Liver Function and Diseases Quiz

Chapter 25: Liver Disease and Gallstones

The liver is the most metabolically active organ.
It processes, stores, and redistributes nutrients from food.
It produces most plasma proteins.
Bile is produced in the liver, emulsifying fat during digestion.
Bile is stored in the gallbladder between meals.
The liver detoxifies drugs and alcohol and processes excess nitrogen to urea for excretion.

Introduction

The liver is the most metabolically active organ.
The liver plays a central role in processing, storing, and redistributing the nutrients provided by the foods we eat.
The liver produces most of the proteins circulating in plasma.
Bile is made in the liver, helps to emulsify fat during digestion, and is stored in the gallbladder.
The liver detoxifies drugs and alcohol and processes excess nitrogen.

Liver Anatomy and Function

The liver receives nutrients from the digestive tract.
The liver processes and stores/distributes throughout the body.
The biliary system (gallbladder and bile ducts) stores and secretes bile.
Bile is transported from the liver to the gallbladder and to the small intestine.
The hepatic portal vein carries nutrient-rich blood from the digestive tract to the liver.
The hepatic artery supplies oxygen-rich blood from the heart to the liver.
The hepatic vein carries blood from the liver to the heart.
The small intestine is missing in image to show placement of Gl tract veins.
Blood vessels that carry oxygen-rich blood from the heart to the intestines are not shown.

Disorders of the Liver

Fatty Liver: Accumulation of fat in the liver due to imbalance between fat production and export. Can be caused by metabolic defects, alcohol use, or drug exposure; insulin resistance is a key factor.
Hepatitis: Liver inflammation caused by virus infection or excessive alcohol, toxic chemicals, and autoimmune conditions. Common causes: Hepatitis A, B, C, D, and E. Can lead to cirrhosis and liver cancer.
- Types of Viral Hepatitis
  - Hepatitis A (HAV) : Fecal-oral transmission
  - Hepatitis B (HBV) : Bloodborne, sexual contact, mother-to-child
  - Hepatitis C (HCV) : Bloodborne, no vaccine

Fatty Liver

Fatty liver is an accumulation of fat in the liver due to an imbalance in fat production and export to the bloodstream.
Defects in metabolism, alcohol abuse, or drug exposure are common causes.
Nonalcoholic fatty liver disease typically involves insulin resistance.
Other causes can include protein-energy malnutrition (PEM), and long-term total parenteral nutrition (TPN).
Some cases are asymptomatic, while others cause inflammation, liver enlargement, and fatigue.
ALT (alanine aminotransferase) and AST (aspartate aminotransferase) are the liver enzymes typically elevated in laboratory tests.

Treatment of Fatty Liver

Eliminate causative factors (e.g., alcohol, drugs).
Lowering blood lipid levels, weight loss, exercise, and medication (to improve insulin sensitivity).
Rapid weight loss is generally discouraged.

Hepatitis

Liver inflammation, often from damage to liver tissue.
Caused by viral infection (A, B, C, D, E), excessive alcohol intake, exposure to toxic chemicals, and autoimmune conditions; fatty liver disease may also contribute.
Many cases are asymptomatic , Mild/chronic vs acute inflammation.
Long-term hepatitis can lead to cirrhosis and liver cancer. Symptoms include fatigue, nausea, vomiting, anorexia, pain in the liver area, jaundice, fever, muscle weakness, skin rashes, and joint pain.

Jaundice

Jaundice is a yellow discoloration of tissues caused by a build-up of bilirubin in the bloodstream.
Bilirubin is a breakdown product of hemoglobin, and its metabolism is normally processed and removed by the liver.
Liver dysfunction disrupts bilirubin metabolism, resulting in its accumulation in the blood.

Cirrhosis

Late-stage chronic liver disease characterized by extensive scarring (fibrosis) of liver tissue.
Long-term liver disease destroys liver tissue leading to scarring.
Impaired liver function can potentially lead to liver failure.
Causes include alcoholic liver disease, autoimmune hepatitis, bile duct obstructions, cystic fibrosis, galactosemia, glycogen storage diseases, hemochromatosis, and Wilson's disease; non-alcoholic fatty liver disease and viral hepatitis can also contribute.

Consequences of Cirrhosis

Portal Hypertension: Scarred liver tissue impedes blood flow, resulting in increased blood flow in nearby arterioles, leading to greater portal blood volume and high pressure in the hepatic portal vein. Collateral blood vessels can form.
Collateral Vessels and Gastroesophageal Varices: Diverted blood flow leads to enlarged veins (varices) in the esophagus and/or stomach area that can rupture and bleed.
Ascites: Accumulation of fluid in the abdominal cavity due to portal hypertension and impaired liver function. This causes discomfort, early satiety, and malnutrition problems.
Hepatic Encephalopathy: Abnormal neurological function, particularly due to high levels of ammonia in the blood. Normally, the liver converts ammonia into urea. Liver impairment results in ammonia accumulation, impairing neurological function.

Treatment of Cirrhosis

Correcting the underlying cause of the disease and treating related complications.
Abstinence from alcohol.
Liver transplantation.
Medical therapies (e.g., diuretics, beta blockers).

Nutrition Therapy for Cirrhosis

Protein-energy malnutrition and muscle wasting are common.
Energy: 25-40 kcal/kg of dry body weight.
Protein: 1-1.5 grams per kg of dry body weight.
Carbohydrate and fat: Similar to general population (for managing insulin resistance).
Sodium: Restricted (2000 mg/day) when ascites are present but can sometimes use a higher sodium intake or fluid removal if too low.
Vitamins and minerals: Supplements may be required.
Enteral and parenteral nutrition: Support may be needed.

Gallstone Disease

Functions of Gallbladder: Formation of gallstones.
Types of Gallstones:
- Cholesterol: Majority of cases form from biliary sludge (thickened bile) and are caused by rapid weight loss, long-term TPN, or pregnancy.
- Pigment: Calcium salt (calcium bilirubinate) and are caused by biliary tract infections, cirrhosis, or sickle cell anemia.; often soft and easy to crush.

Consequences of Gallstones

Symptoms: Mostly asymptomatic; pain (steady and severe) may occur after consuming fatty meals.
Complications: Distension and inflammation of the gallbladder; perforation of the gallbladder; peritonitis (inflammation of the peritoneum); fistulas.

Risk Factors for Cholesterol Gallstones

Genetic factors
Estrogen increases cholesterol secretion in bile.
Hormonal changes: increased estrogen and progesterone.
Gallstones do not dissolve spontaneously.
Increased cholesterol synthesis in liver, resulting in higher cholesterol concentrations in bile.

Treatment Options for Gallstones

Gallbladder surgery: Removal of the gallbladder.
Medication: Ursodeoxycholic acid (ursodiol) to dissolve gallstones.
Shock wave lithotripsy: Break apart gallstones with shock waves to pass into intestines without causing symptoms.

Anemia

Definition: Insufficient number of red blood cells, resulting in lower oxygen-carrying capacity of blood.
Associated with: Many diseases.
Common in: Hospitalized patients.

Nutritional Anemias in Illness

Blood loss: Iron deficiency
Nutrient malabsorption: Iron, vitamin B12, intrinsic factor.

Anemia of Chronic Disease

Chronic diseases can cause anemia.
Anemia can be an initial sign of a chronic disease.
Characteristics include hepcidin.
Blood tests help to differentiate between anemia types.

Medications and Anemia

Drug-nutrient interactions
Impaired coagulation: Anticoagulants
Aplastic anemia: Drug categories
Hemolytic anemia: Cephalosporin (antibiotics), Fludarabine (anti-leukemia agent)

Liver Transplantation

Common illnesses prior to transplantation: Hepatitis C and alcoholic liver disease.
Nutrition status of transplant patients: Check for malnutrition prior to transplantation.
Post-transplant concerns: Organ rejection and infection, immunosuppressant drugs, and potential malnutrition.