GI disorders review GERD

1. GERD is exacerbated in the night time and client should avoid eating in

the night time (like 2 to 3 hrs before).

2. Heartburn (pyrosis) and regurgitation are frequent symptoms of GERD.

3. The client should elevate the head of the bed on blocks to keep gastric acid in the stomach and prevent reflux into the esophagus. 4. Client should eat small, frequent meals and limit fluids with meals to prevent reflux into the esophagus. 5. Clients should avoid alcohol, peppermint, chocolate, spicy, acidic (orange juice, tomatoes, etc), milk, high fat foods. 6. Adult-onset asthma is caused by GERD.
7. Barretts esophagus is a complication of GERD; this is a precursor to

esophageal cancer. 8. Eructation is belching, a symptom of GERD. 9. Water brash is hypersalivation and flatulence is gas all symptoms of GERD. 10. PPI drugs esomeprazole (Nexium) decrease stomach acid production. Promotility drugs metoclopramide (Reglan) increase the rate of gastric emptying. Cryoprotective drugs medications such as sucralfate (Carafate) protect the stomach by creating a mucosal barrier. Antacids neutralize stomach acid by increasing the pH acid (over 3.5). 11. All zoles are proton pump inhibitors.

12. All antacids should be given 1 3 hrs after meal and at bedtime with

water or milk. 13. Histamine 2 receptors antagonists, the dines should be administered 1 hr apart from antacids.
14. Cimetidine (Tagamet) should be administered slowly (IV); IV

administration can cause hypotension and dysrhythmias.

15. Cimetidine crosses the blood brain barrier causing CNS side effects. 16. Food slows the absorption of Cimetidine. Ranitidine (Zantac) is not affected by food. Zantac by IV administration should be administered slowly with NS. The other dines do not need to be administered by food.
17. Misoprostol (Cytotec) is administered with meals; Sucralfate (Carafate)

is administered on an empty stomach. 18. Cytotec should be avoided when pregnant and Mg-containing antacids should be avoided as well. 19. Prilosec, a PPI should be taken before breakfast and dairy should be avoided. Pregnant women and patients with liver problems should avoid this.

HIATAL HERNIA
1. HH is a herniation of a portion of the stomach into the esophagus through the opening or hiatus in the diaphragm.
2. Sliding hernia is the most common. GERD is a common symptom of

sliding hernias.
3. Parasophageal hernia occurs when the greater curvature of the stomach

rolls alongside the esophagus. GERD is not a common symptom. Severe pain may result from incarceration that may lead to perforation, volvulus or strangulation. This is a medical emergency. 4. Surgical interventions for GERD and hiatal hernias are NISSEN fundoplication and TOUPET fundoplication.
5. For diagnostic procedures, client should remain NPO after midnight. A

laxative may be given to help pass the barium and increase fluid intake. Monitor stools for barium (stools will appear chalk white) since it can cause bowel obstruction. Monitor for complications during postprocedure such as perforation (hematemesis, pain, dyspnea, tachycardia, hypotension)

GASTRITIS
1. Gastritis is the inflammation of the stomach or gastric mucosa. 2. Acute gastritis is caused by highly seasoned food, disease-causing organism or NSAID overuse. 3. Chronic gastritis is caused by H. pylori or malignant ulcers, autoimmune diseases, medications and alcohol abuse. 4. The difference between acute and chronic gastritis is that chronic gastritis has a vitamin B12 deficiency. 5. Cobalamin injections are needed for a lifetime and prevents the development of pernicious anemia (vitamin B12 deficiency). 6. The incidence of stomach cancer is higher in clients with chronic gastritis. 7. Monitor for hemorrhagic gastritis such as hematemesis, tachycardia and hypotension.

PUD (Peptic Ulcer Disease)

1. A peptic ulcer is ulcerations in the mucosal wall of the stomach, pylorus, duodenum or esophagus. Erosion may extend to the muscle. 2. Most common ulcers are gastric and duodenal ulcers.
3. The three main causes for PUD are Helicobacter pylori, the overuse of

NSAIDs, alcohol, smoking and Zollinger-Ellison syndrome (a pathologic hypersecretory disorder). 4. Gastric symptoms consist of pain in left midepigastric region occurring 30 to 60 minutes after a meal; food accentuates the pain.
5. Duodenal symptoms consist of cramping pain in the midepigastric area

1 to 3 hours after a meal or during the night. Pain is relieved by ingestion of food. 6. Hematemesis is common with gastric ulcers; melena is common with duodenal ulcers.

7. PUD w/ H. pylori is treated with antibiotics H2 receptor antagonists

and/or proton pump inhibitors. An example of this combination is amoxicillin, clarithromycin and omeprazole for 14 days. 8. PUD clients may be anemic due to the loss of blood accompanying ulceration.
9. A mucosal barrier protectant such as sucralfate (Carafate) should be

administered 1 hour before meal which will protect the lining. 10. Diagnostic tests include EGD, barium swallow and IgG serologic test (urea breath and stool culture test; may also show elevated WBC) 11. IF GI bleeding occurs, maintain NPO status and assist with the NG tube for decompression and lavage access w/ NS. Administer vasopressin (Pitressin) using IV.
12. If perforation occurs (the contents leak into the peritoneal cavity), this is

peritonitis which is a surgical emergency. The abdomen is tender, rigid and board-like. Patient should assume the knee chest position (hypovolemic and/or septic shock on the way).
13. Surgeries for PUD includes gastrectomy (removal of stomach w/ the

attachment of esophagus to jejunum or duodenum), vagotomy (surgical division of the vagus nerve), gastric resection (removal of lower half of stomach, with a vagotomy), Billroth 1 ( -to the duodenum) and Billroth II ( -to the jejunum), pyloroplasty (enlargement of the pylorus). 14. (After the surgery) a. IF the NG tube isnt functioning, dont reposition and notify the physician. b. Monitor input and output, especially NG drainage. c. NPO until peristalsis returns.
d. Monitor for dehydration, sodium, potassium deficiency and

metabolic alkalosis, which occurs secondary to gastric suction. e. The client is at high risk for the following complications: hemorrhage, shock, iron, folate or VIT B12 deficiency anemia and dumping syndrome.

15. Dumping syndrome is the rapid gastric emptying of food into the small

intestine. 16. Assessment of dumping syndrome includes symptoms occurring 30 minutes after eating; N&V, feelings of fullness, explosive diarrhea, diaphoresis, flatulence, palpations and borborygmi (loud gurgles indicating hyperperistalsis)
17. How to prevent dumping syndrome? Client should should lie down after

meals, drink between meals (not with them), avoid large amounts of carbohydrates. Avoid sugar, salt and milk. Eat high protein, high fat and low-carb meals. Take antispasmodic medications to delay gastric emptying. Monitor for hypoglycemia.

HEPATITIS/JAUNDICE
18. Hemolytic jaundice is caused by increased production of bilirubin

followed by RBC destruction. Indirect (unconjugated) serum bilirubin is more than 0.8mg/dL. (sickle cell, blood transfusions, hemolytic anemia)
19. Hepatocellular jaundice is caused by the dysfunction of hepatocytes

which reduces their ability to remove bilirubin from blood and form into bile. Associated with hepatitis. (hepatitis, cirrhosis, hepatocellular carcinoma)
20. Obstructive jaundice is caused by an obstruction of the flow of bile out of

the liver. Direct serum bilirubin is more than 0.3mg/dL. 21. Jaundice is a discoloration of body tissues from increased serum bilirubin levels (more than 2.5mg/dL). 22. The urine will be dark and brownish because of the increased excretion of urobilinogen.
23. The stools will be clay colored because of the absence of bile in the

intestine (it doesnt get absorbed).

24. HAV and HEV are oral-fecal (enteric) route.

25. 26.

Chronic infection markers are present for HBV, HCV and HDV. HBV has the longest incubation period which is 6 to 24 weeks.

27. HAV and HBV have vaccines. 28. To prevent the transmission of hepatitis (especially A and B): a. Proper hand-washing and the use of gloves when handling

contaminated items (bed pans, fecal matter, bed linens). b. Clients should have own bathroom. c. Clients should consume small meals high in carbs and low in fat. d. Client cannot prepare or share foods and utensils for/with anyone. e. Should avoid alcohol, Tylenol and sedatives. f. Client may never donate blood. g. Avoid sexual contact.
h. Medication therapy is aimed towards symptom relief, like anti-

emetics (since most analgesics is metabolized by liver) i. If the liver is compromised, client should avoid protein and salt. 29. 30. Hepatitis B is a STD and is a major risk of liver cancer. HBV can be transmitted from mother to fetus.

31. Avoid sexual contact with a client if he/she test positive for HBV surface antigen (HBsAG). 32. HDV depends on HBV to replicate.

CIRRHOSIS
33. Cirrhosis is irreversible and chronic liver disease by diffuse inflammation and fibrosis of liver tissue.
34. Laennec cirrhosis is also called alcoholic, portal, nutritional cirrhosis.

35. Biliary cirrhosis is caused by obstruction of bile and results in necrosis and fibrosis; caused by gallstones, tumors or chronic pancreatitis. 36. Post-necrotic cirrhosis results from severe liver disease such as hepatitis. 37. Symptoms of cirrhosis vary but the following are major, late signs: a. Skin: pruritis, spider angiomas, palmer erythema, caput medusa, sclera icterus, petechie, jaundice b. Endocrine: testicular atrophy, gynecomastia, loss of chest and axillary hair, increased aldosterone, estrogen, antidiuretic c. Hemotologic: bleeding tendencies, decreased clotting factors d. GI/abdomen: tenderness in RUQ, ascites e. Neurological: (complication, end-stage) hepatic encephalopathy, asterixis, DTR, coma f. Miscellaneous: Portal hypertension, bleeding esophageal varices, DIC, hepatic encephalopathy, hepatorenal syndrome, death. 38. Bleeding esophageal varices: keep a pair of scissors by the bedside. 39. 40. Biopsy is the only definitive way to diagnose the type of cirrhosis. Liver biopsy: a. Vital signs q 15 min X 4 hrs b. Apply direct pressure to biopsy site immediately after procedure c. Position on right side for compression over biopsy site d. Maintain NPO for 2 hrs e. Bedrest 24hrs f. Avoid activities that increase intra-abdominal pressure like coughing, lifting, straining, for 1 to 2 weeks. 41. Ascites: paracentesis performed on severe ascites. To prevent reaccumulation, a LaVeen shunt or transjugular intrahepatic

portosystemic shunt (TIPS); these shunts help to relieve portal hypertension. 42. Clients with ascites are fluid restricted, salt-restricted and proteinrestricted. 43. Clients with ascites: monitor weight, I&O and abdominal girth

44. Lactulose decreases the pH of the bowel, hence decreasing ammonia and facilitating excretion of bowel. 45. Clients may get paracentesis if ascites is very severe.

CHOLECYSTITIS
46. Cholecystitis is the inflammation of the gallbladder. 47. Cholelithiasis is associated with gallstones along with acute inflammation. 48. The hallmark symptom of cholecystitis is epigastric pain that radiates to the scapula 2 to 4 hrs after eating a fatty meal and may persist for 4 to 6 hr after.
49. Murphys sign is when client cannot take a deep breath when

examiners fingers are passed below the hepatic margin of pain.

50. Billary obstruction are dark, tea-colored urine, steatorrhea, clay-colored

stools and jaundice. 51. 52. Maintain NPO status during N&V episodses. Cholecystectomy is the removal of the gallbladder.

53. Choledocholithotomy requires the incision into the common bile duct. 54. Caring for the T-tube: a. Semi-fowlers position. b. Monitor for foul and pus filled drainage.

c. Keep drainage below gallbladder. d. Avoid irrigation, aspiration or clamping without an order. e. Clamp tube before a meal and unclamp if N&V occurs. 55. Eat small, low fat meals with chronic cholecystitis.

56. Post op interventions after a cholecystectomy and choledocholithotomy: a. Encourage deep breath and coughing. b. Instruct the client about splinting the abdomen to prevent discomfort during coughing. c. Encourage early ambulation. d. Maintain NPO status/nasogastric tube suction as prescribd. e. Monitor T-tube drainage.

PANCREATITIS
57. Acute pancreatitis is the inflammation of the pancreas associated with pancreatic enzymes digesting tissue. 58. Chronic pancreatitis will reveal further destruction of tissue, leaving behind scar tissue. 59. Abdominal pain includes sudden onset at midepigastric orLUQ with radiation to back, 60. The pain is aggravated by a fatty meal, alcohol or lying in recumbent position. 61. Cullens sign is the discoloration of the abdomen and periumbilical area. 62. 63. Turners is the bluish discoloration on the flanks. Absent bowels are sometimes associated with pancreatitis.

64. Elevated WBC, glucose, bilirubin, alkaline and urinary amylase levels are associated with pancreatitis. 65. Elevated serum lipase and amylase levels.

66.

Exacerbation of acute pancreatitis: a. Maintain NPO status. b. IV fluid administration. c. Administer Demorol for pain. d. Administer antacids, H2 rceptor antagonists, etc to prevent activation of pancreatic enzymes. e. Avoid alcohol.
f. Notify physician if acute abdominal pain, jaundice, clay-colored

stools or dark, tea colored urine develops. 67. Chronic pancreatitis; assessment includes left upper quandrant mass, steatorrhea and foul-smelling stools, weight loss, jaundice and signs of diabetes mellitus. 68. Interventions for chronic pancreatitis: a. Fat and protein intake must be limited. b. Avoid alcohol and heavy meals. c. Provide vitamins and minerals. d. Administer pancreatic enzymes to help digest and absorb fat and protein. e. Administer oral hypoglycemic or insulin if DM develops. f. Instruct the client to notify the HCP of increased steatorrhea, abdominal distension, cramping or skin breakdown develops.