Cirrhosis and Hepatitis Quiz

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Questions and Answers

What is one of the primary consequences of cirrhosis affecting the liver?

Reduced digestion due to liver impairment (correct)

Increased ability to metabolize hormones

Improved blood coagulation functions

Enhanced protein synthesis leading to higher plasma oncotic pressure

Which statement best describes the role of aldosterone in cirrhosis?

The liver typically clears aldosterone effectively under normal conditions.

Aldosterone has no significant effect on fluid balance in liver disease.

High levels of aldosterone lead to sodium retention and fluid reabsorption. (correct)

Aldosterone levels decrease significantly during cirrhosis.

What is a common type of cirrhosis primarily linked to alcohol consumption?

Alcohol-related liver disease (correct)

Post-necrotic cirrhosis

Biliary cirrhosis

Hepatitis cirrhosis

Which complication is NOT typically associated with cirrhosis?

Increased hepatic detoxification capacity Signup and view all the answers

How does cirrhosis affect blood coagulation?

Causes defects in blood coagulation Signup and view all the answers

Which symptom is NOT typically associated with jaundice?

Local soreness Signup and view all the answers

What is the primary method of preventing Hepatitis A?

Vaccination Signup and view all the answers

Which of these is considered a risk factor for primary liver cancer?

Cirrhosis of the liver Signup and view all the answers

What dietary recommendation is suggested for patients with hepatitis?

Low-fat, high-carbohydrate diet Signup and view all the answers

What is a common nursing intervention for a patient experiencing pruritus related to hepatitis?

Keep nails short and clean Signup and view all the answers

Which condition is primarily associated with chronic obstruction or inflammation of the bile ducts?

Primary biliary cirrhosis Signup and view all the answers

What is a common symptom experienced when liver damage is severe?

Headache Signup and view all the answers

What laboratory finding is likely to be present in patients with liver cirrhosis?

Prolonged PT Signup and view all the answers

What dietary modification is indicated for patients with advanced liver disease?

Low-fat and low-sodium diet Signup and view all the answers

Which of the following is a manifestation of portal hypertension?

Splenomegaly Signup and view all the answers

What is the primary risk associated with performing a paracentesis?

Hypovolemic shock Signup and view all the answers

What is the purpose of a peritoneal jugular shunt?

To alleviate ascitic fluid buildup Signup and view all the answers

Which of the following is a potential complication of surgical shunting procedures?

Worsening hepatic encephalopathy Signup and view all the answers

What is a common treatment approach for managing elevated ammonia levels in hepatic encephalopathy?

Using lactulose to remove excess ammonia Signup and view all the answers

What immediate action should be taken before performing a paracentesis to decrease the risk of bladder puncture?

Ensure the patient voids Signup and view all the answers

What is the main therapeutic goal of administering lactulose in patients with cirrhosis?

To improve mental status Signup and view all the answers

Which of the following nursing interventions is least appropriate for a patient with ineffective tissue perfusion related to impaired blood coagulation?

Encourage vigorous physical activity Signup and view all the answers

What dietary modifications should be made for a patient with cirrhosis?

Low-protein, low sodium, high carbohydrate Signup and view all the answers

Which hepatitis virus is primarily transmitted through fecal contamination?

Hepatitis A Signup and view all the answers

What potential risk increases with the use of sedatives in patients with hepatic encephalopathy?

Worsening of mental status Signup and view all the answers

Study Notes

Cirrhosis

Etiology/Pathophysiology: Chronic, degenerative liver disorder caused by generalized cellular damage. Fibrous tissue covers liver lobes, parenchyma degenerates, and fat infiltrates lobules. Restricted blood flow leads to further destruction—first, hepatomegaly, then liver shrinkage. The liver's inability to perform functions causes digestive and metabolic disturbances, blood coagulation issues, fluid/electrolyte imbalances (ascites), and problems metabolizing hormones and detoxifying chemicals.
Development: Cirrhosis progresses slowly through stages of destruction, inflammation, fibrotic regeneration, and hepatic insufficiency. While liver cells regenerate, repeated scarring reduces their ability to replace destroyed cells. Alcohol is the primary cause but other etiologies exist.
Types:
- Alcohol-related: Most common, often affecting men more than women. Heavy alcohol consumption and the amount needed to damage the liver varies from person-to-person. Risk increases with more than 3-4 drinks per day.
- Post-necrotic: Caused by viral hepatitis, hepatotoxins, or infections. Found worldwide.
- Biliary/Obstructive:
  - Primary: Results from chronic bile duct inflammation or obstruction. More common in women.
  - Secondary: Caused by obstructions from gallstones, tumors, or biliary atresia (in children).
  - Cardiac: Associated with severe right-sided heart failure (CHF), cor pulmonale, constrictive pericarditis, and tricuspid insufficiency.
- Nonalcoholic fatty liver disease (NAFLD): Increasingly common due to obesity.
Symptoms: Occur with severe liver damage, manifesting as anorexia, nausea/vomiting, indigestion, diarrhea/constipation, palpable liver, abdominal pain, changes in bowel habits, fatigue, weakness, weight loss, ascites (fluid buildup in abdomen), and peripheral edema. Dilated abdominal veins (caput medusae) and splenomegaly are also observed.
Portal Hypertension Manifestations: Distended abdominal vessels, esophageal, stomach, and rectal varices (enlarged veins). Increased risk of bleeding from GI tract (hematemesis, blood in stools), bruising, and anemia.
Jaundice: Yellow discoloration of tissues due to high bilirubin levels (liver's inability to conjugate and excrete bilirubin). Visible when serum bilirubin is 2.5 mg/dl or higher. Stools become clay-colored, and urine darkens.
Skin Changes: Spider telangiectases, palmar erythema, pruritus, and hair loss.
Renal Function: Can be impaired.
Assessment: Subjective (early/late stages including nausea, vomiting, loss of appetite, weakness, indigestion, flatulence, constipation/ diarrhea, and dyspnea) and Objective (early/late stages including anemia, fever, jaundice, weight loss, epistaxis, purpura, hematuria, spider hemangiomas, bleeding gums, ascites, coagulopathy, hemorrhage, splenomegaly, disorientation, abnormal behavior, or speech).
Diagnostic Tests: Liver enzyme elevations (ALT, AST, LDH, GGT), decreased serum albumin, elevated ammonia, abnormal CBC, prolonged PT, abnormal urinalysis, visualization tests (ERCP, esophagoscopy with barium esophagography, scans, liver biopsy), and paracentesis.
Medical Management: Eliminating causes, managing fluid buildup (bed rest, sodium/fluid restriction, diuretics (spironolactone, Lasix, hydrochlorothiazide), albumin infusions, shunting procedures), preventing further damage (avoiding alcohol/toxins), and providing supportive care (high-calorie/carbohydrate, low-fat/low-sodium diet with supplemental vitamins, antiemetics).
Esophageal Varices Management: Medical emergencies requiring airway management, IV fluids, vasoconstrictors (vasopressin, nitroglycerin), gastric lavage, endoscopic sclerotherapy, and Sengstaken-Blakemore tube placement.
Surgical Shunting Procedures: Portacaval, splenorenal, and mesocaval shunts (high mortality and complications).
Hepatic Encephalopathy: Liver failure-related CNS manifestations (coma, death) caused by ammonia buildup. Ammonia detoxification impaired by decreased liver function. Therapies include low-protein diet, removing intestinal protein/blood (lactulose, enemas), antibiotics, and maintaining fluid/electrolyte balance.

Hepatitis

Etiology/Pathophysiology: Liver inflammation due to viral agents, toxins, or alcohol abuse. Can be acute or chronic. Viral hepatitis is most common. Hepatitis viruses (A, B, C, D, E, F, and G) are distinguished by transmission and incubation period.
Transmission:
- Hepatitis A: Fecal-oral route (contaminated food/water)
- Hepatitis B: Blood/body fluids (blood, semen, vaginal secretions, saliva, breast milk, needles/equipment)
- Hepatitis C: Blood/body fluids (needles/blood transfusions)
- Hepatitis D: Blood/body fluids (progresses often to cirrhosis).
- Hepatitis E: Fecal-oral route (contaminated water, common in developing regions).
- Hepatitis F & G: Blood/transfusion (also water/food contamination).
Pathology: A diffuse inflammatory reaction causes liver cell degeneration and death. Liver functions decrease as cells are lost. Viral virulence, pre-existing liver conditions, and early healthcare affect outcomes.
Symptoms: Vague manifestations, including malaise, joint pain (arthralgia), headaches, chills, photophobia, right upper quadrant discomfort. Some patients are asymptomatic.
Assessment: Subjective data include malaise, arthralgia, headaches, chills, discomfort, photophobia, anorexia, nausea, diarrhea, and constipation. Objective data include jaundice (yellow skin, sclera), pruritus, dark urine, clay-colored stools, hepatomegaly, and lymphadenopathy.
Diagnosis: Elevated liver enzymes (bilirubin, GGT, AST, ALT, LDH, Alkaline phosphatase), prolonged prothrombin time, leukopenia, and hypoglycemia. Serum tests for presence/absence of hepatitis associated antigens (HAA). No test for Hepatitis E.
Medical Management: Supportive care, preventing transmission, bed rest, one-year alcohol abstinence, avoiding medications that are detoxified by the liver.
Diet: Low-fat, high-carbohydrate diet with vitamin supplements (C, B complex, K).
Prevention: Hand hygiene, universal precautions, sanitation and hygiene improvements, and hepatitis vaccine (A & B are common).

Liver Abscesses

Etiology/Pathophysiology: Infections (bacterial) spreading from the GI tract (appendicitis, diverticulitis, perforated colon) or other sites (blood, bile ducts, trauma). Organisms penetrate the liver, creating pus-filled lesions (abscesses). The liver's immune response causes cell death and abscess formation.
Symptoms: Vague signs (fever, chills, abdominal pain), right upper quadrant tenderness, unintentional weight loss, jaundice, and weakness.
Assessment: Subjective infection (fever, chills, dull abdominal pain, abdominal tenderness.) Objective: fever, hepatomegaly, jaundice, anemia, clay colored stool, dark urine.
Diagnosis: Ultrasound, CT scans, liver scans, liver biopsy, bilirubin levels, liver enzymes, blood cultures, and CBC.
Treatment: IV antibiotics, percutaneous or surgical drainage.
Nursing: Continuous monitoring, symptom management, reporting worsening issues, patient education including preparation and response to treatments.

Gallbladder

Structure: Pear-shaped organ (7-10 cm) located under the liver, connected by areolar tissue. Stores and releases bile (30-50 mL) into the duodenum for fat digestion.
Cholelithiasis: Gallstones (sand-sized to 1-inch); more common in women (Native American, white, African American), obese, pregnant, and diabetic individuals.
Cholecystitis: Inflammation of the gallbladder, often caused by gallstone obstruction.
Symptoms: Acute: severe, colicky pain (RUQ/shoulder/scapula), nausea/vomiting, indigestion. Chronic: mild pain, fat intolerance.
Assessment: Subjective: indigestion after fatty foods, abrupt onset (2-4 hrs) right RUQ/ epigastric pain spreading to scapula region, anorexia, nausea, vomiting, flatulence and tachycardia/tachypnea. Some may appear like MI. Objective: fever, leukocytosis, mild jaundice, fatty stools, dark urine, tachycardia.
Diagnosis: History and physical examination, fecal studies (decreased bile), serum bilirubin tests (elevated), imaging studies (ultrasonography, cholecystograms, cholangiography, MRI/CT scans, HIDA scans, ERCP), and endoscopic sphincterotomy or gallbladder removal.
Medical Management: Diet/fluid restriction, pain control (demerol, antiemetics, IV fluids), antibiotics (prophylactic/treatment), ESWL (extracorporeal shock wave lithotripsy), endoscopic sphincterotomy, or surgical intervention.
Surgical Management: Cholecystectomy (preferred laparoscopic cholecystectomy for less invasive procedure), and post-surgical care.
Post-operative Complications: Bleeding, elevated temperature, wound infection; abdominal distention, bleeding or bile leakage/drainage from puncture site.

Pancreatitis

Etiology/Pathophysiology: Inflammation of the pancreas, ranging from mild edema to severe enzymatic autodigestion. Caused by blockage of the pancreatic duct (bile reflux, stones, scar tissue). Leads to inflammation, swelling, and activation of digestive enzymes within the pancreas, causing further damage.
Causes: Structural/vascular anomalies, trauma, infections, metabolic disorders (hyperlipidemia, hypercalcemia), inflammatory bowel disease, heredity, excessive alcohol intake, certain drugs, refeeding (prolonged fasting/anorexia).
Symptoms: Severe upper abdominal pain (radiates to back/LUQ, relieved by leaning forward), nausea/vomiting, fever, hypotension, jaundice (if bile duct obstructed), diminished bowel sounds, abdominal distention/tenderness.
Assessment: Severe abdominal pain radiating to back, nausea, vomiting, low-grade fever, hypotension, jaundice, diminished bowel sounds, abdominal distention, tenderness.
Diagnosis: Abdominal CT/ultrasound, endoscopy, pancreatic enzymes (serum/urine), elevated serum amylase and lipase, leukocytosis, elevated hematocrit, hypocalcemia/hypoalbuminemia, hyperglycemia, ERCP.
Medical Management: Pain relief (NPO, NG suction, analgesics/antispasmodics, anticholinergics, antacids, antibiotics), fluid/electrolyte replacement (IV fluids, albumin), complication prevention (antibiotics, pseudocyst aspiration), and dietary management (low-fat/low-protein, clear liquids progressing to regular diet once pain controlled).
Complications: Respiratory distress syndrome, bleeding abnormalities.

Pancreatic Cancer

Etiology/Pathophysiology: Commonly originates at the head but can metastasize. Late diagnosis is a primary factor in poor prognosis.
Causes: Smoking, chemical exposures, diabetes, cirrhosis, chronic pancreatitis, high red meat/processed meat intake, coffee, obesity, genetics, African American male.
Pathophysiology: The cancer, often affecting the head of the pancreas, compresses and blocks the common bile duct causing jaundice. Rapid growth can invade surrounding structures. The resulting complications include biliary obstruction, secondary issues in the stomach/GI tract/vascular system and possible diabetes if islet cells involved.
Symptoms: Insidious onset with vague symptoms: anorexia, malaise, nausea, fatigue, abdominal pain (mid-epigastric/back), potential diabetes.
Assessment: Psychosocial history with at-risk populations, subjective: anorexia, fatigue, nausea, flatulence, changes in bowel movements, and steady dull/aching pain in epigastrium or back. Objective data: weight loss, jaundice.
Diagnosis: Transabdominal ultrasound, CT, endoscopic ultrasound (with fine-needle biopsy), ERCP, tumor markers.
Treatment: Often inoperable by time of diagnosis. Radical surgical resection like pancreatoduodenectomy (Whipple procedure) for head of pancreas tumors. Total pancreatectomy with resecting other parts of the GI tract for more diffuse concerns. Palliative care measures are important when cure is not possible.
Prognosis: 5-12 month median survival; poor prognosis is caused by late diagnosis and aggressive disease, low five-year survival rate.

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Test your knowledge on cirrhosis and hepatitis, including their symptoms, complications, and nursing interventions. This quiz covers important aspects like dietary recommendations and laboratory findings related to liver conditions. Perfect for healthcare students and professionals seeking to reinforce their understanding of liver diseases.