Gastrointestinal Problems

Question 1

Functions of the GI system

Answer 1

• process food substances
• absorb the products of digestion into the blood
• excrete unabsorbed materials
• provide an environment for microorganisms to synthesize nutrients, such as vit K.

Question 2

Stomach

Answer 2

• contains the cardia, fundus, body, and pylorus.
• hydrochloric acid kills microorganisms, breaks food into small particles, and provides a chemical environment that facilitates gastric enzyme activation.
• pepsin is the chief coenzyme of gastric juice, which converts proteins into proteoses and peptones,
• intrinsic factor comes from parietal cells and is necessary for the absorption of vit B12.
• gastrin controls gastric acidity.

Question 3

Small and large intestine

Answer 3

• the duodenum contains the openings of the bile and pancreatic ducts; small intestine terminates in the cecum.
• large: absorbs water and eliminates wastes; intestinal bacteria play a vital role in the synthesis of some B vitamins and vit K; the ileocecal valve prevents contents of the large intestine from entering the ileum.

Question 4

Pancreatic intestinal juice enzymes

Answer 4

• amylase digests starch to maltose.
• maltase reduces maltose to monosaccharide glucose.
• lactase splits lactose into galactose and glucose.
• sucrase reduces sucrose to fructose and glucose.
• nucleases split nucleic acids to nucleotides.
• enterokinase activates trypsinogen to trypsin.

Question 5

Liver

Answer 5

• largest gland in the body.
• contains Kupffer cells, which remove bacteria in the portal blood.
• synthesizes glucose, amino acids, and fats.
• aids in the digestion of fats, carbohydrates, and proteins.
• stores and filters blood (200-400ml of blood)
• secretes bile to emulsify fats (500-1000ml of bile/day).
• hepatic ducts: deliver bile to the gallbladder via the cystic duct and to the duodenum via the common bile duct.

Question 6

Gallbladder

Answer 6

• stores and concentrates bile and contracts to force bile into the duodenum during the digestion of fats,
• the sphincter of Oddi is located at the entrance to the duodenum.
• the presence of fatty materials in the duodenum stimulates the liberation of cholecystokinin, which causes contraction of the gallbladder and relaxation of the sphincter of Oddi.

Question 7

Pancreas

Answer 7

• exocrine gland: secretes sodium bicarbonate to neutralize the acidity of the stomach contents that enter the duodenum; pancreatic juices contain enzymes for digesting carbohydrates, fats, and proteins.
• endocrine gland: secretes glucagon to raise blood glucose levels and secretes somatostatin to exert a hypoglycemic effect; the islets of Langerhans secrete insulin; insulin is secreted into the bloodstream and is important for carbohydrate metabolism.

Question 8

Diagnostic Procedures: Upper GI Tract Study

Answer 8

• examination of the upper GI tract under fluoroscopy after the client drinks barium sulfate.
• preprocedure: withhold foods and fluid for 8h prior to the test.
• postprocedure: a laxative may be prescribed; increase oral fluid intake to help pass the barium; monitor stools for the passage of barium (appear chalky white for 24 to 72h) because barium can cause a bowel obstruction.

Question 9

Diagnostic Procedures: Capsule Endoscopy

Answer 9

• a procedure that uses a small wireless camera shaped like a med capsule that the client swallows; the test will detect bleeding or changes in the lining of the small intestine.
• the camera travels through the entire digestive tract and sends pictures to a small box that the client wears like a belt.
• preprocedure: a bowel preparation will be prescribed; the client will need to maintain a clear liquid diet on the evening before the exam; additionally, NPO status is maintained for 3h before and after swallowing the capsule.

Question 10

Diagnostic Procedures: Gastric Analysis

Answer 10

• requires the passage of a NG tube into the stomach to aspirate gastric contents for the analysis of acidity (pH), appearance, and volume.
• the entire gastric contents are aspirated, and then specimens are collected every 15 min for 1h.
• histamine or pentagastrin may be adm SC to stimulate gastric secretions.
• esophageal reflux may be diagnosed; a probe is placed just above the the lower esophageal sphincter and connected to an external recording device, which provides a computer analysis and graphic display of results.
• preprocedure: fasting for at least 12h, use of tabacco and chewing gun is avoided for 24-48h.
• postprocedure: may resume normal activities; refrigerate gastric samples if not tested within 4h.

Question 11

Diagnostic Procedures: Upper GI endoscopy

Answer 11

• following sedation, an endoscope is passed down the esophagus to view the gastric wall, sphincters, and duodenum; tissue specimens can be obtained.
• prepro: NPO for 6-8h; local anesthetic (spray or gargle) is adm along with med that provides moderate sedation.
• client is positioned on the left side to facilitate saliva drainage and to provide easy access of the endoscope.
• airway patency is monitored and emergency equipment should be readily available.
• postpro: NPO until gag reflex returns (1-2h); monitor for signs of perforation and maintain bed rest for the sedated client until alert.

Question 12

Diagnostic Procedures: Fiberoptic Colonoscopy

Answer 12

• study in which the linning of the intestine is visually examined; biopsies and polypectomies can be performed.
• client is positioned on the left side with knees drawn up to the chest.
• prepro: cleansing of the colon is necessary; a clear liquid diet is started ont he day before and NPO should start 4-6h prior the test (avoid red, orange and purple liquids).

Question 13

Diagnostic Procedures: Endoscopic retrograde cholangiopancreatography (ERCP)

Answer 13

• examination of the hepatobiliary system is performed via a flexible endoscope inserted into the esophagus to the descending duodenum.
• prepro: NPO 6-8h and moderate sedation during.
• postpro: monitor VS, return of gag reflex, and signs of perforation or peritonitis.

Question 14

Diagnostic Procedures: Magnetic resonance cholangiopancreatography (MRCP)

Answer 14

• uses magnetic resonance to visualize the biliary and pancreatic ducts in a noninvasive way.
• pre and postprocedure: same as ERCP.

Question 15

Diagnostic Procedures: Computed tomography (CT) Scan

Answer 15

• noninvasive cross-sectional view that can detect tissue densities in the abd, including in the liver, spleen, pancreas, and biliary tree.
• can be performed with or without contrast medium.
• prepro: NPO for at least 4h.
• postpro: no specific care.

Question 16

Diagnostic Procedures: Paracentesis

Answer 16

• prepro: informed consent; obtain VS and weight; void; position upright.
• during: assist PHCP; monitor VS; and provide comfort.
• postpro: weigh the client maintain bed rest; measure fluid collected, describe, and record; label and send to lab; apply a dry sterile dressing to the insertion site and monitor for bleeding; monitor for hypovolemia, electrolyte loss, mental status changes, or encephalopathy, and hematuria.
• the rapid removal of fluid from the abd cavity during paracentesis leads to decreased abd presure, which can cause vasodilation and resultant shock; therefore, HR and BP must be monitored closely.

Question 17

Diagnostic Procedures: Liver Biopsy

Answer 17

• a needle is inserted through the abd wall to the liver to obtain a tissue sample for biopsy and microscopic examination.
• prepro: assess results of coagulation tests; adm sedative; place client in the supine or left lateral position during the procedure to expose the right side of the upper abd.
• postpro: assess VS and site for bleeding; monitor for peritonitis; maintain bed rest for several hours; place the client on the right side with a pillow under the costal margin for 2h to decrease the risk of bleeding, and instruct the client to avoid coughing and straining; avoid heavy lifting and strenuous exercise for 1 week.

Question 18

Diagnostic Procedures: Stool specimens

Answer 18

• includes inspecting the specimen for consistency, color, and occult blood.
• tests for fecal urobilinogen, fat, nitrogen, parasites, pathogens, food substances, and other substances may be performed.
• quantitative 24-72h collections must be kept refrigerated until taken to the lab.
• some specimens require that a certain diet be followed or that certain meds be withheld.

Question 19

Diagnostic Procedures: Urea breath test

Answer 19

• detects the presence of Heliobacter pylori, the bacteria that cause peptic ulcer disease.
• client consumes a capsule of carbon-labeled urea and provides a breath sample 10-20 min later.
• certain meds may need to be avoided:
  = antibiotics and bismuth subsalicylate for 1 month before the test;
  = sucralfate and omeprazole for 1 week before;
  = cimetidine, famotidine, ranitidine, and nizatidine for 24h before.
• H.pylori can also be detected by assessing serum antibody levels.

Question 20

Diagnostic Procedures: Esophageal pH testing for gastroesophageal reflux disease

Answer 20

• used to diagnose or evaluate the treatment for heartburn or reflux disease.
• a probe is inserted into the nostril and is situated in the esophagus.
• pH is tested over a period of 24-48h.

Question 21

Diagnostic Procedures: Liver and pancreas lab studies

Answer 21

• liver enzyme levels are elevated with liver damage or bilary obstruction.
  = ALP 38-126 U/L
  = AST 0-35 U/L
  = ALT 4-36 U/L
• prothrombin time is prolonged with liver damage.
  = normal: 11-12.5 seconds
• serum ammonia level assesses the ability of the liver to deaminate protein byproducts.
  = normal: 10-80 mcg/dL
• an increase in cholesterol level indicates pancreatitis or biliary obstruction.
  = normal: < 200mg/dL
• an increase in bilirubin level indicates liver damage or biliary obstruction.
  = total 0.3-1.0 mg/dL
  = indirect 0.2-0.8 mg/dL
  = direct 0.1-0.3 mg/dL
• increased values for amylase and lipase levels indicate pancreatitis.
  = amylase 60-120 su/dL
  = lipase 0-160 U/L

Question 22

Gastroesophageal Reflux Disease

Answer 22

• backflow of gastric and duodenal contents into the esophagus; caused by an incompetent lower esophageal sphincter (LES), pyloric stenosis, or motility disorder.
• assessment: heartburn, epigastric pain, dyspepsia, nausea, regurgitation, pain, difficulty with swallowing, hypersalivation.
• interventions: avoid factors that decrease LES pressure or cause esophageal irritation, such as peppermint, chocolate, coffee, fried or fatty foods, carbonated beverages, alcoholic beverages, and cigarette smoking; eat a low-fat, high-fiber diet and to avoid eating or drinking 2h before bedtime (also elevate head of bed 15-30cm); avoid the use of anticholinergics, which delay sstomach emptying; also NSAIDs and other meds that contain AAS need to be avoided; instruct client regarding prescribed meds such as antacids, H2-receptor antagonists, proton pump inhibitors, and prokinetic meds (which accelerate gastric emptying).
• surgery may be required in extreme cases.

Question 23

Gastritis: description and assessment

Answer 23

• inflammation of the stomach or gastric mucosa.
• acute gastritis is caused by the ingestion of food contaminated with disease-causing microorganisms or food that is irritating or too highly seasoned, the overuse of aspirin or other NSAIDs, excessive alcohol intake, bile-reflux, or radiation therapy.
• chronic gastritis is caused by benign or malignant ulcers or by the bacteria H.pylori, and also may be caused by autoimmune diseases, dietary factors, meds alcohol, smoking, or reflux.
  Assessment:
• acute: abd discomfort, anorexia, nausea, vomiting, headche, hiccupping, reflux.
• chronic: anorexia, nausea, vomiting, belching, heartburn after eating, sour taste in the mouth, vit B12 deficiency.

Question 24

Gastritis: interventions

Answer 24

• acute: food and fluids may be withheld until symptoms subside; afterward, ice chips can be given, followed by clear liquids, and then solid food.
• monitor for signs of hemorrhagic gastritis.
• avoid irritating foods, fluids, and other substances, such as spicy and highly seasoned foods, caffeine, alcohol, and nicotine.
• instruct the use of ATB for H.pylori and information about vit B12 injections if a deficiency is present.

Question 25

Peptic Ulcer Disease

Answer 25

• is an ulceration in the mucosal wall of the stomach, pylorus, duodenum, or esophagus in portions accessible to gastric secretions; erosion may extend through the muscle.
• may be referred to as gastric, duodenal, or esophageal, depending on its location.

Question 26

Gastric Ulcers

Answer 26

• involves ulceration of the mucosal lining that extends to the submucosal layer of the stomach.
• predisposing factors: stress, smoking, use of corticosteroids, NSAIDs, alcohol, history of gastritis, family history of gastric ulcers, or infection with H.pylori.
• complications: hemorrhage, perforation, and pyloric obstruction.
• assessment: sharp pain in or to the left of the midepigastric region occurs 30-60 min after a meal (food ingestion accentuates the pain); hematemesis is more common than melena.
• interventions: adm small, frequent bland feedings during the active phase; adm H2-receptor antagonists or proton pump inhibitors (to decrease the secretion of gastric acid), antacids (to neutralize gastric secretions), anticholinergics (to reduce gastric motility), mucosal barrier protectants (1h before each meal), prostaglandins (protective and antisecretory actions) as prescribed; avoid alcohol, caffeine, and chocolate, smoking, aspirin or NSAIDs, and reduce stress.
• during active bleeding maintain NPO status and adm IV fluids.

Question 27

Gastric Ulcers: Surgical Interventions

Answer 27

• total gastrectomy
• vagotomy
• gastric resection
• gastroduodenostomy (Billroth I)
• gastrojejunostomy (Billroth II)
• Pyloroplasty
• postop interventions: fowler’s position, monitor NG suction, maintain NPO status for 1-3 days until peristalsis returns; progress diet from NPO to sips of clear water to 6 small meals a day; monitor for complications (hemorrhage, dumping syndrome, diarrhea, hypoglycemia, and vit B12 deficiency).

Question 28

Duodenal ulcers

Answer 28

• is a break in the mucosa of the duodenum.
• risk factors and causes: infection with H.pylori; alcohol intake; smoking; stress; caffeine; and the use of aspirin, corticosteroids, and NSAIDs.
• complications: bleeding, perforation, gastric outlet obstruction, and intractable disease.
• assessment: burning pain occurs in the midepigastric area 1.5-3h after a meal and during the night; melena is more common than hematemesis; pain is often relieved by the ingestion of food.
• interventions: - instruct bland diet, with small, frequent meals; avoid smoking, alcohol, caffeine, use of aspirin, corticosteroids, and NSAIDs; adm antacids, H2-receptor or proton pump inhibitors as prescribed.
• surgery is performed only if the ulcer is unresponsive to meds or if hemorrhage, obstruction, or perforation occurs.

Question 29

Dumping Syndrome

Answer 29

• the rapid emptying of the gastric contents into the small intestine that occurs following gastric resection.
• assessment: symptoms occurring 30 min after eating, nausea, vomiting, feelings of abd fullness and cramping, diarrhea, palpitations and tachycardia, perspiration, weakness and dizziness, borborygmi (loud gurgling sounds resulting from bowel hypermotility).
• client education: avoid sugar, salt, and milk; eat a high-protein, high-fat, low-carbohydrate diet; eat small meals and avoid consuming fluids with meals; lie down after meals; take antispasmodic meds as prescribed to delay gastric emptying.

Question 30

Bariatric Surgery

Answer 30

• surgical reduction of gastric capacity or absorption ability that may be performed on a client with morbid obesity to produce long-term weight loss.
• obese clients are at increased risk for pulmonary and thromboembolic complications and death.
• surgery can prevent complications of obesity and the client needs to agree to modify their lifestyle, lose weight and the weight off, and obtain support from available community resources.
• types: vertical banded gastroplasty; gastric banding; vertical sleeve gastroplasty; bilopancreatic diversion with duodenal switch; roux-en-Y gastric bypass.
• postop interventions: similar to abd surgery; start with clear liquids (as tolerated and after bowel sounds return and client passes flatus), followed by pureed foods, juices, thin soups, and milk 24-48h after clear fluids are tolerated ( the diet is usually limited to liquids or pureed foods for 6 weeks).

Question 31

Hiatal Hernia

Answer 31

• a portion of the stomach herniates through the diaphragm and into the thorax; results from weakening of the muscles and is aggravated by factors that increase abd pressure such as pregnancy, ascites, obesity, tumors, and heavy lifting.
• complications include ulceration, hemorrhage, regurgitation and aspiration of stomach contents, strangulation, and incarceration of the stomach in the chest with possible necrosis, peritonitis, and mediastinitis.
• assessment: heartburn, regurgitation or vomiting, dysphagia, feeling of fullness.
• interventions: small frequent meals and limit the amount of liquids taken with meals, advise not to recline for 1h after eating, avoid anticholinergics.

Question 32

Cholecystitis: description and assessment

Answer 32

• inflammation of the gallbladder (may be acute or chronic process); acute is associated with gallstones; chronic results when inefficient bile emptying and gallbladder muscle wall disease cause a fibrotic and contracted gallbladder.
• acalculous cholecystitis occurs in the absence of gallstones and is caused by bacterial invasion via the lymphatic or vascular system.
• assessment: nausea, vomiting, indigestion, belching, flatulence, epigastric pain that radiates to the right shoulder or scapula, pain the the right upper quadrant, murphy’s sign, elevated temp, tachycardia, and signs of dehydration.
• biliary obstruction: jaundice, dark orange and foamy urine, steatorrhea and clay-colored feces, pruritus.

Question 33

Cholecystitis: interventions

Answer 33

• maintain NPO status during nausea and vomiting episodes and NG decompression for severe vomiting.
• adm antiemetics, analgesics, antispasmodics (anticholinergics).
• eat small, low-fat meals and avoid gas-forming foods.
• surgical: cholecystectomy and choledocholithotomy (requires incision into the common bile duct to remove the stone).

Question 34

Cirrhosis

Answer 34

• a chronic, progressive disease of the liver characterized by diffuse degeneration and destruction of hepatocytes; repeated destruction of hepatic cells causes the formation of scar tissue.
• cirrhosis has many causes and is due to chronic damage and injury to liver cells; the most common are chronic HepC, alcoholism, nonalcoholic fatty disease, and nonalcoholic steatohepatitis.
• complications: portal hypertension (develops as a result of obstruction to flow); ascites (accumulation of fluid in the peritoneal cavity); bleeding esophageal varices; coagulation defects; jaundice (because liver is unable to metabolize bilirrubin); portal systemic encephalopathy; hepatorenal syndrome.

Question 35

Cirrhosis: interventions

Answer 35

• elevate the head of the bed
• if ascites and edema are absent, provide a high-protein diet supplemented with vitamins.
• provide B complex, vit A, C, K, and folic acid; and thiamine as prescribed.
• restrict sodium and fluid intake, initiate enteral or parenteral nutrition as prescribed.
• adm diuretics, monitor intake and output.
• weigh client and measure abd girth daily.
• monitor level of consciousness.
• monitor for asterixis and fetor hepaticus.
• maintain gastric intubation to assess bleeding.
• adm blood products, antacids, lactulose, ATB as prescribed.
• avoid meds such as opioids, sedatives, and barbiturates and any hepatotoxic meds or substances.
• prepare for paracentesis.

Question 36

Esophageal Varices

Answer 36

• dilated and tortuous veins in the submucosa or the esophagus.
• caused by portal hypertension, often associated with liver cirrhosis; are at risk for rupture if portal circulation pressure rises (emergency).
• goal of treatment is to control bleeding, prevent complications, and prevent the recurrence of bleeding.
• assessment: hematemesis, melena, ascites, jaundice, hepatomegaly and splenomegaly, dilated abd veins, signs of shock.
• interventions: elevate the head of the bed; monitor for orthostatic hypotension, lung sounds, level of consciousness, Hb and Ht; adm O2; maintain NPO status; adm fluids, blood or clotting factors as prescribed; assist inserting of an NG tube or a balloon tamponade; avoid activities that will initiate vasovagal responses; prepare for endoscopic procedure.

Question 37

Esophageal Varices: endoscopic injection (sclerotherapy)

Answer 37

• the procedure involves the injection of a sclerosing agent into and around bleeding varices.
• complications include chest pain, pleural effusion, aspiration pneumonia, esophageal stricture, and perforation of the esophagus.

Question 38

Esophageal Varices: endoscopic variceal ligation

Answer 38

• the procedure involves ligation of the varices with an elastic rubber band.
• sloughing, followed by supperficial ulceration, occurs in the area of ligation within 3-7 days.

Question 39

Esophageal Varices: shunting procedures

Answer 39

• shunt blood away from the esophageal varices.
• portacaval shunting involves anastomosis of the
  portal vein to the inferior vena cava, diverting blood from the portal system to the systemic circulation.
• distal splenorenal shunt: shunt involves anastomosis of the splenic vein to the left renal vein; the spleen conducts blood from the high-pressure varices to the low-pressure renal vein.
• mesocaval shunting involves a side anastomosis of the superior mesenteric vein to the proximal end of the inferior vena cava.
• transjugular intrahepatic portosystemic shunt (TIPS): this procedure uses the normal vascular anatomy of the liver to create a shunt with the use of a metallic stent; the shunt is between the portal and systemic venous system in the liver and is aimed at relieving portal hypertension.