Chapter 2 Cellular Responses To Stress, Injury, And Aging Flashcards

1
Q

What are the cellular responses to persistent stress?

A

They occur singly or in combination, may lead to atrophy, hypertrophy, hyperplasia, metal plasma and dysplasia. Also include infra cellular accumulations and storage of products in abnormal amounts.

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2
Q

What is atrophy?

A

When confronted with a decrease in work demands or adverse environmental conditions, most cells are able to revert to a smaller size and a lower and more efficient level of functioning, Thats is compatible with survival.
When a sufficient number of cells are involved, the entire tissue atrophies

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3
Q

What are the general causes of atrophy?

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  1. Disuse - occurs when there is a reduction in skeletal muscle use, 2. Denervation - is a form of disuse atrophy that occurs in muscles of paralyzed limbs, 3. Loss of endocrine stimulation - produces a form of disuse atrophy such as women the loss of estrogen stimulation during menopause results in strophic changes in the reproductive organs. 4. Inadequate nutrition - , 5. Is he is or decreased blood flow. - cells decrease their size and energy requirements as a means of survival.
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4
Q

What is Hypertrophy? What is physiologic and pathological hypertrophy?

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It represents an increase in cell size, and with it an increase in the amount of functioning tissue mass. It 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 through mitotic division and formation of more cells
Physiologic - increase in muscle mass associated with exercise. Pathological occurs as the result of disease conditions and may be adaptive or compensatory. Adaptive is Thickening of the urinary bladder from long continued obstruction of urinary outflow or my paradise hypertrophy from valvular heart disease or hypertension. Compensatory is the enlargement of a remaining organ or tissue after a portion has been surgically removed or rendered inactive, ex one kidney removed, the remaining kidney enlarges to compensate for the loss.

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5
Q

What is hyperplasia? The stimuli may be physiologic or nonphysiologic?

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Refers to an increase in the number of cells in an organ or tissue. It occurs in tissues with cells that are capable of mitotic division, such as the epidermis, intestinal epithelium and glandular tissue. There is evidence that hyperplasia involves activation of genes controlling cell proliferation and the presence of intracellular messengers that control cell replication and growth. It is a controlled process that occurs in response to an appropriate stimulus and ceases after the stimulus has been removed.
Two common types of physiologic are hormonal and compensatory - Breast and uterine enlargement during pregnancy - regeneration of the liver that occurs after partial hepatectomy. No physiologic are due to excessive hormonal stimulation or the effects of growth factors on target tissues. Excessive estrogen production can cause endometrial hyperplasia .

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6
Q

What is metaplasia?

A

Represents a reversible change in which one adult cell type is replaced by another adult cell type. These changes are thought to involve the reprogramming of undifferentiated stem cells that are present in the tissue undergoing the metaplastic changes. 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. But doesnt overstep the boundaries of the primary tissue. Ex is the adaptive substitution of stratified squamous epithelial cells for the the ciliated columnar epithelial cells in the trachea and large airways of a habitual cigarette smoker.

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7
Q

What’s is Dysplasia?

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Is characterized by the deranged cell growth of a specific tissue that results in cells that vary in size, shape, and organization. Minor degrees of dysplasia are associated with chronic irritation or inflammation. Is most frequently encountered in areas of metaplastic squamous epithelium of the respiratory tract and uterine cervix. It is strongly implicated as a precursor of cancer. But they can revert to their former structure and function.

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8
Q

What is intracellular accumulation? What are the 3 categories?

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Represent the buildup of substances that cells cannot immediately use of eliminate. The substances may accumulate in the cytoplasm or in the nucleus. In some cases the accumulation may be an abnormal substance that the cell has produced, and in other cases the cell may be storing exogenous materials or products of pathologic processes occurring elsewhere in the body.

  1. Normal body substances such as lipids, proteins, carbohydrates, melanin, and bilirubin, that are present in abnormally large amounts.
  2. Abnormal endogenous products, such as those resulting from inborn errors of metabolism.
  3. Exogenous products, such as environmental agents and pigments that canning by broken down by the cell. They may accumulate transiently or permanently and they may be harmless or in some cases, toxic.

May accumulate abnormal amounts of various substances because they are synthesized at a rate that exceeds their metabolism or removal. Intracellular accumulation can result from genetic disorders that disrupt the enzymatic degradation of selected substances or their transport to other sites. Pigments are coloured substances that may accumulate in cells. They can be endogenous or exogenous such as jaundice

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9
Q

What is pathologic calcifications? What are the two types?

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Involves the abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium and other minerals.
Dystrophic represents the macroscopic deposition of calcium salts in injured tissue. It is often visible to the naked eye as deposits that range from gritty sand-like grains to firm, hard, rock-like material. The pathogens is of dystrophic calcification involves the intracellular or extra cellular formation of crystalline calcium phosphate. It is commonly seen in atheromatous lesion of advanced atherosclerosis,
Metastatic calcification which in contrast occurs in injured tissues, occurs in normal tissues as the result of increased serum calcium levels. Almost any condition that increase the serum calcium level can lead to calcification in inappropriate sites.

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10
Q

What are the causes of cell injury? Injury from physical agents? Injury from radiation?

A
  1. Injury from physical agents 2. Radiation injury, 3 chemical injury, 4. Injury from biological agents 5. Injury from nutritional imbalances.
  2. Mechanical forces - injury or trauma due to mechanical forces occurs as the result of body impact with another object. These types of injuries split and tear tissue, fracture bones, injure blood vessels, and disrupt blood flow.
  3. Extremes of temperature - of heat and cold cause damage to cell, its organ cells and its enzyme systems.
  4. Electrical forces - injuries due to electrical forces can affect the body through extensive tissue injury and disruption of neural and cardiac impulses. It is mainly determined by its voltage, the type of current, its amperage, the resistance of the intervening tissue, the pathway of the current, and the duration of exposure.

Radiation injury - electromagnetic radiation comprises a wide spectrum of wave propagated energy, ranging from ionizing gamma rays to radiofrequency waves. A photon is a particle of radiation energy.

With frequencies above the UV range is called ionizing radiation because the photons have enough energy to knock electrons off atoms and molecules. It affects cells by causing ionization of molecules and atoms in the cell, by directly hitting the target molecules in the cell, or by producing free radical that destabilize molecules in critical cell components.

Non ionizing radiation refers to radiation energy at frequencies below those of visible light. Includes infrared light, ultrasound, microwaves and laser energy. It exerts its effects by causing vibration and rotation of a atoms and molecules. Used in radar, television, industrial operations, household appliances.

UV radiation represents the portion of the spectrum of electromagnetic radiation just above the visible range. Contains increasingly energetic rays that are powerful enough to disrupt intracellular bonds, cause sunburn, and increase the risk of skin cancers. The risk depends on type , intensity of exposure and the amount of protective melanin pigment in the skin.

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11
Q

What are chemical injury? What are the types?

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Chemicals capable of damaging cells are everywhere around us. Pollutants in the air, water, and would, such as carbon monoxide, pesticides, and trace metals are capable of tissue injury. Can injure the cell membrane and other cell structures

  1. Lead toxicity - is a particularly toxic metal. Small amounts accumulate to reach toxic levels. There are innumerable sources of lead in the environment. It is absorbed through the GI tract or the lungs into the blood. 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 Gi tract, the kidneys and the nervous system. Can cause severe and poorly localized form of acute abdominal pain, diffuse kidney damage leading to renal failure, hypertension. In the nervous system, it is characterized by demyelination of cerebral and cerebellar while matter and death of brain cells.
  2. Mercury toxicity - has been used for industrial and medical purposes for hundreds of years. It is toxic, and the hazards of mercury associated occupational and accidental exposures are well known. Exposure from eating certain fish, amalgams used in dentistry and vaccines. Present in four forms: mercury valid, inorganic rivals the mercury, methyl mercury, and ethyl mercury. Toxicity involving the CNS and kidney can occur.
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12
Q

The last two injury are biologic agents and nutritional imbalances?

A

Biologic agents differ from other injurious agents in that they are able to replicate and can continue to produce their injurious effect. They range from submicroscopic viruses to the larger parasites. They can injure cells by diverse mechanisms. Viruses enter the cell and incorporate its genetic material into their cellular DNA, which then enable synthesis fo new viruses.

Nutritional imbalance excesses and deficiencies predispose cells to injury. Obesity and diets high in saturated fats are thought to predispose persons to atherosclerosis.

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13
Q

What are the mechanisms of cell injury?

A
  1. Free radical injury - These circumstances include ischemia reperfusion injury, chemical and radiation injury, toxicity from oxygen and other gases, cellular aging, responses to microbial infection and tissue injury, caused by inflammation. They are highly reactive chemical species with an unpaired electrons in the outer orbit or the molecule. It causes free radicals to be unstable and highly reactive, so that they reach no specifically with molecules in the vicinity. Free radicals can establish chain reaction consisting of many events that’s generate new free radicals. They can react with proteins, lipids and carbohydrates thereby damaging cell membranes , inactivaating enzymes and damaging nucleotide acids that make up DNA.
  2. Hypoxic cell injury - It deprives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP. The actual time necessary to produce irreversible cell damage depends on the degree of oxygen deprivation and the metabolic needs of the cell. Brain cells can only go 4-6 minutes without oxygen before damage occurs. It can result from inadequate amount of oxygen in the air, respiratory disease, ischemia, anemia, edema or inability of the cells to use oxygen
  3. Impaired calcium homeostasis - Calcium functions as an important second messenger and cytosolic signal for many cell responses. P41
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14
Q

What is reversible cell injury and cell death? What are the two mechanisms?

A

The mechanisms of cell injury can produce sub lethal and reversible cellular damage or lead to irreversible injury with cell destruction or death.
Apoptosis - which is designed to remove injured or worn out cells. Cell death or necrosis - which occurs in irreversibly damaged cells.

  1. Reversible cell injury - although impairing cell function, doesn’t result in cell death. Two patterns of reversible cell injury can be observed under the microscope: cellular swelling - occurs with impairment of the energy dependent Na+ K+ ATPase membrane pump, usually as the result of hypoxic cell injury. and fatty change - are linked to intracellular accumulation of fat. When fatty changes occur, small vacuoles of fast disperse throughout the cytoplasm. It is usually more ominous than cellular swelling and although it is reversible, it usually indicates 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.
  2. Programmed cell death - most normal non tumor cells, the number of cells in tissues in regulated by balancing cell proliferation and cell death. Occurs by necrosis or a form of programmed cell death apoptosis. Apoptosis greek “fallen apart”. Is a highly selective process that eliminates injured and aged cells,thereby controlling tissue regenerationShrining and condensation of the nucleus and cytoplasm occur, The chromatin aggregates at the nuclear envelope, and DNA fragmentation occurs. Then, the cell becomes fragmented into multiple apoptotic bodies in manner that maintains the integrity of the plasma membrane and doesn’t initiate inflammation. Changes in the plasma membrane induce phagocytosis of the apoptotic bodies by macrophages and other cells. It’s thought to be responsible for the programmed destruction of cells during embryonic development, hormone dependent involution of tissues, death of immune cells, cell death by cytotoxic T cells, and cell death in proliferating cell populations. Two basic pathways for it are extrinsic pathway - which is death receptor dependent involves extra cellular signaling proteins that bind to cell surface molecules tumor necrosis factor receptor and the Fas ligand receptor. and intrinsic pathway - which is death receptor independent is activated by conditions such as DNA damage, ROS, hypoxia, dec ATP levels, cellular senescence and activation of the p53 protein by DNA damage.
  3. Necrosis - refers to cell death in an organ or tissue that is still part of a living person. Differs from apoptosis in that is involves unregulated enzymatic digestion of cell components, loss of cell membrane integrity with uncontrolled release of the products of cell death into the extra cellular space, and initiation of the inflammatory response. It often interferes with cell replacement and tissue regeneration. There are marked changes in the appearance of the cytoplasmic contents and the nucleus. A. Liquefaction necrosis occurs when some of the cells die but their catalytic enzymes are not destroyed. Coagulation necrosis, acidosis develops and denatures the enzymatic and structural proteins of the cell. Is characteristic of hypoxic injury and is seen in infarcted areas. Infarction occurs when an artery supplying an organ or part of the body become occluded and no other source of blood supply exists. Caseous necrosis is a distinctive form of coagulation necrosis in which the dead cells persist indefinitely as soft, cheese-like debris from tuberculosis.
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15
Q

What is gangrene? What are the types?

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Is applied when a considerable mass of tissue undergoes necrosis. May be classified as dry or moist.

Dry gangrene - the part becomes dry and shrinks, the skin wrinkles and its color changes to dark brown or black. The spread of is slow, and its symptoms are not as marked as those of wet. The irritation caused by the dead tissue produces a line of inflammatory reaction. Usually results from interference with arterial blood supply to a part without interference with venous return and is a form of coagulation necrosis. Is confined almost exclusively to the extremities

Wet gangrene - the area is cold, swollen and pulseless. The skin is moist, black and under tension. Blebs form on the surface, liquefaction occurs, and a foul odour is caused by bacterial action. There is no line of demarcation between the normal and diseased tissues and the spread of tissue damage is rapid. Systemic symptoms are usually severe, and dearth may occur unless the condition can be arrested. Primarily results from interference with venous return in the development of wet gangrene and is responsible for many of its prominent symptoms. May affect the internal organs or the extremities. If bacteria invade the necrotic tissue , dry may be converted to wet.

Gas gangrene is a special type of gangrene that results from infection of devitalized tissues by one of several Clostridium bacteria, most commonly Clostridium perfringens. These anaerobic and spore - forming organisms are widespread in nature, particularly in soil; gangarene is prone to occur in trauma and compound fractures in which dirt and debris are embedded. The bacteria produce toxins that dissolve cell membranes, causing death of muscle cells, massive spreading edema, hemolysis of red blood cells, hemolytic anemia, hemoglobinuria, and renal failure. Characteristic of this disorder are the bubbles of hydrogen shocked gas that form in the muscle. Is a serious and potentially fatal disease.

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16
Q

What is cellular aging? What are the theories of aging?

A

Aging is a complex natural process in which there are physiologic and structural alteration in almost all organ systems. Beginning in the fourth decade of life, there is a progressive decline in muscle strength, cardiac reserve, vital capacity, nerve conduction time, and glomerular filtration rate.

Replicative senescence - implies that cells have a limited capacity for replication. At the cellular level, Hayflick and Moorhead observed more than 40 years ago that cultured human fibroblasts have a limited ability to replicate and then die. Before achieving this maximum, they slow their rate of division and manifest identifiable and predictable morphological changes characteristic of senescent cells. Is remaster to the length of the outermost regions of each chromosome, Telomeres, that contain short repeat sequences of DNA bases. During mitosis the molecular machinery that replicates DNA can’t copy the extreme ends of the chromosome. Thus , with each cell division, a small segment of telomeric DNA is lost. It is theorized that over time the telomeres broke progressively shorter.

Genetic influences - interest in genes that’s determine longevity. Longevity genes have been found in fruit flies and roundworms, organisms that have attracted considerable attention from scientists because of their short lifespan and their well - characterized genomes.

Accumulation of ENvironmental and Genetic Damage - May be determined by a balance between cellular damage resulting from metabolic events occurring within the cell and molecular responses that’s repair the damage. The damage eventually accumulates to a level sufficient to result in the physiologic decline associated with aging. Somatic mutation theory of aging, which states that the longevity and function of cells in various tissues of the body are determined by the double - stranded DNA molecule and its specific repair enzymes. DNA undergoes continuous change in response to both exogenous agents and intrinsic processes. It has been suggested that aging results from conditions that produce mutations in DNA or deficits in DNA repair mechanisms.

17
Q

What are the syndromes of premature aging?

A

Progeria - represent a range of phenotypes seen in usual aging, but with much earlier ages of onset and more rapid rates of progression. Hutchinson-Gifford progeria syndrome is a rare fatal genetic disorder characterized by accelerated aging in children. Is caused by a mutation in the LMNA gene, which codes for a precursor of lamin A - a scaffolding protein that lines the nucleus. The mutant gene leads to abnormal nuclear structure and altered gene regulation and DNA replication. Werner syndrome, (adult progeria). Which doesn’t have an onset until the late teens, with a life span into the 40-50s. The gene responsible for the disorder has been localized to chromosome 8 and appears to code for an enzyme involved in unwinding DNA, a process that is necessary for DNA repair and replication.