Restricting the carbohydrates will reduce the synthesis of VLDL

thus, increased VLDL synthesis is mechanism of action in alchoholic fatty liver!!

20. Liver: cirrhotic liver with fatty change Note the diffuse nodularity of the liver and the yellowish discoloration representing fatty change. This patient was most likely an alcoholic, since alcohol is the most common cause of fatty change and cirrhosis of the liver. Refer to the class notes for the pathophysiology of fatty change.

21. Liver: fatty change secondary to alcoholism

The accumulation of triglyceride (TG) in the liver or fatty change is a reversible reaction induced by a number of different agents, the most common of which is alcohol. Its favored location in hepatocytes around the central veins in the liver (see arrow on left side of the slide) is closely linked to the mechanics of blood flow from the portal triads to the central vein. Hepatic artery and portal vein tributaries in the portal triads (see arrow on the right side of the slide) discharge blood into the liver sinusoids, which are located in-between cords of hepatocytes. The sinusoidal blood drains into the central veins, which coalesce to form the hepatic vein . Hepatocytes located around the central veins receive less O₂ and other nutrients than those surrounding the more peripherally located portal triads, which benefit by having the first exposure to the blood. This structural arrangement renders the central vein-associated hepatocytes more susceptible to drugs or chemicals, whose metabolic products form free radicals or toxic substances, also fatty change secondary to alcohol and tissue hypoxia. Note how the fatty change (see middle arrow) is located around the central veins rather than the portal triad.

In general, the two primary mechanisms involved in the production of fatty change in the liver relate to (1) increased synthesis of TG secondary to an increase in key substrates, such as fatty acids and glycerol 3-phosphate, ex. Alcoholics and (2) problems in the secretion of TG from the hepatocyte into the plasma (e.g., deficiency of apolipoproteins=kwashiorkor). Sources of fatty acids include excess lipolysis of adipose tissue (e.g., corticosteroids, starvation, alcohol), increased production of acetate (a product of alcohol metabolism), and increased synthesis of fatty acids from acetyl CoA (a product of alcohol metabolism).

Kwashiorkor: reduce protien intake ---> dec apolipoproteins --> needed to cover the VLDL so that it can become soluble in blood!! ---> VLDL cant go out of the liver –-> huge fatty liver

also dec. oncotic pressure ---> Ascites

---> big prutuberant abdomen

Cell Injury
Post 4: (Dated: Jan 15 - 2009)

You need proteins around lipids to dissolve in water.

Other causes of fatty liver: CO poisoning, shock, reye’ syndrome, drugs(tetracycline, amiodarone)

Ferritin: soluble form of iron ---> best marker for diagnosis of iron dificiency anemia or hemosiderosis, hemochromatosis.

Hemosiderin (Insoluble iron storage), Stored in MacroPhages and BM, stained with Prussian Blue

		29. Liver: microscopic section of liver in hemochromatosis Note the golden brown pigment in the liver parenchymal cells (see arrow) and the inflammatory infiltrate. Recall that iron enhances the synthesis of hydroxyl free radicals, which in turn damage the tissue. In this case, the damage is in the form of fibrosis, which results in cirrhosis of the liver. Hemochromatosis is the second most common genetic disease (AR inheritance) in the United States. It is due to an unrestricted reabsorption of iron from the duodenum.
		31. Lungs: chronic pulmonary congestion with hemosiderin laden alveolar macrophages Note the rusty colored material in the alveolar macrophages. This patient had chronic pulmonary edema from left heart failure. The increased hydrostatic pressure in the pulmonary capillaries causes them to rupture, hence releasing RBCs into the alveoli. Alveolar macrophages phagocytose the RBCs and hemosiderin accumulates in the cytoplasm. In the setting of heart failure, these cells are called heart failure cells, which are frequently expectorated and produce a rusty colored sputum.

Dystrophic calcification: Calcium loves to calcify damaged tissue, normal serum calcium.... (Fat necrosis, ATH, aortic stenosis, hemolytic anemia)

ORNISH DIET??? Can reverse atheromatous plaques!!!?

Aortic stenosis: in bicuspid --> two valves doing job of 3 ---> stenosis ---> Dystrophic calcification

Cong bicuspid aortic valve most common cause of aortic stenosis in USA ---> 2 valves instead of 3.

35. Aortic valve: bicuspid aortic valve with dystrophic calcification leading to aortic stenosis Note that the aortic valve has two rather than three cusps. This is a congenital bicuspid aortic valve. Since two cusps are doing the job of three cusps, they are damaged over time and develop dystrophic calcification (see arrow), which narrows the orifice of the valve leading to stenosis. Aortic stenosisresults in problems with opening of the valve and the ejection of blood during systole. Left ventricular hypertrophy with concentric pathologic hypertrophy is a response to the valve stenosis.

Examples:

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