Gastric/Hepatic lec 7

What is the difference between nausea and vomiting?

Nausea: subjective epigastric discomfort/urge to vomit; Vomiting (emesis): forceful ejection of stomach contents.

What are common causes of nausea and vomiting?

GI infections/disorders; CNS or motion problems; pregnancy; cardiac or metabolic disorders; medications, anesthesia, chemotherapy; psychological factors.

What does anorexia mean in GI assessment?

Loss of appetite, not necessarily the psychiatric eating disorder anorexia nervosa.

Why does vomiting of stomach contents cause metabolic alkalosis?

Loss of gastric hydrochloric acid (HCl) removes acid from the body, increasing blood pH.

When can vomiting produce metabolic acidosis instead?

When small-intestinal contents containing bicarbonate are lost, bicarbonate loss can produce metabolic acidosis.

What complications can occur with prolonged vomiting?

Dehydration, weight loss, electrolyte imbalance, decreased plasma volume, hypotension, possible circulatory failure, and aspiration.

What do bright-red versus coffee-ground emesis suggest?

Bright red: fresh/active bleeding; Coffee-ground: blood has remained in the stomach and been altered by gastric acid.

What is the difference between regurgitation and projectile vomiting?

Regurgitation: relatively effortless return of contents; Projectile vomiting: forceful expulsion, sometimes without preceding nausea.

What nursing interventions have priority for persistent vomiting?

Protect the airway/aspiration precautions; NPO initially; IV fluids; assess emesis; monitor vital signs, hydration, electrolytes, and intake/output; NG suction if ordered.

How should a vomiting patient be positioned to prevent aspiration?

Alert patient: upright or semi-Fowler’s; reduced consciousness: side-lying/rescue position (professor emphasizes left lateral).

How is oral intake advanced after severe vomiting resolves?

Start clear liquids and small sips; advance as tolerated to full liquids, bland/soft foods, then usual diet; avoid carbonation, fatty meals, and overeating.

What should the nurse monitor for a patient with NG suction?

Record drainage and total intake/output; monitor dehydration, BP, pulse, and electrolytes; replace NG losses mL-for-mL if specifically ordered.

What is GERD and its main pathophysiologic cause?

Repeated reflux of acidic stomach contents injures the esophagus; the primary problem is an incompetent/weak lower esophageal sphincter (LES).

What factors can worsen GERD or LES function?

Obesity, smoking, hiatal hernia, large/fatty meals, caffeine, alcohol, certain trigger foods, and lying flat after meals.

What are the main manifestations of GERD?

Pyrosis (heartburn), upper-abdominal discomfort (dyspepsia), sour/bitter regurgitation, and sometimes sore throat or hoarseness.

Why must new chest discomfort resembling GERD be evaluated carefully?

GERD pain can mimic angina and spread toward the throat or jaw; cardiac causes must be ruled out first.

What esophageal complications result from untreated GERD?

Esophagitis, ulcers, scar tissue/strictures with dysphagia, and Barrett’s esophagus.

What is Barrett’s esophagus and why is it important?

Metaplasia of the esophageal lining caused by chronic reflux; increases risk of esophageal cancer.

What respiratory and dental problems can GERD cause?

Microaspiration/acid irritation can cause cough, bronchospasm, asthma-like symptoms, or pneumonia; refluxed acid can erode tooth enamel.

What lifestyle teaching helps manage GERD?

Eat small, low-fat meals; avoid personal triggers, caffeine, alcohol, and smoking; manage weight/stress; stay upright 2–3 hours after meals; elevate head of bed.

Which drug classes are emphasized for GERD?

Proton pump inhibitors (PPIs) and H2-receptor blockers reduce gastric acid; antacids offer symptomatic relief.

What is peptic ulcer disease (PUD)?

Erosion/ulceration of GI mucosa exposed to gastric acid and pepsin; often affects the stomach or duodenum.

How do acute and chronic peptic ulcers differ?

Acute: more superficial mucosal erosion; Chronic: deeper injury, scar/fibrous tissue, and recurrent or persistent disease.

What are major risk factors for peptic ulcers?

Helicobacter pylori infection, NSAID/aspirin use, and other gastric irritants; increased acid exposure contributes.

Where do gastric and duodenal ulcers usually occur?

Gastric: stomach, often antrum; Duodenal: first 1–2 cm of the duodenum.

How does pain differ in gastric versus duodenal ulcers?

Gastric: upper epigastric pain about 1–2 hours after meals; food may worsen. Duodenal: burning/cramping pain about 2–5 hours after meals; food may temporarily relieve.

What symptoms may occur with either gastric or duodenal ulcers?

Bloating, nausea/vomiting, and early fullness; some ulcers are silent, especially with older adults or NSAID use.

What are the three major PUD complications?

Hemorrhage (most common); perforation (most lethal); gastric outlet obstruction. All can require emergency treatment.

What findings suggest a perforated peptic ulcer?

Sudden severe abdominal pain, possible radiation to back/shoulders, rigid boardlike abdomen, absent bowel sounds, shallow respirations, and weak rapid pulse.

Why is ulcer perforation life-threatening?

GI contents spill into the peritoneal cavity, causing peritonitis, fluid shifts/hypovolemia, and possible sepsis.

What is gastric outlet obstruction and its key manifestation?

Blockage near distal stomach/duodenum prevents gastric emptying; causes distention, increasing discomfort, and projectile vomiting with dehydration.

What is the most reliable test to locate a peptic ulcer?

Upper GI endoscopy; directly visualizes the ulcer and can also assess healing.

What is the purpose of PPIs and H2 blockers in PUD?

Decrease gastric acid so the injured mucosa can heal; acid suppression alone will not eradicate H. pylori.

How is H. pylori-associated PUD managed?

Test for H. pylori (e.g., breath test); treat with a prescribed antibiotic combination plus a PPI; complete the full treatment course (lecture discusses 14 days).

What patient education reduces PUD recurrence?

Avoid NSAIDs/aspirin unless specifically directed; stop smoking, limit alcohol/irritants, take prescribed medicines completely, and report recurrent pain or GI bleeding.

What is dumping syndrome following gastric surgery?

Rapid delivery of a large hypertonic bolus into the small intestine draws fluid into the bowel, causing distention and decreased plasma volume.

What are manifestations and timing of early dumping syndrome?

About 15–30 minutes after eating: cramping, diarrhea/urgent defecation, borborygmi, weakness, sweating, dizziness, and palpitations.

What dietary measures help reduce dumping syndrome?

Small, frequent meals and rest after eating; monitor for diarrhea, fluid loss, and dehydration.

Why can gastrectomy cause vitamin B12 deficiency and anemia?

Loss of stomach parietal cells decreases intrinsic factor needed for B12 absorption; B12 replacement may be needed, especially after total gastrectomy.

What do hematemesis, melena, and occult GI blood mean?

Hematemesis: vomiting blood; Melena: black tarry stools from digested GI blood; Occult blood: hidden bleeding detected by testing.

What does coffee-ground vomitus indicate compared with bright-red blood?

Coffee-ground: blood exposed to gastric acid; Bright red: fresher bleeding that may still be active.

Why are some older adults at increased risk for upper GI bleeding?

Frequent NSAID/aspirin exposure can damage gastric mucosa and contribute to ulceration or bleeding.

How does the lecture define a massive GI bleed?

More than about 1,500 mL of blood loss or 25% of intravascular blood volume.

What shock findings should the nurse assess during active GI bleeding?

Tachycardia, weak pulse, hypotension, cool extremities, delayed capillary refill, anxiety/apprehension, and altered perfusion.

Why is hourly urine output important with upper GI bleeding?

It reflects kidney perfusion and is a useful indicator of reduced circulating blood volume and developing shock.

What are priority treatments for a severe upper GI bleed?

Frequent hemodynamic assessment, oxygen as needed, IV isotonic fluid resuscitation, blood products when indicated, and endoscopic control of the source.

What findings suggest GI perforation or peritonitis during a bleed?

Tense/rigid abdomen, worsening severe pain, abnormal or absent bowel sounds, guarding, and clinical instability.

What are the principal nursing goals after upper GI bleeding?

Stop further bleeding; identify/treat its cause; restore stable hemodynamics and tissue perfusion; prevent recurrence.

What is the most common histologic type of colorectal cancer?

Adenocarcinoma.

What risk factors for CRC were highlighted in lecture?

Increasing age, family history, smoking, high intake of processed meat, low-fiber diet, and inflammatory bowel disease.

Why is early colorectal cancer often missed?

It can be asymptomatic or cause vague fatigue, anemia, poor appetite, and weight loss until more advanced.

What bowel changes can signal colorectal cancer?

Rectal bleeding, altered constipation/diarrhea patterns, and narrowed/pencil-thin stools caused by a constricting mass.

How do right-sided and left-sided CRC manifestations differ?

Right: occult bleeding/iron-deficiency anemia and diarrhea; Left: fresh red blood in stool and obstructive symptoms.

When does the lecture recommend starting average-risk CRC screening?

At age 45; higher-risk individuals need earlier or more frequent screening based on their risk factors.

What is the lecture’s gold-standard examination for CRC screening?

Colonoscopy, which visualizes the colon and allows detection/removal of polyps or tissue sampling.

Why is bowel preparation important before colonoscopy?

It clears feces so the examiner can see mucosa and lesions; inadequate preparation can hide abnormalities.

What alternatives to colonoscopy are discussed for average-risk screening?

Stool-based occult-blood and DNA testing (such as Cologuard); abnormal screening still requires diagnostic follow-up.

How is CRC generally treated according to stage?

Early: resection with healthy margins and possible bowel anastomosis; higher-risk/stage III: add chemotherapy; advanced unresectable disease: palliation, systemic treatment, and/or radiation.

What is irritable bowel syndrome (IBS)?

A functional GI disorder with recurrent abdominal pain and altered bowel habits (diarrhea, constipation, or both).

What factors can contribute to or trigger IBS symptoms?

Stress, GI infections, food intolerances (e.g., lactose), and individual dietary triggers; exact cause is unknown.

What are the Rome IV features cited for IBS diagnosis?

Recurrent abdominal pain at least 1 day/week over 3 months, associated with changes in defecation, stool frequency, or stool form.

What are the four IBS subtypes?

IBS-C (constipation), IBS-D (diarrhea), IBS-M (mixed), and IBS-U (unsubtyped).

What GI manifestations are common with IBS?

Cramping abdominal pain, constipation/diarrhea, bloating, gas, mucus in stool, and sensation of incomplete evacuation.

What non-GI symptoms may accompany IBS?

Fatigue, headaches, and sleep disturbances.

How is IBS managed?

Individualize care: identify food triggers/food diary, consider low-FODMAP diet, address stress, provide support, and use symptom-directed drugs such as antispasmodics or stool regulators.

What is inflammatory bowel disease (IBD)?

Chronic inflammation of the GI tract with alternating exacerbations and remission; includes Crohn’s disease and ulcerative colitis (UC).

How is IBD different from IBS?

IBD involves actual GI inflammation and possible tissue damage/complications; IBS is a functional bowel disorder.

Where does Crohn’s disease occur compared with ulcerative colitis?

Crohn’s: anywhere mouth to anus, often distal ileum/proximal colon; UC: colon only, typically beginning at rectum and spreading continuously.

Which bowel wall layers are affected by Crohn’s versus UC?

Crohn’s: full thickness (transmural); UC: primarily the mucosal/innermost layer.

What are skip lesions and cobblestoning in Crohn’s disease?

Skip lesions: normal segments between diseased areas; cobblestoning: deep ulcers producing uneven inflamed mucosa.

Why are fistulas and strictures associated with Crohn’s disease?

Transmural inflammation causes deep injury, scarring/narrowing (strictures), and abnormal connections (fistulas).

What are common manifestations of Crohn’s disease?

Diarrhea, cramping abdominal pain, weight loss/malabsorption, fatigue, and possible rectal bleeding.

What are pseudopolyps in ulcerative colitis?

Tongue-like projections of regenerating/inflamed mucosa within the colon.

What manifestation most strongly distinguishes UC from Crohn’s in the lecture?

Frequent BLOODY diarrhea in UC, often with mucus; Crohn’s more often emphasizes cramping, diarrhea, and malabsorption.

How does the lecture describe mild versus severe UC?

Mild: fewer than ~4 stools/day, little blood; Severe: ~10–20 bloody stools/day with fever, anemia, weight loss, tachycardia, and dehydration.

What local complications can occur with IBD?

Hemorrhage, strictures, obstruction, perforation/peritonitis, abscesses, fistulas, and toxic megacolon.

Why do patients with IBD need ongoing colorectal cancer screening?

Chronic bowel inflammation raises colorectal cancer risk, so regular surveillance is important.

What systemic or nutritional complications are noted with IBD?

Malnutrition/malabsorption, anemia, electrolyte and fluid loss, liver disease, and osteoporosis; monitor nutritional status and bone health.

What are the treatment goals for IBD?

Rest bowel when needed; control inflammation, treat infection, correct malnutrition/fluids, relieve symptoms, and improve quality of life.

Which medication groups are discussed for IBD?

Corticosteroids for flares; aminosalicylates especially in UC; biologic/immunomodulating drugs; other therapies selected by disease location and severity.

Why can colectomy cure UC but not Crohn’s disease?

UC is confined to the colon; Crohn’s may affect any GI segment and can recur after surgery.

What nursing teaching is key for IBD flare nutrition or an ileostomy?

Replace fluid/electrolyte losses, choose easily tolerated foods during flares, inspect peristomal skin, and change ostomy appliances as needed—not automatically every day.

What does hepatitis mean, and what can cause it?

Inflammation of liver tissue; causes include viruses, alcohol, drugs/chemicals, autoimmune disease, and metabolic problems.

How does hepatitis A transmission differ from hepatitis B and C?

Hepatitis A: fecal–oral/contaminated food; hepatitis B and C: primarily exposure to infected blood or relevant body fluids.

How is hepatitis B (HBV) commonly transmitted?

Blood and sexual/body-fluid exposure, needlesticks/percutaneous exposure, and perinatal transmission; it can be acute or chronic.

What are HBV prevention priorities?

Vaccination, safe sexual and sharps practices, blood/exposure precautions, and screening for people at risk.

How is hepatitis C (HCV) most commonly acquired?

Percutaneous blood exposure, especially shared injection equipment; also occupational exposure and older unscreened transfusions (before 1992).

(T/F) There is a vaccine for hepatitis B but not hepatitis C.

True. HBV vaccination is a major preventive tool; no HCV vaccine was described in the lecture.

What happens to hepatocytes in acute versus chronic hepatitis?

Acute: infected hepatocytes may be destroyed but regenerate after recovery; Chronic: ongoing injury causes fibrosis and may progress to cirrhosis.

What are common manifestations of viral hepatitis?

Anorexia, nausea/vomiting, fatigue/malaise, joint or muscle pain, RUQ tenderness, and possible hepatomegaly.

What do icteric versus anicteric hepatitis mean?

Icteric: jaundice present, sometimes with dark urine, pale/clay-colored stools, and pruritus; Anicteric: no visible jaundice.

What is notable about the acute phase of hepatitis?

It is the phase of greatest infectivity; patients may have few symptoms and the phase may last months.

What occurs during the convalescent phase of hepatitis?

Jaundice fades, but tiredness and malaise can persist for weeks to months; enlarged liver may remain temporarily.

What serious complications can follow chronic hepatitis B or C?

Cirrhosis, portal hypertension, liver failure, and hepatocellular cancer; chronic hepatitis C is particularly emphasized in the lecture.

What nursing teaching is important during recovery from hepatitis?

Rest, adequate nutrition/hydration, avoid alcohol and hepatotoxic agents, monitor fatigue, and teach ways to prevent transmission.

How are chronic hepatitis C infections treated or prevented?

Direct-acting antiviral therapy was discussed; prevention centers on reducing blood exposure and screening because no vaccine is available.

What is cirrhosis?

Late-stage chronic liver injury in which normal hepatocytes are replaced by fibrous scar tissue and regenerative nodules, reducing liver function.

What causes cirrhosis besides alcohol?

Chronic viral hepatitis, fatty liver/metabolic disease, obesity, malnutrition, and other chronic liver insults; alcohol is not the sole cause.

Why may early compensated cirrhosis be hard to recognize?

Few symptoms; fatigue or enlarged liver may be the only signs, and routine liver tests may initially appear near normal.

What findings indicate more advanced cirrhosis?

Jaundice, edema, ascites, portal hypertension, bleeding problems, skin changes, and neurologic or endocrine symptoms.