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Week 1 Altered Cellular and Tissue Biology

by: Jordan Smith

Week 1 Altered Cellular and Tissue Biology Nursing 240

Jordan Smith
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About this Document

These notes cover our chapter over Altered Cellular and Tissue Biology.
Pathophysiology N240
Dr. Jo Anne Pritchett
Class Notes
pathophysiology, Nursing, patho, Biology, tissue, altered cellular and tissue biology




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This 5 page Class Notes was uploaded by Jordan Smith on Wednesday March 30, 2016. The Class Notes belongs to Nursing 240 at Southern Illinois University Edwardsville taught by Dr. Jo Anne Pritchett in Spring 2016. Since its upload, it has received 29 views. For similar materials see Pathophysiology N240 in Nursing and Health Sciences at Southern Illinois University Edwardsville.

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Date Created: 03/30/16
Chapter 3: Altered Cellular and Tissue Biology  Cellular Alterations  Injury to cells and their surrounding environment (called the extracellular matrix)  leads to tissue and organ injury  Cells can adapt to physiologic demands or stress to maintain a steady state called  homeostasis  Adaptation is a reversible, structural, or functional response both to normal or  physiologic conditions  Example: uterus adapts to pregnancy—a normal physiologic process—by enlarging  Example: in adverse condition such as hypertension, myocardial cells are stimulated to enlarge by increased work of pumping and are usually only temporarily successful  Cellular Adaptation  Physiologic vs. pathogenic o Atrophy – decrease or shrinkage in cell size and consequently in size of affected organ o Hypertrophy­ increase in size of cells and consequently in the size of the affected organ o Hyperplasia­ increase in number of cells form increased rate of cell division o Dysplasia­ abnormal changes in size, shape, and organization of mature cells o Metaplasia­ reversible replacement of one mature cell type by another, sometimes less differentiated cell type Cellular Injury  Reversible  Irreversible  Cellular Injury Mechanisms  Hypoxic injury—single most common cause of cellular injury o Ischemia—reduced blood supply o Anoxia­ total lack of oxygen o Cellular responses  Decrease in ATP, causing failure of sodium­potassium pump and  sodium­calcium exchange (allows calcium to enter into the cell,  killing the cell)  Cellular swelling  Vacuolation­ is the formation of vacuoles within or adjacent to cells,  and, in dermatopathology, often refers to the basal cell­basement  membrane zone area. o Reperfusion injury­ restoration of oxygen that results from generation of  oxygen free radicals that can cause further cell membrane damage and  mitochondrial calcium overload   Chemical injury o Carbon tetrachloride­ now banned, used in industries such as refrigeration  and pesticides  o Lead—paint, soil, pottery, mining o Carbon monoxide—hypoxic asphyxiation, odorless, colorless, deadly o Ethanol—alcohol intoxication/poisoning  o Mercury—fish consumption and dental amalgams  o Social or street drugs—heroin, meth, cocaine  Unintentional and Intentional Injuries  Blunt force injuries o Application of mechanical energy to the body resulting in the tearing,  shearing, or crushing of tissues  o Contusion vs. hematoma  Contusion­ bruise caused by bleeding into skin or underlying tissues  Hematoma­ is a collection of blood in soft tissue  o Abrasion – wound or scrape cause by superficial damage to the skin, no  deeper than the epidermis  o Laceration­ tear or rip in tissue; ragged & irregular with abraded edges  caused by blunt trauma  Extreme example is an avulsion where a wide area is pulled away;  organ injuries can also become lacerated from blunt force  o Fractures­ breakage of bone from blunt force trauma   Sharp injuries o Incised wounds  Longer than it is deep   Straight or jagged with sharp, distinct edges without abrasions  Usually produces significant external bleeding and little internal  bleeding  May see superficial incisions in same area called “hesitation marks” o Stab wounds  Penetrating sharp force injury that is deeper than it is long  External bleeding small due to almost immediate tissue pressure over  site  o Puncture wounds  Made by objects with sharp points but without sharp edges   Prone to infection  Can be deep (stepping on nail)  o Chopping wounds  Made by heavy, edged instruments such as hatchets, propeller blades  Produces a combination of sharp and blunt force characteristics  Unintentional and Intentional Injuries—Gunshot Wounds  Contact rang entrance wounds occur when gun is held so that the muzzle rests or  presses on the skin surface o Searing of edges of wounds from flame/smoke in addition to hole  o Wounds is gaping and/or jagged which is called blow back that mirror the  imprint of the weapon   Intermediated range entrance wound: surrounded by gunpowder stippling/tattooing  that results from fragments of burning or unburned pieces of gunpowder exiting gun  barrel and forcibly striking skin  Exit Wounds  Shored exit wounds Unintentional and Intentional Injuries  Asphyxia injuries—caused by a failure of cells to receive or use oxygen o Suffocation­ choking asphyxiation  o Strangulation – hanging, ligature, and manual strangulation  o Chemical asphyxiants – carbon monoxide most common, cyanide, and  hydrogen sulfide (sewer gas) o drowning  Infectious Injury  Pathogenicity of a microorganism  Disease­producing potential o Invasion and destruction o Toxin/endotoxin production o Production of hypersensitivity reactions  Immunologic and Inflammatory Injury  Phagocytic cells  Immune and inflammatory substances o Histamine, antibodies, lymphokines, complement, and proteases  Membrane alterations  WILL DISCUSS DETAILS IN IMMUNE SYSTEM Cellular Death  Necrosis: sum of cellular changes after local cell death and the process of cellular  auto­digestion o Coagulative necrosis  Kidneys, heart, and adrenal glands  Protein denaturation  Usually caused by ischemia or infarction caused by chemical injury  o Liquefactive necrosis  Ischemic injury to neurons and glial cells of the brain and is digested  by enzymes  Hydrolytic enzymes break down protein, carbs, and fat  Bacterial infection  Staphylococci, streptococci, and Escherichia coli o Caseous necrosis  Tuberculous pulmonary infection  Combination of coagulative and liquefactive necrosis  Cottage cheese appearance and is soft and granular o Fat necrosis  Breast, pancreas, and other abdominal organs  Action of lipases break down fat in these organs o Gangrenous necrosis  Death of tissue from severe hypoxic injury commonly from  arteriosclerosis or blockage of major arteries, esp. those in legs  Dry gangrene dries and shrinks skin and color turns to dark brown or  black  Wet gangrene develops when WBCs invade the site, usually internal  organs causing site to become cold, swollen, and back with foul odor  Gas gangrene­ refers to special type of gangrene caused by  infection of injured tissue by the bacteria clostridium   Death is caused by shock Apoptosis (programmed cell death) vs. necrosis Aging  Cellular aging o Atrophy, decreased function, and loss of cells   Tissue and systemic aging o Progressive stiffness and rigidity o Sarcopenia—loss of muscle tissue R/T aging  Frailty o Mobility, balance, muscle strength, motor activity, cognition, nutrition,  endurance, falls, fractures, and bone density Somatic Death  Algor mortis—post mortem reduction of body temperature; takes about 24 hours until the body temperature equals that of the environment   Livor mortis—gravity causes blood to settle in the most dependent or lowest tissues  which develop a purplish discoloration   Rigor mortis—occurs over 6­ 14 hours; muscle stiffening with smaller muscles being  affected first   Putrefaction usually occurs between 24­48 hours after death as rigor mortis gradually  diminishes   Body becomes flaccid in 36­62 hours 


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