Transcript Document

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.
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 .
Cell Adaptation to Injury
Five Cellular Adaptations to Injury:
1. Atrophy
2. Hypertrophy
3. Hyperplasia
4. Metaplasia
5. Dysplasia
Cell Adaptation to Injury
1) Atrophy
•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 پذیر‬process,
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.
Cell Adaptation to Injury

Increase in cell size and tissue mass.

Occurs when a cell or tissue is
3) Hypertrophy
exposed to an increased workload)‫(بار کاری‬.

Occurs in tissues that cannot
increase cell number as an adaptive response.)‫ ورزشکاران‬،‫(عضله قلبی‬

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)‫ (جبرانی‬process, when one kidney is removed,
for example, the remaining kidney hypertrophies to increase its
functional capacity.
Cell Adaptation to Injury2) Hyperplasia

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.
Cell Adaptation to Injury
4) Metaplasia
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.
Cell Adaptation to Injury
5) Dysplasia
• A derangement)‫ (اختالل‬of 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.
.‫ سلول های دیسپالستیک به ساختار و عملکرد سابق خود بازمی گردند‬،‫در بسیاری از موارد‬
Classification of Cellular injury

Physical injury
•
•
•

Chemical injury
•
•

•
Ionizing radiation — gamma rays, X rays
Non-ionizing radiation — microwaves, infrared, laser
Biologic agents
•

Chemicals, toxins, heavy metals, solvents, smoke,
pollutants, drugs, gases
Radiation injury
•

Mechanical trauma
Temperature extremes (burn injury, frostbite)
Electrical current
Bacteria, viruses, parasites
Nutritional injury
•
•
Malnutrition
Obesity
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 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.
Cellular injury
1)Free radical injury
 Free radicals are highly reactive and can injure cells through:
1. Destruction)‫ (تخریب‬of 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.
 )‫ تابش و سموم دفع آفات‬،‫ آالینده ها‬،‫ حالل های آلی‬،‫(توتون و تنباکو دود‬
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.
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:
1. reversible, if oxygen is quickly restored,
2. Or irreversible)‫ (برگشت ناپذیر‬and 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.
Cellular injury

2)Hypoxic cell injury
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 calciumdependent protease enzymes present within cells that become
activated in the presence of excess calcium and begin to digest
important cellular constituents.
Reversible and Irreversible Cell Injury
Reversible:
Irreversible:
 Decrease generation
Sever
of ATP
mitochondrial
 Loss of cell
membrane integrity Persistent or changes
Extensive damage
excessive
 Defects in protein
injury
synthesis, and DNA
to plasma membranes
damage
Swelling of lysosomes
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.
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).
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.
‫‪1) Apoptosis‬‬
‫‪Cell death‬‬
‫‪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
‫‪It‬فعال نمایید‪ ،‬در نتیجه کشته شدن سلول میزبان و آلوده به ویروس‪.‬‬
‫‪has been theorized that cancer may arise as a failure of‬‬
‫‪normal apoptosis in damaged or mutated cells.‬‬
‫‪‬‬
Cell death
2) Necrosis

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
 Caseous
necrosis
necrosis
 Coagulative
necrosis
Cell death
2) Necrosis
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.
Cell death


Caseous necrosis‫نکروز پنیری‬
Occurs in conditions
like tuberculosis
where there is
prolonged inflammation
and immune activity.
2) Necrosis
Cell death
 Coagulative

2) Necrosis
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.
‫‪Gangrene‬‬
‫که منطقه وسیعی از بافت تحت نکروز است‪ .‬قانقاریا ممکن است به عنوان گانگرن خشک و یا‬
‫گانگرن مرطوب طبقه بندی می گردد‬
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
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
30

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.
31

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.
32
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.
33

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.
34
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.
35
Systemic factors
influencing
wound healing
Local factors
influencing
wound healing
Nutrition
1. Infection
1.
2.
3.
Metabolic status
Circulatory status
4.
Hormones
2. Mechanical factors
3. Foreign bodies
4. Size, location
and types of wound
Tissue repair
Factors That Impair Wound Healing:
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)
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
38
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.
39

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).
40
Figure (28-4( • A )Wound dehiscence( B )Wound evisceration).
41
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.
42
Dressings

A dressing purposes:
 Keeping
the wound clean
 Absorbing
drainage
 Controlling
 Protecting
 Holding
the wound from further injury
medication in place
 Maintaining

bleeding
a moist environment
The most common wound coverings are gauze,
transparent, and hydrocolloid dressings.
43
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.
44

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).
45
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.
46
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. 286).
47
Figure 28-6 • Transparent dressing.
48
Hydrocolloid Dressings

Hydrocolloid dressings are self-adhesive, opaque ( ( ‫م ُد‬
َ ‫أَ ْك‬
‫اللَّ ْون‬, air- and water-occlusive wound coverings (Fig. 287). 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.
49
Figure 28-7 • A hydrocolloid50dressing 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.
51
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
52
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).
53
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.
54
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.
55
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.
56

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.
57
Figure 28-10( • A )Technique for suture removal( .B )Technique for staple removal
58
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.
59
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.
60
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.
61
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.
62
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.
63
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
64
65
66
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.
67

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).
68
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
69

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).
70
Figure 28-17 • Locations where pressure ulcers commonly form( .A )
Supine position( .B )Side-lying position(
.C )Sitting position.
71

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.
72
Stages of Pressure Ulcers

Pressure ulcers are grouped into four stages according
to the extent of tissue injury (Fig. 28-18).
73
Figure 28-18 • Pressure sore stages( .A )Stage I( .B )Stage II( .C )Stage III( .D )Sta
74

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.
75

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).
76
Figure 28-19 • Example of stage IV pressure sore.
77
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.
78
79
80
Nursing Implications

Acute Pain

Impaired Skin Integrity

Ineffective Tissue Perfusion

Impaired Tissue Integrity

Risk for Infection
81