Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Altered Cellular and Tissue.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Adaptation  Physiologic vs. Pathogenic  Atrophy - decrease or shrinkage in cell & organ size Example – skeletal muscle deprived of innervation. Example – skeletal muscle deprived of innervation.  Hypertrophy - increase in the size of cells & organ Example – skeletal and cardiac muscle (due to increased workload). Example – skeletal and cardiac muscle (due to increased workload).

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Adaptation  Physiologic vs. Pathogenic  Hyperplasia - increase in number of cells Examples: Liver enlarges to compensate if part is removed. Liver enlarges to compensate if part is removed. Breasts enlarge due to hormonal signals during pregnancy. Breasts enlarge due to hormonal signals during pregnancy.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Adaptation  Metaplasia - reversible replacement of one mature cell type by another cell type (sometimes less differentiated).  This can be reversible, or it can progress to dysplasia and neoplasia (cancer).  Example – in the bronchi smoking can cause pseudostratified ciliated columnar ep. to change to stratified squamous ep.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Adaptation  Dysplasia - abnormal changes in size, shape and organization of mature cells.  Not a true adaptive change.  Due to persistent severe irritation.  Often reversible if stimulus is removed.  Can progess to neoplasia (cancer).  Example – cervical dysplasia due to human papillomavirus.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity Match each description with one of the processes above. Circle the letter of any that are pathologic. a) Excessive hormonal stimulation causes cells in the ducts of the breast to change their shape, size and arrangement. b) During childhood, the thymus decreases in size. c) During puberty, the male and female reproductive organs grow and develop into their mature forms.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity - Key a) Excessive hormonal stimulation causes cells in the ducts of the breast to change their shape, size and arrangement. Dysplasia b) During childhood, the thymus decreases in size. Atrophy c) During puberty, the male and female reproductive organs grow and develop into their mature forms. Hyperplasia

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury  Reversible  Cells can recover if injurious stimuli ceases  Irreversible  Cells die due to injury

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Hypoxic injury – due to lack of sufficient oxygen, usually from ischemia.  Ischemia - reduced blood supply; if gradual, then adaptation can occur. Example – a growing thrombus which gradually blocks a vessel. Example – a growing thrombus which gradually blocks a vessel.  Anoxia – total lack of oxygen. This is not well tolerated by most tissues. Example – an embolus which lodges in a vessel. Example – an embolus which lodges in a vessel.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms Cellular responses:  Decreased ATP levels – lack of oxygen impairs cellular respiration. This results in:  Failure of sodium-potassium pump and sodium- calcium exchange – Na + and Ca ++ accumulate inside cells, K + outside cells.  Cellular swelling –  Due to movement of Na + into cells.  Decreased protein synthesis  Decreased membrane transport  These changes are reversible if oxygen is restored.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Vacuolation – if O 2 is not restored, vacuoles accumulate in the cytoplasm.  Vacuoles – membrane-bound spheres that may contain fluid, lipids or other materials.  Organelles swell causing ribosomes to detach from the endoplasmic reticulum.  Swelling may lead to rupture of lysosomes.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Mitochondrial damage – due to swelling which damages mitochondrial membrane. Results in:  Changes in membrane permeability  Loss of membrane potential  Decreased ATP production  Between the outer and inner membranes of the mitochondria are proteins that can activate the cell's suicide pathways, called apoptosis.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Accumulation of calcium  Normally intracellular cytosolic calcium concentrations are very low.  Ischemia and certain chemicals cause an increase in cytosolic Ca ++ concentrations.  Ca ++ causes intracellular damage by activating a number of enzymes that further deplete ATP levels, and cause membrane and DNA damage.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Damage is irreversible when there is:  Severe swelling of the mitochondria.  Severe damage to plasma membranes.  Rupture of lysosomes and release of lysosomal enzymes.  Cells may undergo either necrosis or apoptosis, depending on the cause.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Reperfusion injury due to oxidative stress  When O 2 is restored, reactive oxygen intermediates damage organelles.  Can be prevented using antioxidants.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Free radicals and reactive oxygen species  Electrically uncharged atom or group of atoms having an unpaired electron  Cause damage by: Lipid peroxidation – damages membranes of cell and organelles, increases permeability. Lipid peroxidation – damages membranes of cell and organelles, increases permeability. Alteration of proteins – especially those for ion pumps and transport proteins. Alteration of proteins – especially those for ion pumps and transport proteins. Alteration of DNA – fragmenting of DNA reduces protein synthesis. Alteration of DNA – fragmenting of DNA reduces protein synthesis. Mitochondrial damage – allows liberation of calcium into cytosol. Mitochondrial damage – allows liberation of calcium into cytosol.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Radiation  Ionizing radiation can knock electrons out of orbit.  This produces free radicals.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Chemical injury  Carbon tetrachloride (CCl 4 ) Liver converts this to a toxic free radical Liver converts this to a toxic free radical Causes lipid peroxidation → damage to membranes, release of lysozyme, and mitochondrial damage Causes lipid peroxidation → damage to membranes, release of lysozyme, and mitochondrial damage These result in fatty liver, cellular autodigestion, and decreased ATP production. These result in fatty liver, cellular autodigestion, and decreased ATP production.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Chemical injury  Lead – causes: Neurological problems (interferes with neurotransmitter release) Neurological problems (interferes with neurotransmitter release) Anemia Anemia Renal problems Renal problems

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Chemical injury  Carbon monoxide Prevents oxygen from binding to hemoglobin → hypoxic injury Prevents oxygen from binding to hemoglobin → hypoxic injury Cherry red coloring of skin. Cherry red coloring of skin.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Chemical injury  Ethanol Ethanol → acetaldehyde and free radicals in liver Ethanol → acetaldehyde and free radicals in liver Causes inflammation, fatty liver, membrane damage Causes inflammation, fatty liver, membrane damage Depresses CNS by acting on reticular formation which normally inhibits unacceptable behaviors. Depresses CNS by acting on reticular formation which normally inhibits unacceptable behaviors.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Injury Mechanisms  Chemical injury  Mercury Causes birth defects and brain damage in fetuses and small children. Causes birth defects and brain damage in fetuses and small children.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity Indicate whether each of these is primarily associated with a lack of oxygen (–) or with free radicals and oxidative stress (+). a) CO poisoning b) Damage by CCl 4 c) Cellular swelling d) Damage to DNA e) Formation of vacuoles f) Decreased ATP production

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity - Key Indicate whether each of these is primarily associated with a lack of oxygen (–) or with free radicals and oxidative stress (+). a) CO poisoning – b) Damage by CCl 4 + c) Cellular swelling – d) Damage to DNA + e) Formation of vacuoles – f) Decreased ATP production –

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Unintentional and Intentional Injuries  Blunt force injuries  In ER most are from falls and car accidents  Application of mechanical energy to the body resulting in the tearing, shearing, or crushing of tissues  Contusion – “bruise” (release of blood into tissues from damaged vessels without break in skin)  Hematoma – a collection of blood in soft tissues or an enclosed space (subdural space, etc.)

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Unintentional and Intentional Injuries  Blunt force injuries (cont.)  Abrasion – “scrape” (removal of the superficial layers of skin due to friction)  Laceration – a rip or tear of the skin; irregular edges. Avulsion – an extreme laceration. Avulsion – an extreme laceration. May also occur in internal organs due to blunt impact trauma with no external signs on skin. May also occur in internal organs due to blunt impact trauma with no external signs on skin.  Fractures – breakage of bone tissue.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Unintentional and Intentional Injuries Patterned abrasion Avulsion (an extreme laceration)

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Unintentional and Intentional Injuries  Sharp injuries  Incised wounds – a cut that is longer than it is deep.  Stab wounds – a penetrating sharp-force injury that is deeper than it is long.  Puncture wounds – caused by pointed objects without sharp edges.  Chopping wounds – caused by axes, hatches, propeller blades, etc.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Unintentional and Intentional Injuries  Gunshot wounds  Entrance wounds – usually have an abrasion collar. Contact range entrance wound. Contact range entrance wound.  Muzzle touching skin.  Blow-back and muzzle imprint. Intermediate range entrance wound Intermediate range entrance wound  Muzzle not touching skin; less than 48 inches away.  Tattooing and stippling – fragments of gunpowder driven into skin or cause abrasion.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Gunshot Wounds ← Contact range entrance wound ← Tattooing and stippling ↓ Indeterminate range entrance wound

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Unintentional and Intentional Injuries  Gunshot wounds  Entrance wounds (cont.) Indeterminate range entrance wound Indeterminate range entrance wound  Only bullet hits body  May occur through clothes  Exit wounds– usually are clean without an abrasion collar, except: Shored exit wound – abrasion around exit wound as skin pushes against something. Shored exit wound – abrasion around exit wound as skin pushes against something.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Unintentional and Intentional Injuries  Asphyxial injuries  Caused by a failure of cells to receive or use oxygen  Suffocation Caused by lack of oxygen in environment or blockage of external airways. Caused by lack of oxygen in environment or blockage of external airways. Choking asphyxiation – blockage of internal airways. Choking asphyxiation – blockage of internal airways.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Unintentional and Intentional Injuries  Asphyxial injuries  Strangulation Caused by compression and closure of blood vessels and air passageways by external pressure Caused by compression and closure of blood vessels and air passageways by external pressure Death due to lack of blood flow to brain. Death due to lack of blood flow to brain. Hanging – caused by suspension Hanging – caused by suspension Ligature – caused by cord around neck Ligature – caused by cord around neck Manual strangulation – caused by hands Manual strangulation – caused by hands

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Unintentional and Intentional Injuries  Asphyxial injuries  Chemical asphyxiants Prevent delivery or utilization of oxygen in tissues Prevent delivery or utilization of oxygen in tissues Cyanide – CN prevents O2 binding to cytochrome oxidase in mitochondria → cherry red coloring like CO poisoning. Cyanide – CN prevents O2 binding to cytochrome oxidase in mitochondria → cherry red coloring like CO poisoning.  Drowning Alteration of oxygen delivery due to breathing fluid into lungs Alteration of oxygen delivery due to breathing fluid into lungs Death occurs more rapidly in warm water than in very cold water. Death occurs more rapidly in warm water than in very cold water.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Infectious Injury  Pathogenicity of a microorganism  Disease-producing potential depends on organisms ability for:  Invasion and destruction  Toxin production  Production of hypersensitivity reactions

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Immunologic and Inflammatory Injury  Phagocytic cells  Immune and inflammatory substances  Examples - Histamine, complement, and proteases  Membrane alterations  Cause leakage of K + out of cell and influx of Na + and water.  Antibodies - can trigger immune attack and lysis.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Manifestations of Cellular Injury  Cellular accumulations (infiltrations)  Pathologic accumulations can occur due to: 1) excess production of normal substance, 2) the substance not being broken down due to lack of an enzyme, or 3) accumulation of harmful exogenous substances.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Accumulations  Water – enters cells due to lack of ATP and failure of Na + /K + pump, causing cellular swelling.  Oncosis (hydropic degeneration) – Water accumulates in endoplasmic reticulum forming vacuoles separate from cytoplasm (vacuolation). Water accumulates in endoplasmic reticulum forming vacuoles separate from cytoplasm (vacuolation). Visually the organs appear pale. Visually the organs appear pale.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Accumulations  Lipids and carbohydrates – accumulate (usually in spleen, liver and CNS) due to metabolic disorders like Tay-Sachs and Niemann-Pick disease.  Fatty change - can be caused by disruptions of normal lipid metabolism.  Liver appears yellow.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Accumulations  Glycogen – occurs in disorders of glucose and glycogen metabolism,  including diabetes mellitus.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Accumulations  Proteins – accumulate during pathological change in:  Renal tubules - during glomerular disorders that cause proteinuria.  B lymphocytes - excess antibodies form in multiple myeloma cells.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Accumulations  Pigments – accumulation may be normal or signal pathological changes.  Melanin Normal – suntan Normal – suntan Pathologic – melanoma Pathologic – melanoma  Hemoproteins, hemosiderin and bilirubin (from RBC breakdown) Pathologic: Pathologic:  Bruising  Jaundice

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Accumulations  Calcium – occurs due to hypoxia or excess levels of calcium.  Dystrophic calcification - occurs in dying and dead tissues, advanced atherosclerosis, etc.  Metastatic calcification - mineral deposits that occur in undamaged normal tissues as the result of hypercalcemia.  Urate – due to increased levels of uric acid from purine catabolism  Causes gout.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Death  Necrosis – cellular dissolution  Sum of cellular changes after local cell death and the process of cellular autodigestion

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Cellular Death  Processes  Karyolysis Nuclear dissolution and chromatin lysis Nuclear dissolution and chromatin lysis  Pyknosis Clumping of the nucleus Clumping of the nucleus  Karyorrhexis Fragmentation of the nucleus Fragmentation of the nucleus

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Coagulative Necrosis  Coagulative necrosis  Occurs in - kidneys, heart, and adrenal glands  Protein denaturation - results from hypoxia caused by severe ischemia or chemical injury (for example, mercuric chloride intake). Kidney

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Liquefactive Necrosis  Liquefactive necrosis  Occurs in - neurons and glial cells of the brain  Hydrolytic enzymes – from lysozyme in dying cells  Bacterial infection Staphylococci, streptococci, and Escherichia coli Staphylococci, streptococci, and Escherichia coli

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Liquefactive Necrosis http://library.med.utah.edu/WebPath/CINJHTML/CINJ025.html

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Caseous Necrosis  Caseous necrosis - “cheese-like”  Occurs in - tuberculosus pulmonary infection  Combination of coagulative and liquefactive necrosis  Cells disintegrate but are not completely digested

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Fat Necrosis  Fat necrosis  Occurs in - breast, pancreas, and other organs that have lipase enzyme.  Action of lipases - releases free fatty acids that react with Ca 2+, Mg 2+ and Na + → soaps

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Gangrenous Necrosis  Gangrenous necrosis  Death of tissue from severe hypoxic injury – often due to atherosclerosis or trauma Dry gangrene → coagulative Dry gangrene → coagulative Wet gangrene → liquefactive necrosis (internal organs) Wet gangrene → liquefactive necrosis (internal organs)  Gas gangrene –bacteria produce hydrolytic enzymes and create gas bubbles in muscles Clostridium – anaerobic bacteria responsible Clostridium – anaerobic bacteria responsible

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity Which type of necrosis would most likely occur in each of the following situations? a) Damage to a tissue rich in hydrolytic enzymes. b) Damage to a tissue rich in lipid digesting enzymes. c) Tissue destruction by a chemical that denatures protein.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity - Key Which type of necrosis would most likely occur in each of the following situations? a) Damage to a tissue rich in hydrolytic enzymes. Liquefactive necrosis b) Damage to a tissue rich in lipid digesting enzymes. Fat necrosis c) Tissue destruction by a chemical that denatures protein. Coagulative necrosis

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Apoptosis  Apoptosis – death of unnecessary cells due to action of enzymes produced within cell.  Programmed cellular death – prevents overgrowth of cells.  Defects in apoptosis – can cause overgrowth of cells, resulting in cancer.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Apoptosis  Physiologic (normal) –  During embryonic development  As a result of hormonal changes (for example, after childbirth)  In nutrient deprived tissues  Pathologic - due to:  Severe cell injury  Accumulation of misfolded proteins  Viral infections  Obstruction of tissue ducts

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Apoptosis  Normal, genetically programmed cell death.  Usually involves individual, scattered cells.  Cellular enzymes cleave key cellular proteins; cells shrink and fragment.  Cellular debris remains bound in a membrane forming apoptotic bodies which are removed by neutrophils and macrophages.  This process does not stimulate the inflammatory response.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Necrosis  Due to damage from exogenous injury.  Usually involves many cells in area of injury.  Cell membranes rupture, releasing cell contents into tissue.  Triggers inflammatory response.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity Identify whether each of the following is more likely to involve apoptosis (A) or necrosis (N). Atrophy of breast tissue after weaning of an infant. Atrophy of breast tissue after weaning of an infant. Burn injuries. Burn injuries. Leakage of mitochondrial outer membrane. Leakage of mitochondrial outer membrane. Viral infection. Viral infection. Tuberculosis infection. Tuberculosis infection. Hypoxia. Hypoxia.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity - Key Identify whether each of the following is more likely to involve apoptosis (A) or necrosis (N). A Atrophy of breast tissue after weaning of an infant. A Atrophy of breast tissue after weaning of an infant. N Burn injuries. N Burn injuries. A Leakage of mitochondrial outer membrane. A Leakage of mitochondrial outer membrane. A Viral infection. A Viral infection. N Tuberculosis infection. N Tuberculosis infection. N Hypoxia. N Hypoxia.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Aging and Altered Cellular and Tissue Biology  Aging – time-dependent loss of structure and function that proceeds slowly due to accumulated small injuries.  The question is at what point does this become disease? There is some overlap.  Disease – abnormal dysfunction due to injury.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Aging and Altered Cellular and Tissue Biology  Normal life span- across cultures the maximal life span is 80-100 years.  Gender differences – females have a life expectancy about 5 years greater than males.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Theories and Mechanisms of Aging 1. Genetic and Environmental-Lifestyle Factors  Includes three basic mechanisms:  Programmed aging – cells have a finite lifespan with a finite number of possible divisions, after which the DNA loses the capacity for mitosis.  Somatic mutation hypothesis  Catastrophic or error-prone theory

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Theories and Mechanisms of Aging  Somatic mutation hypothesis – repetitive injury to the DNA causes progressive mutations that interfere with the ability of the cell to repair itself and maintain DNA and protein synthesis.  Catastrophic or error-prone theory – the enzymes responsible for transcription and translation become increasingly abnormal, leading to increasing errors in protein synthesis.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Theories and Mechanisms of Aging 2. Alterations of cellular control mechanisms  Neuroendocrine theory – the genetic program for aging is encoded in the brain and is controlled and relayed to peripheral tissues through hormonal and neural signals.  Immune theory - with aging, there is decreased immunity to invaders and cancer and increased autoimmunity (immune system attacks self).

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Theories and Mechanisms of Aging 3. Degenerative extracellular and vascular changes  Binding of collagen – crosslinking, decreased synthesis and increased breakdown of collagen  Free radical effects (oxidative stress) – damage to DNA → malignancies and cell death  Alterations in peripheral blood vessels – decreased vessel integrity and atherosclerosis

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Aging  Cellular aging – characterized by:  Atrophy, decreased function, and loss of cells  Tissue and systemic aging - every physiologic process declines in efficiency with age.  Progressive stiffness and rigidity – arterial, pulmonary, and musculoskeletal systems.  Sarcopenia – loss of muscle mass and strength.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Aging  Frailty  Decreased mobility, balance, muscle strength, motor activity, cognition, nutrition, endurance and bone density result in increased falls and fractures.  Accompanied by declining hormone levels and increased levels of proinflammatory cytokines

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Somatic Death  Death of an entire person  Postmortem changes – after death, diffuse changes that do not involve the inflammatory response.  Algor mortis – postmortem reduction of body temperature. Body temp drops by 1- 1.5 °F per hour.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Somatic Death  Livor mortis – purplish discoloration of tissues due to accumulating blood drawn down by gravity.  Rigor mortis – stiffening of muscles due to depletion of ATP; begins after 6 hours and continues until about 36 hours after death.  Postmortem autolysis – digestion of body tissues due to release of lysozymal enzymes causing liquefactive changes and putrification.

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity A coroner examines a body at the scene of a murder and takes note of the following: the core body temperature is 95 °F, the surface resting on the ground is purplish, and there is no abnormal stiffening of the muscles. Roughly how long ago did death occur?

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Activity - Key A coroner examines a body at the scene of a murder and takes note of the following: the core body temperature is 95 °F, the surface resting on the ground is purplish, and there is no abnormal stiffening of the muscles. Roughly how long ago did death occur? Less than 6 hours (but probably more than 2 hours, since body temp drops by 1-1.5 °F per hour).

Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Altered Cellular and Tissue.

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Elsevier items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc. Some material was previously published. Altered Cellular and Tissue.

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