Cellular+Biology

Back to Home Page

Cellular Biology, Unit One. Pages 1-60 by Prashanthi Dsilva, pages 61-122 by Cori Warner http://library.thinkquest.org/12413/

STARTING PAGE 61 of Chapter 2 Altered Cellular and Tissue Biology

Cited references are for the information on the linked pages. All information on the main Cellular Biology pages comes from the textbook (McCance & Huether, 2006).

UNINTENTIONAL AND INTENTIONAL INJURIES
 * Death due to injury more common in men than women
 * Death due to injury more common in blacks, then whites, then other races
 * Death due to injury peaks for young adults and elderly
 * Disability resulting in injury is also significant
 * Types of injuries
 * Blunt Force Injuries (Internet Pathology Laboratory for Medical Education)- caused by application of mechanical injury resulting in shearing, tearing or crushing of tissues
 * Contusions-(bruise) (Internet Pathology Laboratory for Medical Education) bleeding into the skin or underlying tissues as a result of a a blow that squeezes or crushes soft tissues
 * Collection of blood in tissues is a hematoma.
 * Subdural hematoma- collection of blood in between the dura and the brain
 * Epidural hematoma-collection of blood between the dura and the skull
 * Abrasion-removal of superficial layers of the skin between the skin and injuring object.
 * Abrasions and Contusions may have a patterned appearance (Internet Pathology Laboratory for Medical Education)that mirrors the shape of the injuring object
 * Lacerations- (Internet Pathology Laboratory for Medical Education) is a tear or rip resutling when the the tensile strength of the skin is exceeded
 * Sharp Force Injuries- caused by cutting or piercing, either accidental or intentional
 * Incised wounds (Internet Pathology Laboratory for Medical Education) - longer than it is deep
 * Stab wounds- (Internet Pathology Laboratory for Medical Education) deeper than it is long
 * Puncture- (International Centre for Eye Health) caused by sharp object without edges
 * Chopping wound- (Survive Outdoors, Inc) has characteristics of both blunt force and sharp wounds
 * Gunshot Wounds (Internet Pathology Laboratory for Medical Education, Google search)
 * Entrance wound-bullet goes in
 * Appearance determined by range; contact, close, intermediate or distant ranges will result in distintive patterns of injury
 * Exit wound-bullet goes out
 * More tissue trauma on exit, particularly if bullet is designed to flatten and cause more damage
 * Asphyxial wounds- caused by failure of cells to recieve or utilize oxygen
 * suffocation-O2 fails to reach the blood, due to lack of O2 in environment or obstruction of airways, such as in choking.
 * suffocation-O2 fails to reach the blood, due to lack of O2 in environment or obstruction of airways, such as in choking.
 * strangulation-caused by compression and closure of blood vessels and airway from external pressure on the neck
 * hanging-body suspended and weight causes constriction
 * ligature- petichiae more common because of intermittent opening and closing of blood vessels
 * manual-contusions and abrasions, petichiae common
 * Chemical-prevent delivery of O2 or block its utilization
 * Drowning-major method of injury is hypoxia, can be caused by vagal-nerve mediated laryngospasms, where very little water enters the lungs; called dry-lung drowning.

INFECTIOUS INJURIES IMMUNOLOGIC AND INFLAMMATORY INJURY INJURIOUS GENETIC FACTORS INJURIOUS NUTRITIONAL IMBALANCES INJURIOUS PHYSICAL AGENTS
 * Pathogenicity of a microorganism lies in its ability to invade, survive, and proliferate in the human body
 * Disease producing potential depends on
 * ability to invade and destroy (or take over) cells
 * ability to produce toxins
 * ability to produce hypersensitivity reactions
 * [|Link to article on looming threat of bird flu pandemic] (NY Daily News.com) Scary Stuff (this link takes you out of WIkispaces, use the back button on your browser to return)
 * Cell membranes injured by contact with products on inflammation or autoimmunity, such as phagocytic cells, histamines, complement, and proteases.
 * Commonly found in diabetes (causes peripheral vascular disease and neuropathy) and autoimmune disorders
 * Genetic disorders may be result of genetic factors that alter a cell's nucleus and the prlas membranes' stucture, shape, receptors, or transport mechanisms. Ex: Sickle cell anemia.
 * See Table 2-7
 * Essential nutrients- protiens, carbohydrates, lipis, fats, vitamins, and minerals are required for cells to function normally. Too little or too much can create pathologic conditions. (BTW, called essential because its ESSENTIAL that we consume them, we can not make them in our own body)
 * Some pathologic nutritional states
 * Hyperglycemia -too much sugar in the blood
 * Hypolipidemia -not enough lipids, so body uses fat stores, and creates ketones, can cause ketoacidosis, kidney damage or death (this is the state that ATKINS diet puts your body into; not really a good method to lose weight; kidneys are important....)
 * Hyperlipidemia- high lipid protiens, causes plaques in the vascular system
 * Temperature extremes
 * hypothermia- causes chemical changes (p70) and microvascular constriction resulting in localized necrosis (frostbite)
 * Hyperthermic injury
 * heat cramps-result of salt and water loss
 * heat exhaustion-result of hemoconcentration due to fluid loss
 * heat stroke-life threatening condition associated with high heat and humidity. marked peripheral vasodilation reduces circulating blood volume
 * Burns caused by local heat injury, severity depends on depth and amount of body surface affected
 * Atmospheric pressure
 * blast injury-tranmitted by air or water, increase in pressure such as an explosion
 * decompression sickness- the "bends" caused by rising to quickly to the surface from deep water
 * Ionizing Radiation- any radiation capable of removing orbital electrons from atoms.
 * xray
 * gamma ray
 * radiant sunlight
 * others, see page 71
 * High doses of radation result in skin redness or burns, chromsomal damage, and may occur within hours or days
 * Long term long doses may not show injury for years
 * somatic, involving entire body, ie leukemia
 * genetic, involving offspring
 * fetal, if exposed in utero
 * Illumination
 * fluorescent light may damage eyes and cuase headaches
 * in vitro toxicity of halogen lamps
 * Mechanical Stresses
 * see table 2-9
 * Noise
 * most common injury is hearing impariment (gee, ya think?)
 * acoustic trauma- instantaneous cause by single rising was of sound, ie gunfire
 * noice induced hearing loss- prolonged exposure to high levels of noise (such as what comes out of your teen's stereo)
 * If noise not too loud or too long, hearing will return to previous level. this is called a temporary threshold shift (TTS)
 * If noise is prolonged, may result in a permanent threshold shift (PTS) and long term hearing loss

MANIFESTATIONS OF CELLULAR INJURY
 * Cellular Accumulations- infiltrations occur as result of injury to cells or as a result of inefficient cell function
 * usually an increase in already present substances such as fluides, electrolytes, lipids, etc
 * normal substance is excessively produced
 * endogenous substance not properly catabolized
 * harmful exogenous materials such as heavy metals accumulate because of inhalation, ingestion, or infection
 * Water
 * Cellular swelling-caused by shift of extracellular water into cells. Considered sublethal
 * vacuolation-cisternae of the endoplasmic reticulum become distended, rupture, and coalesce to form vacuoles to isolate the water from the cytoplasmic membrane
 * Oncosis-vacuolar degeneration, or degeneration by water
 * Lipids and Carbohydrates
 * Abnormal accumulations usually found in the spleen, liver and CNS due to certain metabolic disorders
 * Neimann-Pick
 * Gaucher
 * Lipds may accumulate in the heart or kidneys, but most commonly found in the liver, resulting in "fatty liver" which results in pathologic changes. See page 75 for list of mechanisms that may cause this.
 * Common cause is endoplasmic reticulum by free radicals released by alcohol's toxic effect on the liver. (More useless trivia: even moderate alcohol consumption can cause these changes temporarily, causing the liver to have a "nutmeg" appearance. Long term causes cirrhosis.
 * Glygogen is seen in genetic disorders, most commonly in diabetes mellitus.
 * Protien accumulates primarily in the epithelial cells of the renal convoluted tubule and in ß lymphocytes of the immune system.
 * proteinuria-protien in the urine
 * Russell bodies- aggreagates of brotien created during active synthesis of antibodies during immune response. Implicated in multiple myeloma.
 * Pigments may be normal or abnormal, exogenous or endogenous
 * Melanin accumulates in ketinocytes of the skin and retina, protects skin against sunlight exposure
 * stored in melanosomes which are abundant in prjections of melancytic cytoplasm called dendrites from which they are transmitted to neighboring kertinocytes.
 * also accumulates in melanphores, macrophages, or other phagocytic cells in the dermis. This is what causes freckles
 * accumulates in pigmented moles called nevi
 * decrease of absence of melanin production is called albinism
 * Hemoprotiens are one of the most essential endogenous pgiments. Include hemoglobin and cytochromes
 * excessive accumulation caused by excessive storage of iron which enters the blood through tissue stores, the intestingal mucosa, and macrophages that remove and destroy dead blood cells. Amount in blood also determined by levels of the major iron-transport protien transferrin.
 * Hemosiderin is a yellow-brown pigment derived from hemoglobin (makes bruises yellow). may accumulate in the lungs and spleen after congestion caused by heart failure
 * Hemosiderosis is condition in which excess iron is stored as hemosiderin in the cells of multiple organs and tissues. Common after multiple transfusions or parenteral infusions of iron.
 * Bilirubin is a normal yellow-to-green pigment of bile.
 * excessive amounts cause icterus (jaundice)
 * hyperbilirubinemia occurs with destruction of red blood cells, diseases affecting excretion of bilirubin in the liver, and diseases that obstruct the common bile duct, such as gall stones or pancreatic tumor
 * Calcium salts accumulate in both injured and dead tissues. Damage occurs when calcium salts clump and harden. See page 77 for the chemical explanation of this process
 * Dystrophic calcification is the calcification of dying and dead tissues and occurs in chronic TB of the lungs and lymph nodes, in arteris with advanced artherosclerosis and often in injured heart valves
 * Metastatic calcification consists of mineral deposits in normal tissue as a result of hypercalcemial
 * hyperparathyroidism
 * toxic levels of vitamin D
 * hyperthyroidism
 * Addisons
 * systemic sarcoidosis
 * milk-alkali syndrome
 * bone tumors
 * Urate (uric acid) is a normal end product of purine metabolism
 * disturbance in maintaining serum urate levels result in hyperuricemia and deposits of sodium urate crystals in the tissues, known as gout.
 * Systemic manifestations of cellular injury include genral sense of fatigue and mailaise, loss of well-being and appetite and fever. See table 2-10
 * CELLULAR DEATH
 * Necrosis- cellular dissolution
 * autolysis- cellular self-digestion
 * karolysis-nuclear dissolution an dlysis of chromatin for the action of hydrolytic enzymes
 * pyknosis-shrinking of the nucleus into a small dense mass of genetic material that eventually dissolves through kayorrhexis
 * coagluative necrosis-occurse primarily in the kidneys, heart and adrenal glands commonly caused by hypoxia or chemical injury. Caused by protien denaturation which causes albumin to change from gelantinous to firm.
 * liquefactive necrosis (WSU Medical Science)- results from ischemic injury to neurons and glial cells in the brain. Dead brain tissue quickly becomes soft, liquifies and is walled off from healthy tissue and forms cysts. (has a consistency like a melted milkshake)
 * may also be caused by bacterial infection like staph, strep, or e-coli
 * caseous necrosis- (WSU Medical Science) common in TB is a combination of coagulative and liqificative necrosis. The dead cell disintergrates, but is not digested completely by the hydrolases. Tissue then appears soft and granular and rsemble clumped cheese.
 * fat necrosis- (Salhab, et al. 2005) occurs in breast, pancreas and other abdominal structures is caused by lipases which break down triglycerides. Free fatty acids combine with calcium, magnesium, and sodium ions to for soaps (saponification). The necrotic tissue appears opaque and chalk white.
 * Gangrenous necrosis refers to death of tissue related to severe hypoxic injury and bacterial invasion.
 * dry gangrene (Watret & Armitage, 2001) is usually the result of coagulative necrosis. Skin becomes dry and shrinks,and changes to dark brown or black.
 * wet gangrene (Watret & Armitage, 2001) occurs when neutrophils invade the site and cause liquefactive necrosis. Usually occurs in internal organs, site becomes cold, swollen, and black, with foul odor caused by pus. If infection becomes systemic, it can be fatal.
 * gas gangrene- (Barnes, n.d.) special type of gangrene caused by anaerobic bacteria Clostridium. Smells knock-you-over bad. Can cause death because of toxic by-products of the bacteria.
 * Apoptosis~ (Cells Alive!)is a unique type of cell death. It is an active process of self-destruction called programmed cell death. It can be both a normal and a pathologic process. See page 82, and fig 2-36 for description and diagram of process.
 * AGING AND ALTERED CELLULAR AND TISSUE BIOLOGY
 * Aging is defined as the normal process which depnds on irreversable and universal processes at the cellular level.
 * Aging theory 1- aging is the result of the accumulation of multiple injuries and events at the cellular level
 * Aging theory 2- aging is the result of genetically controlled developmental and self-destructive processes
 * See page 83 for theory 3
 * Norman life span is between 80 and 100 and doesn't vary significantly between populations, but requires optimal living conditions to reach the maximal life span.
 * Life span and gender differences
 * Life expectancy for females exceeds that of males except in Bangladesh, Bhutan, India, Nepal, and Pakistan
 * Female advantage is about 4-8 years
 * Whites have a longer life expectancy than blacks, given the same living conditions
 * Theories and mechanisms of aging
 * Table 2-11 for list of various theories on aging and their proponents
 * three areas of the mechanism of aging have retained their appeal
 * cellular changes produced by genetic, environmental, and behavioural factors
 * changes in cellular regulatory mechanisms
 * degenerative extracellular and vascular alterations
 * Somatic mutation hypothesis proposes that aging in the result of DNA damage, inefficiency of repair, and loss of integrity of DNA synthesis
 * Neuroendocrine theory of aging puports that a genetic profram for agin in encoded in the brain and control and relayed to peripheral tissues through hormonal and neuronal agents.
 * Cellular Aging
 * Changes include atrophy, decreased function, loss of cells, possibly by apoptosis. Loss of cells causes hypertrophy and hyperplasia of remaining cells, which can cause metaplasia, dysplasia, and neoplasia. Lack of DNA repair may contribute to development of mutations that are lethal.
 * Tissues and systemic aging
 * every system in the body functions less efficiently as we age. Many tissues become rigid and stiff with age, and many processes slow. Immunity is reduced, reproductive function ceases, muscles decrease in size and strength (sarcopenia).
 * Frailty is imprecisely defined as a wasting syndrome of aging, leaving a person vulnerable to falls, functional decline, disease, and death. Women are more likely to become frail than men, due to metabolic differences
 * Somatic death is death of the entire body. Postmortem changes occur within minutes and leave know doubt that death has occured.
 * algor mortis-drop in body temp after death
 * livor mortis- blood moves to dependent tissues
 * rigor mortis-muscle stiffness due to depeltion of ATP
 * postmortem autolysis- lytic dissolution of tissues due to release of enzymes

CLICK HERE TO GO TO CHAPTER THREE NOTES