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Cell injury

Cell injury. Cell injury. When the cell is exposed to any injurious agent or stress ,a consequence of events follows, that is loosely termed cell injury. Cell injury is reversible up to certain point.

vivian-wilkerson
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Cell injury

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  1. Cell injury

  2. Cell injury • When the cell is exposed to any injurious agent or stress ,a consequence of events follows, that is loosely termed cell injury.Cell injury is reversible up to certain point. • To survive, cells must have the ability for adaptation to variable conditions. This process of adaptation can involve changes in cellular size, number or type. • If the stimulus persist or severe enough from the beginning , cell death occur .

  3. Five Cellular Adaptations to Injury: • Atrophy • Hypertrophy • Hyperplasia • Metaplasia • Dysplasia Cell Adaptation to Injury

  4. 1) Atrophy Cell Adaptation to Injury • It means Decrease or shrinkage in cellular size. • That is either Physiological or Pathological • Pathologic atrophy occur due to ↓ ↓ ↓ in : • Workload(اندام گچ گرفته) • Pressure • Use • Blood supply • Nutrition • Hormonal Stimulation • Nervous Stimulation • Atrophy is generally a reversible(برگشت پذیر) process, except for atrophy caused by loss of nervous innervations to a tissue. • Causes of atrophy include prolonged bed rest, disuse of limbs or tissue, poor tissue nutrition and ischemia.

  5. 3) Hypertrophy Cell Adaptation to Injury • Increase in cell size and tissue mass. • Occurs when a cell or tissue is exposed to an increased workload(بار کاری). • Occurs in tissues that cannot increase cell number as an adaptive response.(عضله قلبی، ورزشکاران) • Hypertrophy may be : • normal physiologic response, such as the increase in muscle mass that is seen with exercise • pathologic as in the case of the cardiac hypertrophy that is seen with prolonged hypertension. • or compensatory(جبرانی) process, when one kidney is removed, for example, the remaining kidney hypertrophies to increase its functional capacity.

  6. 2) Hyperplasia Cell Adaptation to Injury • Increase in number of cells resulting from increased rate of cellular division.(افزایش سلولهای جدید) • It is either: • Physiologic process, as in the breast and uterine hyperplasia that occurs during pregnancy, • Pathologic: such as Benign Prostatic Hyperplasia (BPH) and gingival hyperplasia (overgrowth of gum tissues) that maybe seen in certain patients receiving the drug phenytoin. • or compensatory mechanism:for example, when a portion of the liver is surgically removed, the remaining hepatocytes (liver cells) increase in number to preserve the functional capacity of the liver.

  7. 4) Metaplasia Cell Adaptation to Injury • The conversion of one cell type to another (تغییر یک سلول بالغ) cell type that might have a better chance of survival under certain circumstances. • Metaplasia occurs in response to chronic irritation or inflammation. • An example of metaplasia is: • in the respiratory passages of chronic cigarette smokers.

  8. 5) Dysplasia Cell Adaptation to Injury • A derangement(اختلال) of cell growth that leads to tissues with cells of varying size, shape and appearance. • Generally occurs in response to chronic irritation and inflammation. Dysplasia may be a strong precursor to cancer such as in the cervix or respiratory tract. However, dysplasia is an adaptive process and as such does not necessarily lead to cancer. در بسیاری از موارد، سلول های دیسپلاستیک به ساختار و عملکرد سابق خود بازمی گردند.

  9. Classification of Cellular injury • Physical injury • Mechanical trauma • Temperature extremes (burn injury, frostbite) • Electrical current • Chemical injury • Chemicals, toxins, heavy metals, solvents, smoke, • pollutants, drugs, gases • Radiation injury • Ionizing radiation — gamma rays, X rays • Non-ionizing radiation — microwaves, infrared, laser • Biologic agents • Bacteria, viruses, parasites • Nutritional injury • Malnutrition • Obesity

  10. Cellular injury Although the causes of cellular injury are many , the underlying mechanisms of cellular injury usually fall into one of two categories: • free radical injury • hypoxic injury

  11. Cellular injury 1)Free radical injury • Free radicals are highly reactive chemical species that have one or more unpaired electrons in their outer shell. • Examples of free radicals includesuperoxide (O−2),hydroxyl radicals (OH−) and hydrogen peroxide(H2O2). • Free radicals are generated as by-products of normal cell metabolism and are inactivated • Injury to cells occur when: • excess free radicals are formed from exogenous sources or • the free radical protective mechanisms fail.

  12. Cellular injury 1)Free radical injury • Free radicals are highly reactive and can injure cells through: 1. Destruction(تخریب) of membrane lipids. 2. Damage of cellular proteins. 3. Mutation of cellular DNA. • Exogenous sources of free radicals include tobacco smoke, organic solvents, pollutants, radiation and pesticides. • (توتون و تنباکو دود، حلال های آلی، آلاینده ها، تابش و سموم دفع آفات)Free radical injury has been implicated as playing a key role in: 1.The normal aging process. 2.Number of disease states such as diabetes mellitus, cancer, atheroscelrosis, Alzheimer’s disease and rheumatoid arthritis.

  13. Cellular injury 2)Hypoxic cell injury • Hypoxia is: a lack of oxygen in cells and tissues that generally results from ischemia. • The hypoxic cellular injury process is either: • reversible, if oxygen is quickly restored, • Or irreversible(برگشت ناپذیر) and lead to cell death. Certain tissues such as the brain are particularly sensitive to hypoxic injury. Death of brain tissues can occur only 4 to 6 minutes after hypoxia begins.

  14. Cellular injury 2)Hypoxic cell injury • During periods of hypoxia: • Aerobic metabolism of the cells begins to fail. • This leads to dramatic decreases in energy production (ATP) within the cells. • Hypoxic cells begin to swell as energy-driven processes begin to fail, (such as ATP-driven ion pumps). • The pH of the extracellular environment begins to decrease as waste products begin to accumulate, such as lactic acid, a product of anaerobic metabolism. • Accumulation of intracellular calcium, which is normally closely regulated within cells. There are a number of calcium-dependent protease enzymes present within cells that become activated in the presence of excess calcium and begin to digest important cellular constituents.

  15. Reversible and Irreversible Cell Injury Irreversible: Reversible:  Decrease generation Sever of ATP mitochondrial  Loss of cell changes membrane integrity Persistent or Extensive damage excessive  Defects in protein to plasma membranes injury synthesis, and DNA damage Swelling of lysosomes

  16. Manifestation of Cellular injury • 1. Cellular swelling • Caused by an accumulation of water due to the failure of energy driven ion pumps. Breakdown of cell membrane integrity and accumulation of cellular electrolytes may also occur. • Cellular swelling is considered to be a reversible change.

  17. Manifestation of Cellular injury • 2. Cellular accumulations • In addition to water, injured cells can accumulate a number of different substances as metabolism and transport processes begin to fail. • Substances that can be accumulated in injured cells may include fats, proteins, glycogen, calcium, uric acid and certain pigments such as melanin. • These accumulations are generally reversible but can indicate a greater degree of cellular injury. Accumulation of these substances can be so marked that enlargement of a tissue or organ may occur (for example, fatty accumulation in an injured liver).

  18. Cell death Cell death falls into two main categories: • Apoptosis: controlled, “pre-programmed” cell death • Necrotic cell death: unregulated, enzymatic digestion of a cell and its components.

  19. Cell death 1) Apoptosis • A controlled, “pre-programmed” cell death that occurs with aging and normal wear and tear of the cell. • آپوپتوز ممکن است یک مکانیسم برای از بین بردن فرسوده و یا سلول های آسیب دیده ژنتیکی. برخی از عفونت های ویروسی (ویروس ابشتاین بار، به عنوان مثال) ممکن است آپوپتوز در سلول های آلوده را فعال نمایید، در نتیجه کشته شدن سلول میزبان و آلوده به ویروس.It has been theorized that cancer may arise as a failure of normal apoptosis in damaged or mutated cells.

  20. 2) Necrosis Cell death • Occurs as a result of irreversible cellular injury. • Involves the unregulated, enzymatic digestion (“autolysis”) of a cell and its components. • Different types of tissues tend to undergo different types of necrosis. • Three main types of necrosis have been identified: • Liquefaction necrosis • Caseous necrosis • Coagulative necrosis

  21. 2) Necrosis Cell death Main types of necrosis have been identified: • Liquefaction necrosis • Digestive enzymes released by necrotic cells soften and liquefy dead tissue. • Occurs in tissues, such as the brain, that are rich in hydrolytic enzymes.

  22. 2) Necrosis Cell death • Caseous necrosisنکروز پنیری • Occurs in conditions like tuberculosis where there is prolonged inflammation and immune activity.

  23. 2) Necrosis Cell death • Coagulative necrosis • Often occurs when cell death results from ischemia and hypoxia. The acidosis denatures cellular proteins and hydrolytic enzymes. • Seen with myocardial infarction, for example.

  24. Gangrene که منطقه وسیعی از بافت تحت نکروز است. قانقاریا ممکن است به عنوان گانگرن خشک و یا گانگرن مرطوب طبقه بندی می گردد

  25. Effects of necrosis  Loss of function of dead area (kidney, brain).  Necrotic area can become a focus for infection.  May evoke certain systematic changes (inflammation, fever).  Necrotic tissue often leak its constituent enzyme in to the blood stream (CPK,ESR, AST).

  26. Wound Care

  27. Wound Repair • The process of wound repair proceeds in three sequential phases: • inflammation, • proliferation • remodeling.

  28. Inflammation • Inflammation, the physiologic defense immediately after tissue injury, lasts approximately 2 to 5 days. It’s purposes are to • limit the local damage, • remove injured cells and debris, and • prepare the wound for healing. Inflammation progresses through several stages

  29. blood vessels constrict to control blood loss and confine the damage • . Shortly after, the blood vessels dilate to deliver platelets that form a loose clot. • The membranes of the damaged cells become more permeable, causing release of plasma and chemical substances that transmit a sensation of discomfort. • The local response produces the characteristic signs and symptoms of inflammation: swelling, redness, warmth, pain , and decreased function.

  30. A second wave of defense follows the local changes when leukocytes and macrophages (types of white blood cells) migrate to the site of injury, and the body produces more and more white blood cells to take their place.

  31. Proliferation • Proliferation (period during which new cells fill and seal a wound) occurs from 2 days to 3 weeks after the inflammatory phase. It is characterized by the appearance of granulation tissue (combination of new blood vessels, fibroblasts, and epithelial cells), which is bright pink to red because of the extensive projections of capillaries in the area.

  32. Granulation tissue grows from the wound margin toward the center. It is fragile and easily disrupted by physical or chemical means. As more and more fibroblasts produce collagen (a tough and inelastic protein substance), the adhesive strength of the wound increases.

  33. Remodeling • Remodeling (period during which the wound undergoes changes and maturation) follows the proliferative phase and may last 6 months to 2 years. During this time, the wound contracts, and the scar shrinks.

  34. Systemic factors influencing wound healing Local factors influencing wound healing • Infection • Mechanical factors • Foreign bodies • Size, location and types of wound • Nutrition • Metabolic status • Circulatory status • Hormones

  35. Tissue repair Factors That Impair Wound Healing: • Malnutrition • Poor blood flow and hypoxia • Impaired immune response (immunosuppressive drugs, diseases affecting immune function such as HIV and diabetes) • Infection of wound • Foreign particles in the wound • Old age (decreased immune activity, poor circulation, poor nutrition)

  36. Wound Healing • Several factors affect wound healing: • Type of wound injury • Expanse or depth of wound • Quality of circulation • Amount of wound debris • Presence of infection • Status of the client's health

  37. Wound Healing Complications • Factors that may interfere include compromised circulation; infection; purulent, bloody, or serous fluid accumulation that prevent skin and tissue approximation, and drugs like corticosteroids, and obesity.

  38. The nurse assesses the wound to determine whether it is intact or shows evidence of unusual swelling, redness, warmth, drainage, and increasing discomfort. • Two potential surgical wound complications include dehiscence (separation of wound edges) and evisceration (wound separation with protrusion of organs) (Fig. 28-4).

  39. Figure (28-4 • (A) Wound dehiscence (B) Wound evisceration).

  40. Wound Management • Wound management involves changing dressings, caring for drains, removing sutures or staples when directed by the surgeon, applying bandages and binders, and administering irrigations.

  41. Dressings • A dressing purposes: • Keeping the wound clean • Absorbing drainage • Controlling bleeding • Protecting the wound from further injury • Holding medication in place • Maintaining a moist environment • The most common wound coverings are gauze, transparent, and hydrocolloid dressings.

  42. Gauze Dressings • Gauze dressings are made of woven cloth fibers. Their highly absorbent nature makes them ideal for covering fresh wounds that are likely to bleed or wounds that exude drainage. • Unfortunately, gauze dressings obscure the wound and interfere with wound assessment.

  43. Gauze dressings usually are secured with tape. If gauze dressings need frequent changing, Montgomery straps (strips of tape with eyelets) may be used (Fig. 28-5).

  44. Figure 28-5 • ( • The adhesive outer edge of Montgomery straps are applied to either side of a wound. • The inner edges of Montgomery straps are tied to hold a dressing over a wound. They prevent skin breakdown and wound disruption from repeated tape removal when checking or changing a dressing.

  45. Transparent Dressings • Transparent dressings are clear wound coverings. One of their chief advantages is that they allow the nurse to assess a wound without removing the dressing (Fig. 28-6).

  46. Figure 28-6 • Transparent dressing.

  47. Hydrocolloid Dressings • Hydrocolloid dressings are self-adhesive, opaque (أَكْمَدُ ( اللَّوْن, air- and water-occlusive wound coverings (Fig. 28-7). They keep wounds moist. Moist wounds heal more quickly because new cells grow more rapidly in a wet environment. If the hydrocolloid dressing remains intact, it can be left in place for up to 1 week.

  48. Figure 28-7 • A hydrocolloid dressing absorbs drainage into its matrix.

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