Histopathology: Cell necrosis and cytoplasmic accumulations These presentations are to help you identify basic histopathological features. They do not contain the additional factual information that you need to learn about these topics. This presentation contains images of basic histopathological features of cell necrosis and examples of cytoplasmic accumulations. Before viewing this presentation you are advised to review relevant sections of a pathology textbook, histopathology atlas and lecture notes. Copyright University of Adelaide 2011 (The histopathology of cell necrosis and cytoplasmic accumulations is introduced in semester 1, year 1)
CB viable dead Necrosis is always pathologic and involves irreversible injury to cells. Generally a group of cells or a region of tissue is affected There are many causes. Ischaemia is a common cause. This is a low power view from the edge of a myocardial infarction.
Malignant lesions frequently demonstrate necrosis, which may or may not be visible macroscopically. The necrotic area here is outlined by the black lines. The dead cells are shrunken and more eosinophilic than the viable cells and they have karyorrhectic (pyknotic and fragmented) nuclei.
Apoptosis, or programmed cell death, of which there are also many causes, may be physiologic or pathologic. Apoptotic cells typically occur singly. Apoptotic cells (black arrows) in dysplastic epidermis are displayed here. The cells appear shrunken and deeply eosinophilic with a pyknotic nucleus.
CB viable dead There are various types of necrosis. Infarcts demonstrate coagulative necrosis. The architecture of the dead tissue is retained until it is phagocytosed. On low power the infarcted cells appear more eosinophilic (lower right of image) compared to viable cells (top left) due to increased binding of eosin to denatured cytoplasmic proteins.
Types of necrosis: coagulative. On higher power the nuclei of the dead cells have undergone karyolysis (the nuclei become paler then disappear). Causes of coagulative necrosis include ischaemia and burns.
Types of necrosis: liquefactive. Liquefactive necrosis is associated with pyogenic infection causing acute suppurative or purulent inflammation and is partly caused by the action of lysosomal enzymes from neutrophils. Liquefactive necrosis also follows coagulative necrosis in cerebral infarction. This is not attributable to the action of neutrophils but is possibly related to the lysosomal content of cells of the CNS. The image above is a low power view of a microbascess in the kidney. It contains necrotic tissue and bacteria (black star) and is surrounded by neutrophils (yellow star).
Types of necrosis: caseous. Caseous necrosis refers to a type of necrosis classically associated with tuberculosis, which macroscopically appears like soft cheese. Microscopically the dead cells fail to retain their outlines, instead forming an amorphous mass of cytoplasmic and nuclear debris (grey star). The necrosis at least partly probably results from the action of activated macrophages.
Types of necrosis: fibrinoid. Fibrinoid necrosis refers to an alteration of injured blood vessels, typically occurring in vasculitis or accelerated/malignant hypertension. Injury allows plasma proteins to insudate into and accumulate in the wall, resulting in intense eosinophilic staining (F), here seen in the wall of a renal arteriole in malignant hypertension. From Stevens et al: Core Pathology 3rd ed. Copyright 2009 by Mosby, an imprint of Elsevier, Ltd.
Types of necrosis: fat necrosis. Fat necrosis occurs in adipose tissue and results from the action of digestive enzymes in acute pancreatitis or trauma (sometimes unnoticed) in the breast. In the breast (above) it may induce a granulomatous inflammatory response.
In the living patient, necrotic cells are generally removed by enzymatic digestion and phagocytosis of remaining debris. In some cases the dead or degenerate tissue is not removed and calcium salts are deposited within (dystrophic calcification). This is common in the necrotic tissue of tuberculosis, atherosclerosis and in certain breast lesions. Image above: atherosclerosis. There is significant narrowing with thrombosis of the lumen (yellow star). Black stars: fibrous tissue. Yellow arrows (dark blue material): calcification. Blue star: lipid core
Area of dystrophic calcification (yellow star) within a breast duct showing ductal carcinoma in situ. Such calcification can be seen radiologically.
Sometimes accumulations of various substances may be seen in the cytoplasm of cells. This may be physiological or pathological. Normal liver, medium power view. Black arrows: lipofuscin pigment (yellow-brown) in hepatocytes (physiological). Yellow star: terminal portal venule in portal tract Yellow arrows: bile ductules (note simple cuboidal epithelium) in portal tract Red arrow: terminal hepatic artery in portal tract. Note smooth muscle in wall. The endothelial lining is not readily appreciated here.
Intracellular accumulations. Macrophages containing carbon (black) in the lung.
Intracellular accumulations. Macrophages containing haemosiderin (golden brown) (black arrows) Red arrows: lymphocytes. Yellow arrows: plasma cells
Intracellular accumulations. Macrophages containing melanin (brown pigment) in a malignant melanoma (medium-high power). Many of the cells here are malignant melanocytes, however, much of the melanin made by the melanocytes has been phagocytosed by macrophages.
Intracellular accumulations. Macrophages that contained lipid giving the cytoplasm a foamy appearance (foamy macrophages). The lipid has dissolved out during processing of the sections. Such lipid may be derived from cell membranes following phagocytosis of cells in various degenerative states, from the blood in hyperlipidaemia, from the phagocytosis of myelin in the CNS or from bile in the case of cholesterolosis of the gallbladder.