Gallbladder/Pancreas/Liver - Outline

Cholelithiasis (Gallstones)

• Definition: Formation of stones (calculi) in the gallbladder or bile ducts.

• Common Disorder: Most common disorder of the biliary system.

• Cause: Unknown, but typically occurs when the balance of cholesterol, bile salts, and calcium in the bile is disrupted.

• Types of Gallstones:

  • Cholesterol Stones (most common): Result from excess cholesterol in bile.

  • Pigment Stones: Form when unconjugated bilirubin precipitates in bile.

Pathophysiology

• Cholesterol Stones: Develop due to ↓ bile acid synthesis and ↑ cholesterol synthesis in the liver, leading to bile supersaturation.

• Pigment Stones: Form due to excess unconjugated bilirubin in bile.

Clinical Manifestations

• Symptoms: Can be asymptomatic or severe.

  • Biliary Colic: Severe pain due to stones obstructing ducts.

  • Pain: Usually after a heavy meal or when lying down.

  • Systemic Signs: Tachycardia, diaphoresis, fever if cholecystitis (inflammation) occurs.

• Pain: Often sharp, sudden, and located in the upper right abdomen, radiating to the back or right shoulder.

Diagnostic Tests

• Non-invasive:

  • Ultrasound: Most common, quick, and accurate.

  • MRCP: Magnetic resonance cholangiopancreatography (non-invasive imaging).

• Invasive:

  • ERCP: Endoscopic retrograde cholangiopancreatography (diagnostic and therapeutic, can remove stones).

  • Percutaneous Transhepatic Cholangiography: Used to diagnose obstructive jaundice and locate stones (more expensive, less commonly used now).

• Labs:

  • WBC: Increased due to inflammation.

  • Liver Function Tests: Elevated ALT, AST, alkaline phosphatase.

  • Bilirubin: Elevated.

  • Serum Amylase: Elevated if pancreas is involved.

Care of the Client Undergoing Gallbladder Surgery

• Surgical Goal: Relief of pain, prevention of complications, improved biliary drainage, and adequate nutrition.

• Postoperative Interventions:

  • Positioning: Low Fowler’s position to help expel gas from the abdomen after laparoscopic cholecystectomy.

  • NG Tube: May be in place post-op but typically removed before recovery room.

  • Diet: NPO until bowel sounds return. Soft, low-fat, high-carb diet afterward.

    • Fat reintroduced after 4-6 weeks.

  • Pain Management: Administer analgesics and encourage ambulation, deep breathing, and splinting.

  • Biliary Drainage Care: Ensure proper management if a T-tube is placed.

Client Teaching

• Medications: Instruct on prescribed medications for pain management and bile flow support.

• Diet: Avoid excess fat until advised by the physician. Fat restriction is lifted in 4-6 weeks.

• Wound Care: Teach how to care for the surgical site, including dressing changes and T-tube care (if applicable).

• Signs to Report:

  • Changes in stool or urine color.

  • Fever, unrelieved pain, nausea, vomiting.

  • Redness, swelling, or signs of infection at the incision site.

Risk Factors (5 F’s):

• Female: More common in women.

• Fertile: Increased risk during reproductive years.

• Fat: Obesity increases risk.

• Fair: Higher risk in fair-skinned individuals.

• Forty: Common in individuals over 40 years old.

Pancreatitis

• Definition: Inflammation of the pancreas, which is triggered by the release of pancreatic enzymes into the pancreas itself, leading to vasodilation, increased vascular permeability, necrosis, erosion, and hemorrhage.

• Beta islet cells (in pancreas) may be affected by inflammation.

• Mortality Rate: 2%-10% depending on the severity of the condition.

• Types:

  • Acute pancreatitis: Sudden onset, can be severe but reversible.

  • Chronic pancreatitis: Long-term inflammation, causing permanent damage and loss of pancreatic function.

• Risk Factors:

  • Alcoholism: Chronic alcohol use damages pancreatic tissue, leading to inflammation.

  • Gallstones: Stones that become impacted at the duodenal papilla can obstruct the outflow of pancreatic enzymes. This obstruction increases pancreatic pressure and causes injury to pancreatic cells. Over time, this injury triggers pancreatitis.

Acute Pancreatitis

Pathophysiology:

• Autodigestion of the pancreas: The pancreas digests itself due to the premature activation of digestive enzymes (e.g., trypsin, lipase, amylase) inside the organ. This leads to tissue damage, inflammation, and in severe cases, hemorrhage and necrosis.

• Recurrent Attacks: Patients with acute pancreatitis may experience recurrent pancreatic attacks, which could increase the risk of progressing to chronic pancreatitis.

  • 5%-10% of acute pancreatitis cases develop into chronic pancreatitis over time.

Clinical Manifestations:

• Abdominal Pain: Severe, constant pain in the upper abdomen, especially after meals. Pain is often unrelieved by antacids and may radiate to the back.

• Tenderness: Abdominal tenderness and guarding, which worsens with palpation.

• Nausea and Vomiting: Often associated with abdominal pain.

• Fever: May be present due to the inflammatory process.

• Jaundice: In some cases, particularly with gallstone-induced pancreatitis, the bile duct can become obstructed, leading to jaundice.

• Complications:

  • Fluid and Electrolyte Imbalance: Due to vomiting, diarrhea, and third spacing of fluid (edema in the abdomen).

  • Infection: Bacterial infections may occur due to pancreatitis or secondary to pseudocyst formation.

  • Pseudocysts: Fluid-filled sacs that develop in the pancreas, which can lead to infection, rupture, or hemorrhage.

  • Respiratory Failure: Painful deep breathing due to abdominal distension, which affects the diaphragm’s ability to function properly.

  • Shock: Hypovolemic shock due to fluid loss and hemorrhage within the pancreas.

Chronic Pancreatitis

Pathophysiology:

• Progressive Damage: Chronic pancreatitis is characterized by permanent structural and functional damage to the pancreas. Over time, the pancreas loses its ability to secrete digestive enzymes and insulin (leading to potential diabetes).

• Increased fibrosis: The pancreatic tissue becomes fibrotic and scarred, reducing pancreatic function.

Clinical Manifestations:

• Recurring Attacks: Severe upper abdominal and back pain, often recurring in nature.

• Nausea and Vomiting: Persistent vomiting and difficulty keeping food down due to the damaged pancreas.

• Elevated Blood Glucose: Due to pancreatic damage, the endocrine function (insulin production) can be compromised, leading to hyperglycemia and potential development of diabetes mellitus.

• Steatorrhea: Fatty stools due to poor absorption of fats (resulting from insufficient pancreatic enzyme production).

• Weight Loss: Resulting from malnutrition, decreased food intake due to pain, and fat malabsorption.

• Complications:

  • Bleeding: From damage to blood vessels in the pancreas.

  • Malnutrition: Due to the impaired ability to digest and absorb nutrients, especially fat.

  • Weight Loss: Due to malabsorption and difficulty eating due to pain.

  • Drug Addiction: Chronic pain management may lead to narcotic dependence in some patients.

  • Pancreatic Cancer: Chronic inflammation increases the risk of pancreatic cancer.

Differences Between Acute and Chronic Pancreatitis

• Acute Pancreatitis:

  • Self-limiting condition that resolves with treatment.

  • No long-term pancreatic damage once the inflammation resolves.

  • Reversible with proper care.

• Chronic Pancreatitis:

  • Progressive and permanent damage to pancreatic tissue.

  • Results in functional loss (e.g., insulin production) and permanent scarring.

  • Irreversible damage.

Collaborative Care and Interventions

Diagnostic Tests:

• History: A thorough history of abdominal pain and risk factors (alcohol use, gallstones).

• MRI and CT Scan: Imaging to assess the extent of pancreatic damage and complications.

• Lipase and Amylase Levels: Elevated lipase and amylase levels (3x normal) within 24 hours are indicative of acute pancreatitis.

• X-rays: To check for gallstones or complications.

• ERCP (Endoscopic Retrograde Cholangiopancreatography): Especially useful in diagnosing chronic pancreatitis or obstructions.

Treatment:

• Acute Pancreatitis:

  • NPO (Nothing by Mouth): Rest the pancreas by not stimulating it with food.

  • Hydration: IV fluids to maintain fluid balance and prevent dehydration.

  • NG Tube: To relieve nausea, vomiting, and abdominal distention.

  • Analgesics: Pain management with opioids or non-opioid medications.

  • Antiemetics: For nausea.

  • Enzyme Replacement: May be needed in chronic pancreatitis.

  • TPN (Total Parenteral Nutrition): For patients who cannot tolerate oral intake for extended periods.

• Chronic Pancreatitis:

  • Prevent acute exacerbations by managing risk factors (e.g., alcohol cessation).

  • Nutritional support, including enzyme replacement therapy.

  • Treatment of diabetes if it develops.

  • Pain management: Often requires long-term use of analgesics, potentially opioids.

Medications:

• Analgesics: For pain relief.

• Antiemetics: To control nausea.

• Proton Pump Inhibitors (PPIs): Such as Prilosec or Prevacid to decrease gastric acid secretion.

• Insulin: If diabetes develops due to pancreatic dysfunction.

Monitoring:

• Blood Glucose: Monitor every 6 hours, especially with TPN administration.

• Electrolytes: Regular checks to prevent imbalances.

Nursing Diagnoses

1. Pain: Related to pancreatic inflammation and tissue damage.

2. Altered Nutrition: Less Than Body Requirements: Due to nausea, vomiting, and malabsorption.

3. Risk for Fluid Volume Deficit: Due to vomiting, diarrhea, and third-space fluid loss.

4. Risk for Altered Home Management/Maintenance: Due to the need for lifelong dietary modifications and possibly insulin therapy.

5. Ineffective Breathing Pattern: Due to abdominal pain and respiratory distress.

6. Ineffective Coping: Due to chronic pain, potential addiction to pain medications, and lifestyle changes.

Hepatitis

Definition

• Inflammation of the liver

Causes

• Viral (Types: A, B, C, D, E, G)

• Medications, alcohol, chemicals

• Autoimmune liver disease

• Rarely caused by bacteria

Types of Hepatitis

Hepatitis A (HAV)

• Transmission: Fecal-oral route

• Sources: Contaminated food, water, shellfish, poor hygiene, crowded conditions

• High-Risk Areas: Daycares, poor sanitation areas

• Infectious Period: 2 weeks before symptoms appear

Hepatitis B (HBV)

• Transmission: Blood, body fluids (semen, vaginal secretions, saliva), sexual contact, perinatal, IV drug use, needle-stick injuries

• Infectious Body Fluids: Blood, semen, vaginal secretions, saliva

Hepatitis C (HCV)

• Transmission: Blood exposure (IV drug use, transfusions, organ transplants, hemodialysis, high-risk sexual behavior)

• Most Common Mode: IV drug use

• Infectious Period: 2-5 weeks before symptoms and throughout the clinical course

Hepatitis D (HDV)

• Also Called: Delta virus

• Requires HBV to survive

• Transmission: Blood exposure, sexual contact, perinatal transmission

Hepatitis E (HEV)

• Transmission: Fecal-oral route (esp. contaminated drinking water)

• Common in: Developing countries (India, Asia, Mexico, Africa)

• Diagnosis: No commercial test available in the U.S.

Hepatitis G (HGV)

• Transmission: Blood exposure, sexual contact

• Source: Found in some blood donors, can be transmitted via transfusion

Care of the Client with Hepatitis

Collaborative Care & Treatment

• Diagnostic Tests:

  • Liver function tests: GTT, GTTP, AST (10-40)

• Medications:

  • Immunizations & Vaccines for prevention (HAV, HBV)

  • Antiviral drugs for treatment

Nursing Care

• Prevention Education:

  • Hand hygiene (esp. food handlers)

  • Blood and body fluid precautions

  • Vaccination for high-risk individuals

• Rest & Activity Management:

  • Frequent rest periods

  • Gradual increase in activity

• Nutritional Support:

  • High-calorie diet

  • Small, frequent meals

  • Nutritional supplements

Nursing Diagnoses & Interventions

1. Risk for Infection

   • Strict hand hygiene

   • Report contagious disease to health department

2. Fatigue

   • Encourage rest and energy conservation

3. Imbalanced Nutrition: Less than Body Requirements

   • Provide small, frequent, high-calorie meals

   • Encourage nutritional supplements

4. Body Image Disturbance

   • Provide emotional support

Cirrhosis (Scarring of the Liver)

Definition:

• End-stage of chronic liver disease

• Progressive and irreversible

• U.S. Impact: ~27,000 deaths per year

Pathophysiology

• Alcohol is the major causative factor → excessive scar tissue replaces functioning liver tissue

• Types of Cirrhosis:

  • Alcoholic Cirrhosis – Scar tissue surrounds the portal area

  • Biliary Cirrhosis – Scarring around bile ducts due to chronic biliary obstruction & infection (least common)

  • Posthepatic Cirrhosis – Broad bands of scar tissue

Clinical Manifestations

Early Symptoms

• GI disturbances: anorexia, nausea & vomiting (N&V), fever, dyspepsia, flatulence, diarrhea/constipation

• Abdominal pain, lassitude (weakness), slight weight loss

• Hepatomegaly (enlarged liver) & splenomegaly (enlarged spleen)

Late Symptoms

• Jaundice

• Peripheral edema & ascites

• Skin lesions – Spider angiomas (dilated blood vessels with a red center and spider-like branches)

• Hematologic disorders: Thrombocytopenia, anemia, coagulation disorders

• Endocrine issues: Gynecomastia, testicular atrophy, impotence, loss of axillary & pubic hair

• Peripheral neuropathies

Diagnostic Studies

• Liver Enzymes: ↑ Alkaline phosphatase, AST (SGOT), ALT (SGPT), GGT

• PT (Prothrombin Time): Elevated

• Liver Biopsy

• Ascitic Fluid Analysis – via paracentesis (needle aspiration of abdominal cavity)

Treatment & Management

General Management

• No cure – focus on symptom management

• Rest

• Sodium restriction

• Diuretics & Paracentesis – Fluid removal

• Peritoneovenous Shunt – Reinfuses ascitic fluid into venous system

• Avoid Alcohol & Aspirin

Esophageal Varices Prevention & Management

• Beta-blockers (e.g., Inderal) – Prophylaxis

• Blood products via endoscopy

• Endoscopic ligation/banding

• Balloon Tamponade – Controls hemorrhage via compression

Medications

• Vitamin K (AquaMEPHYTON) – To aid coagulation

• H2 Receptor Blockers (e.g., Tagamet) – Reduce gastric acidity

• Lactulose (Cephulac) – Prevents hepatic encephalopathy by trapping ammonia in the gut

• Dietary Management:

  • Restrict Protein (to prevent ammonia buildup)

  • High-Caloric, Low-Fat, Low-Protein, Low-Sodium Diet

Complications

1. Portal Hypertension – Obstruction to normal blood flow

2. Esophageal Varices – Enlarged veins in esophagus due to portal hypertension; can lead to life-threatening bleeding

3. Peripheral Edema – Can occur in ankles & presacral area

4. Ascites – Accumulation of serous fluid in the peritoneal cavity

   • Manifested by abdominal distension, weight gain, everted umbilicus, striae, & distended abdominal veins

5. Hepatic Encephalopathy (Coma) – Due to ammonia entering systemic circulation

   • Signs: Disorientation, asterixis (flapping tremors of arms/hands)

Collaborative Care & Interventions

• Diagnostic Testing – Liver function tests, imaging, biopsy

• Medication Management – Diuretics, beta-blockers, lactulose, vitamin K

• Dietary & Fluid Management – Restrict sodium & protein, high-calorie diet

• Management of Complications – Control of ascites, varices, and encephalopathy

Nursing Diagnoses

• Fluid Volume Excess

• Altered Thought Process (due to hepatic encephalopathy)

• Ineffective Protection (risk of bleeding)

• Impaired Skin Integrity (due to edema, ascites)

• Imbalanced Nutrition: Less than Body Requirements