Nurs 212a - Pathophys (Pp) - Chapter 2: Cell Response To Stress, Injury, & Aging

Hypertrophy may occur as the result of NORMAL physiologic or ABNORMAL pathologic conditions. The increase in MUSCLE MASS associated with EXERCISE is an example of physiologic hypertrophy.

Disuse atrophy, particularly in MUSCLE TISSUE, is related to workload. When confronted with a decrease in work demands or adverse environment conditions, most cells are able to revert to a smaller size and lower and more efficient level of functioning that is compatible with survival. As the workload of a cell diminishes, oxygen consumption and protein synthesis decreases. Cells that are atrophied reduce their oxygen consumption and other cellular functions by decreasing the number and size of their organelles and other structures. An extreme example of disuse atrophy is seen in muscles of extremities that have been encased in plaster casts. Because atrophy is ADAPTIVE and REVERSIBLE, muscle size is restored after the cast is removed and muscle use is resumed (p. 30).

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True. a LIMIT is eventually reach beyond which further enlargement of the tissue mass is no longer able to compensate for the increased work demands. The limiting factors for continued hypertrophy might be related to limitations in blood flow. for example, in hypertension the increased workload required to pump blood against an elevated arterial pressure results in a progressive increase in left ventricular muscle mass (p. 31).

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Hypertrophy represents an INCREASE in CELL SIZE as well as an increase in the amount of FUNCTIONING TISSUE MASS. Also hypertrophy may occur as the result of NORMAL PHYSIOLOGIC or ABNORMAL PATHOLOGIC conditions (p. 31).

Hypoxia deprives the cell of oxygen and interrupts OXIDATIVE METABOLISM and the generation of ATP. Can include ischemia; ischemia is characterized by impaired oxygen delivery and impaired removal of metabolic end-products. In contrast to PURE HYPOXIA, which affects the ocygen content of the blood and affects all of the cells in the body, ISCHEMIA commonly affects blood flow through small numbers of blood vessels and produces LOCAL tissue injury. Hypoxia literally causes a power failure in the cell, with widespread effects on the cell's funtional and strucutral components. As oxygen tension in the cell falls, OXIDATIVE METABOLISM ceases, and the cell reverts to ANAEROBIC METABOLISM, using its limited GLYCOGEN stores in an attempt to maintain vital cell functions. Cellular pH FALLS as lactic ACID accumulates in the cell. The nuclear chromatin clumps (p. 35).

An extreme example of disuse atrophy is seen in muscles of extremities that have been encased in plaster casts. Because atrophy is ADAPTIVE and REVERSIBLE, muscle size is restored after the cast is removed and muscle use is resumed (p. 30).

FALSE. Once the stimulus for adaptation is removed, the effect on expression of the differentiating genes is removed and the cell RESUMES its previous state of specialized function. Whether adaptive cellular changes are normal or abnormal depends on whether the response was mediated by an appropriate stimulus. NORMAL ADAPTIVE RESPONSES occur in response to need and an appropriate stimulus. After the need has been removed, the adaptive response ceases (p. 30).

f. It is also important to distinguish cellular atrophy from organ atrophy that is due to irreversible loss of cells. For example, atrophy of the brain in Alzheimer disease is secondary to extensive cell death, and the size of the organ cannot be restored (p. 30).

METAPLASIA represents a REVERSIBLE change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type. Metaplasia is thought to involve the reprogramming of UNDIFFERENTIATED STEM CELLS that are present in the tissue undergoing the metaplastic changes. Metaplasia usually occurs in response to chronic irritation and inflammation and allows for substitution of cells that are better able to survive under circumstances in which a more fragile cell type might succumb. However, the conversion of cell types never oversteps the boundaries of the primary groupus of tissue (e.g. one type of epithelial cell may be converted to another type of epithelial cell, but not to a connective tissue cell) (p. 32).

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CELL DEATH can involve apoptosis or necrosis. APOPTOTIC CELL DEATH involves controlled cell DESTRUCTION and is involved in NORMAL cell deletion and renewal. Apoptic cell death, which is equated with cell suicide, eliminates cells that are worn out, have been produced in excess, have developed improperly, or have genetic damage. It also provides the space needed for cell replacement. Initiation of apoptosis occurs principally by sinals from 2 pathways: INTRINSIC (aka mitochondrial pathway) or EXTRINSIC (receptor-initated) pathway.

All of the answers are true. The general causes of cell atrophy include disuse and reduced functional demand, loss of trophic stimuli, insufficient nutrients, decreased blood flow, persistent cell injury, and aging (p. 30).

In ATP depletion and decreased ATP synthesis, after cellular swelling occurs, the cellular changes caused by ischemia are reversible if oxygenation is restored. However, if the oxygen supply is not restored, there is a continued loss of essential enzymes, proteins, and ribonucleic acid through the hyperpermeable membrane. Injury to the lysosomal membrane results in leakage of destructive lysosomal enzymes into the cytoplasm and enzymatic digestion of cell components (p. 38).

Hyperplasia refers to an increase in the NUMBER of cells in an organ or tissue. It occrs in tissues with cells that are capable of MITOTIC DIVISION, such as the epidermis, intestinal epithelium, and glandular tissue. Nerve cells and skeletal and cardiac muscle cells do NOT divide and therefore have NO capacity for hyerplastic growth. There is evidence that hyperplasia involves activation of genes controlling cell proliferation. As with other normal adaptive cellular responses, hyperplasia is a controlled process that occurs in response to an appropriate STIMULUS and CEASES after the stimulus has been removed (p. 31).

All are true except the information regarding electrical damage. It is generally believed that the GREATER the skin resistance, the GREATER is the amount of local skin burn, and the LESS the resistance, the GREATER are the deep and SYSTEMIC effects. Thick, dry skin is more resistance to the flow of electricity than thin, wet skin (p. 36).

Gas gangrene is due to Clostridium infection which produces toxins and H2S bubbles (lecture)

Dysplasia is strongly implicated as a PRECURSOR of cancer. SEVERE DYSPLASIA is considered an indication for aggressive preventative therapy to remove the underlying cause or to surgically remove the affected tissue. However, it is important to point out that dysplasia is an adaptive process and as such does NOT NECESSARILY LEAD TO CANCER. In many cases, the dysplatic cells REVERT to their former structure and function (p. 32).

The deviant protein structure MAY RESULT from an inherited mutation that alters a normal amino acid sequence OR may reflect an acquired DEFECT in protein folding (p. 32).

One of the hallmarks of AGING, particularly in non-replicating cells such as the BRAIN AND HEART, is cell atrophy. There is a DECREASE in the size of most body organs. The size of the brain is invariably decreased, and in the very old, the size of the heart may be greatly diminished.

All of the above are true (p. 32).

PERSISTENT CELL INJURY is most commonly caused by chronic inflammation associated with prolonged viral or bacterial infections. Chronic inflammation may also occur in other conditions, such as IMMUNOLOGIC and GRANULOMATOUS disorders (p. 30-31).

None of the above are true. Many injurious agents exert their damaging effects through a reactive chemical species called a FREE RADICAL. A free radical is a highly reactive chemical species arising from an atom that has a SINGLE unpaired electron in an OUTER orbit. In this state, the radical is highly unstable and can enter into reactions with cellular constituents, particularly key molecules in cell membranes and nucleic acids. Free radical is a BYPRODUCT of many NORMAL cellular reactions in the body, including energy generation, breakdown of lipids and proteins, and inflammatory processes. Free radical formation is a particular THREAT to tissues in which the blood flow has been interrupted and then restored. During the period of interrupted flow, the intracellular mechanisms that control free radicals are inactivated or damaged. When blood flow is restored, the cell is suddenly confronted with an excess of free radicals that it cannot control. DEFENSES include vitamin E, Vitamin A (retinoids), and Vitamin C (ascorbic acid) (p. 38-39).

Normally, intracellular calcium levels are kept extremely LOW compared with extracellular levels. These low intracellular levels are maintained by energy-dependent, membrane-associated calcium/magnesium ATPase exchange systems. Ischemia and certain toxins lead to an increase in cytosolic calcium. The increased calcium level activates a number of enzymes with potentially damaging effects. The enzymes include the phospholipases (damaging phospholipids in cell membrane), proteases (damage cytoskeleton and membrane proteins), ATPase (breaks down ATP), and endonucleases (fragments chromatin) (p. 39).

All are true. One of the most common exogenous pigments is carbon in the form of coal dust. Lipofuscin is endogenous pigments (yellow-brown pigments). Lead poisoning is exogenous. Tattoos are exogenous pigments (insoluble pigments introduced into the skin, where they are engulfed by macrophages and persist for a lifetime) (p. 33).

Clostridium infection is related to gas gangrene.

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Pathologic calcification involves the abnormal tissue deposition of CALCIUM SALTS, together with smaller amounts of iron, magnesium, and other minerals. It is known as DYSTROPHIC CALCIFICATION when it occurs in dead or dying tissue. It is known as METASTATIC CALCIFICATION when it occurs in normal tissue (p. 33).

Icterus, also called JAUNDICE, is a YELLOW discolouration of tissue caused by the retention of BILIRUBIN, and ENDOGENOUS bile pigment. This condition may result from increased bilirubin production from red blood cell destruction, obstruction of bile passage into the intestine, or toxic disease that affect the liver's ability to remove bilirubin from the blood (p. 33).

False. PATHOLOGIC HYPERTROPHY occurs as a result of disease conditions and may be adaptive or compensatory. Examples of ADAPTIVE HYPERTROPHY are the thickening of the urinary bladder from long-continued obstruction of urinary outflow and the MYOCARDIAL HYPERTROPHY that results from valvular heart disease or HYPERTENSION. COMPENSATORY HYPERTROPHY is the enlargement of a remaining organ or tissue after a portion has been surgically removed or rendered inactive. For instance, if one kidney is removed, the remaining kidney enlarges to compensate for the loss (p. 31).

LEAD is a particularly toxic metal. Small amounts accumulate to reach toxic levels. Lead crosses the PLACENTA, exposing the fetus to lead levels comparable with those of the mother. The toxicity of lead is related to its multiple biochemical effects. It has the ABILITY to inactivate enzymes, compete with calcium for incorporation into bone, and interfere with nerve transmission and brain development. The MAJOR TARGETS are the red blood cells, the gastrointestinal tract, the kidneys, and the nervous system. Some of the MANIFESTATIONS of lead toxicity include anemia, acute abdominal pain, signs of kidney damage, and cognitive deficits and neuropathies resulting from demyelination of cerebral and cerebellar white matter and death of cortical nerve cells (p. 36).

Dry gangrene is a condition characterized by tissue death due to lack of arterial blood supply, which leads to tissue coagulation. It occurs when there is no venous flow present to remove waste products. Therefore, all of the given options (A, B, and C) are correct and contribute to the development of dry gangrene.

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In general, the genes expressed in all cells fall into two categories: "housekeeping" genes that are necessary for the normal function of a cell, and genes that determine the differentiating characteristics of a particular cell type. In many adaptive cellular responses, the EXPRESSION OF THE DIFFERENTIATION GENES IS ALTERED, whereas that of the housekeeping genes remains unaffected (p. 29).

Fatty changes are linked to intracellular accumulation of fat. When fatty changes occur, small vacuoles of fat disperse throughout the CYTOPLASM. The process is more OMINOUS than cellular swelling, and although it is REVERSIBLE, it usually indicates MORE severe injury. These fatty changes may occur because normal cells are presented with an increased fat load or because injured cells are unable to metabolize the fat properly. In obese people, fatty infiltrates often occur within and between the cells of the LIVER and HEART because of an increased fat load.

Hypertrophy results from an increased workload imposed on an organ or body part and is commonly seen in CARDIAC and SKELETAL MUSCLE tissue, which cannot adapt to an increase in workload though MITOTIC DIVISION and formation of more cells (p. 31).

The function of many cells depend on trophic stimulation, such as those transmitted by the NERVOUS SYSTEM and ENDOCRINE SYSTEM. DENERVATION ATROPHY is a form of atrophy in paralyzed limbs that results from loss of NERVOUS SYSTEM STIMULI. Lack of ENDOCRINE STIMULATION produces a form of DISUSE atrophy. In women, the loss of estrogen stimulation during menopause results in atrophic changes to the reproductive organs (p. 30).