturally swollen or distended veins in the anorectal region. hernia A weakness in the abdominal muscle wall through which a segment of the bowel or other abdominal structure protrudes. hernioplasty A surgical hernia repair procedure performed to reinforce the weakened outside abdominal muscle wall with a mesh patch. herniorrhaphy Surgical repair of a hernia. intussusception Telescoping of a segment of the intestine within itself. irreducible (incarcerated) hernia A hernia that cannot be reduced or placed back into the abdominal cavity. Any hernia that is not reducible requires immediate surgical evaluation. irritable bowel syndrome A functional GI disorder that causes chronic or recurrent diarrhea, constipation, and/or abdominal pain and bloating. mechanical obstruction A condition in which the bowel is physically blocked by problems outside the intestine (e.g., adhesions), in the bowel wall (e.g., Crohn's disease), or in the intestinal lumen (e.g., tumors). minimally invasive inguinal hernia repair (MIIHR) Surgical hernia repair through a laparoscope. nonmechanical obstruction A condition in which peristalsis is decreased or absent because of neuromuscular disturbance, resulting in a slowing of the movement or a backup of intestinal contents; also known as paralytic ileus. obstipation No passage of stool. polyps In the intestinal tract, small growths covered with mucosa and attached to the surface of the intestine; although most are benign, they are significant because some have the potential to become malignant. reducible hernia A hernia that can be reduced or placed back into the abdominal cavity. strangulated obstruction Bowel obstruction or hernia that has compromised blood flow (can be life-threatening). volvulus Twisting of the intestine.

ch 52 key terms

abscess A localized infection in which there is a collection of pus. appendectomy The removal of the inflamed appendix by one of several surgical approaches. appendicitis An acute inflammation of the vermiform appendix that occurs most often among young adults. celiac disease A chronic inflammation of the small intestinal mucosa that can cause bowel wall atrophy, malabsorption, and diarrhea. Crohn's disease (CD) A chronic inflammatory disease of the small intestine (most often), the colon, or both; the terminal ileum is most often affected. diverticulitis The inflammation or infection of diverticula. diverticulosis The presence of many abnormal pouchlike herniations (diverticula) in the wall of the intestine. effluent Drainage. fissure A tear, crack, or split in skin and underlying tissue. fistula Abnormal opening (tract) between two organs or structures. gastroenteritis A very common health problem worldwide that causes diarrhea and/or vomiting related to inflammation of the mucous membranes of the stomach and intestinal tract. ileostomy A procedure in which a loop of the ileum is placed through an opening in the abdominal wall (stoma) for drainage of fecal material into a pouching system worn on the abdomen. intestinal malabsorption (malabsorption syndrome) The inability of essential nutrients to be absorbed through a diseased intestinal wall, causing anemia and malnutrition (most common in Crohn's disease). laparoscopy A minimally invasive surgery (MIS) with one or more small incisions near the umbilicus through which a small endoscope and tools are placed. laparotomy An open surgical approach requiring a large abdominal incision. ostomate A person who has an ostomy. peritonitis A life-threatening, acute inflammation and infection of the visceral/parietal peritoneum and endothelial lining of the abdominal cavity. progressive multifocal leukoencephalopathy (PML) A deadly infection that affects the brain. steatorrhea Fatty diarrheal stools. tenesmus An unpleasant and urgent sensation to defecate. toxic megacolon Massive dilation of the colon and subsequent colonic ileus that can lead to gangrene and peritonitis. ulcerative colitis (UC) A disease that creates widespread chronic inflammation of the rectum and rectosigmoid colon but can extend to the entire colon when the disease is extensive.

ch 54 key terms

acute pancreatitis A serious, and at times life-threatening, inflammation of the pancreas. biliary colic Severe right upper abdominal pain caused by obstruction of the cystic duct or movement of one or more gallstones. cholecystectomy The surgical removal of the gallbladder. cholecystitis An inflammation of the gallbladder that may be acute or chronic. cholelithiasis Gallstones (also known as calculi). chronic pancreatitis A progressive, destructive disease of the pancreas that has remissions and exacerbations ("flare-ups"). dyspepsia An epigastric burning sensation, often referred to as "heartburn." eructation Belching. flatulence Gas (flatus) in the lower GI tract. icterus Yellow coloration of the eye sclera. jaundice Yellow coloration of the skin and mucous membranes. pancreatic abscess Suppuration (pus formation) of pancreatic tissue caused by secondary bacterial invasion; often occurs in patients with acute or chronic pancreatitis. pancreatic pseudocyst A condition in which infected pancreatic fluid becomes walled off by fibrous tissue. partial pancreatectomy Surgical removal of part of the pancreas. postcholecystectomy syndrome (PCS) A complication of cholecystectomy that causes increased abdominal or epigastric pain and vomiting and/or diarrhea weeks to months after surgery. splenectomy Surgical removal of the spleen. steatorrhea Fatty stools. Whipple procedure (radical pancreaticoduodenectomy) Extensive surgical procedure used most often to treat cancer of the head of the pancreas; entails removal of the proximal head of the pancreas, the duodenum, a portion of the jejunum, the stomach (partial or total gastrectomy), and the gallbladder, with anastomosis of the pancreatic duct (pancreaticojejunostomy), the common bile duct (choledochojejunostomy), and the stomach (gastrojejunostomy) to the jejunum.

ch 53 key terms

alcohol withdrawal A condition that occurs after stopping heavy and prolonged alcohol intake, which often results in tremors, acute confusion, psychotic behaviors (such as delusions and hallucinations), and autonomic symptoms including tachycardia, elevated blood pressure, and diaphoresis. ascites The collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension. asterixis A coarse tremor characterized by rapid, nonrhythmic extensions and flexions in the wrists and fingers (hand flapping). cirrhosis A disease characterized by widespread fibrotic (scarred) bands of connective tissue that change the liver's anatomy and physiology. ecchymoses Large purple, blue, or yellow bruises. esophageal varices A complication of cirrhosis in which fragile, thin-walled esophageal veins become distended and tortuous from increased pressure (portal hypertension). fetor hepaticus The distinctive breath odor of chronic liver disease and hepatic encephalopathy that is characterized by a fruity or musty odor. hepatic encephalopathy (also called portal-systemic encephalopathy [PSE]) is a complex cognitive syndrome that results from liver failure and cirrhosis. hepatitis Widespread inflammation and infection of liver cells. hepatomegaly Liver enlargement that commonly occurs in patients with early cirrhosis. hepatopulmonary syndrome A complication of cirrhosis caused by excessive ascitic volume and manifested by dyspnea as a result of intraabdominal pressure, which limits thoracic expansion and diaphragmatic excursion. hepatorenal syndrome A late complication of cirrhosis affecting the kidneys and manifested by oliguria, elevated blood urea nitrogen (BUN) and creatinine levels, and increased urine osmolarity. icterus Yellow coloration of the eye sclerae. jaundice Yellowish coloration of the skin caused by increased serum bilirubin. nonalcoholic fatty liver disease (NAFLD) A rapidly growing liver disease that is associated with obesity, diabetes mellitus type 2, and metabolic syndrome. paracentesis An invasive procedure performed to remove abdominal fluid in patients who have massive ascites. petechiae Round, pinpoint, red-purple hemorrhagic lesions. portal hypertension A major complication of cirrhosis resulting in persistent increase in pressure within the portal vein >5 mm Hg. splenomegaly Spleen enlargement. spontaneous bacterial peritonitis (SBP) An infection that results from bacteria collected in ascitic fluid. transjugular intrahepatic portal-systemic shunt (TIPS) An interventional radiologic procedure performed for patients who have not responded to other modalities to manage hemorrhage or long-term ascites. ultrasound transient elastography A noninvasive imaging test that measures liver stiffness, which helps the primary health care provider determine the amount of liver disease present.

ALP

alkaline phosphatase Increased values indicate possible: • Cirrhosis • Biliary obstruction • Liver tumor

ch 50 key terms

dumping syndrome A postgastrectomy condition that refers to a group of vasomotor symptoms that occur after eating. dyspepsia An epigastric burning sensation, often referred to as "heartburn." gastrectomy Surgical removal of all (total gastrectomy) or part (subtotal gastrectomy) of the stomach. gastritis The inflammation of gastric mucosa (stomach lining). hematemesis Vomiting bright red or coffee-ground blood. melena Dark, "tarry" (sticky) stool, indicating occult blood caused by digestion of blood within the small intestine. peptic ulcer disease A condition that results when GI mucosal defenses become impaired and no longer protect the epithelium from the effects of acid and pepsin. peritonitis An abdominal infection in which the abdomen is tender, rigid, and boardlike. stress ulcer Acute gastric mucosal lesion occurring after an acute medical crisis or trauma, such as sepsis or a head injury, or surgery.

Types of Ulcers KNOW TREATMENT OF ULCERS

how to treat? things that are gonna coat the stomach/decrease stomach acid Gastric - Gastric ulcers usually develop in the antrum of the stomach near acid-secreting mucosa (see Fig. 50.1). When a break in the mucosal barrier occurs (such as that caused by H. pylori infection ), hydrochloric acid injures the epithelium. Gastric ulcers may then result from back-diffusion of acid or dysfunction of the pyloric sphincter. Without normal functioning of the pyloric sphincter, bile refluxes (backs up) into the stomach. This reflux of bile acids may break the integrity of the mucosal barrier, which leads to mucosal inflammation. Toxic agents and bile then destroy the membrane of the gastric mucosa. Gastric emptying is often delayed in patients with gastric ulceration. This causes regurgitation of duodenal contents, which worsens the gastric mucosal injury. Decreased blood flow to the gastric mucosa may also alter the defense barrier and thereby allow ulceration to occur. uDuodenal - Duodenal ulcers occur more often than other types. Most duodenal ulcers present in the upper portion of the duodenum. They are deep, sharply demarcated lesions that penetrate through the mucosa and submucosa into the muscularis propria (muscle layer). The floor of the ulcer consists of a necrotic area residing on granulation tissue and surrounded by areas of fibrosis (McCance et al., 2019) (Fig. 50.1). The main feature of a duodenal ulcer is high gastric acid secretion, although a wide range of secretory levels are found. In patients with duodenal ulcers, pH levels are low (excess acid) in the duodenum for long periods. Protein-rich meals, calcium, and vagus nerve excitation stimulate acid secretion. Combined with hypersecretion, a rapid emptying of food from the stomach reduces the buffering effect of food and delivers a large acid bolus to the duodenum. Inhibitory secretory mechanisms and pancreatic secretion may be insufficient to control the acid load. uStress - Stress ulcers are acute gastric mucosal lesions occurring after an acute medical crisis or trauma, such as sepsis or a head injury. In the patient who is NPO for major surgery, gastritis may lead to stress ulcers. Patients who are critically ill, especially those with extensive burns (Curling ulcer), sepsis (ischemic ulcer), or increased intracranial pressure (Cushing ulcer), are also susceptible to these ulcers. Stress ulcers are associated with lengthened hospital stay and increased mortality rates. Therefore most patients who have major trauma or surgery receive IV drug therapy (e.g., PPIs) to prevent stress ulcer development. Bleeding caused by gastric erosion is the main manifestation of acute stress ulcers. Multifocal lesions associated with stress ulcers occur in the stomach and proximal duodenum. These lesions begin as areas of ischemia and evolve into erosions and ulcerations that may progress to massive hemorrhage.

Ammonia levels

liver problems make ammonia go up due to liver problems. Causes encephalopathy - check LOC. Pts are confused, and combative, vomiting, and seizures. nothing works well cause brain isn't working- early stages REPORT SEIZURES! late stage - coma, death normal is less than 30 at 89 we have issues How to get it down? give lactulose

Autodigestion

process of autodigestion in acute pancreatitis.

Colostomy Care

right side? - ileostomy, liquid, from small intestine and job is to digest so its liquid left side? - colostomy, thick and more stool like. Stoma should be beefy red!!!! NOT PURPLE. Report any of these early postoperative stoma problems to the surgeon: • Stoma ischemia and necrosis (dark red, purplish, or black color; dry) • Continuous heavy bleeding • Mucocutaneous separation (breakdown of the suture line securing the stoma to the abdominal wall) Normal appearance of stoma uSigns and symptoms of complications uMeasurement of stoma A healthy stoma should be reddish pink (or dark red to pink) and moist and protrude about 1 to 3 cm from the abdominal wall but most commonly about ¾ inch (2 cm) For example, stool from an ascending colon colostomy continues to be liquid, stool from a transverse colon colostomy becomes pasty, and stool from a descending colon colostomy becomes more solid (similar to stool expelled from the rectum). uChoice, use, care, application of appropriate appliance to cover stoma uMeasures to protect skin uDietary measures to control gas and odor uResumption of normal activities If he or she had the open surgical approach, the patient should avoid driving and vigorous physical activity for 4 to 6 weeks while the incision heals. Patients who have had laparoscopy can usually return to all usual activities in 1 to 2 weeks. Action Alert A stool softener may be prescribed to keep stools soft in consistency for ease of passage. Teach patients to note the frequency, amount, and character of the stools. In addition to this information, teach those with colon resections to watch for and report signs and symptoms of intestinal obstruction and perforation (e.g., cramping, abdominal pain, nausea, vomiting). Advise the patient to avoid gas-producing foods and carbonated beverages. The patient may require 4 to 6 weeks to establish the effects of certain foods on bowel patterns.

SCD

sequential compression device Mimic calf moving to prevent blood clots

Liver Trauma

stab wounds, shootings, accidents with seatbelt Most common organ injured during abdominal trauma uObserve for early signs of hypovolemic shock. - tachycardia, hypotension uSigns and Symptoms uAnxiety or agitation, Cool, clammy skin. Confusion. Decreased or no urine output. Generalized weakness. uPale skin color (pallor), Rapid breathing, Sweating, moist skin. uMay require enhanced critical care monitoring, surgery, blood replacement, volume infusion how to fix hypovolemia? - blood, pressers, IV fluids

Assessment Techniques

uAbdominal examination starting at RUQ uInspection, auscultation, palpation uDo not palpate if appendicitis or abdominal aneurysm is suspected. uHealth care providers, APRNs perform percussion and deep palpation. Action Alert If a bulging, pulsating mass is present during assessment of the abdomen, do not touch the area because the patient may have an abdominal aortic aneurysm, a life-threatening problem. Notify the health care provider of this finding immediately! Physiological Integrity While performing an abdominal assessment on a client, the nurse notes a bruit over the aorta. What is the appropriate nursing action? A. Consult another nurse to verify the bruit. B. Auscultate each quadrant for 5 minutes each. C. Notify the health care provider of the findings. D. Perform light palpation to further assess the pulsation.

Problems of the Biliary System and Pancreas

uCholecystitis uCholecystectomy uPancreatitis uPancreatic Abscess uPancreatic Pseudocyst uPancreatic Cancer

Colorectal Cancer

uColorectal—refers to colon and rectum, which together make up large intestine uMost CRCs are adenocarcinomas umalignant tumor formed from glandular structures in epithelial tissue. uEtiology uAge > 50 years uGenetic predisposition uPersonal/family history of cancer Familial adenomatous polyposis risk factors: family history, poor diet, being older than 50, history of diabetes, sedentary lifestyle, polyps Health Promotion and Maintenance The nurse is talking with a group of older clients about colorectal cancer (CRC) risk factors. Which of the following factors are considered to be common CRC risk factors? Select all that apply. A. High-fat diet B. Crohn's disease C. Smoking D. Alcoholism E. Family history of cancer F. Obesity Interprofessional Collaborative Care Assessment Physical Assessment uBleeding and change in stool (most common signs) Psychosocial Assessment Laboratory Assessment uFecal occult blood test (FOBT) - A positive test result for occult (microscopic) blood in the stool (fecal occult blood test [FOBT] or fecal immunochemical test [FIT]) indicates bleeding in the GI tract. uCarcinoembryonic antigen (CEA) - Carcinoembryonic antigen (CEA), an oncofetal antigen, is elevated in many people with CRC. The normal value is less than 5 ng/mL Imaging Assessment uSigmoidoscopy - A sigmoidoscopy provides visualization of the lower colon using a fiberoptic scope. Polyps can be visualized, and tissue samples can be taken for biopsy. Polyps are usually removed during the procedure. A colonoscopy provides views of the entire large bowel from the rectum to the ileocecal valve. As with sigmoidoscopy, polyps can be seen and removed, and tissue samples can be taken for biopsy. Colonoscopy is the definitive test for the diagnosis of colorectal cancer. T Colonoscopy - CT-guided virtual colonoscopy is growing in popularity. This test is noninvasive and includes a CT scan of the rectum and colon. Analysis: Interpreting uPotential for metastasis due to colorectal cancer uPotential for grieving due to cancer diagnosis Planning and Implementation: Responding uPrevent/Control Metastasis uRadiation Therapy - The administration of preoperative radiation therapy has not improved overall survival rates for colon cancer, but it has been effective in providing local or regional control of the disease. However, as a palliative measure, radiation therapy may be used to control pain, hemorrhage, bowel obstruction, or metastasis to the lung in advanced disease. For rectal cancer, unlike colon cancer, radiation therapy is often a part of the treatment plan. Reinforce information about the radiation therapy procedure to the patient and family and monitor for possible side effects (e.g., diarrhea, fatigue). uChemotherapy Adjuvant chemotherapy after primary surgery is recommended for patients with stage II or stage III disease to interrupt the DNA production of cells and destroy them. The drugs of choice are IV 5-fluorouracil with leucovorin (5-FU/LV), capecitabine, and irinotecan hydrochloride Cetuximab and panitumumab are monoclonal antibodies known as epidermal growth factor receptor (EGFR) inhibitors (EGFRIs), and may also be given in combination with other drugs for metastatic disease uSurgical Management The most common surgeries performed are colon resection (removal of the part of the colon and regional lymph nodes) with reanastomosis, partial colectomy with a colostomy (temporary or permanent) or total colectomy with an ileostomy/ileoanal pull-through, and abdominoperineal resection. A colostomy is the surgical creation of an opening (stoma) of the colon onto the surface of the abdomen to allow passage of stool. An abdominoperineal (AP) resection is performed when rectal tumors are present. In this procedure, the surgeon removes the sigmoid colon, rectum, and anus through combined abdominal and perineal incisions. uAssist with Grieving Process uCare Coordination and Transition Management

Complications of Ulcers

uHemorrhage - Hemorrhage is the most serious complication. It tends to occur more often in patients with gastric ulcers and in older adults. uPerforation - Perforation occurs when the ulcer becomes so deep that the entire thickness of the stomach or duodenum is worn away. The stomach or duodenal contents can then leak into the peritoneal cavity. Sudden, sharp pain begins in the mid-epigastric region and spreads over the entire abdomen. The amount of pain correlates with the amount and type of GI contents spilled. The classic pain causes the patient to be apprehensive. The abdomen is tender, rigid, and boardlike as a result of this infection ( peritonitis ). The patient often assumes a "fetal" position to decrease the tension on the abdominal muscles. He or she can become severely ill within hours. Bacterial septicemia and hypovolemic shock can follow. Peristalsis diminishes, and paralytic ileus develops. Peptic ulcer perforation is a surgical emergency and can be life threatening! uPyloric obstruction - Pyloric (gastric outlet) obstruction (blockage) occurs in a small percentage of patients and manifests with vomiting caused by stasis and gastric dilation. Obstruction occurs at the pylorus (the gastric outlet) and is caused by scarring, edema, inflammation, or a combination of these factors. Symptoms of obstruction include abdominal bloating, nausea, and vomiting. When vomiting persists, the patient may have metabolic alkalosis from loss of large quantities of acid gastric juice (hydrogen and chloride ions) in the vomitus uIntractable disease - intractability may develop from complications of ulcers, excessive stressors in the patient's life, or an inability to adhere to long-term therapy. He or she no longer responds to conservative management, or recurrences of symptoms interfere with ADLs. In general, the patient continues to have recurrent pain despite treatment The nurse is caring for a client diagnosed with peptic ulcer disease (PUD). For which potential complications will the nurse monitor? Select all that apply. A. Pneumonia B. Peritonitis C. Anemia D. Stroke E. Hypotension F. Cirrhosis Etiology and Genetic Risk uH. pylori uNSAIDs uOther substances that alter gastric secretion Peptic ulcer disease is caused most often by bacterial infection with H. pylori and long-term use of NSAIDs such as ibuprofen. NSAIDs break down the mucosal barrier and disrupt the mucosal protection mediated systemically by cyclooxygenase (COX) inhibition. Assessment: Noticing uAssess risk factors, including alcohol and tobacco intake; increased stress; dietary habits. uHistory of H. pylori, GI surgeris uPrescription and OTC drugs uPhysical Assessment uEpigatric tenderness, dyspepsia uRigid, boardlike abdomen w/rebound tenderness and pain = perforation into peritoneal cavity uGastric versus duodenal ulcer pain uAssess for fluid volume deficit If perforation into the peritoneal cavity is present, the patient typically has a rigid, boardlike abdomen accompanied by rebound tenderness and intense pain (peritonitis). Initially, auscultation of the abdomen may reveal hyperactive bowel sounds, but these may diminish with progression of the infection. Perform a comprehensive pain assessment. Dyspepsia is the most commonly reported symptom associated with PUD. It is typically described as sharp, burning, or gnawing pain. Some patients may perceive discomfort as a sensation of abdominal pressure or of fullness or hunger. Psychosocial Assessment uAssess impact of ulcer disease on lifestyle, occupation, family, social, leisure activities. uEvaluate impact of necessary lifestyle changes. Diagnostic Assessment uTesting for H. pylori uChest, abdomen x-ray series (if perforation is suspected) uEGD uNuclear medicine test (if GI bleeding is suspected) The major diagnostic test for PUD is esophagogastroduodenoscopy (EGD), which is the most accurate means of establishing a diagnosis. Direct visualization of the ulcer crater by EGD allows the primary health care provider to take specimens for H. pylori testing and biopsy and cytologic studies for ruling out gastric cancer. The rapid urease test can confirm a quick diagnosis because urease is produced by the bacteria in the gastric mucosa. EGD may be repeated at 4- to 6-week intervals while the primary health care provider evaluates the progress of healing in response to therapy. Chapter 48 describes this test in more detail. GI bleeding may be tested using a nuclear medicine scan. No special preparation is required for this scan. The patient is injected with a contrast medium Analysis: Interpreting uAcute pain or chronic noncancer pain due to gastric and/or duodenal ulceration uPotential for upper GI bleeding due to ulceration Planning and Implementation:Responding uManaging acute pain or chronic non-cancer pain uDrug therapy - uProton Pump Inhibitors ublock acid production and promote healing uH2 Blockers ureduce acid the stomach produces uAntibiotics for H pylori-related gastritis uClarithomycin, metronidazole, amoxicillin The primary purposes of drug therapy in the treatment of PUD are to (1) provide pain relief, (2) eliminate H. pylori infection, (3) heal ulcerations, and (4) prevent recurrence. Several different regimens can be used. Although numerous drugs have been evaluated for the treatment of H. pylori infection, no single agent has been used successfully against the organism. A common drug regimen for H. pylori infection is PPI-triple therapy, which includes a proton pump inhibitor (PPI), such as lansoprazole, plus two antibiotics such as metronidazole and tetracycline or clarithromycin and amoxicillin for 10 to 14 days. Bismuth subsalicylate inhibits H. pylori from binding to the mucosal lining and stimulates mucosal protection and prostaglandin production. Teach patients that they cannot take aspirin while on this drug because aspirin is a salicylic acid and could cause an overdose of salicylates. Patients should also be taught that bismuth may cause the stools and/or tongue to be discolored black. This discoloration is temporary and harmless. A proton pump inhibitor (PPI) is the drug class of choice for treating patients with acid-related disorders. Omeprazole, lansoprazole, and esomeprazole are each available as delayed-release capsules designed to release their contents after they pass through the stomach. Omeprazole and lansoprazole may be dissolved in a sodium bicarbonate solution and given through any feeding tube. Bicarbonate protects the dissolved omeprazole and lansoprazole granules in gastric acid. Therefore the drugs are still absorbed correctly. uNutrition therapy- uFoods rich in antioxidants (berries, bell peppers) Teach the patient with peptic ulcer disease to follow healthy nutrition habits and avoid substances that increase gastric acid secretion. This includes caffeine-containing beverages (coffee, tea, cola). Both caffeinated and decaffeinated coffees should be avoided because coffee contains peptides that stimulate gastrin release uComplementary and integrative therapies - reduce stress, including hypnosis and imagery. For example, the use of yoga and meditation techniques has demonstrated a beneficial effect on anxiety disorders. uManaging Upper GI bleeding-slow bleed versus acute Emergency: upper GI bleeding. The patient who is actively bleeding has a life-threatening emergency and needs supportive therapy to prevent hypovolemic shock and possible death KNOW HOW TO FIX GI BLEED Recognize that your priority for care of the patient with upper GI bleeding is to maintain a irway, b reathing, and c irculation (ABCs). Respond to these needs by providing oxygen and other ventilatory support as needed, starting two large-bore IV lines for replacing fluids and blood, and monitoring vital signs, hematocrit, and oxygen saturation. The purpose of managing hypovolemia is to expand intravascular fluid in a patient who is volume depleted. Carefully monitor the patient's fluid status, including intake and output. Fluid replacement in older adults should be closely monitored to prevent fluid overload. Serum electrolytes are also assessed because depletions from vomiting or nasogastric suctioning must be replaced. Volume replacement with isotonic solutions (e.g., 0.9% normal saline solution, lactated Ringer's solution) should be started immediately. The primary health care provider may prescribe blood products such as packed red blood cells (PRBCs) to expand volume and correct a low hemoglobin and hematocrit. For patients with active bleeding, fresh frozen plasma may be given if the prothrombin time is 1.5 times higher than the midrange control value A combination of several different treatments, including nasogastric tube (NGT) placement and lavage, endoscopic therapy, interventional radiologic procedures, and acid suppression, can be used to control acute bleeding and prevent rebleeding. If the patient is actively bleeding at home, he or she is usually admitted to the emergency department. After the bleeding has stopped, H2-receptor antagonists and proton pump inhibitors are the primary drugs used. Nasogastric tube placement and lavage. Upper GI bleeding or obstruction often requires the primary health care provider or nurse to insert a large-bore NGT to: • Determine the presence or absence of blood in the stomach • Assess the rate of bleeding • Prevent gastric dilation • Administer lavage Although not performed as commonly today, gastric lavage requires the insertion of a large-bore NGT with instillation of a room-temperature solution in volumes of 200 to 300 mL. Treatment of pyloric obstruction is directed toward restoring fluid and electrolyte balance and decompressing the dilated stomach. Obstruction related to edema and spasm generally responds to medical therapy. First, the stomach must be decompressed with nasogastric suction. Next, interventions are directed at correcting metabolic alkalosis and dehydration. The NGT is typically clamped after about 72 hours. Check the patient for retention of gastric contents. If the amount retained is not more than 50 mL in 30 minutes or other prescribed parameters, the primary health care provider may allow oral fluids. In some cases, surgical intervention may be required to treat PUD. uNonsurgical management-triple therapy -as above uSurgical management-Endoscopic therapy first -(cauterize or clip) Endoscopic therapy. Endoscopic therapy via an esophagogastroduodenoscopy (EGD) can assist in achieving homeostasis during an acute hemorrhage by isolating the bleeding artery to embolize (clot) it. The endoscopist can insert instruments through the endoscope during the procedure to stop bleeding in three different ways: (1) inject chemicals into the bleeding site; (2) treat the bleeding area with heat, electric current, or laser; or (3) close the affected blood vessels with a band or clip. During the EGD, a specialized endoscopy nurse and technician assist the physician with the procedure. After esophagogastroduodenoscopy (EGD), monitor vital signs, heart rhythm, and oxygen saturation frequently per agency protocol until they return to baseline. In addition, frequently assess the patient's ability to swallow saliva. The patient's gag reflex may initially be absent after EGD because of anesthetizing (numbing) of the throat with a spray before the procedure. After the procedure, do not allow the patient to have food or liquids until the gag reflex has returned! Interventional radiologic procedures.For patients with persistent, massive upper GI bleeding or those who are not surgical candidates, catheter-directed embolization may be performed. This endovascular procedure is usually done if endoscopic procedures are not successful or available. A femoral approach is most often used, but brachial access may be used. An arteriogram is performed to identify the arterial anatomy and find the exact location of the bleeding. Evaluation: Reflecting uDoes not have active PUD or complications uVerbalizes pain control or relief uAdheres to drug regimen, lifestyle changes Drug therapy. Aggressive acid suppression is used to prevent rebleeding. When acute bleeding is stopped and clot formation has taken place within the ulcer crater, the clot remains in contact with gastric contents. Acid-suppressive agents are used to stabilize the clot by raising the pH level of gastric contents. Several types of drugs are used. H2-receptor antagonists prevent acid from being produced by parietal cells. Proton pump inhibitors prevent the transport of acid across the parietal cell membrane uDoes not experience upper GI bleed Action Alert Teach the patient who has had surgery for PUD to avoid any OTC product containing aspirin or other NSAIDs. Emphasize the importance of following the treatment regimen for H. pylori infection and healing the ulcer and of keeping all follow-up appointments. Help the patient identify situations that cause stress, describe feelings during stressful situations, and develop a plan for coping with stressors.

Assessment: Noticing and Interpreting

uHistory uChanges in appetite, weight, stool uPain (PQRST mnemonic) uAge, gender, culture uGI disorders or abdominal surgeries uMedications, herbs, supplements uSmoking history uTravel uNutrition - nutrition history is important when assessing GI system function. Many conditions arise as a result of alterations in intake and absorption of nutrients. uHistory (Cont.) uHealth problems uAlcohol, caffeine intake uSocioeconomic status Family history, genetic risk Physiological Integrity Which daily behavior of a client with GI problems requires further nursing assessment? Select all that apply. A. Smokes a pack of cigarettes B. Uses Fleet enemas frequently to assist with bowel movements C. Practices intentional relaxation D. Eats multiple servings of fruits E. Takes 325 mg of aspirin at night for arthritic pain F. Exercises for 30 minutes three times weekly G. Travels extensively across the world

Complications of Acute Pancreatitis

uHypovolemia - hypervolemic? Is and Os uHemorrhage uAcute kidney failure uParalytic ileus uHypovolemic or septic shock uPleural effusion, respiratory distress syndrome, pneumonia uMultisystem organ failure uDisseminated intravascular coagulation uDiabetes mellitus

Gastritis

uInflammation of gastric mucosa KNOW - constant changes, CHRONIC GASTRITIS CAN LEAD TO STOMACH CANCER! KNOW THE WORD: ATROPHIC CHANGES. CHANGING THE CELLS IN YOUR STOMACH WHICH LEADS TO STOMACH CANCER, WHICH MEANS THE STOMACH WILL HAVE TO BE TAKEN OUT. uErosive versus nonerosive can be erosive (causing ulcers) or nonerosive uAcute versus chronic inflammation of the gastric mucosa or submucosa after exposure to local irritants or other causes can result in acute gastritis . The early pathologic manifestation of gastritis is a thickened, reddened mucous membrane with prominent rugae, or folds. Various degrees of mucosal necrosis and inflammation occur in acute disease. Chronic gastritis appears as a patchy, diffuse (spread out) inflammation of the mucosal lining of the stomach. As the disease progresses, the walls and lining of the stomach thin and atrophy. With progressive gastric atrophy from chronic mucosal injury, the function of the parietal (acid-secreting) cells decreases, and the source of intrinsic factor is lost. Intrinsic factor is critical for absorption of vitamin B12. When body stores of vitamin B12 are eventually depleted, pernicious anemia results. The amount and concentration of acid in stomach secretions gradually decrease until the secretions consist of only mucus and water. uChronic: Type A versus Type B versus atrophic The most common form of chronic gastritis is type B gastritis, caused by Helicobacter pylori infection . A direct correlation exists between the number of organisms and the degree of cellular abnormality present. The host response to the H. pylori infection is activation of lymphocytes and neutrophils. Release of inflammatory cytokines, such as interleukin (IL)-1, IL-8, and tumor necrosis factor-alpha (TNF-α), damages the gastric mucosa uAcid autodigestion Etiology and Genetic Risk Gastritis Prevention • Eat a well-balanced diet and exercise regularly. • Avoid drinking excessive amounts of alcoholic beverages. • Do not take large doses of aspirin, other NSAIDs (e.g., ibuprofen), or corticosteroids. • Avoid excessive intake of coffee (even decaffeinated). • Be sure that foods and water are safe to avoid contamination. • Manage stress levels using complementary and integrative therapies such as relaxation and meditation techniques. • Stop smoking and/or using other forms of tobacco. • Protect yourself against exposure to toxic substances in the workplace such as lead and nickel. • Seek medical treatment if you are experiencing symptoms of gastroesophageal reflux uH. pylori The most common form of chronic gastritis is type B gastritis, caused by Helicobacter pylori infection . A direct correlation exists between the number of organisms and the degree of cellular abnormality present. The host response to the H. pylori infection is activation of lymphocytes and neutrophils. Release of inflammatory cytokines, such as interleukin (IL)-1, IL-8, and tumor necrosis factor-alpha (TNF-α), damages the gastric mucosa uLong-term NSAID use Long-term NSAID use creates a high risk for acute gastritis. NSAIDs inhibit prostaglandin production in the mucosal barrier. Other risk factors include use of alcohol, coffee, and caffeine. Stress and cigarette smoking are considered risk factors for the development of acute gastritis uLocal irritation from radiation therapy Local irritation from radiation therapy and accidental or intentional ingestion of corrosive substances, including acids or alkalis (e.g., lye and drain cleaners), can also cause acute gastritis. Use of drugs such as steroids, aldosterone antagonists, and selective serotonin reuptake inhibitors can contribute to gastroduodenal inflammation and ulceration. uAccidental or intentional ingestion of corrosive materials uAutoimmune causes Health Promotion and Maintenance uBalanced diet - limiting intake of foods and spices that can cause gastric distress, such as caffeine, chocolate, mustard, pepper, and other strong or hot spices. Alcohol and tobacco should also be avoided. Regular exercise maintains peristalsis, which helps prevent gastric contents from irritating the gastric mucosam uRegular exercise uStress-reduction techniques uLimit foods and spices that cause gastric distress. uAvoid tobacco, alcohol. Avoid excessive use of aspirin, NSAIDs. Assessment: Noticing uEpigastric alterations in comfort uNausea, vomiting, upper abdominal or epigastric pain Symptoms of acute gastritis range from mild to severe. Clients typically report a rapid onset of epigastric pain and dyspepsia (an epigastric burning sensation, often referred to as "heartburn"). In some cases, gastric bleeding may occur and manifest as hematemesis (vomiting bright red or coffee-ground blood), or melena (dark, "tarry" [sticky] stool, indicating occult blood caused by digestion of blood within the small intestine). Gastritis or food poisoning caused by endotoxins, such as staphylococcal endotoxin, has an abrupt onset. Severe nausea and vomiting often occur within 5 hours of ingestion of the contaminated food. In some cases gastric hemorrhage is the presenting symptom, which is a life-threatening emergency. Chronic gastritis causes few symptoms unless ulceration occurs. Patients may report nausea, vomiting, or upper abdominal discomfort. Periodic epigastric pain may occur after a meal. Some patients have anorexia. uDiagnostic assessment uEGD uCytologic examination uRapid urease testing Esophagogastroduodenoscopy (EGD) via an endoscope with biopsy is the gold standard for diagnosing gastritis. (See Chapter 48 for discussion of nursing care associated with this diagnostic procedure.) The primary health care provider performs a biopsy to establish a definitive diagnosis of the type of gastritis. If lesions are patchy and diffuse, biopsy of several suspicious areas may be necessary to avoid misdiagnosis. A cytologic examination of the biopsy specimen is performed to confirm or rule out gastric cancer. Tissue samples can also be taken to detect H. pylori infection using rapid urease testing. The results of these tests are more reliable if the patient has discontinued taking antacids and proton pump inhibitors (PPIs) for at least a week Interventions: Responding uAcute gastritis treated with supportive care - Acute gastritis is treated symptomatically and supportively because the healing process is spontaneous, usually occurring within a few days. When the cause is removed, pain and discomfort usually subside. If bleeding occurs, a blood transfusion and fluid replacement may be given. Surgery, such as partial gastrectomy, pyloroplasty, and/or vagotomy, may be needed for patients with major bleeding or ulceration. Eliminating the causative factor(s) is the primary treatment approach for acute gastritis. Nutrition and drug therapy may also be used. Teach the patient to limit intake of any foods and spices that cause distress, such as those that contain caffeine or high acid content (e.g., tomato products, citrus juices) or those that are heavily seasoned with strong or hot spices. Bell peppers and onions are also commonly irritating foods. Most patients seem to progress better with a bland, nonspicy diet and smaller, more frequent meals. Alcohol and tobacco should also be avoided. The primary health care provider often prescribes drugs that block and buffer gastric acid secretions to relieve pain. H 2 -receptor antagonists, such as famotidine and nizatidine, are typically used to block gastric secretions. Sucralfate, a mucosal barrier fortifier, may also be prescribed. Antisecretory agents (proton pump inhibitors [PPIs]), such as omeprazole or pantoprazole, may be prescribed to suppress gastric acid. Antacids used as buffering agents include aluminum hydroxide!!!!! combined with magnesium hydroxide and aluminum hydroxide combined with simethicone and magnesium hydroxide (see the Common Examples of Drug Therapy: Gastritis and Peptic Ulcer Disease box). Calcium carbonate (chewable or liquid) is also a potent antacid, but it triggers gastrin release, causing rebound acid secretion. uChronic gastritis treated based on causative agent Treatment of chronic gastritis varies with the cause. The approach to management includes the elimination of causative agents, treatment of any underlying disease (e.g., chronic kidney disease, Crohn's disease), avoidance of toxic substances (e.g., alcohol, tobacco), and health teaching. Patients with chronic gastritis may require vitamin B12 for prevention or treatment of pernicious anemia. If H. pylori is found, the primary health care provider treats the infection. Current practice for infection treatment is described in the Drug Therapy discussion in the Peptic Ulcer Disease section. DON'T TAKE NSAIDS AND ASPIRIN WITH PEPTO

Diagnostic Assessment

uLaboratory studies uSerum tests-hpylori (gastric cancer) uUrine tests uAmylase can be detected in the urine. In acute pancreatitis, renal clearance of amylase is increased. Amylase levels in the urine remain elevated 5 to 7 days after onset of disease processes, even after serum levels return to normal within 1 to 2 days Amylase can be detected in the urine. In acute pancreatitis, renal clearance of amylase is increased. Amylase levels in the urine remain elevated 5 to 7 days after onset of disease processes, even after serum levels return to normal within 1 to 2 days uStool tests ugFOBT-Fecal Occult Blood test (blood in stool) uFIT-Fecal Immunochemical Test) is a stool test used to look for possible signs of colorectal cancer. uCT, Computed tomography; Endoscopy, esophagogastroduodenoscopy. Options include an annual high-sensitivity fecal immunochemical test (FIT), an annual guaiac-based fecal occult blood test (gFOBT) (such as the Hemoccult II Sensa), or a FIT-DNA test performed every 3 years. These tests use a take-home, multisample method rather than having the test done during a digital rectal examination. These tests use a take-home, multisample method rather than having the test done during a digital rectal examination. The traditionally used gFOBT (e.g., Hemoccult II Sensa) requires an active component of guaiac and is therefore more likely than the FIT (e.g., HemeSelect) to yield false-positive results. In addition, patients having the guaiac-based test must avoid NSAIDs for 7 days prior to and during the collection period, as well as red meat, citrus fruits and juices, and vitamin C in excess of 250 mg/day for 3 days prior to and during the test period As an alternate to the gFOBT or FIT, a stool DNA test (sDNA) can be completed every 3 years (American Cancer Society [ACS], 2018). Available only by prescription, this type of at-home diagnostic kit (such as Cologuard) is shipped directly to the patient after the health care provider has ordered the testing. Although less specific in detection than a colonoscopy, this type of testing can be encouraging to patients who may be fearful of undergoing a traditional colonoscopy or have concerns about financial coverage. • Flexible sigmoidoscopy every 5 years, or • CT colonography (virtual colonoscopy) every 5 years, or • Colonoscopy every 10 years Colonoscopy prep - Bowel prep - NPO since midnight - IV access and hang fluids to prevent dehydration How do you know if a pt can drink after endoscopy? - need a gag reflex - If they can cough, they can gag Which teaching will the nurse provide to a community group about early detection of colorectal cancer? Select all that apply. A. Home testing kits are available with a prescription. B. Sigmoidoscopy should be performed every 10 years. C. People over 40 years old should be tested for colon cancer. D. Bowel preparation is necessary prior to performance of a colonoscopy. E. Virtual colonoscopies (CT colonography) can be performed every 5 years.

Fatty Liver (Steatosis)

uNAFLD versus NASH uNonalcoholic fatty liver disease (NAFLD) is a condition in which fat builds up in your liver. Nonalcoholic steatohepatitis (NASH) is a type of NAFLD. If you have NASH, you have inflammation and liver cell damage, along with fat in your liver. uALT/AST, MRI, US, nuclear medicine are used to diagnose uInterventions include weight loss, glucose control, lipid-lowering agents.

Psychosocial Assessment

uPatients may be embarrassed to discuss elimination problems. uAsk how GI health problem affects life, lifestyle, activities, employment. uAsk about stressful events that preceded or exacerbate GI problems. uPatients with cancer may experience the grieving process.

Cancer of the Liver

uPrimary versus metastatic tumors uOne of the most fatal types of cancer uCirrhosis increases risk uMost people don't have signs and symptoms in the early stages of primary liver cancer. u When signs and symptoms do appear, they may include: uLosing weight without trying uLoss of appetite uUpper abdominal pain uNausea and vomiting uGeneral weakness and fatigue uAbdominal swelling uYellow discoloration of your skin and the whites of your eyes (jaundice) uWhite, chalky stools Diagnostics Elevated AFP and alkaline phosphatase are common. US and contrast-enhanced CT are used. Risks Chronic infection with HBV or HCV. Cirrhosis. Hemochromatosis and Wilson's disease. Diabetes. Nonalcoholic fatty liver disease. Exposure to aflatoxins. Aflatoxins are poisons produced by molds that grow on crops that are stored poorly. Excessive alcohol consumption.

uEsophageal trauma

uThe main causes for esophageal perforation in adults are iatrogenic, traumatic, spontaneous and foreign bodies. uHigh rate of morbidity and mortality

Acute versus Chronic Cholecystitis

uUnderlying cause uGallstones or biliary sludge uSigns/symptoms uSevere pain in upper right or center abdomen that spreads to your right shoulder, nausea, vomiting, fever Patients with cholecystitis have abdominal pain , although symptoms vary in intensity and frequency. Ask the patient to describe the pain, including its intensity and duration, precipitating factors, and any measures that relieve it. Pain may be described as indigestion of varying intensity, ranging from a mild, persistent ache to a steady, constant pain in the right upper abdominal quadrant. It may radiate to the right shoulder or scapula. In some cases the abdominal pain of chronic cholecystitis may be vague and nonspecific. The usual pattern is episodic. Patients often refer to acute pain episodes as "gallbladder attacks." Older adults and patients with diabetes mellitus may have atypical symptoms of cholecystitis, including the absence of pain and fever. Localized tenderness may be the only presenting sign. The older patient may become acutely confused (delirium) as the first symptom of gallbladder disease. Critical Rescue The severe pain of biliary colic is produced by obstruction of the cystic duct of the gallbladder or movement of one or more gallstones. When a stone is moving through or is lodged within the duct, tissue spasm occurs in an effort to get the stone through the small duct. Biliary colic may be so severe that it occurs with tachycardia, pallor, diaphoresis, and prostration (extreme exhaustion). Assess the patient for possible shock caused by biliary colic. Notify the health care provider or Rapid Response Team if these symptoms occur. Stay with the patient and keep the head of the bed flat if shock occurs. In chronic cholecystitis, patients may have slowly developing symptoms and may not seek medical treatment until late symptoms such as jaundice, clay-colored stools, and dark urine occur from biliary obstruction. Icterus may also be present. Steatorrhea (fatty stools) occurs because fat absorption is decreased as a result of the lack of bile. Bile is needed for the absorption of fats and fat-soluble vitamins in the intestine. As with any inflammatory process, the patient may have an elevated temperature of 99°F to 102°F (37.2°C to 38.9°C), tachycardia, and dehydration from fever and vomiting. He or she often will decline food intake because of the resulting pain or other symptoms that may occur. Cholecystitis • Episodic or vague upper abdominal pain or discomfort that can radiate to the right shoulder • Pain triggered by a high-fat or high-volume meal • Anorexia • Nausea and/or vomiting • Dyspepsia • Eructation • Flatulence • Feeling of abdominal fullness • Rebound tenderness (Blumberg sign) • Fever • Jaundice, clay-colored stools, dark urine • Steatorrhea (most common with chronic cholecystitis) uRisk factors ugallstones uRole of diet uHigh Fat and Low Fiber increase the risk Diagnostics Ultrasonography (US) of the right upper quadrant is the best initial diagnostic test for cholecystitis. It is safe, accurate, and painless. Acute cholecystitis is seen as edema of the gallbladder wall and pericholecystic fluid. A hepatobiliary scan (sometimes called a hepatobiliary iminodiacetic acid [HIDA] scan) can be performed to visualize the gallbladder and determine patency of the biliary system. In this nuclear medicine test, a radioactive tracer or chemical is injected IV. About 20 minutes after the injection, a gamma camera tracks the flow of the tracer from the gallbladder to determine the ejection rate of bile into the biliary duct. A decreased bile flow indicates gallbladder disease with obstruction. Teach patients having this test to have nothing by mouth before the procedure. Remind the patient that the camera is large and close to the body for most of the procedure. When the cause of cholecystitis or cholelithiasis is not known or the patient has symptoms of biliary obstruction (e.g., jaundice), an endoscopic retrograde cholangiopancreatography (ERCP) may be performed. Some patients have the less invasive and safer magnetic resonance cholangiopancreatography (MRCP), which can be performed by an interventional radiologist. For this procedure, the patient is given oral or IV contrast material (gadolinium) before having an MRI scan. Before the test, ask the patient about any history of urticaria (hives) or other allergy. MRI is also contraindicated in patients with a pacemaker or other incompatible devices. uUltrasonography (Abdomen) uHIDA Scan uA hepatobiliary iminodiacetic acid (HIDA) scan uimaging procedure used to diagnose problems of the liver, gallbladder and bile ducts. ubile-excreting function of your liver and to track the flow of bile from your liver into your small intestine. uradioactive tracer is injected into a vein in your arm (allergies) uERCP (Endoscopic retrograde cholangio-pancreatography} uused to examine and treat diseases of the liver, bile ducts, and pancreas uInvasive uUses contrast dye uMajor Risk of procedure-pancreatitis uMRCP (Magnetic Resonance Cholangio-Pancreatography) uNon-invasive uNo dye uNo major risks of procedure Analysis: Interpreting uThe priority collaborative problems for patients with cholecystitis include uWeight loss due to pain, nausea, and inflammation uAcute pain due to cholecystitis Planning and Implementation Physiologic Integrity A young adult client admitted with a diagnosis of cholecystitis from cholelithiasis has severe abdominal pain, nausea, and vomiting. Based on these assessment findings, which client problem is the highest priority for nursing intervention at this time? A. Anxiety B. Risk for dehydration C. Acute pain D. Malnutrition Promoting Nutrition uHigh fiber, low fat diet uSmall, frequent meals Manage Pain uNonsurgical Management uDrug Therapy-Antibiotics: To treat gallbladder infections. uMetronidazole . PiperacillinAnalgesics: To manage the pain caused due to gallstones. uOxycodone . AcetaminophenGallstone dissolvers: To dissolve gallstones. uUrsodiol . Chenodiol uLithotripsy uuses shock waves or a laser to break down stones in the kidney, gallbladder, or ureter. uSurgical Management uCholecystectomy Acute biliary pain requires opioid analgesia, such as morphine or hydromorphone (Dilaudid). All opioids may cause some degree of sphincter of Oddi spasm. Ketorolac, a potent NSAID, may be used for mild-to-moderate pain . Be sure to monitor the patient for increased pain, tachycardia, and hypotension because the drug can cause GI bleeding. The primary health care provider prescribes antiemetics to control nausea and vomiting. IV antibiotic therapy may also be given, depending on the cause of cholecystitis or as a one-time dose for surgery. An option for a small number of patients with cholelithiasis (gallstones) is the use of oral bile acid dissolution or gallstone-stabilizing agents. Drugs such as ursodiol and chenodiol may be given as long-term therapy to dissolve or stabilize gallstones (Burchum & Rosenthal, 2019). A gallbladder ultrasound is required every 6 months for the first year of therapy to determine the effectiveness of the drug. Teach patients on this type of drug therapy to report diarrhea, vomiting, or severe abdominal pain, especially if it radiates to the shoulders, to their primary health care provider immediately. Remind them to take the medication with food and milk. For some patients with small stones or for those who are not good surgical candidates, a treatment that is commonly used for kidney stones can be used to break up gallstones—extracorporeal shock wave lithotripsy (ESWL). This procedure can be used only for patients who have a normal weight, cholesterol-based stones, and good gallbladder function. The patient lies on a water-filled pad, and shock waves break up the large stones into smaller ones that can be passed through the digestive system. During the procedure, the patient might have pain resulting from the movement of the stones or duct or gallbladder spasms. A therapeutic bile acid, such as ursodeoxycholic acid (UDCA), may be used after the procedure to help dissolve the remaining stone fragments.

Differences between Ulcerative Colitis and Crohn's

uWhere uUC-limited to colon uChron's occurs anywhere between the mouth and anus uPAIN uUC-confined to left side of abdomen with rectal bleeding uChron's -pain anywhere in the abdomen

uEsophageal diverticula

ua protruding pouch in the lining of the esophagus. It forms in a weak area of the esophagus. The pouch can be anywhere from 1 to 4 inches in length.

Immunity Concept Exemplar: Hepatitis

what organ is it infecting? the liver Are all contagious? no Hepatitis is the widespread inflammation and infection of liver cells. Viral hepatitis, which can be acute or chronic, is the most common type. Less common types of hepatitis are caused by chemicals, drugs, and some herbs. This section discusses hepatitis caused by a virus. Viral hepatitis results from an infection caused by one of five categories of viruses: • Hepatitis A virus (HAV) • Hepatitis B virus (HBV) • Hepatitis C virus (HCV) • Hepatitis D virus (HDV) • Hepatitis E virus (HEV) Some cases of viral hepatitis are not caused by any of these viruses. These patients have non-A-E hepatitis. This section focuses on the most common viral types. Liver injury with inflammation can develop after exposure to a number of drugs and chemicals by inhalation, ingestion, or parenteral (IV) administration. Toxic and drug-induced hepatitis can result from exposure to hepatotoxins (e.g., industrial toxins, alcohol, and drugs). Hepatitis may also occur as a secondary infection during the course of infections with other viruses, such as Epstein-Barr, herpes simplex, varicella-zoster, and cytomegalovirus. Viral hepatitis uToxic and drug-induced hepatitis uClassification uHAV-spread thru fecal-oral transmission or consuming contaminated food or water The causative agent of hepatitis A, hepatitis A virus (HAV), is a ribonucleic acid (RNA) virus of the enterovirus family. It is a hardy virus and survives on human hands. The virus is resistant to detergents and acids but is destroyed by chlorine (bleach) and extremely high temperatures. Hepatitis A usually has a mild course similar to that of a typical flulike infection and often goes unrecognized. It is spread most often by the fecal-oral route by fecal contamination either from person-to-person contact (e.g., oral-anal sexual activity) or by consuming contaminated food or water. Common sources of infection include shellfish caught in contaminated water and food contaminated by food handlers infected with HAV. uHBV-transmitted thru bodily fluids like blood and semen, by unsterile needles and medical/dental equipment, or mother to child during delivery The hepatitis B virus (HBV) is not transmitted like HAV. It is a double-shelled particle containing DNA composed of a core antigen (HBcAg), a surface antigen (HBsAg), and another antigen found within the core (HBeAg) that circulates in the blood. HBV may be spread through these common modes of transmission (CDC, 2020a): • Unprotected sexual intercourse with an infected partner • Sharing needles, syringes, or other drug-injection equipment • Sharing razors or toothbrushes with an infected individual • Accidental needlesticks or injuries from sharp instruments primarily in health care workers (low incidence) • Blood transfusions (that have not been screened for the virus, before 1992) • Hemodialysis • Direct contact with the blood or open sores of an infected individual • Birth (spread from an infected mother to baby during birth) uHCV-is similarly transmitted like HBV through bodily fluids, like blood and semen, and by unsterile needles and medical/dental equipment and procedures. Symptoms of HCV are generally similar to HAV's Hepatitis C (HCV) is the leading cause of end-stage liver disease in the world (Chaney, 2019). The causative virus of hepatitis C is an enveloped, single-stranded RNA virus, which is genetically unstable and has at least six known major genotypes. Transmission is blood to blood. The rate of sexual transmission is very low in a single-couple relationship but increases with multiple sex partners or in men who have unprotected sex with men. HCV is spread most commonly by (Chaney, 2019): • Illicit IV drug needle sharing (highest incidence) • Blood, blood products, or organ transplants received before 1992 • Baby boomers (those adults born between 1945 and 1965) • Needlestick injury with HCV-contaminated blood (health care workers at high risk) • Hemodialysis • Health care workers • People who are incarcerated (prisoners) • Sharing of drug paraphernalia The disease is not transmitted by casual contact or intimate household contact. However, those infected are advised not to share razors, toothbrushes, or pierced earrings because microscopic blood may be on these items. uHDV or Delta hepatitis-coinfection; infections only occur in persons who are also infected with hepatitis B Hepatitis D (delta hepatitis) is caused by a defective RNA virus that needs the helper function of HBV. It occurs only with HBV to cause viral replication. This usually develops into chronic disease. The incubation period is about 14 to 56 days. As with hepatitis B, the disease is transmitted primarily by parenteral routes, especially in patients who are IV drug users. Having sexual contact with someone with HDV is also a high-risk factor uHEV-similar to hepatitis A as it is spread by fecal-oral transmission and consumption of contaminated food and water The hepatitis E virus (HEV) causes a waterborne infection associated with epidemics in the Indian subcontinent, Asia, Africa, the Middle East, Mexico, and Central and South America. Many large outbreaks have occurred after heavy rains and flooding. Like hepatitis A, hepatitis E is caused by fecal contamination of food and water. In the United States, hepatitis E has been found only in international travelers. It is transmitted via the fecal-oral route, and the clinical course resembles that of hepatitis A. uComplications Failure of the liver cells to regenerate, with progression of the necrotic process, results in a severe acute and often fatal form of hepatitis known as fulminant hepatitis. Hepatitis is considered to be chronic when liver inflammation lasts longer than 6 months. Chronic hepatitis usually occurs as a result of hepatitis B or hepatitis C. Superimposed infection with hepatitis D virus (HDV) in patients with chronic hepatitis B may also result in chronic hepatitis. Chronic hepatitis can lead to cirrhosis and liver cancer. Physiological Integrity The nurse is caring for a client diagnosed with hepatitis A. Which transmission-based precautions are required when providing care for this client? Select all that apply. A. Place client in a private room. B. Wear a mask when handling patient bedpan. C. Wear gloves when touching the client. D. Wear a gown when providing personal care to this patient. E. Wear eye goggles when providing care. Prevention of Viral Hepatitis in Health Care Workers • Use Standard Precautions to prevent the transmission of disease between patients or between patients and health care staff (see Chapter 21). • Eliminate needles and other sharp instruments by substituting needleless systems. (Needlesticks are the major source of hepatitis B transmission in health care workers.) • Take the hepatitis B vaccine, which is given in a series of three injections. This vaccine also prevents hepatitis D by preventing hepatitis B. • For postexposure prevention of hepatitis A, seek medical attention immediately for immunoglobulin (Ig) administration. • Report all cases of hepatitis to the local health department. uHAV and HBV are declining due to vaccination. uHCV most common—no vaccine Health Promotion and Maintenance uVaccines for HAV and HBV Hepatitis vaccines for infants, children, and adolescents have helped to decrease the incidence of hepatitis A and hepatitis B. Teach adults the importance of obtaining immunizations for their children. uHAV-specific recommendations uProper handwashing (especially after handling shellfish) Avoid contaminated food or water Assessment: Noticing uAsk about exposure to someone with hepatitis. uAsk about chemical exposure. uInquire about alcohol, drug, herbal use. uInquire about travel, sexual activities, needlestick exposure, drug (IV) use, military service. uAssess for family history of liver disease. uPhysical assessment/signs and symptoms uAbdominal pain uChanges in skin or sclera (icterus) uArthralgia (joint pain) or myalgia (muscle pain) uDiarrhea/constipation uChanges in color of urine or stool uFever uLethargy uMalaise uNausea/vomiting uPruritus (itching) uLaboratory assessment uLiver enzymes uBlood tests specific to hepatitis type uOther diagnostic assessment uLiver biopsy Key Features Viral Hepatitis • Abdominal pain • Yellowish sclera (icterus) • Arthralgia (joint pain) or myalgia (muscle pain) • Diarrhea/constipation • Light clay-colored stools • Dark yellow to brownish urine • Jaundice • Fever • Fatigue • Malaise • Anorexia • Nausea and vomiting • Dry skin • Pruritus (itching) Analysis: Interpreting uWeight loss due to complications associated with inflammation of the liver uFatigue due to decreased metabolic energy production uPotential for infection related to state of immunocompromise Planning and Implementation: Responding uPromoting nutrition uAddressing fatigue uReducing the potential for infection Rest is an essential intervention to reduce the liver's metabolic demands and increase its blood supply. Collaborative care is generally supportive. The patient is usually tired and expresses feelings of general malaise. Complete bedrest is usually not required, but rest periods alternating with periods of activity are indicated and are often enough to promote hepatic healing Action Alert Teach the patient with viral hepatitis and the family to use measures to prevent infection transmission. In addition, instruct the patient to avoid alcohol and check with the primary health care provider before taking any medication or vitamin, supplement, or herbal preparation. Encourage the patient to increase activity gradually to prevent fatigue. Suggest that the patient eat small, frequent meals of high-carbohydrate foods and plan frequent rest periods. Collaborate with the certified infection control practitioner and infectious disease specialist if needed in caring for these patients. These experts can suggest appropriate resources for the patient and family. Care Coordination and Transition Management uHome care management varies depending on type of hepatitis. uEducation regarding infection control is important. Evaluation: Reflecting uMaintain nutritional status adequate for body requirements. uReport increasing energy levels as the liver rests. uRemain infection-free.

Inflammatory Disorders

üAppendicitis üPeritonitis - very serious, can kill your patient. üGastroenteritis üUlcerative colitis üCrohn's Disease üDiverticulosis versus diverticulitis

Focused Inflammatory Disorders

üUlcerative colitis üCrohn's disease