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This document discusses fatty change or steatosis, which describes the abnormal accumulation of triglycerides within parenchymal cells due to an overload of fat and carbohydrates. Causes include alcohol abuse, protein malnutrition, obesity, diabetes, starvation, and toxins. Fatty liver or hepatic steatosis is a reversible condition where large triglyceride molecules accumulate in liver cells, and can be either alcoholic fatty liver disease or nonalcoholic fatty liver disease associated with diabetes and obesity. On gross examination, the liver is enlarged, yellow, and greasy to touch. Microscopically, fat appears as clear areas in hepatocytes ranging from small early vacuoles to large vacuoles pushing the nucleus
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Fatty changes
Fatty change, also known as steatosis, is the abnormal accumulation of triglycerides within parenchymal cells. The most common location is the liver, as it is responsible for fat metabolism. Fatty change can be caused by toxins, alcohol abuse, protein malnutrition, diabetes mellitus, obesity, or anoxia. Alcohol abuse and diabetes associated with obesity are the most common causes of fatty liver. In diabetes, insulin resistance results in triglyceride accumulation in liver cells through impaired fatty acid oxidation, increased fatty acid synthesis and uptake, and decreased secretion of VLDL from the liver. Fat-laden liver cells are sensitive to oxidative stress damage from free radicals, which can cause mitochondrial and cell membrane
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Fatty change, also known as steatosis, is the abnormal accumulation of triglycerides within parenchymal cells. The most common location is the liver, as it is responsible for fat metabolism. Fatty change can be caused by toxins, alcohol abuse, protein malnutrition, diabetes mellitus, obesity, or anoxia. Alcohol abuse and diabetes associated with obesity are the most common causes of fatty liver. In diabetes, insulin resistance results in triglyceride accumulation in liver cells through impaired fatty acid oxidation, increased fatty acid synthesis and uptake, and decreased secretion of VLDL from the liver. Fat-laden liver cells are sensitive to oxidative stress damage from free radicals, which can cause mitochondrial and cell membrane
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LIVER PATHOLOGY
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The document discusses thyroid function tests and thyroid hormones. It describes:
1. The anatomy of the thyroid gland and its histology. Thyroid hormones include T4 and T3, which bind to transport proteins in the blood and act through the hypothalamic-pituitary-thyroid axis.
2. The tests used to evaluate thyroid function, including TSH, T4, and T3 levels, and tests to determine the cause of dysfunction like thyroid antibodies. Signs and symptoms of hyperthyroidism and hypothyroidism are also outlined.
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- TSH stimulates thyroid hormone synthesis and secretion. T4 is converted to T3 in tissues by deiodinase enzymes.
- Thyroid hormones are transported bound to carrier proteins and the free forms enter cells to increase metabolism.
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This document discusses fatty change (steatosis) in the liver. It begins by defining fatty change as the intracellular accumulation of neutral fat within parenchymal cells, especially in the liver. It then lists four types of reversible cell injury, including fatty change. The document goes on to discuss the etiology of fatty liver, which can result from excess fat in the body or from liver cell damage. The pathogenesis involves defects in six steps of normal fat metabolism in the liver that lead to triglyceride accumulation. Morphologically, fatty liver is enlarged with a pale yellow appearance. Microscopically, hepatocytes contain numerous lipid vacuoles of varying sizes.
Fatty liver.ppt
Fatty liver is characterized by the appearance of fat in the cytoplasm of liver cells. It often occurs because the liver plays a key role in fat metabolism. Fatty liver has many potential causes including obesity, diabetes, malnutrition, alcohol abuse, medications, and other illnesses. Microscopically, lipid vacuoles of varying sizes are seen within hepatocytes, sometimes clustered around the nucleus or towards the cell periphery. Special stains can be used to identify fat deposits in liver tissue samples.
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phosphorus estimation
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LIVER PATHOLOGY
IT INCLUDES ANATOMY, PHYSIOLOGY AND PATHOLOGY OF LIVER .
THE SOURCES ARE:-
THE MEDICAL TEXT BOOK OF ROBBIN'S PATHOLOGY
AND OTHERS
IMAGES SOURCE :- ATLAS BOOKS AND INTERNET
Lecture 4
Osmosis, tonicity, and cell volume are regulated by the permeability of cell membranes to water and solutes. Water moves across membranes through aquaporin channels and by osmosis down its concentration gradient. The osmolarity of extracellular fluid is normally 300 mOsm, and cells maintain volume by moving water in or out depending if the extracellular fluid is hypo- or hypertonic. The kidneys help maintain electrolyte and acid-base balance by reabsorbing or secreting ions like sodium, potassium, hydrogen, and bicarbonate to keep fluid volumes and pH within normal ranges.
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The document discusses thyroid function tests and thyroid hormones. It describes:
1. The anatomy of the thyroid gland and its histology. Thyroid hormones include T4 and T3, which bind to transport proteins in the blood and act through the hypothalamic-pituitary-thyroid axis.
2. The tests used to evaluate thyroid function, including TSH, T4, and T3 levels, and tests to determine the cause of dysfunction like thyroid antibodies. Signs and symptoms of hyperthyroidism and hypothyroidism are also outlined.
3. The hormone changes associated with different thyroid conditions - primary and secondary hyperthyroidism and hypothyroidism. TSH,
Amyloidoisis
Amyloidosis is caused by deposition of abnormal amyloid proteins in tissues, damaging their structure and function. There are different types depending on the precursor protein, but all amyloid proteins form insoluble fibrils with beta-pleated sheet structures. The two main types are primary amyloidosis associated with plasma cell dyscrasias and secondary amyloidosis linked to chronic inflammatory conditions. Amyloid deposits can affect many organs like kidneys, heart, liver and spleen, causing organ dysfunction. On staining, amyloid takes up Congo red dye and exhibits apple-green birefringence under polarized light microscopy.
Pathological Calcification
Dystrophic calcification occurs when calcium salts decompose in dead or damaged tissues, as seen in areas of necrosis or injured heart valves. It appears as gritty or hard deposits and results from trauma, infection, or prolonged immobility. Metastatic calcification occurs when high blood calcium levels cause calcium to deposit in normally healthy tissues, as seen with hyperparathyroidism, bone tumors, vitamin D toxicity, or renal failure. Both types of calcification involve the deposition of calcium phosphate or carbonate that can resemble bone mineralization.
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The document discusses thyroid hormones, their biosynthesis, regulation, actions, and peripheral conversion. Some key points:
- Thyroid hormones T4 and T3 are synthesized in thyroid follicles from iodine and tyrosine. T4 is the main secretory product while T3 is the biologically active form.
- TSH stimulates thyroid hormone synthesis and secretion. T4 is converted to T3 in tissues by deiodinase enzymes.
- Thyroid hormones are transported bound to carrier proteins and the free forms enter cells to increase metabolism.
- Thyroid hormone levels are regulated by a negative feedback loop involving the hypothalamus, pituitary and thyroid gland.
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The document discusses fatty liver and the biochemical basis and clinical conditions that can cause fatty liver. It notes that accumulation of abnormal quantities of lipids (>25-30% as triglycerides) in the liver is called fatty liver infiltration. Conditions that can cause fatty liver include starvation, diabetes, obesity from excess calorie intake, alcohol abuse, toxins, drugs, protein-energy malnutrition, and certain hormones. It also discusses lipotropic factors, which are substances that help mobilize fat and prevent its accumulation in the liver, such as choline, betaine, methionine, essential fatty acids, inositol, and some vitamins and minerals. Lipotropic factors can prevent fatty liver but cannot reverse an existing condition
Megaloblastic anaemia
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erythropioesis
Erythropoiesis is the process where red blood cells are produced. It occurs in multiple stages starting with hematopoietic stem cells in the bone marrow. The stem cells differentiate into progenitor cells and then normoblasts as they mature. The stages include the proerythroblast, basophilic, polychromatophilic, and orthochromatic normoblasts. Reticulocytes are released without a nucleus and circulate for a few days before becoming mature erythrocytes. Key regulators of erythropoiesis include erythropoietin, iron, vitamin B12, and folic acid which influence proliferation and maturation of red blood cells.
Rbc
This document discusses the composition and functions of blood. It begins by describing blood as a connective tissue composed of blood cells suspended in plasma. It then discusses the various blood cells (RBCs, WBCs, platelets) and their functions, as well as the components and roles of plasma. The document goes on to provide detailed information about erythropoiesis, hemoglobin, iron metabolism, and specific blood disorders like sickle cell anemia. In summary, the document provides a comprehensive overview of the components and functions of blood.
Mucosal barrier and peptic ulcer
The gastric mucosal barrier protects the stomach from acid damage and is composed of a tight epithelial cell lining, a mucus coating, and bicarbonate ions. Mucus secreted by mucus cells throughout the GI tract acts as a protectant and lubricant. It maintains the alkaline pH of epithelial cells despite gastric acid through its buffering properties. Peptic ulcers occur when this barrier is damaged, such as through excess acid secretion, bacterial infection by Helicobacter pylori, or drug use like NSAIDs. Common symptoms include upper abdominal pain relieved by food or antacids.
Liver function tests and interpretation
The document discusses liver function tests and bilirubin metabolism. It describes that liver function tests are useful for diagnosing and monitoring liver diseases. A battery of tests are needed since the liver has diverse functions including excretion, metabolism, protein and plasma synthesis, and storage. Specific tests mentioned include liver enzymes, albumin, prothrombin time, tumor markers, bilirubin, and dye excretion tests. The types of jaundice - hemolytic, obstructive, and hepatic - are distinguished based on conjugated and unconjugated bilirubin levels as well as other factors. Various inborn errors affecting bilirubin metabolism are also outlined.
Iron metabolism
Iron plays an important role in the body, being essential for hematopoiesis, energy production, and enzyme/hormone synthesis. It exists in protein-bound forms like heme and ferritin or insoluble hemosiderin. Iron levels are tightly regulated through dietary intake and absorption in the small intestine. Deficiency can lead to anemia and other issues, while excess free iron is toxic. The document discusses iron transport, absorption, dietary sources, and factors affecting absorption.
Lipoprotein metabolism
This document discusses lipoprotein metabolism and summarizes the key points. It notes that plasma consists of triglycerides, phospholipids, cholesterol, and other components. There are four major classes of lipoproteins that transport lipids in plasma: chylomicrons, VLDL, LDL, and HDL. The document outlines the formation and catabolism of chylomicrons and VLDL, which involves lipoprotein lipase, and the metabolism of LDL and HDL. Abnormalities in lipoprotein metabolism can lead to hypo- or hyperlipoproteinemia and diseases like atherosclerosis.
Adrenal gland functions and adrenal insufficiency
The adrenal glands sit above the kidneys and are composed of an inner medulla and outer cortex. The cortex secretes corticosteroids like mineralocorticoids and glucocorticoids, and androgenic hormones. Mineralocorticoids regulate sodium and potassium levels while glucocorticoids increase blood glucose and promote fat mobilization. The medulla secretes epinephrine and norepinephrine to stimulate the sympathetic nervous system. Adrenal insufficiency can cause severe renal disorders and electrolyte imbalances due to lack of mineralocorticoid production. Dental management of patients with adrenal insufficiency requires consideration of their corticosteroid needs and risk of stress.
Clinical evaluation calcium
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This document summarizes growth hormone deficiency and excess, including gigantism, acromegaly, and their causes, symptoms, diagnosis, and treatment. Gigantism results from excess growth hormone before epiphyseal fusion and presents with dramatic acceleration of growth. Acromegaly occurs after epiphyseal fusion and presents with soft tissue swelling and coarsening of facial features. Diagnosis involves elevated IGF-1 and failure of GH to suppress with an oral glucose tolerance test. Treatment prioritizes surgical removal of pituitary tumors, while medication includes somatostatin analogues, dopamine agonists, and GH receptor antagonists.
Carbohydrate
The document discusses various methods for analyzing carbohydrates, including qualitative and quantitative tests. It begins by classifying carbohydrates based on carbon atom count, terminal functional groups, number of sugar subunits, and other characteristics. Several common qualitative carbohydrate tests are then described in detail, including the Molisch test, Benedict's test, Barfoed's test, and others. The tests allow identification of carbohydrates by reaction color or formation of characteristic precipitates. The document also mentions quantitative carbohydrate analysis using liquid chromatography-mass spectrometry and biochemical testing specifically for glucose.
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Fatty liver
This document discusses fatty change (steatosis) in the liver. It begins by defining fatty change as the intracellular accumulation of neutral fat within parenchymal cells, especially in the liver. It then lists four types of reversible cell injury, including fatty change. The document goes on to discuss the etiology of fatty liver, which can result from excess fat in the body or from liver cell damage. The pathogenesis involves defects in six steps of normal fat metabolism in the liver that lead to triglyceride accumulation. Morphologically, fatty liver is enlarged with a pale yellow appearance. Microscopically, hepatocytes contain numerous lipid vacuoles of varying sizes.
Fatty liver.ppt
Fatty liver is characterized by the appearance of fat in the cytoplasm of liver cells. It often occurs because the liver plays a key role in fat metabolism. Fatty liver has many potential causes including obesity, diabetes, malnutrition, alcohol abuse, medications, and other illnesses. Microscopically, lipid vacuoles of varying sizes are seen within hepatocytes, sometimes clustered around the nucleus or towards the cell periphery. Special stains can be used to identify fat deposits in liver tissue samples.
liver fatty disorder.ppt pg and mbbs path
Gaucher's disease or Gaucher disease (/ɡoʊˈʃeɪ/) (GD) is a genetic disorder in which glucocerebroside (a sphingolipid, also known as glucosylceramide) accumulates in cells and certain organs. The disorder is characterized by bruising, fatigue, anemia, low blood platelet count and enlargement of the liver and spleen, and is caused by a hereditary deficiency of the enzyme glucocerebrosidase (also known as glucosylceramidase), which acts on glucocerebroside. When the enzyme is defective, glucocerebroside accumulates, particularly in white blood cells and especially in macrophages (mononuclear leukocytes, which is often a target for intracellular parasites). Glucocerebroside can collect in the spleen, liver, kidneys, lungs, brain, and bone marrow.
Manifestations may include enlarged spleen and liver, liver malfunction, skeletal disorders or bone lesions that may be painful, severe neurological complications, swelling of lymph nodes and (occasionally) adjacent joints, distended abdomen, a brownish tint to the skin, anemia, low blood platelet count, and yellow fatty deposits on the white of the eye (sclera). Persons seriously affected may also be more susceptible to infection. Some forms of Gaucher's disease may be treated with enzyme replacement therapy.
The disease is caused by a recessive mutation in the GBA gene located on chromosome 1 and affects both males and females. About one in 100 people in the United States are carriers of the most common type of Gaucher disease. The carrier rate among Ashkenazi Jews is 8.9% while the birth incidence is 1 in 450.[1]
Gaucher's disease is the most common of the lysosomal storage diseases.[2] It is a form of sphingolipidosis (a subgroup of lysosomal storage diseases), as it involves dysfunctional metabolism of sphingolipids.[3]
The disease is named after the French physician Philippe Gaucher, who originally described it in 1882.[4]
Signs and symptoms
Painless hepatomegaly and splenomegaly: the size of the spleen can be 1500–3000 g, as opposed to the normal size of 50–200 g. Splenomegaly may decrease the affected individual's capacity for eating by exerting pressure on the stomach. While painless, enlargement of spleen increases the risk of splenic rupture.
Hypersplenism and pancytopenia, the rapid and premature destruction of blood cells, leads to anemia, neutropenia, leukopenia, and thrombocytopenia (with an increased risk of infection and bleeding).
Cirrhosis of the liver is rare.
Severe pain associated with joints and bones occurs, frequently presenting in hips and knees.
Neurological symptoms occur only in some types of Gaucher's (see below):
Type I: impaired olfaction and cognition
Type II: serious convulsions, hypertonia, intellectual disability, and apnea
Type III: muscle twitches known as myoclonus, convulsions, dementia, and ocular muscle apraxia
Parkinson's disease is recognized as being more common in Gaucher's disease patients and their heterozygous carrier relatives.[5]
Osteoporosis: 75% of p
Lipid metabolism
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
fatty liver grades.pdf
Like diabetes, Fatty liver disease is also considered a Silent Killer disease because people don’t feel any symptoms in the initial stage of fatty liver disease.
It slowly comes into your body and causes chronic liver disease.
The severity of the fatty liver disease depends on fatty liver grades. Your liver condition will become more vulnerable if fatty liver grades get increase.
Fatty liver disease is a metabolic disease where fat gets stored in your hepatocytes or liver cells that, cause inflammation.
There are two main types of fatty liver disease – alcoholic fatty liver disease (AFLD) and non-alcoholic fatty liver disease (NAFLD).
Fatty liver disease is generally graded based on the amount of fat stored and the degree of liver damage. This is called Fatty Liver Grades.
Simply, this fatty liver grade represents stages of fatty liver. There are four grades of fatty liver – Grade 1, Grade 2, Grade 3 and Grade 4.
Fatty liver disease is a silent disease; it comes with no signs or symptoms.
NAFLD (non-inflammatory or Grade 1 fatty liver) is asymptomatic, meaning you don’t feel any symptoms.
Still, you may have fatigue, thirst, anxiety, upper abdominal pain, bloating or discomfort, etc. These are the most common symptoms of NAFLD.
As the disease progresses, symptoms start appearing, usually in advance grading of fatty liver disease such as NASH (inflammatory fatty liver)
If left untreated, you may have a more severe liver condition that gets more complicated.
Although the exact cause of fatty liver is still unclear, but there are certain possible reasons to cause fatty liver.
A bad lifestyle is the most significant risk factor for developing NAFLD (Non-alcoholic fatty liver disease).
The good news is that you can reverse your fatty liver disease and even cure it.
If you get diagnosed early, it can be treated because some fatty liver grades are reversible, such as grade 1, grade 2 and grade 3.
But if you get liver cirrhosis or grade 4 fatty liver, that is irreversible. At this stage, your liver cells cannot reduce fat and can’t return to a healthy liver.
This post will discuss fatty liver grades, types, causes, pathology, symptoms, complications, diagnostic tests and treatment.
3
This document summarizes different types of reversible cellular injury including disorders of cellular water balance and abnormal intracellular accumulations. Cellular swelling and vacuolar degeneration are described as early manifestations of injury due to failure of ion pumps and increased cellular water content. Different patterns of intracellular lipid accumulation are also summarized, including fatty change (steatosis) in the liver, heart and kidneys. The document outlines mechanisms, morphology and significance of reversible fatty changes as well as lipid accumulations in fat cells and macrophages.
Alcoholic liver disease mbbs
1. Alcoholic liver disease progresses through three main stages - fatty liver, alcoholic hepatitis, and fibrosis/cirrhosis.
2. Heavy alcohol use over many years is generally required for severe liver injury to develop.
3. Alcohol is metabolized in the liver, producing toxic metabolites that can cause fat accumulation, inflammation, and scarring of the liver tissue over time.
Metabolic effects of diabetes mellitus
Metabolic changes in diabetes result from insulin deficiency and profoundly affect the liver, muscle, and adipose tissue. This leads to hyperglycemia and ketoacidosis as the liver produces glucose while tissues cannot utilize it. It also causes increased mobilization of fatty acids from adipose tissue and their breakdown in the liver, resulting in the production of ketone bodies. Excess fatty acids are also converted to triglycerides and secreted into the bloodstream. The insulin deficiency shifts energy production away from carbohydrate metabolism and towards fat oxidation, cholesterol synthesis, and ketone body synthesis.
Triglyceride metabolism
Triacylglycerols (TAGs), also known as triglycerides, are the major form of dietary lipids and stored energy in adipose tissue. TAGs are synthesized from glycerol and fatty acids in the liver and adipose tissue. In the liver, TAGs are packaged into VLDL particles and exported, while in adipose tissue TAGs are stored. The rate of TAG synthesis and breakdown is regulated by hormones like insulin and glucagon. During fasting, lipolysis increases in adipose tissue, releasing fatty acids that can be used by other tissues or converted to ketone bodies by the liver.
Carbohydrate.ppt
This document discusses carbohydrates, including their classification, digestion, absorption, and metabolism. It covers monosaccharides, oligosaccharides, polysaccharides, and complex polysaccharides. Specific carbohydrates like starch, glycogen, and cellulose are explained. The roles of carbohydrates in the body and digestion/absorption process are summarized. Causes, symptoms, and types of diabetes and conditions like hypoglycemia and hyperglycemia are defined at a high level. Sources of carbohydrates and recommended intake levels are also provided.
An introduction to alcoholic liver disease part 2
This document provides an overview of alcoholic liver disease (ALD) in multiple parts. It begins by discussing how alcohol is metabolized in the liver and can cause liver dysfunction by damaging hepatocytes and producing toxic byproducts. The major manifestations of ALD are then described, including jaundice, coagulopathy, and encephalopathy, which result from impaired bilirubin metabolism, clotting factor synthesis, and other liver functions. The document outlines the spectrum of ALD from fatty liver to alcoholic hepatitis to cirrhosis. Diagnosis involves assessing alcohol use history and liver enzymes/function. The characteristics of fatty liver, alcoholic hepatitis, and cirrhosis are summarized.
Fatty liver
The document discusses factors that regulate lipid content in the liver and different types of fatty liver. It explains that normal liver lipid content is maintained through a balance of influences on lipid synthesis, mobilization, and utilization. An imbalance can result in abnormal lipid accumulation and fatty liver. Five types of fatty liver are described based on their etiology: type 1 from overfeeding of fat, type 2 from excess carbohydrate metabolism, type 3 from increased lipid mobilization, type 4 from reduced mobilization from liver, and type 5 from reduced lipid utilization in the liver. Causes, characteristics, and examples are provided for each type.
Disorders of lipid metabolism | Hypercholesterolemia | Atherosclerosis | Fatt...
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FATTY LIVER
Fatty liver, or hepatic steatosis, refers to excess triglyceride accumulation in liver cells. This can be caused by increased fatty acid mobilization from adipose tissue, excess fatty acid synthesis in the liver, or reduced removal of fat from the liver. Common causes include obesity, uncontrolled diabetes, high-fat diet, alcoholism, and deficiencies in lipotropic factors like choline, betaine, and inositol. Untreated, fatty liver can progress to non-alcoholic steatohepatitis and fibrosis or cirrhosis of the liver.
Triglyceride metabolism
The document discusses lipids and triglycerides, explaining that triglycerides are composed of a glycerol molecule bonded to three fatty acids and serve as the main form of energy storage. It describes the processes of lipogenesis where triglycerides are synthesized from glucose, and lipolysis where triglycerides are broken down by hormones to release fatty acids. The summary also notes that triglycerides are stored in adipose tissue and mobilized from there to meet energy needs or deposited in the liver in conditions like fatty liver disease.
Malabsorption syndromes
Malabsorption syndromes occur when nutrients are not properly absorbed in the small intestine, leading to deficiencies. Common symptoms include chronic diarrhea and steatorrhea, or excess fat in stool. Malabsorption can result from problems with intraluminal digestion by pancreatic enzymes or bile acids, defects in brush border enzymes, or issues with transcellular transport. Treatment focuses on correcting nutritional deficiencies through supplementation or parenteral nutrition, as well as treating any underlying diseases causing the malabsorption.
Alcoholic Liver Disease- Aditya Pandey
this presentation consists of information about alcoholic liver disease like introduction, risk factors, treatments, and many other things.
so stay tuned
Alcohol
Excessive alcohol consumption can cause serious health issues. It is associated with liver disorders when consumed at more than 20-30g per day. While small amounts may provide some benefits, most of the ingested ethanol is metabolized in the liver to acetaldehyde by alcohol dehydrogenase. Chronic alcohol abuse can lead to fatty liver, alcoholic hepatitis, and alcoholic cirrhosis over time as the toxic byproducts damage liver cells. It also increases risks of certain cancers and causes nutritional deficiencies. Currently, heavy drinking affects millions of Americans and accounts for over 200,000 deaths annually mainly due to liver disease and cancer.
Janssens thesis
This document summarizes the effects of diet and exercise on liver lipid metabolism. It discusses the normal pathways of hepatic lipid metabolism, including lipid influx from adipose tissue and diet, de novo lipogenesis from carbohydrates, and lipid oxidation and secretion. Dietary fat and carbohydrates can accumulate in the liver as triglycerides if uptake and synthesis exceed oxidation and secretion. The roles of different transcription factors and enzymes involved in lipogenesis are also described.
NAFLD non alcoholic fatty liver disease.pptx
This document provides an overview of non-alcoholic fatty liver disease (NAFLD). It discusses that NAFLD is increasingly a cause of liver disease globally, with a prevalence of 25% worldwide and 9-53% in India. NAFLD refers to hepatic fat accumulation in the absence of excessive alcohol use or other known liver diseases. The spectrum of NAFLD ranges from simple steatosis to non-alcoholic steatohepatitis (NASH) which is characterized by inflammation and cellular injury, and can progress to cirrhosis. Genetic and environmental factors contribute to NAFLD pathogenesis. Insulin resistance is a major driver, and comorbidities like obesity, diabetes, and obstructive
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fatty change.pptx
- 2. Fatty change/steatosis Describes abnormal accumulation of triglycerides within parenchymal cells.it is an error of metabolism in which increased intestinal uptake of fats and carbohydrates overloads the fat transport and breakdown system resulting in deposition of large droplets of oil in the liver and renal parenchyma Causes: Alcohol abuse Protein malnutrition Obesity DM Anorexia(starvation) Toxins (CCL4, chloroform, ether) 2
- 3. Fatty liver/Hepatic steatosis Also known as fatty liver disease Reversible condition where large molecules of triglycerides accumulate in the liver cells Two main types: 1) Alcoholic fatty liver disease (AFLD) 2)Nonalcoholic fatty liver disease (NAFLD): Associated with diabetes and obesity Can progress to steatohepatitis and ultimately cirrhosis which are irreversible 3
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- 5. GROSS 5
- 6. Liver is enlarged and yellow Capsule is tense and glistening The cut surface is pale yellow and greasy to touch 6
- 7. MICROSCOPY Fat in the cytoplasm of hepatocytes appears as a clear area At beginning, hepatocytes present small fat vacuoles around the nucleus (microvesicular fatty change) In later stages, size of vacuoles increases, pushing the nucleus to the periphery of the cell, giving characteristic signet ring appearance (macrovesicular fatty change) Sometimes fatty cysts are produced by rupture of adjacent hepatocytes containing fat 7
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- 9. A) NORMAL LIVER B) FATTY LIVER 9
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