Module 7 Responses To Metabolic Gastrointestinal & Liver Alterations PDF

RESPONSES TO METABOLIC GASTROINTESTINAL AND LIVER ALTERATIONS THE GASTROINTESTINAL (GI) SYSTEM (also called the digestive system) consists of the GI tract and its associated organs and glands. Included in the GI tract are the mouth, esophagus, stomach, small intestine, large intestin...

RESPONSES TO METABOLIC GASTROINTESTINAL AND LIVER ALTERATIONS THE GASTROINTESTINAL (GI) SYSTEM (also called the digestive system) consists of the GI tract and its associated organs and glands. Included in the GI tract are the mouth, esophagus, stomach, small intestine, large intestine, rectum, and anus. The associated organs  STRUCTURES AND FUNCTIONS OF GASTROINTESTINAL SYSTEM The GI tract extends approximately 30 ft (9 m) from the mouth to the anus. It is composed of four common layers. From the inside to the outside, these layers are (1) mucosa, (2) submucosa, (3) muscle, and (4) serosa. The muscular coat consists of two layers: the circular (inner) layer and the  The GI tract is innervated by the parasympathetic and sympathetic branches of the autonomic nervous system. The parasympathetic (cholinergic) system is mainly excitatory, and the sympathetic (adrenergic) system is mainly inhibitory.  The abdominal organs are almost completely covered by the peritoneum. The two layers of the peritoneum are the parietal layer, which lines the abdominal cavity wall, and the visceral layer, which covers the abdominal organs.  The two folds of the peritoneum are the mesentery and the omentum. The mesentery attaches the small intestine and part of the large intestine to the posterior abdominal wall and contains blood and lymph vessels. The omentum hangs like an apron from the stomach to the intestines and contains fat and lymph nodes  The main function of the GI system is to supply nutrients to body cells. This is accomplished through the processes of (1) ingestion (taking in food), (2) digestion (breaking down food), and (3) absorption (transferring food products into circulation). Elimination is the process of excreting the waste  The main function of the GI system is to supply nutrients to body cells. This is accomplished through the processes of (1) ingestion (taking in food), (2) digestion (breaking down food), and (3) absorption (transferring food products into circulation). Elimination is the process of excreting the waste INGESTION Ingestion is the intake of food. An appetite center is located in the hypothalamus. It is directly or indirectly stimulated by hypoglycemia, an empty stomach, decrease in body temperature, and input from higher brain centers. The hormone ghrelin released from the stomach mucosa plays a role in appetite stimulation. Another hormone, leptin, is involved in appetite suppression. The sight, smell, and taste of food frequently stimulate appetite.  Deglutition (swallowing) is the mechanical component of ingestion. The organs involved in the deglutition of food are the mouth, pharynx, and esophagus. Mouth- The oral cavity contains the teeth, used in mastication (chewing), and the tongue. The tongue is a solid muscle mass and assists in chewing and moving food to the back of the throat for swallowing  Within the oral cavity are three pairs of salivary glands: the parotid, submaxillary, and sublingual glands. These glands produce saliva, which consists of water, protein, mucin, inorganic salts, and salivary amylase Pharynx- The epiglottis is a lid of fibrocartilage that closes over the larynx during swallowing. During ingestion, the oropharynx provides a route for food from the mouth to the esophagus. When receptors in the oropharynx are stimulated by food or liquid, the swallowing reflex is initiated  Esophagus- The muscular layers contract (peristalsis) and propel the food to the stomach. There are two sphincters: the upper esophageal sphincter (UES) at the proximal end of the esophagus and the lower esophageal sphincter (LES) at the distal end. The LES remains contracted except during swallowing, belching, or vomiting. The LES is an important barrier that normally prevents reflux of acidic gastric contents into DIGESTION AND ABSORPTION The stomach’s functions are to store food, mix food with gastric secretions, and empty contents in small boluses into the small intestine. The stomach absorbs only small amounts of water, alcohol, electrolytes, and certain drugs. It always contains gastric fluid and mucus. The three main parts of the stomach are the fundus (cardia), body, and antrum  The pylorus is a small portion of the antrum proximal to the pyloric sphincter. Sphincter muscles (the LES and the pyloric sphincter) guard the entrance to and exit from the stomach. The pylorus is a small portion of the antrum proximal to the pyloric sphincter. Sphincter muscles (the LES and the pyloric sphincter) guard the entrance to and exit from thThe serous (outer) layer of the stomach is formed by the peritoneum  The muscular layer consists of the longitudinal (outer) layer, circular (middle) layer, and oblique (inner) layer. The mucosal layer forms folds called rugae that contain many small glands. In the fundus the glands contain chief cells, which secrete pepsinogen, and parietal cells, which secrete hydrochloric (HCl) acid, water, and intrinsic factor. The secretion of HCl acid makes gastric juice acidic. This acidic pH aids in the protection against ingested organisms. Intrinsic factor promotes cobalamin (vitamin B12) absorption in the small intestine stomach.  Small Intestine- The two primary functions of the small intestine are digestion and absorption (uptake of nutrients from the gut lumen to the bloodstream). It extends from the pylorus to the ileocecal valve. The small intestine is composed of the duodenum, jejunum, and ileum. The ileocecal valve prevents reflux of large intestine contents into the small intestine.  The digestive enzymes on the brush border of the microvilli chemically break down nutrients for absorption. The villi are surrounded by the crypts of Lieberkühn, which contain the multipotent stem cells for the other epithelial cell types. Brunner’s glands in the submucosa of the duodenum secrete an alkaline fluid containing bicarbonate. Intestinal goblet cells secrete mucus that protects the mucosa. ELIMINATION Large Intestine- The most important function of the large intestine is the absorption of water and electrolytes. The large intestine also forms feces and serves as a reservoir for the fecal mass until defecation occurs  Microorganisms in the colon are responsible for the breakdown of proteins not digested or absorbed in the small intestine. These amino acids are deaminated by the bacteria, leaving ammonia, which is carried to the liver and converted to urea, which is excreted by the kidneys. Bacteria in the colon also synthesize vitamin K and some of the B vitamins. Bacteria also play a part in the production of flatus  When food enters the stomach and duodenum, gastrocolic and duodenocolic reflexes are initiated, resulting in peristalsis in the colon. These reflexes are more active after the first daily meal and frequently result in bowel evacuation. Defecation is a reflex action involving voluntary and involuntary control. Feces in the rectum stimulate sensory nerve endings that produce the desire to defecate. The reflex center for defecation is in the sacral portion of the spinal cord (parasympathetic nerve fibers).  Liver- The functional units of the liver are lobules. The lobule consists of rows of hepatic cells (hepatocytes) arranged around a central vein. The capillaries (sinusoids) are located between the rows of hepatocytes and are lined with Kupffer cells, which carry out phagocytic activity (removal of the toxins and bacteria in the blood).  Biliary Tract- consists of the gallbladder and the duct system. The gallbladder is a pear- shaped sac located below the liver. The gallbladder’s function is to concentrate and store bile. In the intestines, bilirubin is reduced to stercobilinogen and urobilinogen by bacterial action. Stercobilinogen accounts for the brown color of stool.  Bilirubin Metabolism. Bilirubin, a pigment derived from the breakdown of hemoglobin, is constantly produced. Because it is insoluble in water, it is bound to albumin for transport to the liver. This form of bilirubin is referred to as unconjugated. In the liver bilirubin is conjugated with glucuronic acid. Conjugated bilirubin is soluble and is excreted in bile. Bile also consists of water, cholesterol, bile salts, electrolytes, and phospholipids. Bile salts are needed for fat emulsification and digestion.  Pancreas- The pancreas has both exocrine and endocrine functions. The exocrine function contributes to digestion through the production and release of enzymes. The endocrine function occurs in the islets of Langerhans, whose β cells secrete insulin and amylin; α cells secrete glucagon; δ cells secrete somatostatin; and F cells secrete pancreatic polypeptide DIAGNOSTIC TEST  Radiologic Studies Upper Gastrointestinal Series- through provides visualization of the oropharyngeal area, the esophagus, the stomach, and the small intestine via fluoroscopy and x-ray examination. The procedure consists of the patient swallowing contrast medium (a thick barium solution or gastrograffin) and then assuming different positions on the x-ray table. The movement of the contrast medium is observed with fluoroscopy, and several x-rays are taken. An upper GI series is used to identify disorders such as esophageal strictures, polyps, tumors, hiatal hernias, foreign bodies, and peptic ulcers.  Lower Gastrointestinal Series. The purpose of a lower GI series (barium enema) examination is to observe by means of fluoroscopy the colon filling with contrast medium and to observe by x-ray the filled colon. This procedure identifies polyps, tumors, and other lesions in the colon. It consists of administering an enema of contrast medium to the patient. The air- contrast barium enema provides better visualization. Because it requires the patient to retain the barium, it is not tolerated as well in an older or immobile patient.  Virtual colonoscopy combines computed tomography (CT) scanning or magnetic resonance imaging (MRI) with computer software to produce images of the colon and the rectum if a polyp is discovered using virtual colonoscopy, a conventional colonoscopy will then be needed to obtain a biopsy or remove it. A disadvantage of virtual colonoscopy is that it may be less sensitive in obtaining information on the details and color of the mucosa.  Endoscopy refers to the direct visualization of a body structure through a lighted fiberoptic instrument. The GI structures that can be examined by endoscopy include the esophagus, the stomach, the duodenum, and the colon. The pancreatic, hepatic, and common bile ducts can be visualized with an endoscope. This procedure is called endoscopic retrograde cholangiopancreatography (ERCP).  Liver Biopsy- is to obtain hepatic tissue that can be used in establishing a diagnosis or assessing fibrosis. It may also be useful for following the progress of liver disease, such as chronic hepatitis  Liver Biopsy- is to obtain hepatic tissue that can be used in establishing a diagnosis or assessing fibrosis. It may also be useful for following the progress of liver disease, such as chronic hepatitis  INTRAABDOMINAL HYPERTENSION AND ABDOMINAL COMPARTMENT SYNDROME INTRABDOMINAL HYPERTENSION A steady -state pressure concealed within the abdominal cavity IAH is diagnosed when a patient has three documented IAP measurement of 12- 20mmHg , 4-6 hours apart If not treated, it will progressively develop into Abdominal Compartment Syndrome What is an acceptable IAP? Normal= 5mmHg A critically ill patient = 5-7 mmHg Obese patients= 15mmHg It is a complication of an emergency repaired of abdominal aortic aneurysm. Persistent IAH reduce blood flow to the viscera.  ABDOMINAL COMPARTMENT SYNDROME End -organ dysfunction caused by IAH Impaired organ perfusion caused by IAH and resulting to multisystem organ failure How to calculate Abdominal Perforation Pressure (APP)? - Abdominal perfusion pressure is calculated by subtracting the IAP from simultaneous mean arterial pressure (MAP) measurement What are the categories of ACS? Abdominal compartment syndrome can be divided into 3 categories: 1. primary or acute compartment Syndrome occurs when intra-abdominal pathology is directly and proximally responsible for the compartment syndrome 2. Secondary compartment Syndrome occurs when no visible intra-abdominal injury is present but injuries outside the abdomen cause fluid accumulation 3. Chronic abdominal syndrome occurs in the presence of cirrhosis and ascites or related disease states, often CLINICAL PRESENTATION  Marked hypotension  Increased ventilatory pressures, specially increased peak inspiratory pressure  Oliguria  Raise intra-abdominal pressure  Hypoxia, hypercapnia and respiratory acidosis Risk factors  Liver dysfunction/cirrhosis with ascites  Major trauma  Massive fluid resuciattion or fluid overload  Mechanical ventilation  Obesity and increased BMI  Prone positioning  Sepsis  Shock or hypotension How to Measure the IAP? - IAP should be expressed in mmHg and measured at end-expiration in the complete supine position in the complete supine position after ensuring that abdominal muscle contraction is absent and with transducer zeroes at the level of the midaxillary line The Gold Standard for IAP Measurement  IAP monitoring using a Foley’s catheter is known as the gold standard where urinary bladder is acting as the medium for the monitoring  Intermittent or continuous IAP monitoring using bladder is the most commonly used and the recommended method  Uno meter- Abdominal Pressure Kit is needed in measuring IAH If IAH is present, serial measurement should be performed through the patient’s critical illness Measurements should be taken at least four hourly Collaborative Management: Control the situation that leads to IAH Open surgical decompression Percutaneous drainage Conservative measures: intubation, ventilation, patient positioning, gastric decompression, cautious fluid resuscitation, pain management, and temporary hemotransfusion  Uno meter- Abdominal Pressure Kit is needed in measuring IAH If IAH is present, serial measurement should be performed through the patient’s critical illness Measurements should be taken at least four hourly ACUTE LIVER FAILURE ACUTE LIVER FAILURE fulminant hepatic failure, is a clinical syndrome characterized by severe impairment of liver function associated with hepatic encephalopathy The most common cause is drugs, usually acetaminophen in combination with alcohol. People who abuse alcohol are particularly susceptible to detrimental effects of acetaminophen on the liver.  Other drugs that can cause acute liver failure include isoniazid, halothane, sulfa- containing drugs, and NSAIDs. Drugs can cause liver cell failure by disrupting essential intracellular processes or causing an accumulation of toxic metabolic products Viral hepatitis, in particular HBV, is the second most common cause of acute liver failure. Hepatitis A is a less common cause  Acute liver failure is characterized by the rapid onset of severe liver dysfunction in someone with no prior history of liver disease. CLINICAL MANIFESTATIONS AND DIAGNOSTIC STUDIES Manifestations include jaundice, coagulation abnormalities, and encephalopathy. In acute liver failure, changes in mentation are the first clinical sign. Patients are susceptible to a wide variety of complications, including cerebral edema, renal failure, hypoglycemia, metabolic acidosis, sepsis, and multiorgan failure. Serum bilirubin is elevated, and the prothrombin time is prolonged. Liver enzyme levels (AST, ALT) are often markedly elevated. Additional laboratory tests include blood chemistries (especially glucose, since hypoglycemia may be present and require correction), complete blood counts (CBCs), acetaminophen level and screening for other drugs and toxins, viral hepatitis serologies (especially HAV and HBV), serum ceruloplasmin (enzyme synthesized in liver) levels, α1- antitrypsin levels, iron levels, and autoantibodies CT or magnetic resonance imaging (MRI) is helpful in providing information about the liver size and contour, presence of ascites, tumors, and patency of the blood vessels. ENCEPHALOPATHY neuropsychiatric manifestation of liver disease. The pathogenesis is multifactorial and includes the neurotoxic effects of ammonia, abnormal neurotransmission, astrocyte swelling, and inflammatory cytokines. A major source of ammonia is the bacterial and enzymatic deamination of amino acids in the intestines. The ammonia that results from this deamination process normally goes to the liver via the portal circulation and is converted to urea, which is then excreted by the kidneys. When blood is shunted past the liver via the collateral vessels or the liver is unable to convert ammonia to urea, the levels of ammonia in the systemic circulation increase. The ammonia crosses the blood- brain barrier and produces neurologic toxic manifestations. Factors that increase ammonia in the circulation may precipitate hepatic encephalopathy. Clinical manifestations of encephalopathy are changes in neurologic and mental responsiveness; impaired consciousness; and inappropriate behavior, ranging from sleep disturbances to lethargy to deep coma.  Changes may occur suddenly because of an increase in ammonia in response to bleeding varices or infection or gradually as blood ammonia levels slowly increase. A grading system is often used to classify the stages of hepatic encephalopathy A characteristic manifestation of hepatic encephalopathy is asterixis (flapping tremors). This may take several forms, with the most common involving the arms and hands. When asked to hold the arms and hands stretched out, the patient is unable to hold this position and performs a series of rapid flexion and extension movements of the hands Impairments in writing involve difficulty in moving the pen or pencil from left to right and apraxia (the inability to construct simple figures). Other signs include hyperventilation, hypothermia, and grimacing and grasping reflexes. Fetor hepaticus (musty, sweet odor of the patient’s breath) occurs in some patients with encephalopathy. This odor is from the accumulation of digestive by-products that the liver is unable to degrade COLLABORATIVE MANAGEMENT Since acute liver failure may progress rapidly, with hour-by hour changes in consciousness, early transfer to the ICU is preferred once the diagnosis is made. Planning for transfer to a transplant center should begin in patients with grade 1 or 2 encephalopathy because they may worsen rapidly Renal failure is a frequent complication in patients with liver failure and may be due to dehydration, hepatorenal syndrome, or acute tubular necrosis. The frequency of renal failure may be even greater with acetaminophen overdose or other toxins, where direct renal toxicity occurs. Although few patients die of renal failure alone, it often increases the mortality risk and may worsen the prognosis.  Protect renal function by maintaining adequate fluid balance, avoiding nephrotoxic agents (e.g., aminoglycosides, NSAIDs), and promptly identifying and treating infection. Liver transplantation is the treatment of choice for and increases survival rates in patients with acute liver failure. Cerebral edema, cerebellar herniation, and brainstem compression are the most common causes of death. Monitoring and management of hemodynamic and renal function, as well as glucose, electrolytes, and acid-base status, are critical. Conduct frequent neurologic evaluations for signs of elevated intracranial pressure  Position the patient with the head elevated at 30 degrees. Avoid patient stimulation. Maneuvers that cause straining or Valsalvalike movements may increase intracranial pressure (ICP)  Position the patient with the head elevated at 30 degrees. Avoid patient stimulation. Maneuvers that cause straining or Valsalvalike movements may increase intracranial pressure (ICP) Avoid the use of any sedatives because of their effects on mental status. Only minimal doses of benzodiazepines should be used due to their delayed metabolism by the failing liver. Additional measures include padding bedrails to avoid injury from possible seizures, closely observing the patient to prevent injuries, monitoring intake and output for renal function, and providing good skin and oral care to avoid breakdown and infection. Alterations in level of consciousness may compromise nutritional intake. Factors such as coagulation problems may influence whether enteral nutrition is initiated. An NG tube may be irritating to the nasal and esophageal mucosa, thus causing bleeding. PANCREATITIS ACUTE PANCREATITIS is an acute inflammation of the pancreas. The degree of inflammation varies from mild edema to severe hemorrhagic necrosis RISK FACTORS Gallbladder disease Chronic alcoholic disease Smoking is an independent risk factor for acute pancreatitis. Biliary sludge or microlithiasis, which is a mixture of cholesterol crystals and calcium salt hypertriglyceridemia Other less common causes of acute pancreatitis include trauma (postsurgical, abdominal), viral infections (mumps, coxsackievirus B, HIV), penetrating duodenal ulcer, cysts, abscesses, cystic fibrosis, Kaposi sarcoma, certain drugs (corticosteroids, thiazide diuretics, oral contraceptives, sulfonamides, NSAIDs), metabolic disorders (hyperparathyroidism, renal failure), and vascular diseases The most common pathogenic mechanism is autodigestion of the pancreas. The etiologic factors injure pancreatic cells or activate the pancreatic enzymes in the pancreas rather than in the intestine. This may be due to reflux of bile acids into the pancreatic ducts through an open or distended sphincter of Oddi. This reflux may be caused by blockage created by gallstones. Obstruction of pancreatic ducts results in pancreatic ischemia Trypsinogen is an inactive proteolytic enzyme produced by the pancreas. It is released into the small intestine via the pancreatic duct. In the intestine it is activated to trypsin by enterokinase. Normally, trypsin inhibitors in the pancreas and plasma bind and inactivate any trypsin that is inadvertently produced. In pancreatitis, activated trypsin in the pancreas can digest the pancreas and produce bleeding The exact mechanism by which chronic alcohol intake predisposes a person to pancreatitis is not known. It is thought that alcohol increases the production of the digestive enzymes in the pancreas. The pathophysiologic involvement of acute pancreatitis is classified as either mild pancreatitis (also known as edematous or interstitial pancreatitis) or severe pancreatitis (also called necrotizing pancreatitis) CLINICAL MANIFESTATIONS Abdominal pain is the predominant manifestation of acute pancreatitis. The pain is due to distention of the pancreas, peritoneal irritation, and obstruction of the biliary tract. The pain is usually located in the left upper quadrant, but it may be in the midepigastrium. It commonly radiates to the back because of the retroperitoneal location of the pancreas. Abdominal tenderness with muscle guarding is common. Bowel sounds may be decreased or absent.  Paralytic ileus may occur and causes marked abdominal distention. The lungs are frequently involved, with crackles present. Intravascular damage from circulating trypsin may cause areas of cyanosis or greenish to yellow-brown discoloration of the abdominal wall. Other areas of ecchymoses are the flanks (Grey Turner’s spots or sign, a bluish flank discoloration) and the periumbilical area (Cullen’s sign, a bluish periumbilical discoloration). These result from seepage of blood-stained exudate from the pancreas and may occur in severe cases. Shock may occur COMPLICATIONS The severity of the disease varies according to the extent of pancreatic destruction. Some patients recover completely, others have recurring attacks, and others develop chronic pancreatitis. Acute pancreatitis can be life threatening pancreatic pseudocyst is an accumulation of fluid, pancreatic enzymes, tissue debris, and inflammatory exudates surrounded by a wall. Manifestations of pseudocyst are abdominal pain, palpable epigastric mass, nausea, vomiting, and anorexia.  The serum amylase level frequently remains elevated. CT, MRI, and endoscopic ultrasound (EUS) may be used in the detection of a pseudocyst. The cysts usually resolve spontaneously within a few weeks but may perforate, causing peritonitis, or rupture into the stomach or the duodenum. Treatment options include surgical drainage, percutaneous catheter placement and drainage, and endoscopic drainage. A pancreatic abscess is a collection of pus. It results from extensive necrosis in the pancreas. It may become infected or perforate into adjacent organs.  Manifestations of an abscess include upper abdominal pain, abdominal mass, high fever, and leukocytosis. Pancreatic abscesses require prompt surgical drainage to prevent sepsis. The main systemic complications of acute pancreatitis are pulmonary (pleural effusion, atelectasis, pneumonia, and acute respiratory distress syndrome [ARDS]) and cardiovascular (hypotension) complications and tetany caused by hypocalcemia. The pulmonary complications are likely due to the passage of exudate containing pancreatic enzymes from the peritoneal cavity through transdiaphragmatic lymph channels. Enzyme induced inflammation of the diaphragm occurs with the end result being atelectasis caused by reduced diaphragm movement Trypsin can activate prothrombin and plasminogen increasing the patient’s risk for intravascular thrombi, pulmonary emboli, and disseminated intravascular coagulation. When hypocalcemia occurs, it is a sign of severe disease. It is due in part to the combining of calcium and fatty acids during fat necrosis. Trypsin can activate prothrombin and plasminogen increasing the patient’s risk for intravascular thrombi, pulmonary emboli, and disseminated intravascular coagulation. When hypocalcemia occurs, it is a sign of severe disease. It is due in part to the combining of calcium and fatty acids during fat necrosis. DIAGNOSTIC STUDIES The serum amylase level is usually elevated early and remains elevated for 24 to 72 hours. Serum lipase level, which is also elevated in acute pancreatitis, is an important test because other disorders (e.g., mumps, cerebral trauma, renal transplantation) may increase serum amylase levels. Other findings include an increase in liver enzymes, triglycerides, glucose, and bilirubin  Diagnostic evaluation of acute pancreatitis is also directed at determining the cause. An abdominal ultrasound, x-ray, or contrast- enhanced CT scan can be used to identify pancreatic problems. CT scan is the best imaging test for pancreatitis and related complications such as pseudocysts and abscesses. ERCP is used (although ERCP can cause acute pancreatitis), magnetic resonance cholangiopancreatography (MRCP), and angiography. COLLABORATIVE CARE Goals of collaborative care for acute pancreatitis include (1) relief of pain; (2) prevention or alleviation of shock; (3) reduction of pancreatic secretions; (4) correction of fluid and electrolyte imbalances; (5) prevention or treatment of infections; and (6) removal of the precipitating cause, if possible  aggressive hydration, pain management, management of metabolic complications, and minimization of pancreatic stimulation. Treatment and control of pain are very important. IV morphine may be used. Pain medications may be combined with an antispasmodic agent. However, atropine and other anticholinergic drugs should be avoided when paralytic ileus is present because they can decrease GI mobility,  aggressive hydration, pain management, management of metabolic complications, and minimization of pancreatic stimulation. Treatment and control of pain are very important. IV morphine may be used. Pain medications may be combined with an antispasmodic agent. However, atropine and other anticholinergic drugs should be avoided when paralytic ileus is present because they can decrease GI mobility,  If shock is present, blood volume replacements are used. Plasma or plasma volume expanders such as dextran or albumin may be given. Fluid and electrolyte imbalances are corrected with lactated Ringer’s solution or other electrolyte solutions Vasoactive drugs such as dopamine (Intropin) may be used to increase systemic vascular resistance in patients  It is important to reduce or suppress pancreatic enzymes to decrease stimulation of the pancreas and allow it to rest. This is accomplished in several ways. First, the patient is NPO (taking nothing by mouth). Second, NG suction may be used to reduce vomiting and gastric distention and to prevent gastric acidic contents from entering the duodenum.  The inflamed and necrotic pancreatic tissue is a good medium for bacterial growth. In patients with acute necrotizing pancreatitis, infection is the leading cause of morbidity and mortality. Therefore it is important to prevent infections Surgical Therapy. When the acute pancreatitis is related to gallstones, an urgent ERCP plus endoscopic sphincterotomy (severing of the muscle layers of the sphincter of Oddi) may be done. This may be followed by laparoscopic cholecystectomy to reduce the potential for recurrence. Surgical Therapy. When the acute pancreatitis is related to gallstones, an urgent ERCP plus endoscopic sphincterotomy (severing of the muscle layers of the sphincter of Oddi) may be done. This may be followed by laparoscopic cholecystectomy to reduce the potential for recurrence.  CHRONIC PANCREATITIS  Chronic pancreatitis is a continuous, prolonged, inflammatory, and fibrosing process of the pancreas. The pancreas is progressively destroyed as it is replaced by fibrotic tissue. Strictures and calcifications may also occur in the pancreas.  Chronic pancreatitis can be due to alcohol abuse; obstruction caused by cholelithiasis (gallstones), tumor, pseudocysts, or trauma; and systemic diseases (e.g., systemic lupus erythematosus), autoimmune pancreatitis, and cystic fibrosis. Some patients may not have an identifiable risk factor (idiopathic pancreatitis).  The most common cause of obstructive pancreatitis is inflammation of the sphincter of Oddi associated with cholelithiasis. Cancer of the ampulla of Vater, duodenum, or pancreas can also cause this type of chronic pancreatitis. In nonobstructive pancreatitis there is inflammation and sclerosis, mainly in the head of the pancreas and around the  The most common cause of obstructive pancreatitis is inflammation of the sphincter of Oddi associated with cholelithiasis. Cancer of the ampulla of Vater, duodenum, or pancreas can also cause this type of chronic pancreatitis. In nonobstructive pancreatitis there is inflammation and sclerosis, mainly in the head of the pancreas and around the  CLINICAL MANIFESTATIONS abdominal pain. The patient may have episodes of acute pain, but it usually is chronic (recurrent attacks at intervals of months or years). The attacks may become more and more frequent until they are almost constant, or they may diminish as pancreatic fibrosis develops. The pain is located in the same areas as in acute pancreatitis, but is usually described as a heavy, gnawing feeling or sometimes as burning and cramplike. The pain is not relieved with food or antacids.  Other clinical manifestations include symptoms of pancreatic insufficiency, including malabsorption with weight loss, constipation, mild jaundice with dark urine, steatorrhea, and diabetes mellitus. The steatorrhea may become severe, with voluminous, foul-smelling, fatty stools. Urine and stool may be frothy. Some abdominal tenderness may be present  Other clinical manifestations include symptoms of pancreatic insufficiency, including malabsorption with weight loss, constipation, mild jaundice with dark urine, steatorrhea, and diabetes mellitus. The steatorrhea may become severe, with voluminous, foul-smelling, fatty stools. Urine and stool may be frothy. Some abdominal tenderness may be present DIAGNOSTIC STUDIES In chronic pancreatitis the levels of serum amylase and lipase may be elevated slightly or not at all, depending on the degree of pancreatic fibrosis. Serum bilirubin and alkaline phosphatase levels may be increased. There is usually mild leukocytosis and an elevated sedimentation rate  Stool samples are examined for fecal fat content. Deficiencies of fat-soluble vitamins and cobalamin, glucose intolerance, and possibly diabetes may also be found in those with chronic pancreatitis. A secretin stimulation test may be used to assess the degree of pancreatic function COLLABORATIVE CARE It sometimes takes frequent doses of analgesics (morphine or fentanyl patch [Duragesic]) to relieve the pain if dietary measures and enzyme replacement are not effective. Diet, pancreatic enzyme replacement, and control of diabetes are ways to control the pancreatic insufficiency. Small, bland, frequent meals that are low in fat content are recommended to decrease pancreatic stimulation. Smoking is associated with accelerated progression of chronic pancreatitis. Teach the patient not to consume alcohol and caffeinated beverages  Pancreatic enzyme products (PEPs) such as pancrelipase (Pancrease, Zenpep, Creon, Viokase) contain amylase, lipase, and trypsin and are used to replace the deficient pancreatic enzymes. They are usually enteric coated to prevent their breakdown or inactivation by gastric acid. Bile salts are sometimes given to facilitate the absorption of the fat-soluble vitamins (A, D, E, and K) and prevent further fat loss. If diabetes develops, it is controlled with insulin or oral hypoglycemic agents. Acidneutralizing drugs (e.g., antacids) and acid-inhibiting drugs (e.g., H2-receptor blockers, proton pump inhibitors) may be given to decrease hydrochloric acid (HCl) secretion but have little overall effect on patient outcomes. Antidepressants, such as nortriptyline (Aventyl), have been shown to reduce the neuropathic pain associated with chronic pancreatitis  Treatment of chronic pancreatitis sometimes requires endoscopic therapy or surgery. When biliary disease is present or obstruction or pseudocyst develops, surgery may be indicated. Surgical procedures can divert bile flow or relieve ductal obstruction. A choledochojejunostomy diverts bile around the ampulla of Vater, where there may be spasm or hypertrophy of the sphincter.  Another type of surgical diverting procedure is the Roux-en-Y pancreatojejunostomy, in which the pancreatic duct is opened and an anastomosis is made with the jejunum. Pancreatic drainage procedures can relieve ductal obstruction and are often done with ERCP. Some patients may undergo ERCP with sphincterotomy and/or stent placement at the site of obstruction BARIATRIC OBESITY Obesity is an excessively high amount of body fat or adipose tissue The most widely used and endorsed measures are BMI and waist circumference  BMI is calculated by dividing a person’s weight (in kilograms) by the square of the height in meters BMI= weight (kg)÷ height (m) 2  Individuals with a BMI less than 18.5 kg/m2 are considered underweight those with a BMI between 18.5 and 24.9 kg/m2 reflect a normal body weight. A BMI of 25 to 29.9 kg/m2 is classified as being overweight, and those with values at 30 kg/m2 or above are considered obese. The term severely (morbidly, extremely) obese is used for those with a BMI greater than 40 kg/m2. ETIOLOGY AND PATHOPHYSIOLOGY Obesity is an increase in body weight beyond the body’s physical requirements. This results in an abnormal increase and accumulation of fat cells  In obesity, there is an increase in the number of adipocytes (hyperplasia) and an increase in their size (hypertrophy) Adipocyte hypertrophy is a process by which adipocytes can increase their volume several thousand–fold to accommodate large increases in lipid storage.  preadipocytes are triggered to become adipocytes once storage of existing fat cells is exceeded. This process primarily occurs in the visceral (intraabdominal) and subcutaneous tissues. The process of hyperplasia (increase in numbers) of adipocytes is greatest from infancy through adolescence.  a gene known as FTO (fat mass and obesity-associated gene) and BMI. Environmental Factors. Psychosocial Factors. BARIATRIC SURGERY Surgery is currently the only treatment that has been found to have a successful and lasting impact for sustained weight loss for severely obese individual. Criteria guidelines for bariatric surgery include having a BMI of 40 kg/m2 or a BMI of 35 kg/m2 with one or more severe obesity-related medical complications (e.g., hypertension, type 2 diabetes mellitus, heart failure, sleep apnea). CONTRAINDICATION untreated depression, binge eating disorders, and drug and alcohol abuse cancer; end-stage kidney, liver, and cardiopulmonary disease; severe coagulopathy; or inability to comply with nutritional recommendations CATEGORIES Restrictive Surgeries  reduces either the size of the stomach, which causes the patient to feel full more quickly, or the amount allowed to enter the stomach.  In these surgeries, digestion is not altered so the risk of anemia or cobalamin deficiency is low.  The most common restrictive surgeries include adjustable gastric banding and vertical sleeve gastrectomy Adjustable Gastric Banding the most common restrictive procedure done, involves limiting the stomach size with an inflatable band placed around the fundus of the stomach This restrictive procedure can be done using a Lap-Band or Realize Band system. The band is connected to a subcutaneous port and can be inflated or deflated (by fluid injection in the health care provider’s office) to change the stoma size to meet the patient’s needs as weight is lost The restrictive effect of the band creates a sense of fullness as the upper portion of the stomach now accommodates less than the average stomach. The band then causes a delay in stomach emptying, providing patients with further satiety. The procedure can be either modified or reversed at a later date if necessary. AGB is the preferred option for patients who are surgical risks because it is a less invasive approach. Vertical Sleeve Gastrectomy.  about 85% of the stomach is removed, leaving a sleeveshaped stomach  The procedure is not reversible. The removal of the majority of the stomach also results in the elimination of hormones produced in the stomach that stimulate hunger, such as ghrelin. Combination of Restrictive and Malabsorptive Surgery Roux-en-Y Gastric Bypass. is a combination of restrictive and malabsorptive surgery This procedure, which is irreversible, involves creating a small gastric pouch and attaching it directly to the small intestine using a Y-shaped limb of the small bowel. After the procedure, food bypasses 90% of the stomach, the duodenum, and a small segment of jejunum Combination of Restrictive and Malabsorptive Surgery Roux-en-Y Gastric Bypass. is a combination of restrictive and malabsorptive surgery This procedure, which is irreversible, involves creating a small gastric pouch and attaching it directly to the small intestine using a Y-shaped limb of the small bowel. After the procedure, food bypasses 90% of the stomach, the duodenum, and a small segment of jejunum NURSING MANAGEMENT PERIOPERATIVE CARE OF THE OBESE PATIENT Ensure that the patient scheduled for bariatric surgery understands the surgical procedure Prepare the patient before surgery for the possibility of returning with one or more of the following: urinary catheter, IV catheter, compression stockings, and nasogastric tube. Emphasize that vital signs and a general assessment will be conducted frequently to monitor for complications. the patient must understand that he or she will be assisted with ambulation soon after surgery and encouraged to cough and deep breathe to prevent pulmonary complications. Liquids will be started early but only after the patient is fully awake and there is no evidence of any anastomosis leaks. The initial postoperative care focuses on careful assessment and immediate intervention for cardiopulmonary complications, thrombus formation, anastomosis leaks, and electrolyte imbalances the patient’s airway should remain stabilized and attention given to managing the patient’s pain. Maintain the patient’s head at a 35- to 40- degree angle to reduce abdominal pressure and increase lung expansion. turning and ambulation postoperatively will prevent complications from surgery Antiembolic stockings or sequential compression stockings may be ordered along with low-dose heparin to minimize the risk of a DVT. Active and passive range-of-motion exercises are a frequent part of daily care Assess the patient’s skin for any complications related to wound healing. Keep skinfolds clean and dry to prevent dermatitis and secondary bacterial or fungal infections. HYPERGLYCEMIA DIABETES  Is a group of metabolic disease characterized by increased levels of glucose in the blood resulting from defects in insulin secretion, insulin action or both. (American Diabetes Association) It is formerly known as diabetes mellitus.  PANCREAS Insulin – allows glucose to diffuse across cell membrane; converts glucose to glycogen. Glucagon – increases blood glucose by causing gluconeogenesis in the liver; secreted in response to blood sugar.  Insulin is secreted by beta cells, which are one of four types of cells in the islets of Langerhans in the pancreas. Insulin is an anabolic, or storage, hormone. Predisposing factors:  exact cause of diabetes mellitus remain unknown  genetic / hereditary predisposition  viruses  pancreatitis  pancreatic tumor  autoimmune disorder  obesity (overweight people require more insulin to metabolize the food they eat or the number of insulin receptor sites in cells is decreased)  Race/ethnicity (eg, African Americans, Hispanic Americans, Native Americans, Asian Americans, Pacific Islanders) Age ≥45 years Previously identified impaired fasting glucose or impaired glucose tolerance Hypertension (≥140/90 mm Hg) HDL cholesterol level ≤35 mg/dL (0.90 mmol/L) and/or triglyceride level ≥250 mg/dL (2.8 mmol/L) History of gestational diabetes or delivery of babies over 9 lbs 1.INSULIN-DEPENDENT DIABETES MELLITUS (IDDM) 2.NON-INSULIN DEPENDENT DIABETES MELLITUS (NIDDM) 3. Gestational diabetes mellitus. 4. Diabetes mellitus associated with other conditions or syndromes. TYPE 1 DIABETES  It is characterized by destruction of pancreatic beta cells.  Absolute deficiency of insulin  the client is prone to DIABETIC KETOACIDOSIS TYPE 2 DIABETES  It is characterized by relative lack of insulin receptors or resistance to the action of insulin.  It occurs more commonly to people who are older than 30 years  the client is prone to HYPEROSMOLAR, HYPERGLYCEMIC SYNDROME GESTATIONAL DIABETES  Is any degree of glucose intolerance with its onset during pregnancy  Hyperglycemia develops because of secretion of placental hormones MANIFESTATIONS Polyuria, polydipsia and polyphagia Weight loss Blurred vision Recurrent infection, prolonged wound healing Weakness and paresthesia Nausea, vomiting and abdominal pain DIAGNOSTIC TEST Fasting Plasma Glucose Random Plasma Glucose 2 hour post load OGTT ( oral glucose tolerance test) Hgb A1C CRITERIA FOR DIAGNOSIS OF DIABETES  Symptoms of diabetes plus casual plasma glucose concentration equal to or greater than 200mg/dl (11.1 mmol/L)  Fasting plasma glucose greater than or equal to 126 mg/dL (7mmol/L) Two –hour post prandial glucose equal to or greater than 200mg/dL (11..1 mmol/L) during an oral glucose tolerance test. The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water. (American Diabetes Association 2009) MANAGEMENT DIET 1. Follow individualized meal plan and snacks as scheduled  Balanced diabetic diet – 50% CHO, 30% fats, 20% CHON, vitamins and minerals  diet based on pts. size, wt., age, occupation and activity 2. Pt. must have adequate CHO intake to correspond to the time when insulin is most effective 3.Routine blood glucose testing before each meal and at bedtime is necessary during initial control, during illness and in unstable pts. 4.Do not skip meals. 5.Measure foods accurately, do not estimate. 6.Less added fat, fewer fatty foods and low-cholesterol. 7.Advise use of complex carbohydrates to help stabilize blood sugar. Meal should include more fiber and starch and fewer simple or refined sugars. 8.Avoid concentrated sweets, high in sugar (jellies, jams, cakes, ice cream) 9.High Fiber Diet especially vegetables ACTIVITY AND EXERCISE  The benefits of regular pattern exercise are as follows:  increases glucose uptake by the cells  Lowers insulin requirements  Help achieve desirable body weight  Maintain normal serum lipids  Instruct client on dietary adjustments when exercising  Instruct client to monitor blood glucose before during and after exercise  The client who requires insulin should be instructed to eat 15g carbohydrate snack before engaging in moderate exercise to prevent hyperglycemia  If blood glucose level is greater than 250mg/dL and urinary ketones are present (DM type 1), the client is instructed not to exercise until blood glucose is normal and urinary ketones are absent  MEDICATION 1.Oral Hypoglycemic Agent 2.Insulin OHA  Effective for patients who have type 2 diabetes that cannot be treated effectively with diet and exercise. TYPES: FIRST GENERATION SULFONYLUREAS Chlorpropamide (Diabenese) Tolazamide (Tolinase) Tolbutamide (Orinase)  Less commonly used  Used in type 2 diabetes to control blood glucose levels  Stimulate beta cells of the pancreas to secrete insulin  May improve binding between insulin and insulin receptors or increase the number of insulin receptors SECOND-GENERATION SULFONYLUREAS  Glipizide (Glucotrol, Glucotrol XL) Glyburide (Micronase, Glynase, Diaberta) Glimeperide (Amaryl)  May improve binding between insulin and insulin receptors or increase the number of insulin receptors  Used in type 2 diabetes to control blood glucose levels  Have more potent effects than 1st generation sulfonylureas  May be used in combination with metformin or insulin to improve glucose control BIGUANIDES Metformin (Gluphage, Gluphage XL, Fortamet) Metformin with glyburide (Glucovance) Inhibit production of glucose by the liver Increase body tissue sensitivity to insulin Decrease hepatic synthesis of cholesterol Used in type 2 diabetes to control blood glucose levels ALPHA-GLUCOSIDASE INHIBITOR Acarbose (Precose) Miglitol (Glyset)  Delay absorption of complex carbohydrates in the intestine and slow entry of glucose into systemic circualtion  Do not increase insulin secretion  Used in type 2 diabetes to control blood glucose levels Can be used alone or in combination with sulfonylureas, metformin or insulin to improve glucose control Non-sulfonylurea insulin secretagogues Repaglinide ( Prandin) categorized as a miglitinide Nateglinide (Starlix) categorized as a D- phenylalanine derivative  Stimulate pancreas to secrete insulin  Used in type 2 diabetes to control blood glucose levels  Can be used alone or in combination with metformin or thiazolidinediones to improve glucose control Thiazolidinediones or glitazones Pioglitazone (Actos) Rosiglitazone (Avandia) Sensitize body tissue insulin, stimulate insulin receptor sites to lower blood glucose and improve action of insulin May be used alone or in combination with sulfonylurea, metformin or insulin Dipeptidyl peptidase-4 (DPP-4) inhibitors Sitagliptin (Januvia) Vildagliptin (Galvus) Increase and prolong the action of incretin, a hormone that increases insulin release and decreaes glucagon levels, with the result of improved glucose control Oral Antidiabetic Agents  INSULIN Indicated for TYPE 1 Diabetes Indicated in type 2 when diet and weight control are ineffective Regular insulin is the only insulin that can be administered intravenously in the emergency treatment of diabetic ketoacidosis TYPE ONSET PEAK DURATION RAPID-ACTING INSULIN Lispro (Humalog) 10-15 min 1 hour 2-4 hours Aspart(Novolog) 5-15 min 40-50min 2-4 hours Glulisine (Apidra) 5-15 min 30-60min 2-4 hours SHORT-ACTING INSULIN Humulin Regular 0.5-1 hour 2-3 hours 4-6 hours INTERMEDIATE-ACTING INSULIN NPH 2-4 hours 4-12 hours 16-20 hours Humulin N, 3-4 hours 4-12 hours 16-20 hours Novolin N, Iletin II Lente TYPE ONSET PEAK DURATION LONG-ACTING INSULIN Humulin Ultralente 1 hour continuous 24 hours ____________________________________________________ PREMIXED INSULIN 0.5-1 hour 2-12 hours 18-24 hours 70% NPH-30% Regular HUMULIN 50/50 0.5-1 hour 3-5 hours 24 hours (50% NPH/ 50% Regular) LISPRO/PROTAMINE 10-15min 5 hours 24 hours 72/25  The main route of insulin administration is subcutaneous  The main areas for insulin injections are the ABDOMEN, ARMS (posterior surface), THIGHS (anterior surface) and buttocks Administer insulin at 90 degree angle. Most needle gauge 27 to 29 that is about ½ inch long Injection should be ½ apart within the anatomical area. Finish all sites in one anatomical area before going to another area Do not massage injection site Systemic rotation of the site of injection Administer insulin at room temperature Do not shake the vial of insulin Regular insulin may be mixed with any other insulin  To mix insulin, the following nursing actions are done: o Introduce air into the vial of intermediate acting. Do not aspirate yet. o Introduce air into the vial of regular insulin and draw up the insulin o Draw up the intermediate-acting insulin  traditional subcutaneous injections Insulin pen: use small prefilled insulin cartridges that are loaded into a penlike holder Jet injector: deliver insulin through the skin under pressure in an extremely fine stream  Insulin pumps: continuous subcutaneous insulin infusion involves the use of small, externally worn devices that closely mimic the functioning of the normal pancreas.  Future insulin delivery: involved implantable insulin pumps that can be externally programmed according to blood glucose test results. Transplantation of pancreatic cells diabetes who are receiving : transplantation of the whole pancreas or a segment of the pancreas (mostly patients with diabetes who are receiving a kidney transplantation simultaneously) Local Systemic Reactions Systemic Allergic reactions: o these rare reactions are occasionally associated with generalized edema and prophylaxis o Treatment: desensitization with small dose insulin gradually increasing amount Insulin Lipodystrophy Lipoatrophy: is loss of subcutaneous fat and appears as slight dimpling or more serious pitting of subcutaneous fats Lipohypertropy: is the development of fibrous fatty masses at the injection site  Resistance to injected insulin: Lack of tissue sensitivity to the insulin from body which results in hyperglycemia. The client has develop immune antibodies that bind with the insulin, thereby decreasing the insulin available for use TREATMENT: administer more concentrated insulin preparation  Dawn Phenomenon: Reduced tissue sensitivity to insulin that develops between 5 and 8 am TREATMENT: change time of injection of evening intermediate acting insulin from dinner time to bedtime  Somogyi Effect Normal or elevated blood glucose at bedtime, a decrease at 2-3 am to hypoglycemic levels and a subsequent increase which triggers production of counterregulatory hormones By 7am, the blood glucose rebounds to hyperglycemia range. TREATMENT: decrease evening dose of intermediate-acting insulin or increase bedtime snack Insulin Waning Progressive rise in the blood glucose from bedtime to morning TREATMENT: increase evening dose of intermediate or long acting insulin or institute a dose of insulin before the evening meal if one is not already part of the treatment regimen. HYPOGLYCEMIA  Occurs when the blood glucose falls to less than 70mg/dL (3.7 mmol/L) CAUSES: Overdose of insulin or oral hypoglycemic agents Omission of meals or too little food Strenuous exercise or excessive activity Gastrointestinal upset MANIFESTATIONS 1.Sweating, tremor, pallor, tachycardia, palpitations and nervousness caused by release of epinephrine from the CNS when blood glucose falls rapidly 2.Headache, light-headedness, confusion, numbness of lips and tongue, slurred speech, drowsiness, convulsions and coma caused by depression of the CNS because of glucose supply of brain cells  MANAGEMENT 1. Give simple sugar orally if pt. is conscious and can swallow – orange juice, candy, glucose tablets, lump of sugar 2. Give Glucagon (SQ or IM) if pt. is unconscious or cannot take sugar by mouth 3. As soon as pt. regains consciousness, he should be given carbohydrate by mouth 4. If pt. does not respond to the above measures, he is given 50 ml of 50% glucose I.V. or 1000 ml of 5%-10% glucose in water I.V. Preventing Hypoglycemic Reactions Due to Insulin… Instruct the pt. as follows: 1. Hypoglycemia may be prevented by maintaining regular exercise, diet and insulin 2. Early symptoms of hypoglycemia should by recognized and treated 3. Carry at all times some form of simple carbohydrate (orange juice, sugar, candy) 4. Extra food should be taken before unusual physical activity or prolonged periods of exercise 5. Between-meal and bedtime snacks may be necessary to maintain a normal glucose level.  DIABETIC KETIACIDOSIS  Is caused by an absence or markedly inadequate amount of insulin. Life threatening complication of type 1 DM.  the 3 main clinical features of DKA are as follows: Hyperglycemia Dehydration and electrolyte loss acidosis MANIFESTATIONS polyuria, thirst nausea, vomiting, abdominal pain –-- due to acidosis weakness, headache, fatigue --- due to acidosis and F/E imbalance dim vision dehydration, hypovolemic shock (PR, BP, dry skin, wt. loss) hyperpnea (Kussmaul’s breathing) acetone breath (fruity odor) lethargy  COMA Blood glucose level > 300-800 mg/dL HYPEROSMOLAR, HYPERGLYCEMIC SYNDROME  Is a metabolic disorder of type 2 diabetes resulting from a relative insulin deficiency without ketosis and acidosis MANIFESTATIONS Blood glucose level of 600 to 1,200mg/dL Hypotension Dehydration Tachycardia Mental status changes Neurolic deficit seizures Interventions for DKA and Hyperosmolar Coma Regular insulin IV push or IV drip 0.9% NaCl IV – 1 L during the 1st hr, 2-8 L over 24 hrs. administer sodium bicarbonate IV to correct acidosis Monitor electrolyte levels, esp. serum K+ levels administer K+, monitor UO hourly (30ml/hr) MANIFESTATIONS 1.Sweating, tremor, pallor, tachycardia, palpitations and nervousness caused by release of epinephrine from the CNS when blood glucose falls rapidly 2.Headache, light-headedness, confusion, numbness of lips and tongue, slurred speech, drowsiness, convulsions and coma caused by depression of the CNS because of glucose supply of brain cells