d. Parenchymatous degeneration of liverCellular swelling occurs because of marked mitochondrial damage, cessation of ATP production and failure of sodium pump leading to increased osmotic pressure within cells. The alteration is on selective permeability of cellular membranes leading to influx of water molecules. PATHOGENESIS:Acute cell swelling or hydropic degeneration occurs due to failure of the injured cells to maintain electrolyte balance through the "Sodium-Potassium pump". As this mechanism is energy dependent, a fall in ATP in injured cells causes the efflux of Potassium ions. With the influx of Sodium ions, the increasing osmotic pressure in the cytoplasm attracts water molecules. As a result, swelling of the cells occur, and is evident grossly as an enlarged pale and heavy organ. Microscopically, affected cells show vacuoles in the cytoplasm with no distinct borders. The cytoplasm is diluted, and dispersed. This type of degeneration is apt to be present in most types of injury. It is particularly severe in toxic and febrile conditions. The condition is best seen in organs with intense metabolic rates of metabolism such as the liver, kidneys, and brain.MACROSCOPIC APPEARANCE:In cellular swelling, at gross examination, the affected organ is enlarged, pale and soft. MICROSCOPIC APPEARANCE:Microscopically, the cells are enlarged, with a clear cytoplasm (due to the presence of small clear or pale vacuoles, with indistinct shape and limits) and a normal nucleus in central position; blood capillaries are compressed, explaining the organ's pallor.e. Parenchymatous and fatty degeneration of liverFatty liver or steatosis hepatitis is present if the moist mass of the liver contains >10% fat, or if more than 50% of the hepatic cells display medium or large-sized lipid vacuoles and there is a diffuse pattern of distribution.PATHOGENESIS:The causes of the underlying fatty change may be: Exogenous:Increased fat transportIncreased carbohydrate intakeEndogenous:Increased peripheral mobilization of fatInhibited intracellular utilization of fat in the hepatic cellsIncreased fat synthesis in the hepatic cellsDecreased removal of fatMACROSCOPIC APPEARANCE:mild hepatomegaly (in ~75%) attenuation/signal of liver shifted towards that of fat focal fatty sparingislands of normal liver tissue within sea of hepatic steatosisMICROSCOPIC APPEARANCE:At the beginning, the hepatocytes present small fat vacuoles in the vicinity of the endoplasmic reticulum (liposomes) - microvesicular fatty change (photo). In the late stages, the size of the vacuoles increases pushing the nucleus to the periphery of the cell - macrovesicular fatty change. These vesicles are well delineated and optically "empty" because fat solves during tissue processing (paraffin embedding). Large vacuoles may coalesce, producing fatty cysts - which are irreversible lesions.f. Hemorrhagic infarct of lungHemorrhagic infarcts, also called red infarcts are bloody because venous or arterial obstruction occurs in loose, spongy tissue or tissue with a dual blood supply, notably the lung (which has blood supply from the right ventricle through the pulmonary artery and from the left ventricle via the bronchial artery branches from the aorta). In these organs, occlusion of one area can cause infarction, but the other supply continues to pump blood into the dead tissue.PATHOGENESIS:If emboli are small, they may pass through the main pulmonary arteries and become impacted in the peripheral branches, usually in the arteries supplying the lower lobes of the lungs. Smaller emboli impede the flow of blood through the lungs and raise pulmonary artery pressure, but they have a les devastating effect than large emboli. Frequently, the segment of lung supplied by the obstructed pulmonary artery undergoes necrosis, resulting in a pulmonary infarct. The alveolar septa break down, and blood flows from the ruptured capillaries into the pulmonary alveoli which become distended with blood.

MACROSCOPIC APPEARANCE:These infarcts are haemorrhagic (dark brown to black in colour) and the surrounding pulmonary parenchyma is consolidated. Compare this parenchyma with that of the upper lobe which is normal. This consolidation will be a result of the inflammatory response to the infarcts. In areas of consolidation the alveolar air spaces appear more prominent because they are clearly outlined by edematous inter-alveolar septae.

MICROSCOPIC APPEARANCE::Histologically, the hemorrhagic area shows ischemic necrosis of the alveolar walls, bronchioles and vessels. If the infarct is caused by an infected embolus, the neurtrophilic inflammatory reaction can be intense. Such lesions are referred to as septic infarcts, some which turn into abscesses.They appear eosinophilic (pink), homogenous, lacking the nuclei, but keep their shapes - "structured necrosis". Alveolar lumens from infarcted area are invaded by red blood cells

REFERENCES:The Nature of Disease: Pathology for the Health ProfessionsBy Thomas H. McConnellEssentials of Human Disease By Leonard V. CrowleyRobbins & Cotran Pathologic Basis of DiseaseBy Vinay Kumar, Abul K. Abbas, Jon C. Asterhttp://www2.mozcom.com/~emcdvm/path01.htmlhttp://www.pathologyatlas.ro/cellular-swelling-liver.phphttp://www.pathologyatlas.ro/fatty-change-liver-steatosis-pathology.phphttp://radiopaedia.org/articles/diffuse-hepatic-steatosishttp://www.pathologyatlas.ro/hemorrhagic-infarct-lung-pulmonary-pathology.phphttps://secure.health.utas.edu.au/intranet/cds/pathprac/Files/Cases/Respiratory/Case33/Case33.htmRESEARCHER: brainiac