Free fatty acids from adipose tissue or ingested food are normally transported into hepatocytes. In the liver, they are esterified to triglycerides, converted into cholesterol or phospholipids, or oxidized to ketone bodies. Release of triglycerides from the hepatocytes requires apoproteins to form lipoproteins. Excess accumulation of triglycerides within the liver may result from defects in any one of the events in the sequence from fatty acid entry to lipoprotein exit.
Causes of fatty change of the liver
1 .Alcohol is the MCC (most common cause) of fatty change in the liver: alter mitochondrial and SER function and thus inhibit fatty acid oxidation
2. Anoxia inhibits fatty acid oxidation
3. Starvation increases fatty acid mobilization from peripheral stores
Excess immunoglobulin accumulation in RER of plasma cells.
Fuse to form eosinophilic globules known as Russell bodies.
Mallory bodies (=Alcoholic Hyaline)
Are masses of keratin intermediate filaments within hepatocytes.
Seen in patients with alcoholic liver disease.
Refers to arterioles that have a glassy, amorphous eosinophilic material in the vessel wall that often narrows the lumen seen in small vessels in DM and hypertension.
Pigments are colored substances.
Exogenous: from outside the body
Carbon / coal dust
Endogenous: synthesized within the body
Carbon or coal dust
Air pollution® Inhalation of carbon dust ® alveolar macrophages ® accumulation in lymphatics, regional lymph nodes and lungs à blacken the tissues of the lungs (anthracosis) and the involved lymph nodes.
In Coal miners accumulation of coal dust composed of carbon and silicaà induces fibroblastic reaction à lung disease = coal worker’s pneumoconiosis.
Localized pigmentation of skin. Pigments à phagocytosed by dermal macrophages.