NCLEX: Gastrointestinal Disorders

Gastrointestinal Disorders: Common GI Disorders

Focus topic: Gastrointestinal Disorders

Gastrointestinal Disorders: Pancreatitis

Focus topic: Gastrointestinal Disorders

Pancreatitis — inflammation of the pancreas — occurs in acute and chronic forms and may result from edema, necrosis, or hemorrhage. The prognosis is good when pancreatitis follows biliary tract disease but poor when it’s a complication of alcoholism. Mortality reaches 60% when pancreatitis causes tissue destruction or hemorrhage.

What causes it
Most commonly caused by biliary tract disease and alcoholism, pancreatitis also results from:
• pancreatic cancer
• possibly, peptic ulcer, mumps, or hypothermia
• certain drugs, such as glucocorticoids, zidovudine (Retrovir), didanosine (Videx), sulfonamides, chlorothiazide (Diuril), and azathioprine ( Imuran)
• less commonly, from stenosis or obstruction of Oddi’s sphincter, hyperlipidemia, metabolic and endocrine disorders, vascular disease, viral infections, mycoplasmal pneumonia, or pregnancy
• iatrogenic causes, including diagnostic or therapeutic ERCP, which increases the risk of pancreatitis by 3% to 6%.

Pathophysiology
Chronic pancreatitis is a persistent inflammation that produces irreversible changes in the structure and function of the pancreas. It sometimes follows an episode of acute pancreatitis. Here’s what probably happens:
• Protein precipitates block the pancreatic duct and eventually harden or calcify.
• Structural changes lead to fibrosis and atrophy of the glands.
• Growths called pseudocysts, containing pancreatic enzymes and tissue debris, form.
• An abscess results if these growths become infected.

The acute angle

Focus topic: Gastrointestinal Disorders

Acute pancreatitis occurs in two forms:

  • edematous (interstitial), causing fluid accumulation and swelling
  • necrotizing, causing cell death and tissue damage.
    The inflammation that occurs with both types is caused by premature activation of enzymes, which causes tissue damage. Normally, the acini in the pancreas secrete enzymes in an inactive form.

Interesting theories…

Focus topic: Gastrointestinal Disorders

Two theories explain why enzymes become prematurely activated:

  • A toxic agent, such as alcohol, alters the way the pancreas secretes enzymes. This agent increases pancreatic secretion, alters the metabolism of the acinar cells, and encourages duct obstruction by causing pancreatic secretory proteins to precipitate.
  • A reflux of duodenal contents containing activated enzymes enters the pancreatic duct, activating other enzymes and setting up a cycle of more pancreatic damage.

What to look for
Steady epigastric pain centered close to the umbilicus, that radiates between the 10th thoracic and 6th lumbar vertebrae and is unrelieved by vomiting may be the first and only symptom of mild pancreatitis. A severe attack may cause:
• extreme pain
• persistent vomiting
• abdominal rigidity
• diminished bowel activity (suggesting peritonitis)
• crackles at lung bases
• left pleural effusion
• extreme malaise
• restlessness
• mottled skin
• tachycardia
• low-grade fever (100 to 102 F [37.8 to 38.9 C])
• cold, sweaty extremities
• possible ileus.

What tests tell you
• Dramatically elevated serum amylase levels — commonly more than 500 Somogyi units/dl — confirm pancreatitis and rule out perforated peptic ulcer, acute cholecystitis, appendicitis, and bowel infarction or obstruction. Dramatic elevations of amylase levels also occur in urine, ascites, and pleural fluid. Characteristically, amylase levels return to normal 48 hours after the onset of pancreatitis, despite continuing signs and symptoms.
• Serum lipase levels are increased but rise more slowly than serum amylase levels.
• Serum calcium levels are low from fat necrosis and formation of calcium soaps.

• Glucose levels are elevated and may be as high as 900 mg/dl, indicating severe hyperglycemia.
• WBC counts range from 8,000 to 20,000/μl, with increased polymorphonuclear leukocyte levels.
• Hematocrit occasionally exceeds 50% concentrations.
• Abdominal X-rays may show dilation of the small or large bowel or calcification of the pancreas.
• A GI series indicates extrinsic pressure on the duodenum or stomach caused by edema of the pancreas head.
• An ultrasound isn’t usually helpful in providing diagnosis because the pancreas is poorly visualized.
• An abdominal CT scan can help distinguish between cholelithiasis and pancreatitis.

How it’s treated
Treatment must maintain circulation and fluid volume, relieve pain, and decrease pancreatic secretions.
• Emergency treatment for shock (the most common cause of death in early-stage pancreatitis) consists of vigorous I.V. replacement of electrolytes and proteins. Metabolic acidosis secondary to hypovolemia and impaired cellular perfusion requires vigorous fluid volume replacement.
• Hypocalcemia requires infusion of 10% calcium gluconate; s er um glucose levels greater than 300 mg/dl require insulin therapy.
• After the emergency phase, continuing I.V. therapy for 5 to 7 days should provide adequate electrolytes and protein solutions that don’t stimulate the pancreas.

Whenever you’re ready…

Focus topic: Gastrointestinal Disorders

• If the patient isn’t ready to resume oral feedings by then, he may need TPN.
• Nonstimulating elemental gavage feedings may be safer because of the decreased risk of infection and overinfusion.
• In extreme cases, the patient may require laparotomy to drain the pancreatic bed, 95% pancreatectomy, or a combination of cholecystostomy-gastrostomy, feeding jejunostomy, and drainage.

What to do
• Give plasma or albumin, if ordered, to maintain blood pressure.
• Record fluid intake and output, check urine output hourly, and monitor electrolyte levels.
• For bowel decompression, maintain constant NG suctioning and give nothing by mouth. Perform good mouth and nose care.
• Watch for signs of calcium deficiency — tetany, cramps, carpopedal spasm, and seizures. If you suspect hypocalcemia, keep airway and suction apparatus handy and pad the side rails.

• Administer analgesics as needed to relieve the patient’s pain and anxiety.

A case of dry mouth

Focus topic: Gastrointestinal Disorders

• Don’t confuse thirst caused by hyperglycemia (indicated by serum glucose levels of up to 350 mg/dl and glucose and acetone in urine) with dry mouth caused by NG intubation and anticholinergics.
• Watch for complications due to TPN, such as sepsis, hypokalemia, overhydration, and metabolic acidosis.
• Evaluate the patient. He should have normal nutrition and hydration levels, balanced electrolyte levels, and an improved comfort level. He also should understand the need for lifestyle modifications and adjust lifestyle factors that aggravate his disease.

Gastrointestinal Disorders

Gastrointestinal Disorders: Peptic ulcers

Focus topic: Gastrointestinal Disorders

Appearing as circumscribed lesions in the gastric mucosal membrane, peptic ulcers can develop in the lower esophagus, stomach, pylorus, duodenum, or jejunum from contact with gastric juice (especially hydrochloric acid and pepsin). About 80% of all peptic ulcers are duodenal ulcers.

What causes it
The precise cause of peptic ulcer is unknown but may include:
• H. pylori infection
• use of NSAIDs or salicylates
• inadequate protection of mucous membranes
• pathologic hypersecretory disorders.

Factor it in

Focus topic: Gastrointestinal Disorders

Factors that predispose a person to peptic ulcer include:
• blood type (gastric ulcers and type A; duodenal ulcers and type O) and other genetic factors
• exposure to irritants, such as alcohol, coffee, and tobacco
• emotional stress
• physical trauma
• normal aging.

Pathophysiology
In a peptic ulcer due to H. pylori, acid adds to the effects of the bacterial infection. H. pylori releases a toxin that destroys the stomach’s mucus coat, promoting mucosal inflammation and ulceration. Salicylates and other NSAIDs encourage ulcer formation by inhibiting the secretion of prostaglandins (substances that block ulceration).

What to look for
Patients with duodenal ulcers may experience attacks about 2 hours after meals, whenever the stomach is empty, or after consuming orange juice, coffee, aspirin, or alcohol. Exacerbations tend to recur several times a year, then fade into remission. Such patients may report heartburn and localized midepigastric pain, which is relieved after eating.

Gastrointestinal Disorders

What tests tell you
• Upper GI tract X-rays show abnormalities in the mucosa.
• Gastric secretory studies show hyperchlorhydria.
• Upper GI endoscopy confirms the presence of an ulcer.
• Serologic or breath urea test shows presence of H. pylori.
• Biopsy rules out cancer.
• Stool may test positive for occult blood.

How it’s treated
Treatment is essentially symptomatic and emphasizes drug therapy and rest:
• Antacids reduce gastric acidity. Proton pump inhibitors, such as omeprazole (Prilosec) or lansoprazole (Prevacid), or H2-receptor antagonists, such as cimetidine (Tagamet) or ranitidine (Zantac), reduce gastric secretion in short-term therapy (up to 8 weeks).
• Anticholinergics, such as propantheline, inhibit the vagus nerve effect on the parietal cells and reduce gastrin production and excessive gastric activity in duodenal ulcers.
• Physical rest promotes healing.
• Gastroscopy can promote coagulation of the bleeding site by cautery or laser therapy.
• If GI bleeding occurs, emergency treatment begins with passage of an NG tube to allow for iced saline lavage, possibly containing norepinephrine. Sclerotherapy with epinephrine is used to ligate active vessels. Angiography assists placement of an intra-arterial catheter, followed by infusion of vasopressin to constrict blood vessels and control bleeding. This type of therapy allows postponement of surgery until the patient’s condition stabilizes.
• Surgery is indicated for perforation unresponsive to conservative treatment and suspected cancer. Surgical procedures for peptic ulcers include vagotomy and pyloroplasty or distal subtotal gastrectomy.

What to do
• Administer medications as ordered, and watch for adverse effects of cimetidine (dizziness, rash, mild diarrhea, muscle pain, leukopenia, and gynecomastia) and anticholinergics (dry mouth, blurred vision, headache, constipation, and urine retention). Anticholinergics are usually most effective when given 30 minutes before meals. Give sedatives and tranquilizers as needed.

• Evaluate the patient. After successful treatment for peptic ulcers, he should understand the disease process and comply with the treatment regimen. He should recognize the need to avoid factors that may exacerbate his condition and modify his diet and lifestyle to do so. He should also understand the need for followup care and know when to seek immediate attention.

Gastrointestinal Disorders

Gastrointestinal Disorders: Peritonitis

Focus topic: Gastrointestinal Disorders

An acute or chronic inflammation, peritonitis may extend throughout the peritoneum, the membrane that lines the abdominal cavity and covers the visceral organs, or it may be localized as an abscess. Peritonitis commonly reduces intestinal motility and causes intestinal distention with gas. Mortality is 10%. Death usually results from sepsis and progressive organ faiure.

What causes it
• Peritonitis results from bacterial inflammation due to a ruptured appendix, perforated bowel, a strangulated obstruction, an abdominal neoplasm, or a stab wound.
• It may also result from chemical inflammation, as in ruptured fallopian tubes or bladder, perforated gastric ulcer, or released pancreatic enzymes.

Pathophysiology
Although the GI tract normally contains bacteria, the peritoneum is sterile. When bacteria or chemical irritants invade the peritoneum because of inflammation and perforation of the GI tract, peritonitis results. In chemical and bacterial inflammation, accumulated fluids containing protein and electrolytes make the transparent peritoneum opaque, red, inflamed, and edematous. Because the peritoneal cavity is so resistant to contamination, infection is commonly localized as an abscess.

What to look for
The main symptom of peritonitis is sudden, severe, diffuse abdominal pain that tends to intensify and localize in the area of the underlying disorder. Also assess the patient for:
• weakness, pallor, excessive sweating, and cold skin
• decreased intestinal motility and paralytic ileus
• abdominal distention
• an acutely tender abdomen associated with rebound tenderness
• shallow breathing

• diminished movement by the patient to minimize pain
• hypotension, tachycardia, and signs of dehydration
• fever of 103° F (39.4° C) or higher
• possible shoulder pain and hiccups.

What tests tell you
• Abdominal X-rays showing edematous and gaseous distention of the small and large bowel support the diagnosis. With perforation of a visceral organ, the X-ray shows air in the abdominal cavity.
• Chest X-rays may show an elevated diaphragm.
• Blood studies show leukocytosis (more than 20,000 leukocytes/μl).
• Paracentesis reveals bacteria, exudate, blood, pus, or urine.
• Laparotomy may be necessary to identify the underlying cause.

How it’s treated
Early treatment of GI inflammatory conditions and preoperative and postoperative antibiotic therapy prevent peritonitis. After peritonitis develops, emergency treatment aims to stop infection, restore intestinal motility, and replace fluids and electrolytes:
• Massive antibiotic therapy usually includes administration of cephalosporins with an aminoglycoside according to the infecting organisms. Quinolones may also be used.
• To decrease peristalsis and prevent perforation, the patient should be given nothing by mouth and should receive supportive fluids and electrolytes parenterally.
• Supplementary treatment measures include preoperative and postoperative analgesics, such as meperidine; NG intubation to decompress the bowel; and possible use of a rectal tube to help passage of flatus.
• When peritonitis results from perforation, surgery is performed as soon as the patient can tolerate it. Surgery aims to eliminate the infection source by evacuating the spilled contents and inserting drains.
• Occasionally, paracentesis may be needed to remove accumulated fluid.
• Irrigation of the abdominal cavity with antibiotic solutions during surgery may be appropriate.

What to do
• Regularly monitor vital signs, fluid intake and output, and the amount of NG drainage or vomitus.
• Place the patient in semi-Fowler’s position to help him deepbreathe with less pain, which helps to prevent pulmonary complications.

Evacuation procedures

Focus topic: Gastrointestinal Disorders

After surgery to evacuate the peritoneum:
• Watch for signs and symptoms of dehiscence (the patient may complain that “something gave way”) and abscess formation (continued abdominal tenderness and fever).
• Frequently assess peristaltic activity by listening for bowel sounds and checking for gas, bowel movements, and a soft abdomen.
• When peristalsis returns and temperature and pulse rate are normal, gradually decrease parenteral fluids and increase oral fluids. If the patient has an NG tube in place, clamp it for short intervals. If neither nausea nor vomiting results, begin oral fluids as ordered and tolerated.
• Evaluate the patient by assessing for normal fluid and electrolyte balance, normal body temperature and WBC count, lack of bowel obstruction or other complications, and normal oral intake and bowel elimination patterns.

Gastrointestinal Disorders

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Gastrointestinal Disorders: Ulcerative colitis

Focus topic: Gastrointestinal Disorders

An inflammatory, typically chronic disease, ulcerative colitis affects the mucosa and submucosa of the colon. It usually begins in the rectum and sigmoid colon and commonly extends upward into the entire colon. It rarely affects the small intestine, except for the terminal ileum. Severity ranges from a mild, localized disorder to a fulminant disease that may cause a perforated colon, progressing to potentially fatal peritonitis and toxemia.

What causes it
The cause of ulcerative colitis is unknown. Risk factors include a family history of the disease; bacterial infection; allergic reaction to food, milk, or other substances that release inflammatory histamine in the bowel; overproduction of enzymes that break down the mucous membranes; and emotional stress. Autoimmune disorders, such as rheumatoid arthritis, hemolytic anemia, erythema nodosum, and uveitis, may heighten the risk.

Pathophysiology
Ulcerative colitis damages the large intestine’s mucosal and submucosal
layers. Here’s how it progresses:

  • Usually, the disease originates in the rectum and lower colon. Then it spreads to the entire colon.
  • The mucosa develops diffuse ulceration with hemorrhage, congestion, edema, and exudative inflammation. Unlike Crohn’s disease, ulcerations are continuous.
  • Abscesses formed in the mucosa drain purulent pus, become necrotic, and ulcerate.
  • Sloughing occurs, causing bloody, mucus-filled stools.

Close-up on the colon

Focus topic: Gastrointestinal Disorders

As ulcerative colitis progresses, the colon undergoes changes:

  • Initially, the colon’s mucosal surface becomes dark, red, and velvety.
  • Abscesses form and coalesce into ulcers.
  • Necrosis of the mucosa occurs.
  • As abscesses heal, scarring and thickening may appear in the bowel’s inner muscle layer.
  • As granulation tissue replaces the muscle layer, the colon narrows, shortens, and loses its characteristic pouches (haustral folds).

What to look for
Recurrent bloody diarrhea and symptom-free remissions are the hallmarks of ulcerative colitis. The stool typically contains pus and mucus. Assess the patient for other signs and symptoms, such as:
• spastic rectum and anus
• abdominal pain
• irritability
• weight loss
• weakness
• anorexia
• nausea and vomiting
• fever
• occasional constipation (in elderly patients).

What tests tell you
• Sigmoidoscopy shows increased mucosal friability, decreased mucosal detail, and thick inflammatory exudate. Biopsy during sigmoidoscopy helps confirm the diagnosis.
• Colonoscopy helps determine the extent of disease and evaluate strictured areas, pseudopolyps, and precancerous changes.
• A barium enema helps to assess the extent of the disease and to detect complications, such as strictures and carcinoma.
• A stool specimen may reveal leukocytes, ova, and parasites.
• The ESR will be increased in proportion to the severity of the attack.
• Decreased serum levels of potassium, magnesium, hemoglobin, and albumin as well as leukocytosis and increased PT support the diagnosis.

How it’s treated
Treatment seeks to control inflammation, replace nutritional losses and blood volume, and prevent complications.
• Supportive treatment includes bed rest, I.V. fluid replacement, and a clear liquid diet.
• For a patient awaiting surgery or showing signs of dehydration and debilitation from excessive diarrhea, TPN is administered to rest the intestinal tract, decrease stool volume, and restore positive nitrogen balance. The patient may also need blood transfusions or iron supplements to correct anemia.
• Drug therapy to control inflammation includes adrenocorticotropic hormone and adrenal corticosteroids, such as prednisone, prednisolone (Prelone), hydrocortisone (Cortef), and budesonide (Entocort EC).
• If disease is limited to the left side of the colon, topical mesalamine suppositories or enemas or hydrocortisone enemas may be effective.
• Sulfasalazine and mesalamine (Asacol), which have antiinflammatory and antimicrobial properties, may also be used.

Don’t spaz out

  • Antispasmodics, such as tincture of belladonna, and antidiarrheals, such as diphenoxylate, are used only for patients whose ulcerative colitis is under control but who have frequent, troublesome diarrheal stools. These drugs may precipitate massive dilation of the colon (toxic megacolon) and are usually contraindicated.
  • Immunomodulatory agents, such as azathioprine and 6-mercaptopurine, may be effective for patients who have frequent flareups of symptoms despite continuous steroid therapy. Patients with severe disease have also been treated with cyclosporine.These medications require careful monitoring along with serial CBC with differential counts.
  • Surgery is the treatment of last resort if the patient has toxic megacolon, fails to respond to drugs and supportive measures, or finds symptoms unbearable. The most common surgical technique is proctocolectomy with ileostomy. Total colectomy with ileorectal anastomosis is done less often because of its associated mortality (2% to 5%).
  • In pouch ileostomy, a pouch is created from a small loop of the terminal ileum and a nipple valve formed from the distal ileum. The resulting stoma opens just above the pubic hairline; the pouch empties through a catheter inserted in the stoma several times each day.
  • Colectomy to prevent colon cancer is controversial in treatment for ulcerative colitis.

Gastrointestinal Disorders

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