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Cell injury 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. Cell injury is reversible up to certain point.
To survive, cells must have the ability for adaptationadaptation 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 deathcell death occur .
Cell Adaptation to Cell Adaptation to InjuryInjury
Five Cellular Adaptations to Injury:
1. Atrophy
2. Hypertrophy
3. Hyperplasia
4. Metaplasia
5. Dysplasia
Cell Adaptation Cell Adaptation to Injuryto Injury•It means Decrease or shrinkage in cellular size.•That is either Physiological or Pathological•Pathologic atrophy occur due to ↓ ↓ ↓ in :
• Workload( گرفته گچ (اندام• Pressure• Use• Blood supply• Nutrition• Hormonal Stimulation• Nervous Stimulation
•Atrophy is generally a reversible( پذیر ,process (برگشتexcept 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.
1) 1) AtrophyAtrophy
Cell Adaptation Cell Adaptation to Injuryto 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(ج�برانی) process, when one kidney is removed, for example, the remaining kidney hypertrophies to increase its functional capacity.
3) 3) HypertrophyHypertrophy
Cell Adaptation Cell Adaptation to Injuryto 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.
2) 2) HyperplasiaHyperplasia
Cell Adaptation Cell Adaptation to Injuryto InjuryThe conversion of one cell type to another ( بالغ سلول یک (تغییر
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.
4) 4) MetaplasiaMetaplasia
Cell Adaptation Cell Adaptation to Injuryto Injury5) 5) DysplasiaDysplasia
• A derangement(اختالل) of cell growth that leads to tissues with
cells of varying size, shape and appearance.
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.
خود سابق عملکرد و ساختار به دیسپالستیک های سلول موارد، از بسیاری در. گردند بازمی
• Generally occurs in response to chronic irritation and
inflammation.
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
Classification of Cellular Classification of Cellular injury 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
Cellular injuryCellular 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 include superoxide (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.
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.
Free (توتون و تنباکو دود، حالل های آلی، آالینده ها، تابش و سموم دفع آفات) 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.
Cellular injuryCellular injury 1)Free radical injury
Cellular injuryCellular 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:
1. reversible, if oxygen is quickly restored,
2. Or irreversible( ناپذیر and lead to cell (برگشت
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.
During periods of hypoxia:
1. Aerobic metabolism of the cells begins to fail.
2. This leads to dramatic decreases in energy production (ATP) within the cells.
3. Hypoxic cells begin to swell as energy-driven processes begin to fail, (such as ATP-driven ion pumps).
4. The pH of the extracellular environment begins to decrease as waste products begin to accumulate, such as lactic acid, a product of anaerobic metabolism.
5.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.
Cellular injuryCellular injury 2)Hypoxic cell injury
Reversible and Irreversible Cell Injury
Reversible: Irreversible: Decrease generation Sever
of ATP mitochondrial Loss of cell
changes membrane integrity Persistent or Defects in protein excessive Extensive damage synthesis, and DNA injury to plasma membranes damage
Swelling of lysosomes
1. Cellular swelling1. 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.
Manifestation of Cellular Manifestation of Cellular injuryinjury
2. Cellular accumulations2. 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).
Manifestation of Cellular Manifestation of Cellular injuryinjury
Cell death falls into two main categories:
Apoptosis: Apoptosis:
controlled, “pre-programmed” cell death
Necrotic cell death: Necrotic cell death:
unregulated, enzymatic digestion of a cell
and its components.
Cell deathCell death
A controlled, “pre-programmed” cell death that
occurs with aging and normal wear and tear of the cell.
آپوپتxوز ممکن اسxت یxک مکانیسxم بxرای از بین بxردن فرسxوده و یxا سxلول
(ویxروس ویروسxی هxای عفxونت از بxرخی ژنxتیکی. دیxده آسxیب هxای
ابشxتاین بxار، بxه عنxوان مثxال) ممکن اسxت آپوپتxوز در سxلول هxای آلxوده
بxه آلxوده و میزبxان سxلول شxدن کشxته نتیجxه در نماییxد، فعxال را
It has been theorized that cancer may arise as.ویروس
a failure of normal apoptosis in damaged or mutated
cells.
Cell deathCell death 1) ApoptosisApoptosis
Cell deathCell 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
2) NecrosisNecrosis
Cell deathCell deathMain 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.
2) NecrosisNecrosis
Cell deathCell death
Caseous necrosisنکروز پنیری
Occurs in conditions
like tuberculosis
where there is
prolonged inflammation
and immune activity.
2) NecrosisNecrosis
Cell deathCell 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.
2) NecrosisNecrosis
Gangrene
. عنوان به است ممکن قانقاریا است نکروز تحت بافت از وسیعی منطقه که
گردد می بندی طبقه مرطوب گانگرن یا و خشک گانگرن
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).
Wound Care
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Wound Repair
The process of wound repair proceeds in three sequential phases:
inflammation,
proliferation
remodeling.
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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
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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.
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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.
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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.
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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.
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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.
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1. Nutrition
2. Metabolic status
3. Circulatory status
4. Hormones
Systemic factors influencing
wound healing
1. Infection
2. Mechanical factors
3. Foreign bodies
4. Size, location
and types of wound
Local factors influencing
wound healing
Tissue repairTissue repair
1. Malnutrition
2. Poor blood flow and hypoxia
3. Impaired immune response (immunosuppressive drugs, diseases affecting immune function such as HIV and diabetes)
4. Infection of wound
5. Foreign particles in the wound
6. Old age (decreased immune activity, poor circulation, poor nutrition)
Factors That Impair Wound Healing:
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
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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.
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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).
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Figure (28-4 • (A) Wound dehiscence (B) Wound evisceration).
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.
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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.
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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.
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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).
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Figure 28-5 • (
A) The adhesive outer edge of Montgomery straps are applied to either side of a wound.
B) 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.
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).
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Figure 28-6 • Transparent dressing.
Hydrocolloid Dressings
Hydrocolloid dressings are self-adhesive, opaque �و�ن) �م�د� ( الل ْك
� air- and water-occlusive wound ,َأcoverings (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.
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50Figure 28-7 • A hydrocolloid dressing absorbs drainage into its matrix.
Dressing Changes
Nurses change dressings when a wound requires assessment or care and when the dressing becomes loose or saturated with drainage.
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Drains
Drains are tubes that provide a means for removing blood and drainage from a wound. They promote wound healing by removing fluid and cellular debris
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Open Drains Open drains are flat, flexible tubes that provide a pathway for
drainage toward the dressing. Draining occurs passively by gravity and capillary action. Sometimes a safety pin or long clip is attached to the drain as it extends from the wound.
As the drainage decreases, the physician may instruct the nurse to shorten the drain, (Fig. 28-8).
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Figure 28-8 • An open drain is pulled from the wound, and the excess portion is cut. A drain sponge is placed around the drain, and the wound is covered with a gauze dressing.
Closed Drains
Closed drains are tubes that terminate in a receptacle. Some examples of closed drainage systems are a Hemovac.
Closed drains are more efficient than open drains because they pull fluid by creating a vacuum or negative pressure.
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Sutures and Staples
Sutures, knotted ties that hold an incision together, generally are constructed from silk or synthetic materials such as nylon.
Staples (wide metal clips) perform a similar function. Staples do not encircle a wound like sutures; instead, they form a bridge that holds the two wound margins together.
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Sutures and staples are left in place until the wound has healed sufficiently to prevent reopening. Depending on the location of the incision, this may be a few days to as long as 2 weeks.
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Figure 28-10 • (A) Technique for suture removal. (B) Technique for staple removal.
Bandages and Binders
A bandage is a strip or roll of cloth wrapped around a body part. One example is Crib bandage.
A binder is a type of bandage generally applied to a particular body part such as the abdomen or breast.
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Débridement
Some wounds require débridement (removal of dead tissue) to promote healing. The four methods for débriding a wound are sharp, enzymatic, autolytic, and mechanical.
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Sharp Débridement
Sharp débridement is the removal of necrotic tissue (nonliving tissue) from the healthy areas of a wound with sterile scissors, forceps, or other instruments.
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Enzymatic Débridement
Enzymatic débridement involves the use of topically applied chemical substances that break down and liquefy wound debris.
This form of débridement is appropriate for uninfected wounds or for clients who cannot tolerate sharp débridement.
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Wound Irrigation
Wound irrigation generally is carried out just before applying a new dressing. This technique is best used when granulation tissue has formed. Surface debris should be removed gently without disturbing the healthy proliferating cells.
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Heat and Cold Applications
Heat and cold have various therapeutic uses (Box 28-1).
The terms hot and cold are subject to wide interpretation Table 28-2
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Therapeutic Baths
Therapeutic baths (those performed for other than hygiene purposes) help to reduce a high fever or apply medicated substances to the skin to treat skin disorders or discomfort.
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The most common type of therapeutic bath is a sitz bath (soak of the perianal area). Sitz baths reduce swelling and inflammation and promote healing of wounds after a hemorrhoidectomy (surgical removal of engorged veins inside and outside the anal sphincter) or an episiotomy (incision that facilitates vaginal birth).
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Pressure Ulcers
A pressure ulcer is a wound caused by prolonged capillary compression that is sufficient to impair circulation to the skin and underlying tissue. The primary goal in managing pressure ulcers is prevention. Once a pressure ulcer forms, however, the nurse implements measures to reduce its size and to restore skin and tissue integrity
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Pressure ulcers or sores, also referred to as decubitus ulcers, most often appear over bony prominences of the sacrum, hips, and heels. They also can develop in other locations such as the elbows, shoulder blades, back of the head, and places where pressure is unrelieved because of infrequent movement (Fig. 28-17).
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Figure 28-17 • Locations where pressure ulcers commonly form. (A) Supine position. (B) Side-lying position. (C) Sitting position.
The tissue in these areas is particularly vulnerable because body fat, which acts as a pressure-absorbing cushion, is minimal. Consequently, the tissue is compressed between the bony mass and a rigid surface such as a chair seat or bed mattress. If the compression on local capillaries continues without intermittent relief, the cells die from lack of oxygen and nutrition.
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Stages of Pressure Ulcers
Pressure ulcers are grouped into four stages according to the extent of tissue injury (Fig. 28-18).
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Figure 28-18 • Pressure sore stages. (A) Stage I. (B) Stage II. (C) Stage III. (D) Stage IV.
Stage I is characterized by intact but reddened skin. The hallmark of cellular damage is skin that remains red and fails to resume its normal color when pressure is relieved.
A stage II pressure ulcer is red and accompanied by blistering or a skin tear (shallow break in the skin). Impairment of the skin may lead to colonization and infection of the wound.
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A stage III pressure ulcer has a shallow skin crater that extends to the subcutaneous tissue. It may be accompanied by serous drainage (leaking plasma) or purulent drainage (white or greenish fluid) caused by a wound infection. The area is relatively painless despite the severity of the ulcer.
Stage IV pressure ulcers are life threatening. The tissue is deeply ulcerated, exposing muscle and bone (Fig. 28-19). The dead or infected tissue may produce a foul odor. The infection easily spreads throughout the body, causing sepsis (potentially fatal systemic infection).
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Figure 28-19 • Example of stage IV pressure sore.
Prevention of Pressure Ulcers
The first step in prevention is to identify clients with risk factors for pressure ulcers (Box 28-2). The second step is to implement measures that reduce conditions under which pressure ulcers are likely to form. See Nursing Guidelines 28-2.
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Nursing Implications
Acute Pain
Impaired Skin Integrity
Ineffective Tissue Perfusion
Impaired Tissue Integrity
Risk for Infection
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