NCLEX: Gastrointestinal Disorders

Gastrointestinal Disorders: Common GI disorders

Focus topic: Gastrointestinal Disorders

Gastrointestinal Disorders: Crohn’s disease

Focus topic: Gastrointestinal Disorders

An inflammatory disorder, Crohn’s disease can affect any part of the GI tract (usually the terminal ileum), extending through all layers of the intestinal wall. It may also involve regional lymph nodes and the mesentery.

What causes it
The exact cause of Crohn’s disease is unknown. Possible causes include allergies, immune disorders, lymphatic obstruction, infection, and genetic factors. Crohn’s disease is most prevalent in adults ages 20 to 40, but a second peak incidence occurs between ages 55 and 65.

Pathophysiology
In Crohn’s disease, inflammation spreads slowly and progressively. Here’s what happens:
• Lymph nodes enlarge and lymph flow in the submucosa is blocked.

Just skip it

Focus topic: Gastrointestinal Disorders

• Lymphatic obstruction causes edema, mucosal ulceration, fissures, abscesses and, sometimes, granulomas. Mucosal ulcerations are called skipping lesions because they aren’t continuous as in ulcerative colitis.
• Oval, elevated patches of closely packed lymph follicles — called Peyer’s patches — develop on the lining of the small intestine.
• Fibrosis occurs, thickening the bowel wall and causing stenosis, or narrowing of the lumen.

What to look for
Clinical effects vary according to the location and extent of inflammation and at first may be mild and nonspecific.

Gastrointestinal Disorders

• In acute disease, look for right lower abdominal quadrant pain, cramping, tenderness, flatulence, nausea, fever, diarrhea, and bleeding (usually mild but may be massive).
• In chronic disease, look for diarrhea, four to six stools per day, right lower quadrant pain, steatorrhea, marked weight loss, possible weakness and, rarely, clubbing of fingers.

What tests tell you
• Laboratory findings typically indicate increased WBC count and erythrocyte sedimentation rate (ESR), hypokalemia, hypocalcemia, hypomagnesemia, and decreased hemoglobin levels.
• A barium enema showing the string sign (segments of stricture separated by normal bowel) supports this diagnosis.
• Sigmoidoscopy and colonoscopy may show patchy areas or inflammation, thus helping to rule out ulcerative colitis.
• Biopsy results confirm the diagnosis.
• Upper GI series with small-bowel examination helps determine disease in the ileum.

How it’s treated
TPN helps to maintain nutrition while resting the bowel of a debilitated patient. Surgery can correct bowel perforation, massive hemorrhage, fistulas, or acute intestinal obstruction. The patient with extensive disease of the large intestine and rectum may require colectomy with ileostomy.

Take a pill

Focus topic: Gastrointestinal Disorders

Effective drug therapy requires important changes in lifestyle: physical rest, a restricted-fiber diet (low in fruit and vegetables), and elimination of dairy products for lactose intolerance. Drug therapy may include:
• anti-inflammatory corticosteroids and antibacterials, such as sulfasalazine (Azulfidine) and mesalamine (Asacol)
• metronidazole (Flagyl)
• opium tincture and diphenoxylate (Lomotil) to help combat diarrhea (contraindicated in patients with significant intestinal obstruction)
• immunosuppressants, such as azathioprine (Imuran), cyclosporin (Sandimmune), and 6-mercaptopurine (Purinethol), for patients who can’t be controlled on steroid therapy
• infliximab (Remicade), a tumor necrosis factor-alpha, to promote closure of fissures and treat refractory Crohn’s disease flare-ups, given in a monitored setting by I.V. infusion in a cycle of three treatments (at weeks 1, 2, and 6).

What to do
• Record fluid intake and output (including the amount of stool), and weigh the patient daily.
• Watch for dehydration and maintain fluid and electrolyte balance.
• Be alert for signs of intestinal bleeding (bloody stool). Check stool daily for occult blood.
• If the patient is receiving steroids, watch for adverse reactions such as GI bleeding. Remember that steroids can mask signs of infection. Check hemoglobin levels and hematocrit regularly. Also check the WBC count if the patient is on immunomodulators. Give iron supplements, blood transfusions, and analgesics as ordered.
• Watch for fever and pain on urination, which may signal bladder fistula. Abdominal pain, fever, and a hard, distended abdomen may indicate intestinal obstruction.
• Before ileostomy, arrange for a visit by an enterostomal therapist. For postoperative care, see “Bowel surgery with ostomy,” page 450.
• Evalate the patient. After successful treatment for Crohn’s disease, he will maintain optimal nutrition, hydration, and skin integrity. He’ll use positive coping mechanisms to deal with a changed body image. He should be able to identify and avoid foods likely to cause distress. Make sure he can demonstrate proper care of anostomy, if required, and uses appropriate support groups. Evaluate his understanding of the need for follow-up care and when to seek immediate attention.

Gastrointestinal Disorders

Gastrointestinal Disorders: Diverticular disease

Focus topic: Gastrointestinal Disorders

In diverticular disease, bulging, pouchlike herniations (diverticula) in the GI wall push the mucosal lining through the surrounding muscle. Diverticula occur most commonly in the sigmoid colon, but they may develop anywhere, from the proximal end of the pharynx to the anus. Other typical sites are the duodenum, near the pancreatic border or the ampulla of Vater, and the jejunum. Diverticular disease of the stomach is rare and is usually a precursor of peptic or neoplastic disease. Diverticular disease of the ileum (Meckel’s diverticulum) is the most common congenital anomaly of the GI tract.
Diverticular disease has two clinical forms:
• diverticulosis — diverticula present but typically produces no symptoms
• diverticulitis — inflamed diverticula; may cause potentially fatal obstruction, infection, and hemorrhage.

What causes it
The exact cause is unknown, but it may result from:
• diminished colonic motility and increased intraluminal pressure
• defects in colon wall strength.

Pathophysiology
Diverticula probably result from high intraluminal pressure on an area of weakness in the GI wall where blood vessels enter. Diet may be a contributing factor because insufficient fiber reduces fecal residue, narrows the bowel lumen, and leads to high intraabdominal pressure during defecation.

A sad sac

Focus topic: Gastrointestinal Disorders

In diverticulitis, undigested food and bacteria accumulate in the diverticular sac. This hard mass cuts off the blood supply to the thin walls of the sac, making them more susceptible to attack by colonic bacteria. Inflammation follows and may lead to perforation, abscess, peritonitis, obstruction, or hemorrhage. Occasionally, the inflamed colon segment adheres to the bladder or other organs and causes a fistula.

What to look for
The different forms of diverticular disease result in different signs and symptoms:
• Meckel’s diverticulum usually produces no symptoms.
• In diverticulosis, recurrent left lower abdominal quadrant pain is relieved by defecation or passage of flatus. Constipation and diarrhea alternate.
• In diverticulitis, the patient may have moderate left lower abdominal
quadrant pain, mild nausea, gas, irregular bowel habits, low-grade fever, leukocytosis, rupture of the diverticuli (in severe diverticulitis), and fibrosis and adhesions (in chronic diverticulitis).

What tests tell you
• An upper GI series confirms or rules out diverticulosis of the esophagus and upper bowel.
• Barium enema confirms or rules out diverticulosis of the lower bowel. Biopsy rules out cancer; however, a colonoscopic biopsy isn’t recommended during acute diverticular disease because of the strenuous bowel preparation it requires.
• Blood studies may show an elevated ESR in diverticulitis, especially if the diverticula are infected.

How it’s treated
Diverticulosis that produces no symptoms usually doesn’t require treatment. Treatment for diverticular disease depends on the type.
• Intestinal diverticulosis with pain, mild GI distress, constipation, or difficult defecation may respond to a liquid or bland diet, stool softeners, and occasional doses of mineral oil. These measures relieve symptoms, minimize irritation, and lessen the risk of progression to diverticulitis. After pain subsides, the patient also benefits from a high-residue diet and bulk-forming laxatives such as psyllium.

Mild measures

Focus topic: Gastrointestinal Disorders

• Treatment of mild diverticulitis without signs of perforation seeks to prevent constipation and combat infection. It may include bed rest, a liquid diet, stool softeners, a broad-spectrum antibiotic, meperidine to control pain and relax smooth muscle, and an antispasmodic such as dicyclomine to control muscle spasms.

Major management

Focus topic: Gastrointestinal Disorders

Diverticulitis unresponsive to medical treatment requires a colon resection to remove the involved segment.
• Complications that accompany diverticulitis may require a temporary colostomy to drain abscesses and rest the colon, followed by later anastomosis.
• Patients who hemorrhage need blood replacement and careful monitoring of fluid and electrolyte balance. Such bleeding usually stops spontaneously. If it continues, angiography for catheter placement and infusion of vasopressin into the bleeding vessel is effective. Rarely, surgery may be required.

What to do
• If the patient with diverticulosis is hospitalized, observe his stool carefully for frequency, color, and consistency.
• Keep accurate pulse and temperature charts because changes in pulse or temperature may signal developing inflammation or complications.
Management of diverticulitis depends on the severity of symptoms.
• In mild disease, administer medications as ordered, explain diagnostic tests and preparations for such tests, observe stool carefully, and maintain accurate records of temperature, pulse rate, respiratory rate, and intake and output.
• Monitor carefully if the patient requires angiography and catheter placement for vasopressin infusion. Inspect the insertion site frequently for bleeding, check pedal pulses frequently, and keep the patient from flexing his legs at the groin.
• Watch for signs and symptoms of vasopressin-induced fluid retention (apprehension, abdominal cramps, seizures, oliguria, and anuria) and severe hyponatremia (hypotension; rapid, thready pulse; cold, clammy skin; and cyanosis).
• For postsurgical care, see “Bowel resection and anastomosis,”.
• Evaluate the patient. After successful treatment and appropriate teaching, the patient will observe and report the character of the stool, modify his diet as needed, understand the need for followup care, and know when to seek immediate attention.

Gastrointestinal Disorders

Gastrointestinal Disorders: Gastroesophageal reflux disease

Focus topic: Gastrointestinal Disorders

GERD is the backflow of gastric or duodenal contents, or both, past the LES, into the esophagus, without associated belching or vomiting. Reflux may or may not cause symptoms or abnormal changes. Persistent reflux may cause reflux esophagitis (inflammation of the esophageal mucosa).

What causes it
Reflux occurs when LES pressure is deficient or when pressure within the stomach exceeds LES pressure. Predisposing factors include:
• pyloric surgery (alteration or removal of the pylorus), which allows reflux of bile or pancreatic juice
• long-term NG intubation (more than 5 days)
• any agent that decreases LES pressure, such as food, alcohol, cigarettes, anticholinergics (atropine, belladonna, propantheline), and other drugs (morphine, diazepam, and meperidine)
• hiatal hernia (especially in children)
• any condition or position that increases intra-abdominal pressure.

Pathophysiology
Normally, the LES maintains enough pressure around the lower end of the esophagus to close it and prevent reflux. Typically, the sphincter relaxes after each swallow to allow food into the stomach. In GERD, the sphincter doesn’t remain closed (usually due to deficient LES pressure or pressure within the stomach exceeding LES pressure), and stomach contents flow into the esophagus. The high acidity of the stomach contents causes pain and irritation in the esophagus, and stricture or ulceration can occur. If the gastric contents enter the throat and are aspirated, chronic pulmonary disease may result.

What to look for
Gastroesophageal reflux doesn’t always cause symptoms, and in patients showing clinical effects, physiologic reflux isn’t always confirmable.

Achy, breaky heartburn

Focus topic: Gastrointestinal Disorders

The most common feature of gastroesophageal reflux is heartburn, which may become more severe with vigorous exercise, bending, or lying down and may be relieved by antacids or sitting upright. The pain of esophageal spasm resulting from reflux esophagitis tends to be chronic and may mimic angina pectoris, radiating to the neck, jaws, and arms. Other symptoms include:
• odynophagia (pain when swallowing), which may be followed by a dull substernal ache from severe, long-term reflux
• dysphagia from esophageal spasm, stricture, or esophagitis and bleeding (bright red or dark brown)
• rarely, nocturnal regurgitation wakes the patient with coughing, choking, and a mouthful of saliva.

Don’t hold your breath

Focus topic: Gastrointestinal Disorders

Pulmonary symptoms, which result from reflux of gastric contents into the throat and subsequent aspiration include:
• chronic pulmonary disease or nocturnal wheezing
• bronchitis
• asthma
• morning hoarseness and cough.

What tests tell you
• In children, barium esophagography under fluoroscopic control can show reflux. Recurrent reflux after age 6 weeks is abnormal.
• An acid perfusion (Bernstein) test can show that reflux is the cause of symptoms.
• Endoscopy and biopsy allow visualization and confirmation of any abnormal changes in the mucosa.
• An ambulatory pH test measures the acidity of the esophagus.
• Manometry indicates the strength and activity of the lower esophageal sphincter.

How it’s treated
Effective management relieves symptoms by reducing reflux through gravity, strengthening the LES with drug therapy, neutralizing gastric contents, and reducing intra-abdominal pressure. Specific treatments include the following:
• To reduce intra-abdominal pressure, the patient should sleep in a reverse Trendelenburg position (with the head of the bed elevated) and should avoid lying down after meals and late-night snacks as well as wearing tight-fitting clothing around the abdomen. In uncomplicated cases, positional therapy is especially useful in infants and children.

Neutralize the problem

Focus topic: Gastrointestinal Disorders

• Antacids given 1 hour and 3 hours after meals and at bedtime help control intermittent reflux. A nondiarrheal antacid containing aluminum carbonate or aluminum hydroxide (rather than magnesium) may be preferred, depending on the patient’s bowel status.
• Proton pump inhibitors are now a mainstay of therapy for GERD and erosive esophagitis. Other helpful drug treatments include metoclopramide (Reglan) and H2-blockers.
• If possible, the patient should have NG intubation for no more than 5 days because the tube interferes with sphincter integrity and itself allows reflux, especially when the patient lies flat.
• Surgery may be necessary to control severe and refractory symptoms, such as pulmonary aspiration, hemorrhage, obstruction, severe pain, perforation, incompetent LES, and associated hiatal hernia. Surgery is also preferred in some young patients with severe GERD (rather than a lifetime of pharmacologic therapy).

What to do
After surgery using a thoracic approach, follow these steps:
• Carefully watch and record chest tube drainage and respiratory status.
• If needed, give chest physiotherapy and oxygen.
• Position the patient with an NG tube in semi-Fowler’s position to help prevent reflux.
• Evaluate the patient; assess for optimal hydration and nutritional levels, diet modification, positioning, appropriate activity levels, and increased comfort as the patient complies with therapy.

Gastrointestinal Disorders

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Gastrointestinal Disorders: Hepatic encephalopathy

Focus topic: Gastrointestinal Disorders

Hepatic encephalopathy, also known as portosystemic enceph alopathy or hepatic coma, is a neurologic syndrome that develops as a complication of chronic liver disease. It commonly occurs in patients with cirrhosis, resulting primarily from cerebral ammonia intoxication. It may be acute and self-limiting or chronic and progressive. In advanced stages, the prognosis is poor despite vigorous treatment.

What causes it
Rising blood ammonia levels may result from:
• cirrhosis
• excessive protein intake
• sepsis
• constipation or GI hemorrhage, resulting in excessive accumulation of nitrogenous body wastes
• bacterial action on protein and urea to form ammonia.

Pathophysiology
Hepatic encephalopathy follows rising blood ammonia levels. Normally, the protein breakdown in the bowel is metabolized to urea in the liver. However, when portal blood shunts past the liver, ammonia directly enters the systemic circulation and is carried to the brain. Such shunting may result from the collateral venous circulation that develops in portal hypertension or from surgically created portosystemic shunts.

What to look for
Although clinical manifestations of hepatic encephalopathy vary (depending on the severity of neurologic involvement), they develop in four stages:

In the prodromal stage, early symptoms are usually overlooked because they’re subtle. They include slight personality changes (disorientation, forgetfulness, slurred speech), sleep disturbance, diminished affect, and slight tremor.

During the impending stage, tremor progresses into asterixis, the hallmark of hepatic coma. Asterixis is characterized by quick, irregular extensions and flexions of the wrists and fingers when the wrists are held out straight and the hands flexed upward. Lethargy, aberrant behavior, and apraxia also occur.

Hyperventilation occurs in the stuporous stage, and the patient is stuporous, but noisy and abusive when aroused.

In the comatose stage, signs include hyperactive reflexes, a positive Babinski’s sign, fetor hepaticus (musty, sweet breath odor), and coma.

What tests tell you
• Elevated venous and arterial ammonia levels, clinical features, and a positive history of liver disease confirm the diagnosis.
• Arterial blood gas (ABG) analysis shows respiratory alkalosis with central hyperventilation.
• EEG shows slow waves as the disease progresses.
• Other test results that suggest the disorder include elevated serum bilirubin levels and prolonged PT.

How it’s treated
• Treatment aims to improve hepatic function and correct underlying liver disease. Specific steps include the following:
• Adequate calorie intake (1,800 to 2,400 cal/day) in the form of glucose or carbohydrates helps prevent protein catabolism. Protein may be restricted to 40 g/day and advanced to up to 100 g/day as symptoms improve.
• Correction of electrolyte imbalances and management of GI bleeding are also essential.
• Effective treatment stops advancing encephalopathy by reducing blood ammonia levels. Ammonia-producing substances are removed from the GI tract by administering neomycin to suppress bacterial ammonia production, using sorbitol to induce catharsis to produce osmotic diarrhea, continuously aspirating blood from the stomach, reducing dietary protein intake, and administering lactulose to reduce blood ammonia levels.
• Potassium supplements help correct alkalosis (from increased ammonia levels), especially if the patient is taking diuretics.

Toxic cleanup

Focus topic: Gastrointestinal Disorders

• Hemodialysis may temporarily clear toxic blood. Exchange transfusions may provide dramatic but temporary improvement; however, these require a particularly large amount of blood.
• Salt-poor albumin may be used to maintain fluid and electrolyte balance, replace depleted albumin levels, and restore plasma.

What to do
• Frequently assess and record the patient’s LOC.
• Continually orient him to place and time.
• Keep a daily record of the patient’s handwriting to monitor the progression of neurologic involvement.
• Monitor intake, output, and fluid and electrolyte balance. Check daily weight and measure abdominal girth.
• Watch for and immediately report signs of anemia (decreased hemoglobin levels), infection, alkalosis (increased serum bicarbonate levels), and GI bleeding (melena, hematemesis).

• Provide the specified low-protein diet, with carbohydrates supplying most of the calories. Provide good mouth care.
• Promote rest, comfort, and a quiet atmosphere. Discourage stressful exercise.
• Protect the comatose patient’s eyes from corneal injury by using artificial tears or eye patches.
• Provide emotional support for the patient’s family in the terminal stage of hepatic coma.
• Evaluate the patient. He should have adequate hydration and intact skin. His family should have adequate support to deal with his condition.

Gastrointestinal Disorders

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