gi -- exam 1

What is peritonitis?

Inflammation and infection of the peritoneum/endothelial lining of the abdominal cavity.

What is the classic assessment finding of peritonitis?

A rigid, board-like abdomen.

What can cause peritonitis?

Perforation from appendicitis, diverticulitis, PUD, penetration; bowel obstruction; gangrenous bowel/gallbladder; or ascending genital infection.

What complications can occur with peritonitis?

Ileus, bacteremia/sepsis, and respiratory insufficiency.

What assessment findings suggest peritonitis?

Abdominal pain, rigid/board-like abdomen, N/V, anorexia, distention, diminished bowel sounds, tachycardia, decreased urine output, dehydration, and fever.

What labs/diagnostics are associated with peritonitis?

Elevated WBC with high neutrophils, blood cultures, BMP, and abdominal x-ray to look for free fluid or dilated bowel loops.

What are major nursing interventions for peritonitis?

Monitor VS and SaO2, manage pain, give broad-spectrum antibiotics and IV fluids, maintain I&O, use an NG tube as ordered, and encourage ambulation when appropriate.

What is the classic pain pattern of appendicitis?

Pain often begins cramping in the epigastric/periumbilical area and shifts to the RLQ as it becomes more severe.

What does rebound tenderness mean in appendicitis?

Pain occurs after pressure is released, suggesting peritoneal irritation/inflammation.

What other findings support appendicitis?

Anorexia and elevated WBC with high neutrophils.

What diagnostic finding supports appendicitis?

Ultrasound may show an enlarged appendix.

How is appendicitis commonly treated?

Appendectomy/laparoscopy; early ambulation, pain management, and IV/PO antibiotics if peritonitis or an abscess is present.

What is gastroenteritis?

Inflammation of the stomach and intestinal tract, most commonly from viral infection but also from bacterial infection.

How is norovirus gastroenteritis spread?

Fecal-oral transmission through contaminated food/water and contaminated surfaces or objects.

What are the key findings and main fluid/electrolyte concerns with gastroenteritis?

Nausea, vomiting, abdominal cramping, diarrhea, hypokalemia, and hypovolemia/dehydration.

What is the main care for viral gastroenteritis?

It is usually self-limiting; replace oral fluids/electrolytes and emphasize handwashing and surface sanitation.

What is ulcerative colitis (UC)?

An inflammatory bowel disease involving the rectum/rectosigmoid colon, with periods of remission and exacerbation.

What happens to the intestinal lining in UC?

The mucosa becomes hyperemic and edematous and can ulcerate and bleed.

What are classic GI manifestations of UC?

Frequent bloody stools, abdominal pain, nausea, anorexia, malaise, weight loss, and anemia.

What extraintestinal manifestations can occur with UC?

Arthritis, mouth sores, visual problems, and skin disorders.

What can fever and tachycardia suggest in a patient with UC?

Dehydration or possible perforation.

What labs are important in UC?

CRP and/or ESR may be elevated; CBC, electrolytes, and albumin are monitored; stool cultures may be obtained.

What tests can help visualize UC?

MRE and colonoscopy/barium enema can identify distribution, depth, and disease involvement.

What stool/nutrition monitoring is important in UC?

Record stool color, volume, frequency, and consistency; monitor weight 1–2 times weekly; NPO/TPN may be used when indicated.

What diet teaching is included for UC in the lecture?

Low animal fats and sugars, increase fruits/vegetables, and avoid lactose and carbonated drinks.

What lifestyle teaching is important for UC?

Smoking cessation.

What are 5-ASA medications used for UC?

Sulfasalazine and mesalamine; they have an anti-inflammatory effect on the intestinal lining.

What important teaching goes with sulfasalazine?

Folic acid supplementation is needed.

What is important about glucocorticoids for UC?

They are tapered rather than stopped abruptly; prednisone may be given PO or rectally.

Why are immunomodulators used cautiously in UC?

They can cause immunosuppression.

What biologic medications are listed for inflammatory bowel disease?

TNF inhibitors such as infliximab and adalimumab are listed in the lecture.

What is Crohn’s disease?

An inflammatory bowel disease that most often affects the small intestine but can involve the colon or both.

What is a key difference between Crohn’s and UC regarding distribution?

Crohn’s can involve multiple separated areas, producing skip lesions.

What bowel changes occur in Crohn’s?

Thickening, strictures, ulcerations, fistulas, and fibrosis/scarring that can lead to obstruction.

What are classic Crohn’s manifestations?

Frequent/severe diarrhea, abdominal pain or distention, weight loss, fatigue, malabsorption, anemia, and steatorrhea.

What perianal findings can occur with Crohn’s?

Perianal fissures; fistulas and abscesses may also occur.

What can low-grade fever in Crohn’s suggest?

Fistulas, abscesses, or severe inflammation.

Why can Crohn’s cause anemia and nutritional deficiencies?

Bleeding and malabsorption can contribute; folate and vitamin B12 deficiencies are also possible.

What lab abnormalities can occur with Crohn’s?

Elevated CRP/ESR/WBC, fluid and electrolyte changes, low albumin, and anemia.

What diagnostic imaging is emphasized for Crohn’s?

MRE can visualize the bowel lumen, wall, and mesentery; x-ray can show narrowing, ulcerations, strictures, or fistulas.

What nutrition/care measures may be used for severe Crohn’s?

Monitor stools and weight, provide nutritional supplements, and use NPO/TPN when indicated.

What medications are listed for Crohn’s?

Azathioprine, 6-MP, TNF inhibitors such as infliximab/adalimumab, glucocorticoids, and antibiotics such as ciprofloxacin/metronidazole.

What is the easiest high-yield way to distinguish UC from Crohn’s?

UC primarily involves the rectum/rectosigmoid colon and is associated with frequent bloody stools; Crohn’s can affect the small intestine/colon with skip lesions, strictures, fistulas, malabsorption, and steatorrhea.

What are diverticula?

Pouchlike herniations of mucosa through weak points in the muscular bowel wall.

What contributes to diverticular disease?

Aging, low fiber intake, and increased intraluminal pressure associated with constipation.

What is diverticulitis?

Inflammation/infection of diverticula.

What is the classic pain location in diverticulitis?

Left lower quadrant (LLQ) abdominal pain.

What findings can occur with diverticulitis?

LLQ/generalized pain, constipation, N/V, fever/chills, tachycardia, and guarding/rebound if peritonitis develops.

What labs/diagnostics are important for diverticulitis?

WBC may be elevated; Hgb/Hct may be low with bleeding; occult blood may be present; CT/ultrasound can identify abscess or bowel thickening; x-ray can assess for free air/fluid or perforation.

How is an acute diverticulitis flare treated in the lecture?

Bowel rest/low-fiber or clear liquids as ordered, IV fluids, pain management, and broad-spectrum antibiotics such as metronidazole with TMP-SMX or ciprofloxacin.

What diet teaching is used after diverticulitis resolves?

Increase fiber to about 25–35 g/day, use psyllium as appropriate, and maintain adequate fluids.

What is gastritis?

Inflammation of the gastric mucosa that can cause lesions, erosion, or ulceration.

What are common gastritis risk factors?

NSAIDs, alcohol, caffeine, stress, and cigarette smoking.

What are important gastritis manifestations?

Epigastric pain, dyspepsia, nausea/vomiting, hematemesis, melena, and anorexia.

What is the primary cause of chronic gastritis listed in the lecture?

H. pylori infection.

What can chronic gastritis cause through loss of intrinsic factor?

Pernicious anemia.

What diagnostic test is used for gastritis?

EGD with tissue biopsy, including detection of H. pylori.

What should the nurse monitor if gastritis may be causing bleeding?

Blood pressure, heart rate, Hgb/Hct, and fluid/electrolyte balance.

What medications are listed for gastritis/PUD management?

Famotidine (H2 blocker), sucralfate (mucosal barrier fortifier), omeprazole/pantoprazole (PPIs), antacids, and antibiotics for H. pylori.

What is peptic ulcer disease (PUD) commonly associated with?

H. pylori infection and NSAID-related mucosal injury.

What is the most common complication of PUD?

Hemorrhage/bleeding.

What findings suggest significant PUD bleeding?

Hematemesis, melena, decreased Hgb/Hct, decreased BP, increased heart rate, dizziness/vertigo, and mental-status changes.

What can happen if a peptic ulcer perforates?

Peritonitis, bacteremia, sepsis, and shock.

What are the main transmission routes for hepatitis A?

Fecal-oral transmission and contaminated food/water.

What is important to know about hepatitis B?

It can spread through needles/razors, blood exposure, and person-to-person transmission; many clear the virus and develop immunity, while a small percentage become carriers.

What is important to know about hepatitis C?

It is associated with blood/needle exposure and may become chronic; many infected people have few or no symptoms.

Which hepatitis types are strongly associated with chronic infection leading to cirrhosis/liver cancer in the lecture?

Chronic hepatitis B and C.

What is unique about hepatitis D?

It occurs only with hepatitis B infection.

How is hepatitis E transmitted?

Waterborne/fecal-oral transmission through contaminated food or water; it is usually self-limiting.

What are common manifestations of hepatitis?

RUQ pain, jaundice, light-colored stools, dark urine, fatigue, malaise, anorexia, N/V, fever, pruritus, and sometimes arthralgia/myalgia.

What liver enzymes are commonly elevated with hepatitis?

ALT and AST.

How is hepatitis C evaluated according to the lecture?

HCV antibody testing followed by viral load testing.

What is cholecystitis?

Inflammation of the gallbladder; about 95% of cases are calculous from gallstones obstructing the cystic duct.

What is the classic pain pattern/sign for cholecystitis?

RUQ pain that may radiate to the right shoulder/scapula; Murphy’s sign may be positive.

What other cholecystitis findings are high-yield?

N/V, anorexia, fever, tachycardia, dehydration, jaundice, pruritus, clay-colored stools, dark urine, and possible steatorrhea.

Why can jaundice, clay-colored stools, and dark urine occur with biliary obstruction?

Obstructed bile flow causes bilirubin to accumulate in the blood, decreases bile reaching the intestine, and increases bilirubin excretion in urine.

What labs/diagnostic tests are emphasized for cholecystitis?

WBC may increase; AST/ALP/LDH and bilirubin may rise. RUQ ultrasound is the best initial diagnostic test; ERCP may evaluate biliary obstruction.

What is the main treatment for symptomatic cholecystitis in the lecture?

Cholecystectomy, along with IV fluids, pain management, antiemetics, and early ambulation.

What is acute pancreatitis?

Acute inflammation of the pancreas in which digestive enzymes become activated inside the pancreas, causing autodigestion.

What are the major causes of acute pancreatitis emphasized in the lecture?

Gallstones (about 40%) and alcohol (about 30%).

What is the classic pain of acute pancreatitis?

Severe, constant epigastric/LUQ abdominal pain that may radiate to the back; pain may improve with an upright position or bending forward.

What serious complications can occur with acute pancreatitis?

Necrosis/hemorrhage, pancreatic abscess or pseudocyst, hypocalcemia, hyperglycemia, pleural effusion, AKI, sepsis, and shock.

What labs are high-yield in acute pancreatitis?

Amylase and lipase increase; bilirubin/ALT may increase with obstruction; WBC, glucose, and ESR may increase; serum calcium may decrease.

What is a major nursing priority in acute pancreatitis?

Monitor VS for sepsis/shock, pain, SaO2/pulmonary status, fluid status, glucose, and signs of hypocalcemia.

What are important acute pancreatitis interventions?

IV isotonic fluids, NPO as ordered, pain management, antiemetics, H2 blockers/PPIs, and jejunal enteral feeding when indicated to reduce pancreatic enzyme secretion.

What signs can indicate hypocalcemia in acute pancreatitis?

Tetany, twitching, numbness, and irritability.

What is chronic pancreatitis?

A progressive, destructive pancreatic disease with remissions and exacerbations.

What are key manifestations of chronic pancreatitis?

Severe malabsorption, weight loss, muscle wasting, steatorrhea, continuous burning/gnawing pain with acute exacerbations, and diabetes.

What happens to amylase/lipase in chronic pancreatitis?

They may be normal to moderately elevated, unlike the marked elevations expected in acute pancreatitis.

What is pancreatic enzyme replacement therapy (PERT) used for?

To prevent malnutrition, malabsorption, and excessive weight loss in pancreatic insufficiency.

When should pancreatic enzymes be taken?

With all meals and snacks.

What is the general nutrition plan for chronic pancreatitis in the lecture?

High-calorie, carbohydrate- and protein-rich, low-fat intake with small, frequent meals; avoid alcohol.

What is cirrhosis?

Progressive liver damage involving inflammation, fibrosis, and necrosis that impairs hepatocytes and blood flow.

What are common causes of cirrhosis listed in the lecture?

Alcohol use, chronic hepatitis, and bile duct disease.

What is the sequence connecting cirrhosis to portal hypertension complications?

Fibrosis increases resistance to blood flow → portal hypertension → splenomegaly/platelet consumption → ascites → varices → prominent abdominal veins/caput medusae and hemorrhoids.

What causes ascites and edema in cirrhosis?

Loss of intravascular albumin/low serum albumin contributes to fluid shifting out of the vascular space.

What are key bleeding-related findings/labs in cirrhosis?

Thrombocytopenia, bruising, prolonged/high PT/INR, and possible hematemesis or melena.

What is hepatic encephalopathy and what are classic clues?

A cognitive syndrome associated with elevated ammonia; clues include confusion, fruity breath, and asterixis.

What medication is used to reduce ammonia and confusion in hepatic encephalopathy?

Lactulose; neomycin/rifaximin may also be used to reduce intestinal ammonia production.

What are important cirrhosis fluid-management interventions?

Monitor VS, electrolytes, daily weights, and I&O; manage ascites/edema with fluid management and diuretics as ordered.