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Description : It a pathology ppt .Topic name: CELLULAR ADAPTATIONS TO STRESS

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Published on : Jul 03, 2021 | Views : 726 | Downloads : 4

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General pathology Summited To : Mian Mubeen Ali Qadri Summited By : Sundas Jawwad
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CELLULAR ADAPTATIONS TO STRESS
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Cellular adaptation Adaptations are reversible changes in the number, size, phenotype, metabolic activity, or functions of cells in response to changes in their environment. The adaptation may be physiologic or pathologic. Physiologic adaptations usually represent responses of cells to normal stimulation by hormones or endogenous chemical mediators or to the demands of mechanical Stress. Physiologic adaptations:
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Pathologic adaptations: Pathologic adaptations are responses to stress that allow cells to modulatentheir structure and function and thus escape injury, but at the expense of normal function, such as squamous metaplasia of bronchial epithelium in smokers. Four types of morphological adaptations include: Hyperplasia Hypertrophy Atrophy Metaplasia
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Hypertrophy “Hypertrophy is an increase in the size of cells resulting in an increase in the size of the organ” In contrast, hyperplasia is an increase in cell number. Hyperplasia is an adaptive response in cells capable of replication, whereas hypertrophy occurs when cells have a limited capacity to divide. Hypertrophy and hyperplasia also can occur together, and obviously both result in an enlarged organ. Hypertrophy can be physiologic or pathologic and is caused either by increased functional demand or by growth factor or hormonal stimulation.
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The massive physiologic enlargement of the uterus during pregnancy occurs as a consequence of estrogen-stimulated smooth muscle hypertrophy and smooth muscle hyperplasia. Physiologic hypertrophy of the uterus during pregnancy. (1) Gross appearance of a normal uterus (right) and a gravid uterus (left) that was removed for postpartum bleeding. (1)
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(2) Small spindle-shaped uterine smooth muscle cells from a normal uterus. (2) (3) Large, plump hypertrophied smooth muscle cells from a gravid uterus; compare with 2. (3)
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The relationship among normal, adapted, reversibly injured, and dead myocardial cells. The cellular adaptation depicted here is hypertrophy, the cause of reversible injury is ischemia, and the irreversible injury is ischemic coagulative necrosis. All three transverse sections of myocardium were stained with triphenyltetrazolium chloride, an enzyme substrate that colors viable myocardium magenta. Failure to stain is due to enzyme loss after cell death.
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An adaptation to stress such as hypertrophy can progress to functionally significant cell injury if the stress is not relieved. The cause of hypertrophy, a limit is reached beyond which the enlargement of muscle mass can no longer compensate for the increased burden. When this happens in the heart, several degenerative changes occur in the myocardial fibers, of which the most important are fragmentation and loss of myofibrillar contractile elements. The net result of these degenerative changes is ventricular dilation and ultimately cardiac failure.
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2. Hyperplasia “Hyperplasia is an increase in the number of cells in an organ that stems from increased proliferation, either of differentiated cells or, in some instances, less differentiated progenitor cells” Hyperplasia takes place if the tissue contains cell populations capable of replication; it may occur concurrently with hypertrophy and often in response to the same stimuli. Hyperplasia can be physiologic or pathologic in both situations, cellular proliferation is stimulated by growth factors that are produced by a variety of cell types.
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The two types of physiologic hyperplasia are: Types Of Physiologic Hyperplasia Hormonal Hyperplasia, exemplified by the proliferation of the glandular epithelium of the female breast at puberty and during pregnancy. b) Compensatory Hyperplasia,in which residual tissue grows after removal or loss of part of an organ. For example, when part of a liver is resected, mitotic activity in the remaining cell begins as early as 12 hours later, eventually restoring the liver to its normal size. The stimuli for hyperplasia in this setting are polypeptide growth factors produced by uninjured hepatocytes as well as nonparenchymal cells in the liver.
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Most forms of pathologic hyperplasia are caused by excessive hormonal or growth factor stimulation. For example, after a normal menstrual period there is a burst of uterine epithelial proliferation that is normally tightly regulated by the stimulatory effects of pituitary hormones and ovarian estrogen and the inhibitory effects of progesterone. A disturbance in this balance leading to increased estrogenic stimulation causes endometrial hyperplasia, which is a common cause of abnormal menstrual bleeding. In all of these situations, the hyperplastic process remains controlled; if the signals that initiate it abate, the hyperplasia disappears Nevertheless,in many cases, pathologic hyperplasia constitutes a fertile soil in which cancers may eventually arise.
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3. Atrophy “Atrophy is shrinkage in the size of cells by the loss of cell substance” When a sufficient number of cells are involved, the entire tissue or organ is reduced in size, or atrophic . Although atrophic cells may have diminished function, they are not dead. Causes Of Atropy: A decreased workload, loss of innervation, diminished blood supply, inadequate nutrition,loss of endocrine stimulation, and aging.
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Although some of these stimuli are physiologic for-example “the loss of hormone stimulation in menopause” and others are pathologic for-example “denervation” the fundamental cellular changes are similar. Cellular atrophy results from a combination of decreased protein synthesis and increased protein degradation. Protein synthesis decreases because of reduced metabolic activity. The degradation of cellular proteins occurs mainly by the ubiquitin-proteasome pathway. Nutrient deficiency and disuse may activate ubiquitin ligases, which attach multiple copies of the small peptide ubiquitin to cellular proteins and target them for degradation in proteasomes. This pathway is also thought to be responsible for the accelerated proteolysis seen in a variety of catabolic conditions, including the cachexia associated with cancer.
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Atrophy as seen in the brain. (A) (A) Normal brain of a young adult. (B) (B) Atrophy of the brain in an 82- year-old man with atherosclerotic disease. Atrophy of the brain is caused by aging and reduced blood supply. Note that loss of brain substance narrows the gyri and widens the sulci. The meninges have been stripped from the bottom half of each specimen to show the surface of the brain.
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4. Metaplasia “Metaplasia is a change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type” In this type of cellular adaptation, a cell type sensitive to a particular stress is replaced by another cell type better able to withstand the adverse environment. Metaplasia is thought to arise by the reprogramming of stem cells to differentiate along a new pathway rather than a phenotypic change of already differentiate cells.
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Metaplasia need not always occur in the direction of columnar to squamous epithelium; in chronic gastric reflux, the normal stratified squamous epithelium of the lower esophagus may undergo metaplastic transformation to gastric or intestinal-type columnar epithelium Metaplasia also may occur in mesenchymal cells, but in these situations it is generally a reaction to some pathologic alteration and not an adaptive response to stress. For example,bone is occasionally formed in soft tissues, particularly in foci of injury.
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Metaplasia of normal columnar (left) to squamous epithelium (right) in a bronchus, shown Schematically (A) Histologically (B)
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The influences that induce metaplastic change in an epithelium, if persistent, may predispose to malignant transformation. Squamous Metaplasia of the respiratory epithelium often coexists with lung cancers composed of malignant squamous cells. It is thought that cigarette smoking initially causes squamous metaplasia, and cancers arise later in some of these altered foci.
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INTRACELLULAR ACCUMULTIONS
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Under some circumstances, cells may accumulate abnormal amounts of various substances, which may be harmless or may cause varying degrees of injury. The substance may be located in the cytoplasm, within organelles or in the nucleus, and it may be synthesized by the affected cells or may be produced elsewhere. it The main pathways of abnormal intracellular accumulations are inadequate removal and degradation or excessive production of an endogenous substance, or deposition of an abnormal exogenous material.
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Examples Fatty Change: Fatty change, also called steatosis, refers to any accumulation of triglycerides within parenchymal cells. It is most often seen in the liver, since this is the major organ involved in fat metabolism, but also may occur in heart, skeletal muscle, kidney, and other organs. Steatosis may be caused by toxins, protein malnutrition, diabetes mellitus, obesity, or anoxia. Cholesterol and Cholesteryl Esters: Cellular cholesterol metabolism is tightly regulated to ensure normal generation of cell membranes without significant intracellular accumulation. Phagocytic cells may become overloaded with lipid in several different pathologic processes, mostly characterized by increased intake or decreased catabolism of lipids.
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Proteins: Morphologically visible protein accumulations are less common than lipid accumulations; they may occur when excesses are presented to the cells or if the cells synthesize excessive amounts. Glycogen: Excessive intracellular deposits of glycogen are associated with abnormalities in the metabolism of either glucose or glycogen. Glycogen also accumulates within cells in a group of related genetic disorders collectively referred to as glycogen storage diseases, or glycogenosis. Pigments: Pigments are colored substances that are either exogenous, coming from outside the body, such as carbon, or are endogenous, synthesized within the body itself, such as lipofuscin, melanin, and certain derivatives of hemoglobin.
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Lipofuscin: Lipofuscin or “wear-and-tear pigment,” is an insoluble brownish-yellow granular intracellular material that accumulates in a variety of tissues with aging or atrophy. The brown pigment when present in large amounts, imparts an appearance to the tissue that is called brown atrophy. Melanin: Melanin is an endogenous, brown-black pigment that is synthesized by melanocytes located in the epidermis and acts as a screen against harmful UV radiation. Although melanocytes are the only source of melanin, adjacent basal keratinocytes in the skin can accumulate the pigment as can dermal macrophages. Hemosiderin: Hemosiderin is a hemoglobin-derived granular pigment that is golden yellow to brown and accumulates in tissues when there is a local or systemic excess of iron. Hemosiderin pigment represents large aggregates of these ferritin micelles, readily visualized by light and electron microscopy; the iron can be unambiguously identified by the Prussian blue histochemical reaction.
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Mechanisms of intracellular accumulation: (1): Abnormal metabolism, as in fatty change in the liver. (2): Mutations causing alterations in protein folding and transport, so that defective molecules accumulate intracellularly. (3): A deficiency of critical enzymes responsible for breaking down certain compounds, causing substrates to accumulate in lysosomes, as in lysosomal storage diseases. (4): An inability to degrade phagocytosed particles, as in carbon pigment accumulation.
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PATHOLOGIC CALCIFICATION
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“Pathologic calcification, a common process in a wide variety of disease states, is the result of an abnormal deposition of calcium salts” It can occur in two ways: Dystrophic calcification: In this form, calcium metabolism is normal but it deposits in injured or dead tissue, such as areas of necrosis of any type. Dystrophic calcification is initiated by the extracellular deposition of calcium phosphate in membrane-bound vesicles, which may be derived from injured cells, or the intracellular deposition of calcium in the mitochondria of dying cells.
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2. Metastatic calcification: This form is associated with hypercalcemia and can occur in normal tissues. The major causes of hypercalcemia are: Increased secretion of parathyroid hormone, due to either primary parathyroid tumors or production of parathyroid hormone–related protein by other malignant tumors. Destruction of bone due to the effects of accelerated turnover, immobilization, or tumors (increased bone catabolism associated with multiple myeloma, or diffuse skeletal metastases). Vitamin D–related disorders including vitamin D intoxication and sarcoidosis Renal failure, in which phosphate retention leads to secondary hyperparathyroidism
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Hemosiderin granules in liver cells: (A) Hematoxylin-eosin–stained section showing golden-brown, finely granular pigment. (A) (B) Iron deposits shown by a special staining process called the Prussian blue reaction.