Liver Diseases and Pathologies Quiz
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Questions and Answers

Massive damage to the liver can result from toxins, drugs, and viruses.

True (A)

Inflammation of the liver is characterized by a deficiency of inflammatory cells.

False (B)

Fibrosis in the liver can occur due to inflammation or toxicity acting directly on liver tissue.

True (A)

In massive hepatocellular necrosis, liver regeneration can occur only if the reticular network is disrupted.

<p>False (B)</p> Signup and view all the answers

Hydropic degeneration in hepatocytes is often a precursor to other types of dystrophies.

<p>True (A)</p> Signup and view all the answers

Biliary stasis is a form of metabolic disturbance that affects liver function.

<p>True (A)</p> Signup and view all the answers

Vacuolar degeneration in hepatocytes is commonly associated with starvation and hypoxia.

<p>True (A)</p> Signup and view all the answers

Dystrophies can be classified into groups based on the presence or absence of iron pigments.

<p>True (A)</p> Signup and view all the answers

The synthesis of coagulation factors is increased in chronic liver diseases.

<p>False (B)</p> Signup and view all the answers

Vitamin K deficiency in chronic liver diseases is often due to malabsorption of fat-soluble vitamins.

<p>True (A)</p> Signup and view all the answers

In chronic liver diseases, there is an increase in the number of platelets due to hypersplenism.

<p>False (B)</p> Signup and view all the answers

Elevated levels of plasmins indicate an increase in fibrinolysis in patients with liver problems.

<p>True (A)</p> Signup and view all the answers

Factor VIII is consistently low in liver diseases.

<p>False (B)</p> Signup and view all the answers

Thrombocytopenia in chronic liver diseases can result from immune thrombocytolysis.

<p>True (A)</p> Signup and view all the answers

Excessive fibrinolysis is a common condition among patients with liver cirrhosis.

<p>True (A)</p> Signup and view all the answers

Antithrombin III activity decreases in severe liver diseases.

<p>True (A)</p> Signup and view all the answers

Cori type I is associated with glucose-6-phosphatase deficiency, leading to decreased glucose-6-phosphate levels.

<p>True (A)</p> Signup and view all the answers

Pompe disease is characterized by glycogen storage in the liver only.

<p>False (B)</p> Signup and view all the answers

Hyaline degeneration results in the storage of substances predominantly within the cells.

<p>False (B)</p> Signup and view all the answers

Fibrinoid degeneration is characterized by the fragmentation and disintegration of collagen fibers.

<p>True (A)</p> Signup and view all the answers

Amyloid degeneration involves proteins that are stored intracellularly.

<p>False (B)</p> Signup and view all the answers

Generalized glycogenoses result from genetically determined enzyme deficiencies.

<p>True (A)</p> Signup and view all the answers

Increased glycogen content in the liver can lead to organ hypertrophy.

<p>True (A)</p> Signup and view all the answers

Mallory hyaline bodies are primarily associated with acute liver inflammation.

<p>False (B)</p> Signup and view all the answers

Hemosiderosis is characterized by an excessive accumulation of hemosiderin primarily in the liver and pancreas.

<p>True (A)</p> Signup and view all the answers

Hemochromatosis only has a primary form and does not occur secondarily due to other diseases.

<p>False (B)</p> Signup and view all the answers

In hemochromatosis, the excessive absorption of iron can lead to conditions such as liver cirrhosis.

<p>True (A)</p> Signup and view all the answers

Copper accumulation in the liver is a characteristic feature of Hemosiderosis.

<p>False (B)</p> Signup and view all the answers

Prolonged obstructive cholestasis can result in necrosis and the formation of 'bile lakes' in the liver.

<p>True (A)</p> Signup and view all the answers

Hepatic steatosis is only caused by obesity and does not have other contributing factors.

<p>False (B)</p> Signup and view all the answers

Biliary infarction is associated with the accumulation of extravasated bile in the liver.

<p>True (A)</p> Signup and view all the answers

Foamy degeneration in hepatocytes occurs due to the accumulation of bile pigments.

<p>True (A)</p> Signup and view all the answers

Hepatocellular necrosis, fibrosis, and regeneration can lead to the formation of fibrous septa around hepatocytic nodules.

<p>True (A)</p> Signup and view all the answers

Macroscopic examination of granulomatous hepatopathy reveals the presence of nodules larger than 2 mm in diameter.

<p>False (B)</p> Signup and view all the answers

The liver can be affected by a variety of viruses, including hepatitis viruses A, B, C, D, E, F, and G.

<p>True (A)</p> Signup and view all the answers

Langhans cells are characterized by nuclei located at the center of the cells.

<p>False (B)</p> Signup and view all the answers

Pancreatic head adenocarcinoma primarily targets hepatocytes.

<p>False (B)</p> Signup and view all the answers

The giant cells in granulomas are derived from modified fibroblasts.

<p>False (B)</p> Signup and view all the answers

The liver is essential for metabolism of proteins, lipids, and carbohydrates.

<p>True (A)</p> Signup and view all the answers

Fibrosis in the liver takes a very short time to develop.

<p>False (B)</p> Signup and view all the answers

In infectious hepatitis, there is a decrease in albumins and an increase in gammaglobulins.

<p>True (A)</p> Signup and view all the answers

The Ritis Ratio is represented by the ratio of globulins to albumins.

<p>False (B)</p> Signup and view all the answers

In advanced forms of chronic hepatitis, a characteristic 'β-γ' block is present.

<p>True (A)</p> Signup and view all the answers

In hemolytic jaundice, the urine shows an absence of UBG.

<p>False (B)</p> Signup and view all the answers

Mechanical jaundice is associated with high levels of direct bilirubin in the blood.

<p>True (A)</p> Signup and view all the answers

In hepatogenic jaundice, total cholesterol levels are elevated.

<p>False (B)</p> Signup and view all the answers

In the case of cholestasis, the duodenal juice may show a decrease in bile pigments.

<p>True (A)</p> Signup and view all the answers

Hepatogenic jaundice is indicated by increased levels of both direct and indirect bilirubin in the blood.

<p>True (A)</p> Signup and view all the answers

Flashcards

Massive Liver Damage

Severe liver damage caused by toxins, drugs, or viruses.

Ballooned Hepatocytes

Hepatocytes (liver cells) appear swollen and filled with fluid.

Liver Inflammation

Inflammation in the liver characterized by the influx of inflammatory cells.

Liver Regeneration

The liver's ability to regenerate damaged tissue.

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Liver Fibrosis

An excessive buildup of scar tissue in the liver.

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Cirrhosis

A severe form of liver disease characterized by widespread fibrosis and nodule formation.

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Protein Metabolism Degeneration

A type of liver degeneration caused by disturbances in protein metabolism.

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Ionic Imbalance Degeneration

A type of liver degeneration resulting from an imbalance of ions.

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Hypocoagulability in Chronic Liver Diseases

A state of reduced blood clotting ability often seen in chronic liver diseases. It arises due to decreased production of clotting factors by the damaged liver, leading to a deficiency in fibrinogen and prothrombin complex.

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Disseminated Intravascular Coagulation (DIC)

A complex clotting disorder characterized by widespread activation of clotting within blood vessels, leading to consumption of clotting factors, platelet depletion, and ultimately, bleeding.

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Hepatic Clearance Insufficiency

A condition where the liver cannot effectively remove clotting factors from the bloodstream, contributing to the development of DIC in chronic liver diseases.

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Fibrinolysis

A process that breaks down blood clots, which is often excessive in patients with chronic liver disease, leading to increased bleeding.

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Vitamin K Deficiency

A deficiency in vitamin K, often seen in chronic liver diseases, which impairs the synthesis of clotting factors.

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Hypersplenism

A condition where the spleen removes too many platelets from the blood, leading to a low platelet count and contributing to bleeding in chronic liver diseases.

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Thrombasthenia

Impaired platelet aggregation and adhesion, leading to poor clot formation and bleeding in chronic liver diseases.

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Deficient Megakaryopoiesis

A condition characterized by a decrease in the number of megakaryocytes, the cells that produce platelets, leading to thrombocytopenia (low platelet count).

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Hemosiderosis

A condition where iron accumulates in tissues, mainly due to overload or excessive hemosiderin buildup. It can affect the liver, pancreas, kidneys, heart, lymph nodes, and bone marrow. Common causes include hemolytic anemia and iron treatments.

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Hemochromatosis

A genetic disorder that results in excessive iron absorption, leading to iron accumulation in various organs. This can cause liver damage, diabetes, and skin discoloration.

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Iron Deposition in Liver (Hemochromatosis)

A form of liver damage caused by the buildup of iron in the liver, leading to cell death and fibrosis. This can progress to cirrhosis and ultimately liver failure.

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Foamy Degeneration (Bile Pigment Accumulation)

A type of cell degeneration characterized by the accumulation of excess bile pigments (bilirubin) within cells, leading to a foamy appearance.

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Cholestasis

The process of bile accumulation within the bile canaliculi, the tiny channels in the liver that transport bile.

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Obstructive Cholestasis

A severe form of cholestasis where bile is trapped within the liver, leading to liver cell damage, necrosis, and formation of "bile lakes" filled with debris.

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Hepatic Steatosis (Fatty Liver)

Accumulation of fat within liver cells, leading to steatosis, a condition characterized by fatty liver.

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Diffuse Hepatic Steatosis

The development of steatosis where the fatty changes spread throughout the liver lobules, altering the normal structure.

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Generalized Glycogenoses

A group of metabolic disorders where glycogen accumulates abnormally in cells due to enzyme deficiencies.

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Cori Type I

Type of glycogenosis caused by a deficiency in glucose-6-phosphatase, leading to decreased glucose production and hypoglycemia.

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Pompe Disease (Cori Type II)

A type of glycogenosis caused by lysosomal acid alpha-glycosidase deficiency, resulting in glycogen accumulation within lysosomes.

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Hyaline

A glassy, translucent substance found in tissues, often deposited extracellularly. It's often composed of protein or glycoprotein.

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Mallory Hyaline Bodies

The accumulation of hyaline in the cytoplasm of liver cells, often seen in alcohol-related liver disease.

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Fibrinoid

An acellular substance characterized by its acidophilic staining properties and complex structure. It often replaces normal tissue elements.

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Amyloid

A group of proteins that accumulate extracellularly in various tissues. They share unique staining characteristics and complex structures.

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Amyloid Degeneration

Degeneration of tissue characterized by the deposition of amyloid proteins.

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Alcoholic Cirrhosis

A chronic liver disease characterized by the formation of fibrous septa and nodules of varying sizes, leading to a macro- and micronodular appearance.

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Granulomas in Hepatopathy

Nodules in the liver consisting of epithelioid cells, multinucleated giant cells, and fibroblastic proliferation surrounded by lymphocytes and plasma cells.

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Epithelioid Cells

Cells derived from modified histiocytes and fibroblasts, found in granulomas, involved in immune response.

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Multinucleated Giant Cells

Large cells formed by the fusion of epithelioid cells, found in granulomas, play a role in engulfing foreign material.

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Langhans Cells

A type of multinucleated giant cell found in granulomas, with nuclei located at the periphery.

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Foreign Body Giant Cells

A type of multinucleated giant cell found in granulomas, with nuclei scattered throughout the cytoplasm.

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Specific Liver Structure Reactions

The reaction of different liver structures to various aggressions or insults, such as viruses, toxins, or medications.

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Infectious Mononucleosis Virus

A virus that attacks the reticulo-histiocytic system, not hepatocytes, causing infectious mononucleosis.

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Dysproteinemia in Infectious Hepatitis

A protein abnormality in which there are decreased albumin levels and increased gammaglobulins in the blood. This pattern is often seen in infectious hepatitis and reflects the liver's inability to produce albumin and its increased production of antibodies.

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Ritis Ratio

A specific ratio used to evaluate liver function. It is calculated by dividing the albumin level by the globulin level in the blood. A subunit value of the Ritis Ratio is indicative of chronic hepatitis where liver damage has compromised albumin synthesis.

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β-γ Block

A characteristic pattern observed in advanced chronic hepatitis and liver cirrhosis, where there is a reduction in the concentrations of beta and gamma globulins in the blood. This indicates a significant disruption in protein synthesis and liver function.

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Hemolytic Jaundice

A type of jaundice characterized by increased levels of unconjugated bilirubin in the blood. This is due to excessive hemolysis (breakdown of red blood cells) and the inability of the liver to conjugate the bilirubin.

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Mechanical Jaundice

A type of jaundice caused by obstruction of the bile ducts, preventing the flow of bile from the liver to the intestines. This leads to an accumulation of conjugated bilirubin in the blood, resulting in a yellowing of the skin and eyes.

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Hepatogenic Jaundice

A type of jaundice caused by damage to the liver cells themselves, impairing their ability to process bilirubin. This results in an accumulation of both conjugated and unconjugated bilirubin in the blood, indicating a serious liver problem.

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Serum Liver Function Tests

A laboratory test that measures the levels of bilirubin (both direct and indirect), alkaline phosphatase, and cholesterol in the blood. These values are used to assess liver function and identify potential liver damage or disease.

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Urine Liver Function Tests

A laboratory test that examines the presence of bilirubin and bile pigments in the urine. These tests can provide valuable insights into liver function and identify potential liver damage or disease.

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Study Notes

Biochemical Exploration of the Liver

  • The liver is susceptible to various metabolic, toxic, microbial, circulatory, and neoplastic aggressions.
  • Liver damage can be primary (e.g., viral hepatitis, hepatocellular carcinoma) or secondary to other diseases (e.g., heart failure, metastatic cancer, alcoholism, extrahepatic infections).
  • The liver has a large functional reserve, which leads to a latency in the clinical expression of early liver lesions.
  • Expansion of the pathological process can lead to life-threatening consequences due to functional imbalance.

Alteration of Carbohydrate Metabolism

  • Severe hepatopathies impact both glucose production (glycogenolysis, gluconeogenesis) and utilization (glycogenogenesis, triglyceride synthesis).
  • This can result in hypoglycemia, hyperglycemia, or glucose intolerance.
  • In cirrhosis, the number and volume of liver cells decrease, as does glucose intake.

Hypoglycemia

  • Hypoglycemia is less common in cirrhotics but can occur with malnutrition and alcohol abuse.
  • Alcohol inhibits gluconeogenesis.
  • Depletion of glycogen stores results in depressed gluconeogenesis.
  • Hepatic glycogen reserve reduction is linked to the destruction of hepatocytes.
  • Massive liver necrosis is associated with fulminant hepatitis, hypoglycemia, and potential death.
  • Dysfunction of glucose precursors (galactose and fructose) metabolism occurs in cirrhotics.

Alteration of Lipid Metabolism

  • Triglycerides are converted into ketones (prebeta-LP) in the liver in metabolic deficiencies.
  • High levels of ketone bodies (↑ketonemia > 70 mg/dL) exceeds the capacity of tissues (striated skeletal and myocardial).
  • Hyperketonemia can occur due to alcohol consumption (↑ lipolysis).
  • Cholesterol synthesis decreases in severe liver failure.
  • Cholestasis (impaired bile elimination) results in hypercholesterolemia.
  • Bile acid synthesis is reduced in some conditions, resulting in decreased glucuronic acid/taurocholic acid.

Alteration of Protein Metabolism

  • Chronic hepatopathy, especially cirrhosis, significantly reduces albumin synthesis.
  • Albumin levels can decrease due to dilution, alteration in distribution, or increased catabolism.
  • Degradation products are transported to the gastrointestinal tract.
  • The liver is crucial for globulin synthesis, with alpha and beta fractions being predominant.
  • Aggressiveness and cirrhosis cause hypergammaglobulinemia due to lympho-plasmacytic infiltration.

Disturbance of the Coagulation Mechanism

  • Chronic liver diseases often result in hypocoagulability.
  • Coagulation factor synthesis (e.g., fibrinogen, prothrombin, factors II, VII, IX, X) decreases due to hepatocellular insufficiency.
  • Levels of coagulation factors may increase, but these factors may be modified or have reduced function.
  • Vitamin K deficiency contributes to reduced coagulation factor production due to malabsorption.
  • Platelet numbers and function may be diminished.
  • Increased fibrinolysis and vascular fragility can increase the risk for hemorrhage.

Disturbance of Bile Secretion and Excretion

  • Various sites in hepatopathies alter bile secretion and excretion, including multiple locations, affecting:
  • Microsomal biotransfer systems, hepatocyte membranes, and desmosomes.
  • Bile canalicular membrane and canalicular ectoplasm.
  • Inflamed bile canaliculi result in increased bilirubin (direct bilirubin), bile acids, increased ALP, 5-nucleotidase, GGT, LAP activities.
  • Excess bile salts damage hepatocytes.

Alteration of the Bilirubin Capture Stages

  • Alteration of bilirubin's hepatic capture can occur due to liver cell damage, often related to other issues with hepatic metabolism of bilirubin.
  • Causes include conjugation or excretion deficiencies in conditions like Gilbert's syndrome.
  • Hypoactivity of hepatocyte UDP-glucuronyl-transferase is a factor in Gilbert's disease.

Alteration of the Conjugation Stage of Bilirubin

  • Deficiency in microsomal UDP-glucuronyl-transferase activity leads to increased unconjugated bilirubin in the blood.
  • This deficiency can be congenital (Gilbert syndrome, Crigler-Najjar syndrome) or acquired (drugs, infections, toxic agents).

Alteration of the Hepatocytic Excretion Stage of Bilirubin

  • Usually associated with mixed hyperbilirubinemia, primarily affecting the conjugated bilirubin fraction.
  • Issues with bilirubin transport or excretion in the bile ducts lead to this condition.
  • Relevant diseases include Dubin-Johnson syndrome, Rotor syndrome, acquired issues (medications, postoperative, acute and chronic hepatitis), and liver cirrhosis.

Disturbance of Clearance and Detoxification Function

  • The liver is central in detoxification of various substances (endogenous or exogenous).
  • Endogenous substances include hormones, ammonia, and bilirubin.
  • Exogenous substances include drugs and toxins.
  • Liver damage compromises antitoxic function, affected in the parenchyma and hepatic mesenchyme.

Toxic Syndrome

  • Liver cell inability to neutralize and eliminate catabolic and exogenous toxins leads to a toxic syndrome.
  • Reduced liver activity affects other cells and systems (i.e., derivation of the portal angel).
  • Elevated ammonia (NH3) in the blood can cause CNS toxicity, seizures, and potentially death.
  • Drug metabolism modifications in chronic hepatopathies impact oxidation pathways more than conjugation pathways.

Impairment of Pharmacokinetics in Drugs

  • Impairment in drug pharmacokinetics occurs due to intrinsic clearance, liver circulation, portocaval shunt, and plasma protein binding.
  • Three types of reactions occurring in the liver affect bilirubin metabolism:
  • Hemolysis, affecting the binding of bilirubin in white blood cells.
  • Alterations in bilirubin conjugation.
  • Changes in bile excretion and intrahepatic cholestasis.

Direct Hepatotoxicity

  • Direct hepatotoxicity can cause necrosis, with examples such as carbon tetrachloride (CCl4), halothane, chloroform, DDT, TNT, amanita phalloides, and certain drugs.
  • Hepatic steatosis can occur with minimal inflammatory infiltration.
  • Hepatocellular jaundice and death can occur in serious cases.

Disorders of Hormone Metabolism

  • The liver is important for steroid hormone catabolism.
  • Hyperestrogenism, hypercorticism, hyperaldosteronism, and decreased hepatic clearance of hormones can affect hormone balance.
  • The liver converts 17-hydroxysteroids to 17-ketosteroids, affecting androgen synthesis and resulting in potential disruptions and symptoms (such as secondary feminization).
  • Increased aldosterone and antidiuretic hormone (ADH) can lead to edema and ascites.

Hydro-Electrolytic and Acid-Base Balance

  • Liver damage can cause permeability changes, resulting in K+ loss from cells, increased blood K+, and entry of Na+ and H+ into cells.
  • Elevated blood K+ and loss of K+ in urine cause secondary hypokalemia and alkalosis.
  • Additional factors that worsen the situation include hypovolemia, increased Na+ retention, and decreased hormone degradation.

Phospho-Calcium Balance

  • Serum levels of calcium are affected by reduced serine fixation and transport.
  • Insufficient calcium intake (e.g., anorexia) and decreased calcium absorption contribute to hypocalcemia.
  • Impaired secretion of HCI and pancreatic insufficiency can affect vitamin D3 conversion into cholecalciferol, further hindering calcium metabolism.
  • Severe hepatopathies can lead to a rise in extracellular water due to decreased transport or metabolism.

Morphological Models of Hepatic Injury

  • Specific patterns of liver reactions to injury depend on the type of aggression and include:
  • Focal necrosis (often associated with microbial infections).
  • Degeneration (ballooning, edema due to metabolic disorders of proteins, lipids, carbohydrates, hemoglobin).
  • Inflammation (influx of inflammatory cells).
  • Regeneration (thickening of proliferating hepatocyte cords).

Fibrosis and Cirrhosis Outcomes

  • Severe liver necrosis can, in intact connective tissue, result in regeneration of all tissue.
  • Damage to the tissue network requires fibrosis to repair, resulting in fibrosis.
  • Fibrotic deposits lead to the transformation of nodules.
  • Accumulations of substances in the liver due to metabolic problems lead to pathologies.

Morphological Models of Hepatic Dystrophy

  • Dystrophy results from disturbances in protein metabolism, causing increased Na+/water uptake and K+ loss.
  • This results in cell swelling and mitochondrial swelling, seen as (turbid).
  • Such conditions are seen in infections, intoxications, hypoxia, and starvation.
  • Vacuoles result from content loss and free cellular water.

Dystrophies of Hemoglobin Pigments

  • These involve iron-containing pigment accumulations (hemosiderin), either localized or generalized.
  • Other pigments, like bilirubin, can accumulate in the liver, causing distinct dystrophies.
  • These are often associated with conditions like hemolytic anemia or increased iron load.

Hemosiderosis

  • Hemosiderosis occurs due to iron overload, typically from hemorrhages, liver stasis, or excessive iron treatment.
  • Hemochromatosis is a genetic condition leading to iron accumulation.
  • Deposits of iron in the parenchyma and organs result in characteristic complications.

Pigment Dystrophies

  • Excess bile pigments (bilirubin) lead to various changes, including hepatocyte foam cells and swollen bile canaliculi
  • Kupffer cells are crucial in absorbing and phagocytosing these substances.

Prolonged Obstructive Cholestasis

  • Obstruction of bile ducts results in foam-like hepatocyte changes and destruction.
  • Necrosis foci will accumulate cellular debris and bile pigments ("bile lakes").

Hepatic Steatosis

  • Excess fat accumulation may result from various causes (obesity, diabetes, alcohol use, and intoxications)
  • This can occur in different areas of the liver, and microscopic examination reveals hypertrophied liver cells with lipid droplets, which push the nucleus to the cell's periphery.

Degenerative Changes Through Carbohydrate Metabolism

  • Localized and generalized glycogenoses (due to enzyme deficiencies).
  • Type I and type II glycogenoses show generalized and localized glycogen buildup, respectively, causing disruptions in glucose-6-phosphatase and lysosomal acid alpha-glycosidase activity.
  • These conditions may impact many organs (especially heart, muscle, kidneys).

Hyaline Degeneration or Hyalinosis

  • Hyaline is protein or glycoprotein in nature and results in an acellular, homogeneous, translucent, and eosinophilic aspect.
  • Hyaline can accumulate in various locations in the liver and other tissues, and conditions like chronic alcoholism and certain viral infections may contribute
  • Mallory hyaline bodies are an example of hyaline accumulation.

Fibrinoid Degeneration

  • Fibrinoid, with tinctorial affinity, is an acellular substance with acidophilic appearance.
  • Swelling and fragmentation of the fundamental substance are hallmarks of the process, leading to fibrin formation.
  • Systemic lupus erythematosus (SLE) is a prevalent condition associated with fibrinoid dystrophy in the liver.

Amyloid Degeneration

  • Amyloid is a fibrillar protein deposit in tissues.
  • It is normally extracellular and can be morphologically characterized by tinctorial affinities.
  • Different proteins can clump together into amyloid, affecting the tissues.

Global Investigation of Functional Liver Mass

  • Liver transit tests are used to evaluate the functional liver mass, assessing its ability in:
  • Recognizing and processing substances using blood vessels.
  • Processing and transporting materials in sinusoids..
  • Transporting substances through hepatocytes using blood ducts.

Viral Markers in Hepatitis B

  • Viral hepatitis B has specific markers, including HBsAg, which are useful in diagnosis and prognosis.
  • Markers like HBsAg, HBcAg, and HBV DNA are critical in differentiating acute, chronic, and asymptomatic cases.
  • HBeAg is important in assessing the infectious status.

Autoimmune Manifestations

  • A range of various types of autoimmune issues can impact the liver.
  • Diseases like thyroid dysfunction, rheumatoid issues, or vasculitis can be associated.

Autoimmune Effects of IFN

  • IFN can trigger autoimmune responses in patients with chronic HCV infections, affecting various organs (like the thyroid gland).

Renal Manifestations

  • Infections like hepatitis C and B can be associated with various kidney-related conditions (proliferative, membranous glomerulonephritis, acute proliferative glomerulonephritis).

Alcoholic Hepatopathy

  • Chronic alcoholism causes various effects, and the most concerning is the toxic impact on the liver.
  • Steatosis, hepatitis, and cirrhosis can result, with different mechanisms involved (depending on alcohol intake, diet composition, and overall person physiology).

Overview of Liver Structures

  • The liver consists of hepatocytes, Kupffer cells, vessels, and bile canaliculi.

Alcoholic Hepatopathy Mechanisms

  • Excessive alcohol intake results in fat accumulation in liver cells (steatosis).

  • Altering lipid transport interferes with functions.

  • Alcohol metabolism generates potentially damaging substances which damage liver cells

  • Increasing fatty acid accumulation exacerbates problems.

  • Inflammation and fibrosis are common outcomes in alcoholic progression to liver problems.

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Test your knowledge on various liver diseases, their causes, and effects on liver function. This quiz covers topics such as hepatocellular necrosis, hydropic degeneration, and chronic liver disease implications. Understand complex interactions in liver pathology and enhance your learning on this critical organ.

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