GI

Diverticulosis and Diverticulitis Assessment

A patient w/ diverticula, outpounchings found in the descending, sigmoid colon, is said to have diverticulosis. DIvertiula are common in the older adult and may never produce symptoms or complicatons. However, when the outpouchings become inflamed, the condition is called diverticulitis. If left untreated, diverticulitis can lead to perforation of the intestine and can cause peritonitis. Clinical manifestations of diverticulitis include lower left-side abdominal pain, abdominal distention, flatulence, fever, rectal bleeding, and constipation or diarrhea. A patient w/ outpounchings, or diverticula, in their colon is said to have diverticulosis. THis condition is likely related to low intake of dietary fiber and increased pressure in the colon needed to expel the small, low-bulk stool. Diverticulosis is common in older adult patients, though it may never produce complications. Many patients w/ diverticulosis never have any symptoms. Inflammation of the diverticula, or outpouchings of the colon, is called diverticulitis. if left untreated, this condition can lead to perforation of the intestine and can cause peritonitis. Patients may report lower, left sided abdominal pain and cramping. THough uncommon, right sided abdominal pain may also occur. Abdominal bloatig and distention can occur if there is difficulty passing stool thru the affected area of the colon. Flatulence is a common finding in patients w/ diverticular disease. INflammation and infection of the diverticula seen in diverticulitis can produce a fever. DIverticula often contain small blood vessels. When these vessels rupture, diverticula will bleed, causing hematochezia, or bleeding from the rectum. Patients w/ diverticular disease initially experience chronic constipation and then diarrhea. If the diverticula become inflamed and rupture, peritonitis or inflammation of the peritoneum can develop. Hypovolemic shock can occur in patients w/ peritonitis, due to the large fluid shift from the vasculature into the abdominal cavity. Other lab results that may be indicative of an infection related to peritonitis are an elevated C-reactive protein level and leukocytosis w/ a shift to the left (increased number of immature neutrophils).

Acute pancreatitis causes

Acute pancreatitis has numerous etiologies. It occurs when pancreatic enzymes (especially trypsin) that digest food are activated in the pancreas instead of the small intestine. It may be acute-beginning suddenly and lasting a few days. The mneumonic GET SMASHHED is useful in recalling the most common causes Gallstones- gallstones are the most common cause. When gallstones become trapped in the biliary treee, pancreatitis develops due to obstructioin of flow. Ethanol-Ingestion of large amounts of alcohol can lead to acute pancreatitis. ALcohol abuse is also the most common cause of chronic pancreatitis. Trauma- thru the pancreas is one of the least injured organs in abdominal trauma, acute pancreatitis can occur from minimal trauma. Example include blunt force, motor vehicle accident and penetrative injury. Steroids- Corticosteroids, such as prednisolone, are known to induce pancreatitis. MUmps-a virus typically experienced in childhood if unvaccinated, can lead to self-limited acute pancreatitis. Autoimmune disease- a common presntation of acute pancreatitis. It can be particularly challenging to diagnose b/c the way it presents itself closely resembles pancreatic cancer. Scorpion Sting- Scorpion stings lead to a transient, self-limiting acute pancreatitis. Hypercalcemia- Pancreatitis can develop thru translation of inactive trypsinogens to active ones by hypercalcemia. Though not particularly understood, hypercalcemia can occur from hyperparathyroidism, which is also lined to acute pancreatitis. Hypertriglyceridema >1000- Hypertriglyceridemai is the third most common cause of acute pancreatiits (after gallstones and alcohol). A serum triglyceride level > 1000 is an identifiable risk factor for acute pancreatitis. ERCP- can lead to acute pancreatitis, as it is a procedure which involves cannnulation or injection of the pancreatic duct. Drugs- Azathioprine and valproic acid are associated w/ development of acute pancreatitis

types of intestinal obstruction

An intestinal obstruction occurs when the contents of the GI tract cannot pass thru the intestines. Obstructions can be either mechanical, invovling an identifiable blockage, or non mechanical, having neuromuscular or vascular origins. Adhesions are areas of scar tissue that develop on theoutside of the intestine after surgery, or injury to the bowel. INitially, adhesions may not be troublesome; however, movement of the intestine can stretch the scar tissue into a long band. THis band of tissue may eventually encircle the intestine, and squeeze it shut causing an obstruction. When there is an area of weak msucle in the abdomen, a portion of the small intestine can slip thru the muscl efibers causing a hernia. If the protruding hernia becomes pinched, it can cause intestinal obstruction. INtestinal obstruction caused by twisting of the bowel is called a volvolus. THis type of obstructon can often be resolved w/ot surgery. This type of obstruction occurs when a segment of the intestine telescopes of folds into another portion of the intestine. Currant jelly-like stools area characteristic assessment findings, along w/ a palpable sausage-shaped mass in the RUQ. Intussusception is a medical emergency. INtestinal tumors can grow inside the intestine, creating a blockage, or they can develop outside the intestine, pinching it closed. INtestinal obstruction resulting form an arterial occlusion is rare. In most cases, an embolus disrupts blood flow to an area of the intestine, causing a non mechanical blockage. Injury to the spinal cord that disrupts the signals from the brain to the intestines can disrupt peristalsis, causing paralytic ileus. This type of obstruction occurs when intestinal peristalsis is absent; assessment will reveal a lack of bowel soiunds. Paralytic ileus is common after surgery.

complications of cirrhosis

As the liver changes in structure, it begins to compress the heaptic veins and sinusoids, obstructing normal blood flwo. THis leads to increased venous flow in the portal circulation, known as portal htn. Ascites is described as the accumulation of fluid in the peritoneal and abdominal caity, and is commonly seen w/ cirrhosis. It occurs b/c of two reasons. First, there is increased hydrostatic pressure (b/c of portal htn), pushing this fluid out of blood vessels into the tissues. Second, there are decreased proteins in the lympth and blood vessels, which typically hold fluid in the vessels (like albumin ). THis decrease causes fluid to lead out of vasculature, into the tissues. Esophagael Varices are tortuous veins which are enlarged and swollen due to portal htn. Gastric varices are similar, but occur in the upper portion of the stomach. THese vessels tolerate high pressure poorly, and easily hemorrhage. W/ cirrhosis, patients develop decreased liver function. They are unable to normlaly produce clotting factors, and these coagulation defects may display as prolonged bleeding. This is a neuropsychiatric manifestation of cirrhosis, also called hepatic encephalopathy, and is a result of the neurotoxic effects of ammonia. B/c of portal htn, ammonia cannot be deaminated normally, and excess ammonia builds up, leading to symptoms of impaired consciousness, inappropriate behavior,lethargy and coma. Hepatorenal syndrome occurs from cirrhosis, and it is described as a type of renal failure w/ advancing azotemia, oliguria and ascites. This occurs from portal htn, which leads to increased systemic vasodilation and, thus, decreased arterial flow. THis leads to renal vasoconstriction, leading to renal failure.

Colorectal cancer

Colorectal cancer is the third most common cancer in both men and women w/ the majority of cases being adenocarcinoma. Risk factors include family history of colorectal cancer, personal history of inflammatory bowel disease such as ulcerativ colitis or Crohn's disease, diet high in red meat, obesity, alcohol consumption greater than foiur drinks per week, and cigarette smoking. CLinical manifestations of early stage colorectal cancer are usually non specific, while manifestations of late stage colorectal cancer include hepatomegaly, peritonitis, and abdominal pain. Patients aged 50 and older should undergo a colonoscopy once every ten years to assess for polyps and/or the presence of cancer. Colorectal cancer encompasses the 3rd most commonly occurring cancer worldwide, after lung and breast cancer, respectively. Changes in bowel habits vary depending on where the cancer is found. For example, colorectal cancer found in the right side of the intestine is likely to cause diarrhea, while left-sided cancerous lesions typically cause bowel obstructionor constipation. Bowel obstructions can be caused by tumors in patients w/ undiagnosed colorectal cancer. The patient may experience constipatioin before the bowel becomes completely obstructed. Rectal bleeding should not be ignored, as it may be a sign of colorectal cancer. INtestinal polyps that become large enough can bleed, causing stool to appear black or tar-like Rectal bleeding that persists or remains untreated can lead to excess blood loss and iron deficiency anemia. Anemia occurs when there is a decrease in the amount of red blood cells present in the blood. patients who are anemic may feel tired, weak, or SOB. Weight loss in patients w/ colorectal cancer can be attributed to teh increased metabolic needs of the tumor. A patient who experiences an unexplained weight loss of ten pounds or more should contact their hcp. Ascites occurs when there's a collection of fluid in the abdomen or peritoneal space. If cancer of the colon spreads to the liver, hepatomegaly and liver dysfunction may result. Inability of the liver to make proteins necessary to maintian oncotic pressure will cause shifting of fluid from the vasculature into the "third space." Accumulaiton of fluid in the abdomen related to ascites can cause abdominal pain and discomfort. This procedure allows a hcp to look at the inside of the intestine using a colonoscope and is considered the gold standard for screening practices. Patients aged fifty and older should undergo a colonoscopy once every ten years to assess for colon polyps and/or the presence of colon cancer. Fecal occult blood tests and fecal immunochemical tests can be sued to detect blood in a patient's stool, which could indicate the presence of a polyp or cancer. These tests should be conducted yearly.

HIrschsprung's disease

HIrschsprung's disease is a congenital disorder in which there is limited or absent intestinal motility due to a lack of ganglion cells in the intestine. The absence of ganglion cells prevents the intestine form receiving appropriate signals from the nervous sytem, resulting in constant sympathetic stimulation; and therefore, increased bowel tone. B/c the intestine is in a contracted state, peristalsis does not occur. Newborns w/ Hirschsprung's disease do not pass meconium w/n the first 24 hours of birth and may also present w/ a distended abdomen, and a feeding intolerance, or refusal to ffed, w/ bilious vomiting. A digital rectal exam may reveal no stool on the examiners finger; however, the exam can stimulat ethe bowel and subsequently cause forceful expulsion of stool. interventions : surgical resection of the bowel w / possibility of a temporary colostomy. Surgical resection of bowel is typically performed to remove the aganglionic section of the bowel, thus restoring motility and relieving obstruction. Anal strictue and incontinence may occur following a pull thru surgical procedure. CHroinc problems of constipation and fecal incontinence may occur after surgery. The pateint may need a temporary colostomy after surgery is performed to resect the bowel. A colostomy will facilitate waste removal while the bowel heals. The earlier the diagnosis of the condition is made, the proximal bowel may not distend extremely. This allows for a primary pull through (Soave ) surgery and the elimniation of needing to have a temporary colostomy.

IBS interventioins

Irritable bowel syndrome is a chroinc GI disorder characterized by severe abdominal pain and alternating episodes of diarrhea and constipation. goal: decreasing symptoms by increasing dietary fiber and administering meds such as anticholingerics, loperamide, tricyclic antidepressants, and linaclotide. MEds specific to women include lubiprostone, tegaserod, and alosetrone. Identifying and reducing risk factors that exacerbate IBS is critical to help avoid exacerbations of the condition. Identifying a patient's risk factors and triggers is critical for decreasing the symptoms of IBS. By reducing feelings of depression and anxiety, the patient may experience fewer or less severe symptoms. To identify factors triggering IBS symptoms, encourage the patient to keep a diary recording symptoms, diet, and feelings of stress. Determining a pattern will help the pateint avoid triggers and decrease abdominal pain. If the patient can tolerate it, gradually increase the intake dietary fiber to help facilitate the passage of stool. The addition of fiber should be done slowly to prevent gas buildup and abdominal discomfort. Although 30-40g of fiber daily is recommended, the pateint should have a t least 20g of fiber every day. If the pateint expereinces symptoms of abdominal distention and flatulence, teach the patient to avoid gas producing foods such as broccoli. Probiotics may help alleviate symptoms of IBS by altering intestinal flora that may be exacerbating the condition. Yogurt contains probiotics may be a better tolerated source of calcium than milk. IN some cases, antibiotics also help relieve symptoms by adjusting levels of intestinal bacteria. anticholinergics prevent acetylcholine from binding to parasympathetic nerves and cause smooth muscle to contract. THe GI tract is lined by smooth muscle. A common side effect of anticholinergic drugs is constipation, which can help relieve symptoms of diarrhea in patients w/ IBS. Low doses of tricyclic antidepressants (TCA's ) may help relieve symptoms of IBS by decreasing peripheral nerve sensitivity. Example of TCA's include amitriptyline (Elavil) and desipramine (Norpramin). Loperamide (Imodium) is a synthetic opiod that slows down the intestinal tract. The drug is to treat episodes of diarrhea associated w/ rapid peristalsis. Linaclotide (Linzess) is a medication used in patients over age 8 for idiopathic chronic constipation as well as a treatment for IBS w/ constipation. It works as an agonist to guanylate cyclase-c in the intestinal lumen to increase cGMP (cyclic guanosine monophosphate). This increase in cGMP causes an increase in fluid in the intestinal lumen and works to decrease transit time of GI contents thru decreased motor activity. Tegaserod (Zelnorm) increases the movement of stools in the bowels and helps relieve constipation. However, the drug has been withdrawn from the U.S> market and is only indicated for limited emergency situations. Men taking tegaserod did not experience symptom relief. Lubiprostone (Amitiza) is a laxative indicated to relive constipation in woemn diagnosed w/ IBS. The med softens stool and increases motility of the GI tract. Alosetron (Lotronex) is a serotonergic antagonist used to hlep decrease pain and diarrhea. However, the drug has serious side effects such as severe constipatioin and ischemic colitis, which involves decreased blood flow to the intestines. The med is used as a last resort treatment for women who habe not responded to other IBS treatment options. IF constipation occurs, the drug should be discontinued. Instruct the patient taking alosetron to report abdominal pain or bloody stools immediately to the hcp.

peptic ulcer disease interventioins

Peptic ulcers are caused by an erosion of themucosal wall of the GI tract . These ulcers develop when excess hydrochloric acid and digestive enzymes (pepsin) disrupt the gastric mucosal barrier, causing breakdown. Meds to decrease or inhibit hydrochlori (gastric) acid secretion may be used in combination w/ diet and lifestyle modifications to treat peptic ulcer disease (PUD) patients should avoid nsaids as these drugs may cause gastric irritation and bleeding. Triple or quadruple therapy may be used to treat peptic ulcers. Triple therapy involves a proton pump inhibitor (PPI) and two antibiotics, while quadruple therapy uses a PPI, bismuth, tetracycline, and metronidazole. Clarithromycin and amoxicillin are used to treat peptic ulcers caused by H. pylori. These antibiotics are used along w/ a proton pump inhibitor for 7 to 14 days. Patients may require a second round of treatment due to the increased incidence of antibotic resistance. PPIs directly inhibit release of acid into the stomach. A decrease in the secretion of gastric acid will reduce the pain associaed w/ peptic ulcers, while also allowing the ulcers to heal. H2 blockers are used to block histamine receptors on gastric parietal cells, causing a decrease in gastric acid secretion. PPIs also minimize hydrochloric acid secretion; however, these meds work by directly inhibiting the gastric proton pump in the stomach. Patients w/ PUD should avoid NSAIDs, as these drugs may cause gastric irritation and bleeding. Patients who must continue aspirin therapy should take enteric-coated aspirin to reduce the risk of side effects. Dietary modifications to facilitate ulcer healing include leimination of caffeinated, and/or carbonated beverages, and foods that can cause GI upset, such as spicy foods. SMoking cessation, decreased alcohol intake, and stress management are also key in peptic ulcer healing.

diverticulosis and diverticulitis interventions

When a patient is diagnosed w/ diverticular disease, diet and lifestyle modifications must be made to prevent recurrence and/or exacerbatons of the disease. Interventions include eating a diet high in fiber, taking products to soften the stool, reducing intra abdominal pressure, and exercising. In severe instances, bowel resection may be encessary to remove the affected portion of the intestine. Initially NPO status or a clear liquid diet. This allows adequate time for inflammation in the bowel to subside and for ehaling to occur. When the patient is well enough to begin eating solid foods again, a diet high in fiber is recommended. patients may take fiber supplements if their oral fiber intake is not adequate. HIgh fiber foods will increase the bulk of the stool makingit easier to eliminate. Patients w/ diverticular disease should decrease intra-abdominal pressure to reduce the risk of diverticula formationof rupture. These individuals should avoid heavy lifting, bending, vomiting, and straining w/ a bowel movement, if possible. Stool softners should be encouraged to ease passage of stool and to reduce straining w/ bowel movements. Exercise is an important component of the treatment regimen, b/c it can promote gut motility in these patients, while also enouraging weight loss in patients who are obese. Anticholinergic meds may be prescribed to reduce gut cramping or spasms. Antibiotics are used to treat patients w/ signs of infection related to diverticulitis. Typically, antibiotics are given intravenously while in the hospital. If a patient develops an absecess or intestinal obstruction, surgery will be performed to manage the complication. Surgery is only performe din the patient's condition cannot be corrected or resolved by other means.

types of hernia

a hernia occurs when contents of the abdomen, usually a portion of the intestine, protrudes thru an area of weakened muscle or tissue. Types of hernias include; hiatal, infuinal, femoral, umbilical, and incisional. If a hernia becomes strangulated, emergency surgery must be performed to restore blood flow and to prevent bowel necrosis. This type of hernia occurs when a portion of the upper stomach protrudes into the esophagus or thorax thru a weak are aof the diaphragm. Gerd is a complicatioin of a hiatal hernia, causing reflux of stomach acid into the esophagus. Clinical manifestations of this syndrome include hearburn and regurgitation. An inguinal hernai is present when contents of the abdomen protrude thru a weak area in the inguinal cancal where the spermatic cord is present in men, and where the roiund ligament is located in women. INguinal hernias are more common in men that in women due to inherent weakness along the inguinal canal. Femoral hernias present as an area of swelling, or a bulge, in the femora area near the groin. This type of hernia occurs when contents of the abdomen, susually the intestines, push thru a weak spot in the femoral canal. These hernias are more common in women due to the shape and angle of the female pelvis. INcisional or ventral hernias are common i npatients who have had several or repeat surgeries in the same anatomical area, those who are obese, or those who have experienced poor healing. With incisional hernieas. the hernia protrudes thru a weakened scar. An umbilical hernia occurs in persons w/ a weakned recturs abdominis muscle, such as those who are obese or when the umbilical opening fails to close after birth. As the name describes, the hernia occurs at the umbilicus or belly button. When a hernia become spinched, blood flow to the affected area of the bowel may be cut off. When this occurs, emergency surgery is required to prevent bowel tissue necrosis.

Barrett's Esophagus

a syndrome which refers to an abnormal change in the distal esophagus. Cells undergo metaplasia, replacing the normal stratified squamous epithelium w/ columar epithelium (which are found in the lower GI tract)preccipitated by GERD. These new cells are are nonciliated columnar w/ gobletcells It is associated w/ esophagitis and esophageal ulcer, as well as an increased risk of esophageal adenocarcinoma. As this syndrome occurs from chronic exposure to refluxed acid, it is associated w/ esophageal ulcer development in patients. As this is a syndrome of metaplasia, there's always an increased risk of malignancy. Patients w/ Barrett's esophagus are placed at a higher risk of developing esophageal adenocarninoma.

mallory-weiss

a syndrome with mucosal lacerations, leading to bleeding at the junction of the stomach and esophagus. THis often results from forceful vomiting, which may be a consequence of eating disorders or alcoholism. Diagnosis is made via endoscopy, thru which treatment (if needed) can also take place. This syndrome occurs after tears are formed in the mucosa and submucosa of the gastroesophageal junction, leading to bleeding. These tears do not occur in the mucular layer, like in Boerhaave syndrome. The tears occur b/c of forceful vomiting and violent retching, which increases esophageal pressure. Conditions such as alcoholism, hyperemesis gravidarum and eating disorders, which lead to increased vomiting frequency can cause this syndrome. Patients w/ alcoholism are at risk for developing this syndrome. As patients are more intoxicated, they may vomit more often, which can cause these tears. Patients w/ eating disorders, such as bulimia nervosa, who regularly vomit forcefully may develop such tears. A common symptom which may clue-in a provider to this condition is hematemesis. Patients may present w/ an episode of vomiting up blood, and may have a history of retching. Diagnosis of the mucosal teras from Mallory-Weiss syndrome can be made thru endoscop. Treatment is ususally supportive, but in severe bleeds cauterization or eipinephrine injection may also be done during endoscopy.

hep a

acute infectious disease of the liver caused by hep a virus. ITs incidence in the U.S. has declined since vaccination was recommended for children and at risk individuals. Hep A is spread thru the fecal-oral route, likely from ingesting contaminated food or water. INdividuals are most infectious during the two weeks before the onset of symptoms and remain infectious until 1-2 weeks after the start of symptoms. Hep A is ribonucleic acid (RNA) virus primarily transmitted thru the fecal-oral route. Thus, it is present in poverty-stricken countries where clean water and food may not be available. Outbreaks of hep A often occur due to fecal contamination of food or drinking water. COntributing factors include improper handling of food, poor sanitary and hygeine conditions, as well as crowded conditioins. This incubation period for heaptitis A is a range btwn 15-50 days, w/ an average of 28 days (4 weeks). The greatest risk of transmission occurs around two weeks before the onset of symptoms, w/ patients being infectious until 1-2 wks after the start of symptoms. Manifestatioins of hepatitis A often resemble flu-like symptoms and often don't appear until the individual has had the virus for a couple weeks. A low-grade fever may be present. The individual may experience general malaise or a generalized feeling of discomfort. Nausea and vomiting, fatigue, and loss of appetite are common complaints. Symptoms of hep A are rarely severe unless there is underlying liver failure. Some patients may experience hepatomegaly or swelling of the liver beyond normal. Hep A is a self-limiting infection meaning that it usually resolves itself w/ot treatment. It is often detected by the presence of antibodies to hepa A virus. Proper hand washing is one of the most effective ways to prevent the spread of hep A. This is especially important for food handlers.

Acute pancreatitis

acute inflammation of the pancreas commonly caused by gallbladder disease or chronic alcohol intake. symptoms include abdominal pain, nausea, vomiting, anorexia, abdominal guarding and rigidity, decreased or absent bowel sounds. Elvated WBCs, generalized jaundice, and hypotension and tachycardia may also be present. Smoking is considered a risk factor. IN the majority of cases, acute pancreatitis is caused by heavy alcohol use and gallstones. Abdominal pain is usually located in LUQ and commonl radiates to the back b/c of the retroperitoneal location of the pancreas. This pain is due to distention of the pancreas, peritoneal irritation, and obstruction of the biliary tract. It typically has a sudden onset and is described as severe, deep , piercing, and continuous or steady. Patients may complain of nausea, vomiting, and anorexia, which can lead to weight loss. Abdominal tenderness w/ muscle guarding is common as is a rigid, board-like abdomen. Bowel sounds may become decreased or even absent, so be sure to perform a thorough GI assessment. Hypotension and tachycardia may be present in some patients. It si important to monitor for these symptoms, b/c life-threatening shock can occur as aresult of pancreatic hemorrhage, excessive fluid volume shifts, or toxic effects of abdominal sepsis from enzyme damage. Jaundice, or yellowing of the skin, can occur and is typically generalized. Additionally, other skin assessments to look for include Grey Turner's spots or sign ( a bluish flank discoloration on the flanks ) and CUllen's sign (a bluish periumbilical discoloration on the periumbilical area). Elevated WBC (leukocytosis) , is another finding; this may be accompanied by a low grade fever.

cholescystitis interventions

biliary obstruction or bacteria entering the gallbladder. Bile is produced in the liver and stroed and concentrated in the gallbladder. The condition may be acute or chronic depending on the cause. Classic symptoms include RUQ abdominal pain and indigestion. Supportive treatment includes maintaining electrolyte and fluid status and providng a low fat diet. Analgesics may be administered for pain management and antibiotics will help treat the infection. IF cholcystitis is related to stone formation, lithotrispsy may be performed to eliminate the blockage. patients who undergo cholecystectomy may have a TI tube in place to facilitate drainage. Maintaining the patient's fluid and electrolyte balance is critical while providing supportive treatment to the patient w/ cholecystitis. Vomiting associated w/ cholecystitis may lead to metabolic alkalosis and chlorid shift. Administering NaCl will help compensate the shift in chloridelevels. Antibiotics are administered to treat bacterial infection that may be present in cholecystitis. COmmon causative organisms are E.coli, streptococci, and salmonellae, which invade the gallbladder via the vascular or lymphatic system. To prevent flare-ups of biliary colic, eduacte the patient about theimportance of adhering to a diet w/ minimal saturated fats, such as butter, shortening, or lard. Encourage the patient to increase their intake of fiber and calcium. Although a reduced-calorie diet may be recommended for obese patients, avoid rapid weight loss b/c it may cause gallstone formation. Instruct the patient to avoid spicy and fatty foods to prevent gallbladder irritation. Eating smaller, more frequent meals w/ a small amount of fat may assist w/ gallbladder emptying. INserting NG tube in the patient w/ cholecystitis experiencing severe vomiting will help decompress the stomach and minimize gallbladder stimulatioin. Minimizing stimulation will help rest the inflamed organ and prevent further irritation. Painmanagement using analgesics is critical during an acute episode of cholecystitis. Morphine may be initially given for pain management. NSAIDs, such as ketorolac (Toradol), may be administered to help decrease pain associated w/ gallbladder inflammation . Components of bile that precipitate into stones include cholesterol, bile salts, bilirubin, calcium, and protein. If the patient's cholecystitis is caused by the formation of gallstones, lithotripsy may be indicated. After using ultrasound to locate gallstones, high energy shock waves are used to disintegrate the stones. After lithotripsy, the fragments travel thru the common bile duct and into the small intestine for excretioin. A cholescystectomy is the surgical removal of the gallbladder. Usually done laparoscopically ( lap chole), this procedure dissects the gallbladder w/n the abdomen and removes it from the abdominal cavity using grasping forceps. Three or four tiny incisions are made on the abdomen and the patient is often discharged the day of the surgery. After an open or incisional cholecsytectomy via a right subcostal incision, a T tube may be inserted to facilitate drainage of the common bile duct. Patients often remain in the hospital for a couple days following this incisional approach. After gallbladder surgery, a T tube may be inserted into the common bile duct. The T tube allows excess bile to drain as the small intestines adjust to recieving continuous bile flow. The T tube is connected to a closed gravity drainage system and must be observed for proper functionining and drainage. Nursing responsibilities include measuring the amount of drainage and noting its color and consistency. Keep in mind that the usual amount of bile excretion by the liver is btwn 500mL to 1 liter per day, so anticipate a large amount of bile drainage in the collection device.

HEp C

can lead to acute or chroinc states . Acute hep C is typically asymptomatic and msut be diagnosed by lab tests. The most common cause of contraction of this virus is due to injection drug use, but it may also be spread thru exposure to infectious blood or body fluids, as well as perinatally by mothers infected w/ hep c Hep C virus can be spread by exposure to infectious blood. This includes perinatal transmission, which means a mother can pass the virus to the fetus during childbirth. Additionally, accidental needle sticks contaminated w/ infected blood are another source of transmission. Sexual activity w/ infected partners can lead to transmissioin of hep C, though this is a rare occurrence. A history of unprotected sexual activity, especially w/ prostitutes and rough sex leading to microabrasions is usually present in patients who habe had sexual transmission of the disease. Injection drug abusers remain the most common cause of acquiring acute hep C. The virus is easily transmitted thru needles and syringes contaminated w/ infected blood. The incubation period for hep C is a range btwn 14-180 days, w/ an average of 45 days (7weeks). The greatest rask of infectivity occurs 1-2 weeks before the onset of symptoms. 75-85% of patients go on to develop chronic hep C and remain infectioius. The majority of patients w/ hep C develop chronic infection; however, most are unaware of their infeciton potentially for months or years until symptoms of the chronic disease are manifested. LIver cirrhosis or scarring of the liver is a complciation of the chronic disease. Jaundice is often the first sign. Barrier protection is important to help decrease transmission of this disease. Educate high risk patients, such as individuals who have multiple partners to use a condom to prevent spread of this virus.

cirrhosis interventions

care of patiens involves releiving discomfort from ascites, excess fluid volume, skin changes, nutritional deficiencies and preventing complications associated w/ hematologic problems, esophageal and gastric varieces, and hepatic encephalopathy. Patients should avoid alcohol, NSAIDs, and other meds that impair liver function. Patients w/ cirrhosis should have a high carbohydrate diet w/ low fat, as malnutrition is a serious clinical problem they can face. Patients should have a low sodium diet to decrease edema and ascites, and should take B complex vitamins and abstain from alcohol. Paracentesis, which is a needle puncture into the peritoneum, is used as a diagnostic and therapeutic intervention. It helps remove the ascitic fluid, but this fluid can also be tested for infection. There is no specific drug therapy for cirrhosis, but there are several meds used to treat the varous complications of disease. Bleeding varices can be controlled by vasopressin and octreotide, and beta blockers are used to reduce portal venous pressure. Endoscopic band ligation (endoscopic variceal ligation also called banding) or sclerotherapy may be used ot reduce bleeding of varices in patients w/ cirrhosis. LIgation is done by placing an o-ring arouind the base of the enlarged veing, and sclerotherapy involves injecting a sclerosing agent into the varix (base of enlarged vein). Ballon tamponade mechanically compresses the varices, controlling hemorrhage. THis procedure invovles two balloons w/ three lumens, one for the esophageal and one for gastric aspiration (Sengstaken-Blakemore tube). It is an important sfety precaution to label the lumens to avoid confusion during the procedure. TIPS, or transjugular intrahepatic portosystemic shunt is a nonsurgical procedure that creates a shunt. THis shunt connects systemic and and portal venous systems, which redirects portal blood flow to reduce venous pressure. THis is done by puncturing the wall of the heaptic vein and using a catheter to connect it to the portal vein. THis is contraindicated in those w/ severe hepatic encephalopathy. Lactulose is used to eliminate ammonia in the blood stream. It does so by acidifying the feces in the bowel, trapping ammonia, allowing it to be eliminated during defecation. Antibiotics like refaximin (Xifaxan) work to decrease bacterial flora, which normally would form ammonia in the gut. Removing these bacteria decreases ammonia formation.

cholecystitis assessment

caused by biliary obstruction or bacteria entering the gallblader. Bile is produced in the liver and stored and concentrated in the gallbladder. The condition may be acute or chronic depending on the cause . Symptoms include right upper qudrant abdominal pain, nausea, voiting, indigestion, fever, clay colored stools, and jaundice. Instruct the patient to avoid fatty or spicy foods that may exacerbate symptoms. Assess the patient's WBC count and monitor for signs of infection. An ultrasound may be used to determine cholecystitis and rule out other possible causes of the patient's symptoms. As gallstones pass thru the cystic duct or common bil duct, they lodge into the ducts and cause obstruction and visceral pain. Biliary colic refers to severe and constant pain caused by gallstones obstructing the common bile duct. The patient may experience excruciating pain lasting up to an hour w/ symptoms of tachycardia, diaphoresis, and prostration. Ingesting a high fat meal or lying down may induce biliary colic. After the pain subsides, teh patient may experience residual tenderness in teh RUQ of the abdomen as well as abdominal rigidity. Acute pain and tenderness associated w/ cholecystitis is located in the RUQ of the abdomen. The pain often refers to the right shoulder and scapula. Since biliary obstruction prevents bilirubin from reaching the small intestine to be converted to urobilinogen, the patient w/ cholecystitis may excrete clay colored stools. Obstruction of bile flow into the duodenum impairs liver function and manifests as jaundice. The characteristic symptom of jaundice is yellowing of the skin and sclera. Ultrasound may be performed to determine possible liver dysfunction causing jaundice and clay colored stools in teh patient w/ cholecystitis. The patient w/ acute cholecystitis may experience nausea and vomiting. Nausea after eating meals is a common symptoms of cholecystitis. Administering antiemetics will help alleviate symptoms. After the patient vomits, frequent mouth rinses may be done to provide comfort. Manifestations of inflammatioin related to cholecystitis include fever. The patient w/ cholecystitis may also have an elevated WBC count caused by inflammation. The patient w/ cholecystitis may exhibit signs of infection such as fever and increased WBC count. MOnitoring the patient's temp and WBC is critical for early detection and treatment of infection. Indigestion is an initial symptoms of acute cholecystitis. Dyspepsia or heartburn is a common symptom of chronic cholecystitis. IBiliary obstruction prevents bile from entering the small intestine for fat digestion. The patient w/ cholecystitis willd evelop an intolerance to fatty or spicy foods. INgesting fatty foods will cause flare ups of biliary colic w/ symptoms including nausea, anorexia, and a sensation of fullness. The pain frequently occurs 3-6 hours after eating a high -fat meal. Ultrasound may be performed to diagnose cholelithiasis, or gallstones causing gallbladder inflammation. The diagnosis tool may also be completed to ensure the absence of calcification that may indicate cancer. In patients w/ cholecystitis, ultrasound is performed to rule out other possible causes of symptoms. The ultrasound may show biliary sludge or gallbladder wall thickening indicating inflammation.

irritable bowel syndrome IBS

chronic gastrointestinal disorder that includes symptoms of abdominal pain, alterations in bowel patterns, excessive flatulence, and fatigue. However, these symptoms are widely individualized, which makes IBS difficult to diagnose. Symptoms may be exacerbated by psychosocial stressors and certain foods. This condition is more commonly diagnosed in women. ALthough there's no specific test to identify IBS, diagnostic tests for other health conditions are performed to rule them out. Patients w/ IBS experience abdominal pain or discomfort. The pain is usually felt in the lower left quadrant of the abdomen. THe signals btwn the brain and abdomen are poorly coordinated. As the abdomen excessivly stretches from gas or stool, the brain does not anticipate the changes in digestion and reacts bya ctivating pain receptors. When the patient defecates, the intestinal walls relax as stool is released. By decreasing the pressure w/n the intestinal walls, the pain in the abdominal is releived. Individuals w/ IBS experience intermittent episodes of diarrhea and constipation. The patient w/ IBS may have more than 3 bowel movements a day w/ loose and watery stools. W/ constipation, the stools are small and hard, frequently followed by several softer stools. The alterations of bowel patterns cause pain as increased and decreased bowel transit times affect bowel motility and intestinal wall integrity. The chronic changes in bowel patterns may cause fatigue and sleep disturbances. The pateint may experience anxiety and depressioin from their abnormal bowel patterns. The constant abdominal pain activates the stress response and leads to fatigue. Patients w/ IBS experience excessive flatulence, abdominal distention, and bloating. During normal peristalsis, the intestinal walls smoothly coordinate contractons to move digested flood thru the intestinal tract. During IBS, intestinal contractions may be stronger and longer than normal. This causes increased bloating in the abdomen and is released as flatulence. The pateint w/ IBS may feel like they haven't completely emptied their colon after a bowel movement. The constant alterations btwn hard stools during constipation and looser stools w/ diarrhea may affect their sensation of defecation. Psychological stressors such as depression, anxiety, abuse, and post-traumatic stress disorders (PTSD) may contribute to the development and exacerbations of IBS. A majority of patients report worsening symptoms during periods of increased stress. Assess the patient's psychosocial factors, such as stress and axiety, while obtaining a health history. Certain food intolerances are often reported by patients w/ IBS. Chemicals that may exacerbate symptoms of IBS include fructans found in wheat, galactans, lactose, fructose, sorbitol, and xylitol. COnsuming certain types of food may trigger changes in bowel patterns. Other foods that may exacerbate symptoms include chocolate, fat, spices, fruit, dairy, and carbonated beverages. Irritable bowel syndrome affects women 2 to 2.5 times more often than men. Women are more likely to report symptoms such as constipatioin, migraine headaches, insomnia, and fibromyalgis. Since women are more likely to seek professioinal healthcare help, IBS is diagnosed more frequently in women than men. Hormonal changes related tomenstruation may also contribute to IBS. Since there are no accurate tests to identify IBS, obtaining a torough history and physical examination of the patient is critical to initiate supportive therapy to help relieve symptoms. Assess the patient's symptoms, past health history, current meds, family history, and diet history. To rule out other conditions, diagnostic tests for colorectal cancer, IBD, endometriosis, and malabsorption disorders are performed.

Cirrhosis Assessment

chronic liver disease that evolves slowly, has a prolonged course, and occurs asa result of excessive alcohol intake, nonalcoholic fatty liver disease (NFLD), or chronic hepatitic C. As a result of these disorders, cirrhosis stems from degeneration and destruction of liver cells. In cirrhosis there's hepatit damage. the liver cells attempt to regenerate, but this process is unorganized. THis results in abnormal architecture w/ irregular lobules that impede blood flow. THis leads to decreased liver function in patients. Jaundice results from theovergrowth of liver cells and connective tissue, leading to connective tissue overgrowth. As the body is unable to conjugate and excrete bilirubin, jaundice, or yellowing of the skin, occurs. The onset of cirrhosis is insidious, and an early symptom is fatigue. Patients may attribute this to other etiologies and might not be aware of their liver condition. Palmar erythema is described as a red area of skin on the palms that blanches w/ pressure. THis can also develop in cirrhotic pateints as a result of increased estrogen. As a result of increased circulating estrogen and an inability to metabolisze steroid hormones, spider angiomas can develop. These are dilated blood vessesl w/ a bright red center point and spider -like braches, which can occur on the trunk, neck, face, nose, and shoulders. Due to dysfunctional liver cell degeneration, the liver becomes enlarged and fibrosed. This leads to htn in the portal vein (going thru the liver), which leads to increased venous pressure in organs feeding into the liver. This leads to splenomegaly as well. B/c the liver is producing less albumin, and there' more portal htn, fluid is squeezed out of the vasculature into tissues. This is displayed as peripheral edema (ankle, legs), but can also turn into ascites, which is the accumulation of serous fluid in the abdominal cavity. Normally, the liver metabolizes hormones, like estrogen and testosterone. W/ cirrhosis, these hormones are not broken down as normal and excess estrogen leads to gynecomastia (male breasts) in men, while excess twstosterone leads to hirsutism (facial hair development ) in women. Patients display a chane in their LOC , in a complication known as hepatic encephalopathy. Increased circulating ammonia leads to neurotoxic effects, and patients experience changes in mental responsiveness, impaired memory and conssciousness, or even coma.

Cholecystitis Causes

gallbladder inflammation caused by biliary obstruction or bacteria entering the gallbladder. Bile is produced in the liver and stroed and concentrated in the gallbladder. Gallbladder inflammation may be acute or chronic. The 6 F's can help you remember risk factors: female, fair, fat, fertile, forty, and flatulence. INflammation of the gallbladder may be limited to the mucous lining or involve the entire wall of the gallbladder. Acalculous calculous, or gallbladder inflammation not related to an obstruction, is more frequently seen in patients who are older, critically ill, diabetic, or experiencing prolonged immobility or fasting. Acute cholecystitis is often caused by a gallstrone obstructing the common bile duct and causes gallbladder distentioin filled w/ bile or pus. After an acute attack, fibrosis of the gallbladder walls leads to decreased gallbladder fucntion that may develop into chronic cholecystitis. Symptoms of chronic cholcystitis may include a history of fat intolerance, dyspepsia,heartburn, and flatulence. The incidence of this condition is higher in females. Since fat tissues promotes cholesterol secretion in the bile and women tend to accumulate more fatty tissue than men, females have an increased risk of biliary obstruction leadng to cholecystitis. Those w/ fair complexion (caucasians) are more likely to develop cholesterol gallstones, which can later develop into cholecystitis and cholelithiasis. Additionally, the incidence is particularly high in Native American populations, especially in the Navajo and Pima tribes. Since excess fat tissue causes increased secretion of cholesterol in the bile, the obese patient has an increased risk of biliary obstruction leading to cholecystitis. Precipitation of cholesterol leading to biliary obstruction occurs when bile becomes supersaturated w/ cholesterol. Fertile women have a higher risk of developing cholecystitis. Multiparous women w/ multiple pregnancies are more likely to habe gallbladder inflammation. Pregnancy related hormones delay the emptying of the gallbladder, which results in bile stasis. Biliary sludge may develop and cause obstruction. Since hormones may habe an influence in cholecystitis, postmenopausal women receiving estrogen therapy have an increased risk of developing cholecystitis. Advanced age is a risk factor for developing cholecystitis. INdividuals over forty yrs of age have an increased risk. After the age of 50, gender differences in incidence btwn males and females decrease. A dysfunctional gallbladder prevents normal bile flow that is necessary for the digestion of fats. The patient w/ cholecystitis develops an intolerance to fatty foods and may experience flatulence.

ulcerative colitis assessment

inflam bowel disorder primarily affeects colon. The disease is characterized by periodic remissions and exacerbations. symptoms : abdominal pain in lower quadrants of abdomen and pain is crampy of colicky and often relieved w/ defecation. Tenesmus is a very unpleasant sensation of the need to defecate immediately, despit an empty colon. Ulcerative colistis patients may encounter this 10-20 times per day. INflammation of only the superficial layers of the intestinal mucosa cause a loody diarrhea in patients b/c of increased blood flow to the inflammed tissue. THe stool often has flecks of mucus. These patients defecate excessively as often as 10-20 stools per day. Defecating this often causes anxiety and fear of leaving the proximity of a restroom, which may severely affect the patient's lifestyle. Patients often experience fever during acute exacerbations of the disease. THis fever is often low grade. A presentation of a high fever may be indicative of perotonitis related to a bowel perforation. The superficial layers of the intestine are often inflamed and hyperemic due to increased blood flow. THis inflammation may cause weakening of the blood vessels and cause hemorrhage. Patients will present w/ hematochezia or large amounts of frank blood from the rectum

Gastroeinteritis

inflammation of the mucos alining the stomach and small intestine. Bacteria, viruses, and food intolerances may trigger gastroeenteritis and lead to symptoms of abdominal distress including sudden diarrhea, nausea, vomiting, and abdominal cramping. Gastrointeritis caused by bacteria may cause bloody stool, while viral causes may present w/ flu like symptoms including fever, fatigue, headache, and muscle pain. Although the disease is self-limiting w/ symptoms resolving w/n one week, oral rehydration of IV fluid replacement is necessary if dehydration occurs. Prevention techniques, such as hand washing and rotavirus vaccination, are critical in minimizing the spread of gastroenteritis. Viruses are the leading cause of gastroenteritis. Norovirus is the common cause in adults while rotavirus is the leading cause of gastroenteritis in children. Sources of virus transmission include eating contaminated food and touching tainted surfaces. Bacerial causes o gastroeinteritis include Campylobacter jejuni, E.coli, and Salmonella. Toxins released by certain bacteria such as C>difficile may also trigger cases of gastroenteritis. Food intolerances may cause inflammation of the mucosal lining in the stomach and small intestine. Examples include individuals w/ Crohn's disease, people w/ lactose intolerance consuming dairy products, and people w/ Celiac disease eating gluten. Gastroenteritis may present w/ flu-like symptoms, such as fever, fatigue, headache, and muscle pain. FLu-like symptoms are commonly associated w/ some viral causes of infectious gastroenteritis. Symptoms of acute GI distress manifest in patients w/ gastroenteritis. The patient may present w/ sudden diarrhea, nausea, vomiting, and abdominal cramping. Since frequent diarrhea and vomiting may quickly dehydrate the patient,monitoring hydration status is important for prompt intervention. Bacterial causes of gastroenteritis may cause the patient to have blood stools. Contact the patient's hcp if bloody stools occur. Although most cases of gastroenteritis are self-limiting dehydration is a major risk factor. Since electrolytes and fluid are los thru diarrhea and vomit, encourage the patient to drink fluids containing glucose and electrolytes as tolerated. Since older adults and chronicallyill patients may be unable to orally consume adequate amounts of fluid to compensate for fluid loss, IV fluid replacement may be administered as needed. Most cases of gastroenteritis are self-limiting, meaning that it usually resolves itself w/n 1 week after the onset of symptoms. Nursing management is similar to that of a patient w/ acute diarrhea. However, individuals such as older adults and chronically ill patients are at high risk of dehydration. MEds that suppres sintestinal motility (loperamide {Imodium}) should not be given as they prevent the elimination of the infecting organism unles sthe hcp determines that antiperistaltic agents are needed. Preventative measures are critical in minimizing the risk of developing gastroenteritis. Frequent hand washing w/ soap and drinking clean water are techniques to help avoid contacting and spreading infectous gastroenteritis. The rotavirus vaccine is recommended in children to hlep decrease the risk of contracting the virus.

acute pancreatitis interventions

inflammation of the pancreas w/ severity depending on the extent of pancfreatic destruction. Goals of care are to monitor for changes in vitals that can indicate the life threatening emergency of shock, assess ofr changes in LOC related to alcohol withdrawal, relieve abdominal pain, minimize pancreatic stimulus by diety changes to reduce secretions, correct fluid and electrolyte imbalances, prevent or treat infection, and determine and elimate the precipitation cause of the acute episode. NPO w/ NG tube to suction: this is done to reduce or suppress pancreatic enzymes to decrease stimulation of the pancrease and allow for rest. NG set to suction helps reduce vomiting and gastric distention and prevents gastric acidic contents from entering the duodenum. Patients w/ severe pancreatitis who cannot resume oral intake may be supported w/ entereal nutrition. Big complication is paralytic ileus. IV morphine is often used. pain meds can be given w/ an antispasmodic agent; however, atropine and other anticholinergic drugs should be avoided in teh presence of a paralytic ileus due to its effects of decreasing GI mobility. Place the patient in a position of comfort, typicaly on side w/ legs drawn to chest. Albumin is a plasma volume expander, which is often given in the presenc eof shock to help replace blood volume. Lactated Ringer's solution or other electrolyte solutions are given as part of an aggressive hydration treatment plan to help correct fluid and electrolyte imbalances. In patients w/ persistent hypotension, vasoactive drugs such as dopamine may also be used to increase systemic vascular resistance. The replacement of calcium and magnesium may also be needed. Proton pump inhibitors work by decreasing hydrochloric (HCl) acid secretion, as HCl acid stimulates pancreatic activity. A common PPi prescribed is omeprazole (Prilosec). IN the presence of necrotizing pancreatitis, patients often develop infection as the inflamed and necrotic pancreatic tissue is a good medium for bacterial growth. Administer antibiotics as prescribed. Acute pancreatitis related to gallstones requires an endoscopic retrograde cholangiopancreatography (ERCP) plus endoscopic sphincterotomy. THis can be followed by laparoscopic cholecystectomy to prevent reoccurrence. It is important to stay properly nourished to aid w/ recovery. When able to eat, small , frequent high carb , highprotein, low fat meals should be consumed. To avoid irritation, cosume bland foods w/ no spices and avoid GI stimulants, such as caffeine or alcohol.

appendicitis assessment

inflammationof the appendix as a result of an obstruction of the lumen of appendix. Obstruction results in distention, venous engorgement, and the buildup of bacteria and mucus, leading to possible complications, such as peritonitis and sepsis. It results in one of the most common abdominal surgical emergencies that occurs in children w/ the average age being ten years affecting boys and girls equally before puberty. SYmptoms may include periumbilical pain, RLQ pain, nausea, vomiting, anorexia, rebound tenderness, increased white blood cells, and fever. A common cauuse of appendicitis is obstruction of the intestinal lumen by a fecalith (accumulated feces). THis obstruction impairs blood supply and can cause bacterial infection in the wall of the appendix, which may cause gangrene. It is important to relieve the obstruction as soon as possible. general syimptoms: nausea vomiting anorexia An early symptom of appendicitis is periumbilical pain that may be described as a dull and throbbing pain localized around the navel. THis pain may also be referred to as epigastric pain and often progresses to right lower quadrant (RLQ) pain. As swelling in the appendix increases, the pain tends to move toward the right lower abdomen and localizes at McBurney's point (halfway btwn the umbilicus and the right ilia crest). It is often described as pain that is persistent and continuous, progressing over the course of 4-6 hours. COughing, sneezing, and deep inhalation may intensify the pain, while a side lying position w/ abodminal guarding (legs flexed) relieves the pain. in early apendicitis WBCs may be normal but most often a mild elevation will occur. Rebound tenderness refers to pain upon the removal of pressure rather than the application of pressure to the abdomen (the latter is referred to as abdominal tenderness). More simply put, it is pain experienced on deep palpation after a sudden release. It represents aggravation of the pareital layer of the peritoneum by stretching or moving. A low grade fever may or may not be present. It typically occurs as the appendix becomes increasingly inflammd as part of the body's natural immune response. A fever is noted at 100.4 degrees F, while a low grade fever ranges btwn 99-102 F. Peritonitis is inflammation of the peritoneum often occurring from a perforated appendix, which results in a release of its contents into the normally sterile peritoneal cavity. It presents as a sudden relief of pain and then a subsequent increase in pain accompanied by right gaurding of the abdomen. Patients may present w/ a fever, abdominal distention, tachycardia, tachypnea, pallor, chills, restlessness and irritability. Sepsis is a possible complication as bacteria enteres the peritoneal cavity. THis is a serious and deadly condition that must be treated immediately.

Crohn's Disease Assessment

inflammatory bowel disorder that can involve any segment of the GI tract from the mouth ot the anus but preferentially is found in the terminal ileum. THe disease is characterized by periodic remissions and exacerbations. This condition has non-bloody stools w/ patients experiencing 5-6 loose stools per day. Bloody diarrhea is uncommon in Crohn's disease, in contrast to patients w/ ulcerative colitis who often have bloody stools. The stools often contain large amounts of fat due to malabsorption, which is termed steatorrhea. The patient may experience 5-6 soft, loose stools per day, which are usually non bloody. It is important to assess the number of stools along w/ amount, consistency, odor, and color. Abdominal pain characterized w/ cramping occurs often. Abdominal pain is typicallay confined to the lower abdominal quadrants. Transmural inflammation of teh bowel mucosa may cause a fever in some patients and is not required for diagnosis. THis fever is often intermittent and described as low grade 99F- 100F Many patients experience weight loss b/c of frequent stooling and decreased absorption of calories. Patients may also lose weight, b/c they consume less food in anticipation of the fear of future abdominal pain. This weight loss may be profound and is usually unintentional. Frequent stools and intestinal inflammation cause a decreased amount of time for intestinal mucosa to absorb vitamins and nutrients as well as decreased surface area. This leads to nutritional deficiencies, especially of fat soluble vitamins A, D, E, and K. This is b/c this disease often affects the small intestine where these nutrients are absorbed. Anemia is a finding in these patients b/c B12 is primarily absorbed in the terminal ileum, the most common primary site of Crohns' inflammatory process. THe lack of B12 causes a megaloblastic anemia. If the disease process affects the duodenum, then patients may present w/ iron deficiency anemia. Patients often have complications from inflammation which causes scarring and stricture formation. These potentiate megacolon and ileus formations. THis stasis of stool often leads to intestinal obstructions. Intestinal obstructions in these patients often requires surgical intervention. FIstulas are abnormal openings btwn two adjacent hollow organs. They occur in Crohn's disease most commonly as bowel bladder fistulas, which will allos fecal matter into the urine termed fecaluria. Fistulas often create high risk scenarios for urinary tract infections, peritonitis or abscesses depending on where the fistula is located.

Kwashiorkor

malnutriton state which occurs thru severe protein deficiency. Patients develop edema and swollen bellies, as well as liver dysfunction from decreased apolipoprotein synthesis. Patients can become anemic due to decreased protein anabolism, while developing desquamative skin lesions. Develops from a severe deficiency in dietary protein. This disorder typically is seen in areas of famine or poor food supply. An example of this is seen when a mohte rweans a child from breastmilk, replacing the diet w/ starchy carbs. The classic example of this condition is a malnourished child w/ pitting edema of the lowe rlimbs w/ a distended abdomen. The swelling of the gut occurs b/c there's an osmotic imablance in the GI system, which is a consequence of protein deficiency. Retention of water leads to the swollen belly seen w/ this disorder. MEALS acronym: Malnutrition--- from protein deficiency Edema--occurs in abdomen, shins, and ankles. This is so b/c lack of protein leads to an osmotic imbalance, leading to retention of water. Anemia--Decreased protein in the diet limits anabolic processes. B/c of this, blood cell production may be impaired, slowly causing the development of anemia. LIver malfunction--Due to a shortage of amino acids *from protein), there'simpaired synthesis of VLDL apoprotein. This causes accumulation in the liver of unused lipids which would normally participate in lipoprotein synthesis,leading to fatty liver in patients. Skin lesions--low protein intake leads ot various skin lesions in patients who develop this condition. A common condition is ulcerating dermatosis, which is a type of desquamatice rash.

appendicitis interventions

management of appendicitis focuses on early recognition of acute appendicitis. B/c school age children often complain of abdominal pain, it is important to carefully assess for typical symptoms of appendicitis. INterventionis associated w/ properative and postoperative appendectomy care are crucial to a successful outcome. Recovery after surgery is fairly rapid and complete. Removing the appendix is the gold standard treatment for appendicitis. An appendectomy is surgical removal of the appendix. Antibiotics are often given peoperatively to help prevent infection before and after the s urgery. Antibiotic treatment kills bacteria and stronger and longer courses of antibiotics are required if peritonitis occurs. IV fluids are given to maintain fluid and electrolyte balance. Additionallly, patients should be kept on NPO status as the stomach should be empty prior to surgery. The use of enemas or laxatives are dangerous as the resulting peristalsis may cause perforation of the appendix. Placing the patient in Semi-fowler's, especially if there's an infection, is an important intervention. THis allows for the infection to localize in the peritoneum and not ascend to the lungs, heart, etc. THis position is preferred, as high fowler's may not be tolerated by patients. An NG tube is placed until GI motility returns. Be sure to assess bowel sounds. Diet is advanced as tolerated. Pain management is an important intervention not only to keep the pateint comfortable, bu to promote early ambulation, which decreases the risk of developing complications and aids in recovery time. Analgesics are commonly used to manage pain. Ambulation should begin the day of surgery or the first postoperative day. Encouragement of early ambulation decreases the risk of possible postoperative complications and aids in recovery time.

hep b assessment

may be acute or chronic, leading to liver failure, cirrhosis, or hepatocellular carcinoma (liver cancer). The virus is spread by exposure to infectious blood or body fluids, as well as perinatally by mothers infected w/ HBV Close contact w/ infected individuals and their bodily fluids can lead to contraction of the HBV. This includes sexual contact w/ an infected partner in which exposure to saliv, blood, semen, or vaginal secretions enter the body. Additionally, casual contact in the form of open sores or cuts can lead to infection. Hept B can be spread by exposure to infectious blood. This includes perinatal transmisison, which means a mom can pass virus to fetus during childbirth. Additionally, accidental needle sticks contaminate3d w/ infected blood are noather source of transmission. IV drug abusers are increased risk of contracting hep B, as the virus is easily transmitted thru needles and syringes contaminated w/ infected blood. The incubation period for hepatitis B is quite variable w/ a range of 1-6 months (45-180 days), w/ an average of 56-96 days. Patients are infectious for 4-6 months and carriers continue to be infectious for life. Manifestations of hep B often resemble flu-like symptoms and often don't appear until the individual has had the virus for a couple weeks. A low-grade fever may be present. The individual may experience nausea and vomiting, as well as generalized weakness and fatigue, and loss of appetite. Symptoms of hep B are rarely severe unless there is underlying liver failure. Some patients may experience hepatomegaly, or swelling of the liver beyond normal. Approx ten percent of individuals infected w/ HBV, usually immunosuppressed individuals, can develop chronic hep B. Chronic hep B may eventually cause cirrhosis (scarring of the liver). Chronic hep B may also cause hepatocellular carcinoma or liver cancer. Hep B is preventable by vaccination. The incidence of HBC infection has decreased significantly due to the widespread use of the HBV vaccine.

intestinal obstruction

occurs when the contents of the GI tract cannot pass thru the intestines. Signs and symptoms of an obstruction include severe abdominal pain, vomiting, abdominal distension, high pitched or absent bowel sounds, and increased or absent peristalsis. Fluid and acid-base problems accompany an intestinal obstruction w/ metabolic alkalosis occurring when an obstructioin is high (upper duodenum) due to loss of HCL form vomiting and/or nasogastric suction and dehydration when the obstruction is located in the small intestine. Typically, dehydration and electrolyte imbalance does not usually occur w/ a large intestine bowel obstruction. Sudden onset of severe abdominal pain may be an early sign of an obstruction. The frequency of abdominal pain can vary depending on the type and location of the obstructioin; mechanial obstruction of the bowel typically produces intermittent pain. Guarding and abdominal tenderness may be present upon physical examination. Gradual onset of vomiting is characteristic of a distal, small bowel obstruction. IF the obstruction is located higher in the intestine; however, vomiting may be projectile, containing bile and can result in temporary relief of abdominal pain. IF bowel wounds are present in a pateint w/ an intestinal obstruction, they weill be high-ptiched and present above the level of the obstruction. Gurgling bowel sounds called borborygmi may also be audible due to hyperactive intestinal motility. Though clinical manifestations vary depending on the location and type of obstruction, abdominal distention could be an early sign of an intestinal obstruction. Distention usually precedes the onset of constipation. INitially, when the bowel becomes obstructed, peristalsis may increase in an attempt to dislodge or resolve the obstruction. Bowel sounds may be completely absent in some cases of obstruction. Lack of bowel sounds usually indicates cessatioin of intestinal activity. A hcp must listen to each abdominal quadrant for five minutes before concluding that bowel sounds are absent. This occurs when intestinal peristalsis is absent of bowel sounds. Paralytic ileus is common after surgery.

peptic ulcer disease assessment

peptic ulcers are caused by an erosion of the mucosal wall of the GI tract. These ulcers develop when excess hydrochloric acid and digestive enzymes (pepsin) disrupt the gastric mucosal barrier, causing breakdown. A bacteria called Helicobacter pylori (H.pylori) may also contribute to peptic ulcer formation; however, not everyone who is infected w/ this bacteria will develop an ulcer. Patientw w/ this condition may present w/ abdominal pain,heartburn, GI distress, black, tarry stools, and weight loss. H. pylori is a bacteria that lives in the stomach and has been linked to the development of peptic ulcers. Despite this association,not everyone who is infected w/ H.pylori will develop an ulcer. Factors such as diet, environment, and genetic makeup influence a person's repsonse to the bacteria. A person's lifestyle can greatly contribute to the development of peptic ulcers. For example, individuals experiencing stress, or those who consume beverages such as cofee or alcohol, cause an increase in hydrochloric acid secretion, which can lead to ulcerations. Patientw w/ Zollinger-Ellison syndrome, a condition that causes hypersecretion of gastric acid, will also develop ulcers. Though abdominal pain is a common complaints of patients w/ peptic ulcers, timing of the pain varies according to where the ulcer is located. Pain caused by a duodenal ulcer typically occurs 2 to 5 hrs after a meal, and may radiate to the patient's back. Gastric ulcers, however, cause a burning pain 1 to 2 hours after a meal and may be releived by vomiting. HEartburn is a burning sensation in the chest, caused by gastric acid. Patients w/ peptic ulcer disease may notice this burning sensation at night when tehy ar in asupine position. Elevating the head of the bed is recommended, as laying fla can worsen heartburn. Upper GI bleeding related to ulcers can cause patients to have black, tarry stools. Patients should monitor their stool for signs of bleeding and report these changes to their hcp immediately. Hematemesis or vomiting of blood may also occur. Patients w/ peptic ulcer disease, particularly a gastric ulcer, may lose their desire to eat or drink due to unrelieved painin their abdomen. A decrease in food and fluid intake can cause constipation. Duodenal ulcers are more common than gastric ulcers, and can occur in people of all ages. Pain caused by a duodenal ulcer typically occurs 2-5 hours after a meal, b/c eating relieves the pain due to the buffereing effect of food on the sotmach acid. pain is typically located mid-epigastric region and is described as burning or cramp-like. Gastric ulcers cause a burning pain 1-2 hours after a meal, and pain is not relieved by eating. Pain from a gastric ulcer may be relieved by vomiting.

hernia interventions

reducing intra abdominal pressure in patients w/ existing or recently treated hernias helps prevent complications. INcreased abdominal pressure may complicate or exacerbate hernias, so patients are encouraged to sue open mouth sneezing techniques and to avoid lifting or straining. Patients should avoid heavy lifting and staining for 6-8 weeks following a hernia repair. Excessive stain of heavy lifting can increase the patient's risk of developing another hernia. IF sneezing is unavoidable, instruct patients to sneeze w/ their mouth open to reduce intraabdominal pressure. Additionally, patients recovering from a hernia repair should not participate in postoperative coughin. Instead, patients should be encouraged to deep breathe to prevent postoperative complications, such as penumonia. Excision of a hernia, or hernotomy, involves surgical removal of the hernia sac. THis procedure is common w/ hiatal hernias. A herniorrhaphy is a surgical procedure to correct a hernia. Typically, it is done as an outpatient procedure. Be sure the patient has voided prior to discharge, as difficulty voiding following the procedure is common due to edema in the perineal area. Another option for patients undergoing hernia repair is a hernioplasty. This procedure invovles reinforcing the area of weakness w/ wire, fascia, or mesch. Scrotal swelling and edema may develop after repair of an inguinal hernia. To reduce discomfort, patients may use a scrotal support, in addition tointermittent application of an ice pack and other pain relieving measures.

GERD assessment

reflux of gastric contents into the esophagus, which is characterized by inflammatory symptoms resulting from the irritating effects of gastric or duodenal contents on teh esophageal mucosa. Patients who are obese are at increased risk for the disease due to increased intraabdominal pressue, which allows the reflux (backward flow) of stomach contents into the esophagus. INflammation in this disorder causes persistent relaxation of the sphincter at the base of the esophagus. The LES typically constricts to prevent reflux of gastric contents into the esophagus. Chronic inflammation by prolonged GERD can lead to "Barrett's Esophagus/Epithelium," which increases esophageal adenocarcinoma risk. Dyspepsia is a conditioin of impaired digestion. It typially occurs after meals and includes symptoms such as abdominal pain/discomfort, bloating, nausea, heartburn, upper abdominal fullness, and belching. It is important to differentiate the characteristics of upper abdominal pain and chest pain in patients; there's often a correlation w/ dyspepsia and food intake. Commonly gas in the stomach is held in place by the lower esophageal sphincer (LES). Since these patients have poor LES tone they often exhibit belching, which may be excessive after consuming gas-producing foods or beverages. Classicaly GERD is associated w/ syimptoms that are worsened when lying down, like at night. This increased irritation causes coughing, wheezing, and sypnea that may awake the patient from sleep. GERD can mimic asthma or can worsen pre-existing asthma. Patients should be advised to elevate teh head of bed when sleeping. The term dysphagia means difficulty swallowing and may be the result of esophagitis from GERD. DYsphagia also may be presenting complaint of an esophageal stricture, which is a complication GERD. Swallowing may also be painful, termed odynophagia. The pain in GERD is classically described as above the stomach and described by patients as a burning sensation that seems to rise up from the stomach in the center of their chest. THe pain may persist in a wave-like motion. It often mimics angina-like pain but, typically in GERD, these patients have recently ingested a meal. Reversal of food contents in the opposite direction is termed regurgitation.These food contents or stomach acid may lead to aspiration into the respiratory tract or vomiting. Aspirated food contents are common causes of respiratory patients. Another phenomenon is called "water brash" where excess salivation occurs as a reaction to regurgitation. It can be described as that last feeling of salivation reight before you vomit. Heartburn, also known as pyrosis, is painful burning feeling below or behind the breastbone. The pain often rises in one's chest from the stomach and may radiate tot he neck, throat, or jaw region. THis is a frequent symptom. Globus, sometimes referred to as globus pharyngis or globus hystericus, is the subjective feeling or sensation of alump or foreign body in the throat. GERD is often a major cause of globus.

Boerhaave Syndrome

rupture of the esophageal wall, which can be a result of violent retching or iatrogenic injury. It can present w/ chest pain, subcutaneous emphysema, odynophagia and shock. THis is a surgical emergency that requires immediate treatmnt. IN contrast to mallory weiss tears (which are mucosal), Boerhaave syndrome is described by rupture or perforation of the esophagus (thru the mucosal and muscular layers) This rupture is caused thru a sudden rise of internal esophageal pressure during vomiting, and can stem from excessive food and alcohol intake, or bulimia. ANother common cause of this syndrome is iatrogenic perforation. MOst cases of Boerhaave's syndrome occur at the distal (lower third ) esophagus. After vomiting or a procedure, patients may display excruciating retrosternal chest pain, and possibly upper abdominal pain. IN less evident cases where Boerhaave's is susupected, the caregiver may find that the patient presents w/ odynophagia, or painful swallowing of liquids and foods. Though not a very important diagnostic finding, due to its lack of sensitivity, patients w/ this syndrome can develop subcutaneous emphysema, or crepitus, near the mediastinum. If there's bleeding from the esophageal rupture, patients may go into hypovolemic shock from blood loss. This condition is usually a surgical emergency. Due to its high morbidity and mortality, potential for rapid clinical deterioration and fatal outcome w/ot treatment, all patients suspected of having Boerhaave syndrome should have surgical consultation.

marasmus

severe form of malnutrition caused by total calorie malnutrition (protein, carbs and all other nutrients). This results in emaciation, characterized by muscle and tissue wasting, to the point where body weight is less than 60% of normal. Marasmus is caused by total calorie malnutrition, meaning that there is a severe deficiency in nearly all nutrients, including protein and carbs. IN these patients, emaciaiton and tissue wasting occurs to the point that body weight is reduced to less than sixty percent of the normal, expected body weight. Patients w/ marasmus show extensive tissue and muscle wasting. There is notable loss or muscle mass, and skin becomes dry, loose, and hanging. NOtably, there' s drastic loss of body fat (adipose tissue). Areas of normal fatty deposits, such as the buttocks and thighs, show extensive loss of subcutaneous fat. Marasmus is different from kwashiorkor, in that marasmus is total nutrition deficiency, instead of solely portein. There's still protein wasting w/ this disorder, however, and may lead to edema in patients, which may present in multiple variations.