Inflammatory (inflammation)
Definition
Inflammation is a protective
response to local injury or damage caused by the network, which serves destroy,
reduce, or confine (sequestration) both pencedera agent and the injured tissue
(Dorland, 2002).
When tissue injuries such as
burns, sliced or as infectious germs, then the network will happen reaction
sequence which destroy harmful agents that prevent network or agents spread
more widely. These reactions are then also cause tissue injury repaired or
replaced with new tissue. The series is called inflammatory reaction
(Rukmonto, 1973).
Agents that can cause injury to
the tissue, which is then followed by inflammation is a germ (microorganisms),
objects (knives, bullets, etc.), Temperature (hot or cold), various types of
rays (X-rays or ultraviolet light), electric, substance chemicals or
substances, and others. Inflammatory injury caused by various agents
demonstrate the process that has the same points, which happened tissue
injuries such as degeneration (deterioration) or necrosis (death) tissue,
capillary dilation accompanied by capillary wall injury, accumulation of fluid
and cells (plasma fluid , blood cells and tissue cells) in a place that is
accompanied by inflammation of tissue cell proliferation of macrophages and
fibroblasts, the process of phagocytosis, and the immunological changes
(Rukmonto, 1973).
Broadly speaking, the
inflammation is characterized by local vasodilation of blood vessels resulting
in excessive local blood flow, increase in capillary permeability accompanied
by large amounts of fluid leakage into the interstitial space, freezing fluid
in the interstitial space due to fibrinogen and other proteins that leak from
capillaries in copious amounts, the migration of a large number of granulocytes
and monocytes into the tissue, and swelling of the tissue cells. Some
networking products that cause this reaction is histamine, bradykinin,
serotonin, prostaglandins, some kind of reaction products of the complement
system, coagulation reaction products, and a variety of hormonal substances
called lymphokines released by sensitized T cells (Guyton & Hall, 1997) .
Signs of inflammation
(macroscopic)
Overview macroscopic inflammation
has been described almost 2000 years ago. Signs of inflammation is by
Celsus, a Roman scholar who lived in the first century AD, already known and
referred to the main signs of inflammation. Signs of inflammation is still
used to this day. Signs of inflammation include rubor (redness), calor (heat), dolor (pain),
and tumor(swelling). Marks the fifth principal added in the last
century that functio laesa(change function) (Abrams, 1995; Rukmonto, 1973;
Mitchell & Cotran, 2003).
Generally, rubor or redness is
first seen in the area of inflammation.When the inflammatory reactions arise,
dilation of the arterioles that supply blood to the area of inflammation. Allowing
more blood to flow into the local microcirculation and capillary stretch
quickly fills with blood. This is called hyperemia or congestion, causing
local red color due to acute inflammation (Abrams, 1995; Rukmonto, 1973).
Calor coincided with redness of
acute inflammatory reaction. Heat is also caused by increased blood
circulation (active hyperemia). Because blood has a temperature
of 37 ° C is channeled to the surface of the body have more
inflammation than to the normal area (Abrams, 1995; Rukmonto, 1973).
Local pH changes or local
concentrations of certain ions can stimulate nerve endings. Spending
substances such as histamine or other bioactive substances can stimulate the
nerves. The pain is caused also by the pressure rises due to the swelling
of inflamed tissue (Abrams, 1995; Rukmonto, 1973).Actually, this pain precedes
an inflammatory process. This is probably due to the formation of a
substance by mast cells. This substance is useful to increase the
permeability of blood vessel walls.
Hyperemia and swelling partly due
largely caused by the delivery of fluids and cells from the blood circulation
into the interstitial tissues. A mixture of fluid and cells accumulate at
the site of inflammation called inflammatory exudate (Abrams, 1995; Rukmonto,
1973).
Based on his origin, functio
laesa is missing function (Dorland, 2002).Functio laesa an inflammatory
reaction which has been known. But not known in depth the mechanisms
undermining of inflamed tissue (Abrams, 1995).Fungtio laesa can mean reduced
function due to pain caused by nerve stimulated so that the organs are not
functioning. Other causes of decreased function of the body is edema.
The main sign of inflammation is
called the cardinal symptoms and are caused by changes in blood
vessels. Inflammation is a complex process, causing the
occurrence of a change in body tissues. Such processes include:
1. Destruction
process stimuli that are usually accompanied by tissue damage
2. The
process of repair damaged tissue.
Classification Inflammation
a. According
to Clinical Factors or duration of Inflammation
1. Acute
Inflammation
Acute inflammation is a quick and
immediate response to injury didesainuntuk send leukocytes to areas of injury. Leukocytes
clean various microbes that invade and begin the process of dismantling the
necrotic tissue.There are two major components in the acute inflammatory
process, namely the cross-section and structural changes of the blood vessels
as well as the emigration of leukocytes. Changes in blood vessel cross
section will result in increased blood flow and the structural changes at the
micro blood vessels will allow plasma proteins and leukocytes to leave the
blood circulation.Leukocytes from the microcirculation will conduct further
emigration and accumulate at the site of injury (Mitchell & Cotran, 2003).
Immediately after injury, local
arteriolar dilation which may be preceded by a brief vasoconstriction. Prakapiler
sphincter opens with the result that blood flow in the capillaries that have
functioned increased capillary matting and also the opening of previously
inactive. As a result, post-capillary venular woven dilated and filled
with blood flowing. Thus, the microvascular lesion location dilated and
filled with blood unstoppable. Except in very mild injury, increasing
blood flow (hyperemia) in the early stages will be followed by a slowing of
blood flow, changes in intravascular pressure and changes in the orientation of
the elements in the form of blood against the walls of veins. Changes in
blood vessels in terms of time, a lot depends on the severity of the injury. Dilatation
of arterioles arise within a few minutes after injury. Slowing and dam looks
after 10-30 minutes (Robbins & Kumar, 1995).
Increased vascular permeability
accompanied by the release of plasma protein and white blood cells into the
tissue is called exudation and a prominent feature of acute inflammatory
reaction. Micro-vasculature basically consist of continuous channels
endothelial layered branching and anastomosis hold.Endothelial cells covered by
a continuous basement membrane (Robbins & Kumar, 1995).
At the end of the capillary
arterioles, high hydrostatic pressure urging the fluid out into the
interstitial tissue spaces by means of ultrafiltration. This may lead to
elevated concentrations of plasma proteins and cause large increases colloid
osmotic pressure, by pulling back on the base fluid capillary venules.The
normal exchange will leave little fluid in the interstitial tissue that runs
from the room through a network of lymphatic channels. Generally, the
capillary wall can be passed water, salt, and the solution to the density of
10,000 dalton (Robbins & Kumar, 1995).
Inflammatory exudate is the
extravascular fluid with high density (above 1020) and often contain 2-4 mg%
protein and white blood cells that do emigration. These fluids accumulate
as a result of increased vascular permeability (which allows plasma proteins
with large molecules can be separated), increasing the intravascular
hydrostatic pressure as a result of increased local blood flow as well and
complicated series of events that led to emigration of leukocytes (Robbins
& Kumar, 1995).
Hoarding of white blood cells,
particularly neutrophils and monocytes at sites of injury, is the most
important aspect of an inflammatory reaction. White blood cells that are
capable of phagocytosing foreign material, including bacteria and necrotic cell
debris, and lysosomal enzymes contained in it help defend the body in several
ways. Some white blood cell products is driving an inflammatory reaction,
and in certain cases cause significant tissue damage (Robbins & Kumar,
1995).
In the focus of inflammation,
microcirculation early dam would cause red blood cells to clot and form
aggregates larger than leukocytes themselves.According to the laws of physics
of flow, the mass of red blood cells will be located at the center in axial
flow, and white blood cells move to the edge (marginasi). At first, the
white blood cells move and rolled slowly along the endothelial surface in the
flow of stuttering but then the cells will attach and coat the surface of
endothelial (Robbins & Kumar, 1995).
Emigration is the process of
moving the white blood cells that move out of the blood vessels. The main
place of leukocyte emigration is a meeting between endothelial cells. Although
the widening inter-cell meetings facilitate emigration of leukocytes, but
leukocyte able to infiltrate themselves through meetings between the
endothelial cells that seemed closed without any real change (Robbins &
Kumar, 1995).
After leaving the blood vessels,
leukocytes move toward the main lesion location. Migration of white blood
cells are directed is caused by influences that can diffuse chemical called
chemotaxis. Almost all types of white blood cells is affected by
chemotactic factors in varying degrees. Neutrophil and monocyte chemotaxis
most reactive to stimuli. Instead lymphocytes react weak. Several
factors can affect neutrophil chemotaxis and monocytes, the other works
selectively against some types of white blood cells. Chemotactic factors
can be derived from plasma proteins endogenous or exogenous, eg bacterial
products (Robbins & Kumar, 1995).
Once at the site of leukocytes to
inflammation, there was the process of phagocytosis. Although phagocytic
cells can be attached to particles and bacteria without preceded by an
introduction to the typical process, but will be supported if the phagocytosis
of microorganisms covered by opsonin, which is present in the serum (eg, IgG,
C3). After experiencing opsonization of bacteria attached to the surface,
subsequent phagocytic cells will mostly include particles, have an impact on
the formation of deep pockets. These particles are located on the
cytoplasmic vesicles are still bound to the cell membrane, called a phagosome. Although
at the time of phagosome formation, before closing complete, neutrophil
cytoplasmic granules fused with the phagosome and release their contents into
it, a process called degranulation. Most microorganisms that have
undergone pelahapan easily destroyed by phagocytes which resulted in the death
of microorganisms. Although some virulent organisms that can destroy
leukocytes (Robbins & Kumar, 1995).
2. Chronic
inflammation
Chronic inflammation can be
defined as the inflammation that lasts long (weeks to years) and occurs
simultaneously process of active inflammation, tissue injury, and healing. The
difference with acute inflammation, acute inflammation is characterized by
vascular changes, edema, and infiltration of neutrophils in large quantities. While
chronic inflammation is characterized by infiltration of mononuclear cells
(such as macrophages, lymphocytes, and plasma cells), tissue destruction and
repair (including the proliferation of new blood vessels / angiogenesis and
fibrosis) (Mitchell & Cotran, 2003).
Chronic inflammation can occur
through one or two roads. Can occur following acute inflammation, or the
response from the beginning is chronic.Changes in acute inflammation becomes
chronic inflammation takes place when the acute inflammatory response can not
be stopped, due to injury-causing agents that persist or there is interference
with the normal healing process.There are times when chronic inflammation from
the beginning of the primary process. Frequent cause of injury have low
toxicity compared to the causes that give rise to acute inflammation. There
are 3 major groups are the cause, namely persistent infection by specific
intracellular microorganisms (such as the tubercle bacillus, Treponema
palidum, and certain fungi), prolonged contact with materials that can not
be destroyed (eg, silica), an autoimmune disease.When an inflammation lasts
longer than 4 or 6 weeks is called chronic. But as much reliance effective
host response and the nature of injury, the time limit does not make much
sense. The distinction between acute and chronic inflammation should be
based on the morphological pattern of reaction (Robbins & Kumar, 1995).
b. Based
on the network, or Microscopic Changes
1. Exudative
inflammation
In exudative inflammation,
largely dominated by inflammatory exudate, dead tissue only
slightly. There are two kinds of inflammatory exudate exudate exudate
cellular and humoral. Based on cellular exudate, inflammation is divided
into acute inflammation, inflammation subacute, and chronic
inflammation. In acute inflammation, the cells were mainly found is PMN
(polymorphonuclear cells) neutrophils, lymphocytes and monocytes little
while.In subacute inflammation that many are PMN cells eosinophils, while the
number of lymphocytes and monocytes increased. In chronic inflammation,
which is most often found are lymphocytes and monocytes. Sometimes
encountered plasma cells and PMN cells slightly.
2. Degenerative
inflammation
Most of the microscopic picture
consists of necrotic tissue with few inflammatory cells such on diphtheria,
which contains the germ of the tonsils but issued exotoxin which can cause
inflammation of the heart. If to cause death, the heart muscle tissue will
be found in some parts of the tissue necrosis.
3. Proliferative
Inflammation
Microscopically, in addition to
common exudate, inflammation is also composed of a network that can
berproliferatifa. So, here will be visible growth of the network so that
it will form a bulge. Because there exudate inflammation and tissue
proliferation, gambaranya almost the same with granulation
tissue. Excessive granulation tissue will form a bulge called a granuloma
is a time such as tumor tersir over granulation tissue. Because there is
growth of granulation tissue, called granulomatous inflammation.Inflammation
provides an overview of specific and can be found in tuberculosis, syphilis,
leprosy, sarcoidosis, lymphogranuloma inguinal, brucellosis, and actinomycosis.
c. Based
exudate Humoralnya
1. Inflammation
Katarhalis
Exudate exudate is clear form of
lenders, found in organs that produce mucus, such as nasopharyngeal, lung,
intestinal tract, and uterus, for example, on a cold and cholera.
2. Fibrinous
inflammation
Exudate composed largely of
fibrin, inflammatory cells are usually only slightly. But there is also a
disease with microscopic picture exudate composed of fibrin but many contain
PMN, eg lobar pneumonia. In this disease, pleuranya often come
inflamed. Such circumstances called pleurisy sika (yellow).
3. Serous
inflammation
Eksudatnya seems serous and
clear. Fibrinnya slightly, remains liquid and the liquid should be
vacuumed frequently. Can be found for example in the tuberculosis which
would cause pleurisy eksudatnya.
4. Purulent
inflammation
Exudate composed largely of pus,
found in ulcers and bronchopneumonia or pneumonia lobularis. In lobularis
pneumonia, although there PMN neutrophils are life and death, there is also a
germ, but ridak cause pus or purulent inflammation, because there are no dead
or necrotic tissue.
Instead, the existing pneumonia
Salain lobularis PMN and fibrin, necrotic tissue so also there is no pus. As
a result, the healing can occur with pneumonia lobularis flawless, although
there is always scarring.
5. Inflammation
Haemorrhagik
In this inflammation eksudatnya
red because it contains erythrocytes, usually much tissue damage that will be
formed new capillaries and lymph channels. But if the inflammation has
subsided or cured, will constrict capillaries and disappear again.
6. Inflammation
Pseudomembranous
This inflammation appears
characteristics with the formation of a false membrane is formed of a fibrin
clot, necrotic epithelial and leukocyte cell death. Inflammation is only
found on mucosal surfaces, such as the pharynx, larynx, trachea, bronchial and
intestinal tract, due to the existence of a gene or a strong irritant eg diphtheria
germs. In this inflammation will be necrosis and then freezes so inflamed
tissue surface to be coated by a layer of necrotic grayish white. This
membrane is called pseudomembranous.
d. Based
on the location
1. Abscess
An abscess is a purulent
inflammation are gathered in one place in the body so that it is in the pus
cavity anatomically no. If found pus in a body cavity existing
anatomically, called empiemia, for example epiemia peritonni, empimia
perikardii, and often is empymia thiracii. Set of pus in the thoracic
cavity is called empimia only.
2. Phlegmon
or cellulitis
Phlegmon a purulent or
suppurative inflammation of the average spread in all parts of the body, such
as acute appendicitis flegmonosa. Cellulitis is an acute inflammation of
the connective tissue that is found in rare, spread evenly and widely, and
often under the skin without the formation of pus.There are some authors who
consider the same cellulitis with phlegmon and gives the following definition:
acute inflammatory phlegmon is spread evenly across a network beranyaman
mnungkin rarely accompanied by the formation of pus.
Ulcer or ulcer is a local defect
of a surface of an organ or tissue due to the presence of an inflammatory
necrotic tissue gushing out. Ulceration can occur only if the chronic
inflammation that can come out or close to the surface so it can be
penetrated. Ulcers occur if the tissue surface partially disappear so that
the surrounding tissue is inflamed. Tissue necrosis can be caused by
toxins or capillary blockage caused by inflammation.
Ulcers are common in the state:
There
is a focus of necrotic inflammation in the oral mucosa, stomach, and
intestines.
Subcutaneous
inflammation of the lower limbs in patients with impaired elderly circulation
is a factor predisposing to the occurrence of extensive necrosis.
On
the cervix, in the mouth (ulcers dekubitalis), stomach (peptic ulcer), and skin
(ulcers)
Healing
A. Recovery
Network
Network recovery is the end of an
inflammatory process toward healing, while healing is a process or way of
repairing damaged tissue.
Cells that replace damaged
tissues derived from two sources. Yes It Is:
1. Parenchyma
tissue
2. Stromal
tissue
The healing process of parenchymal
cells occurs by replacing damaged cells with new cells and the same, so that
the body functions and the network will be restored to perfection. Healing
so-called regeneration. As for network storma damaged cells or
tissues are replaced by connective tissue. This process is calledorganization. At
the organization will be formed granulation tissue which then will form the
connective tissue.
Parenchyma cells differentiated
into:
labile
cells
is a cell that is at any given
moment experiencing mikrosis but will experience pembaharusan happens
periodically and the cells will be replaced with the same cells through a
process called regeneration physiological
stable
cell
is the parenchymal cells
contained in the gland cells in the body, including the liver, pankrean,
edndokrin gland, kidney tubular cells, and glands of the skin.
permanent
cell
In unstable or stable cell
regeneration will be changes that will turn adult cells into young or embryonic
cells that can proliferate
B. Factors
Inhibiting Healing
1. General
Factors
a. Age
Usually slower healing in the
elderly. Munkin due to lack of blood supply in the elderly.
b. Diet
By the time people eat less
protein causes protein levels in the blood are very low. This situation
causes are difficult to heal wounds and cause more severe
injuries. Important substance is a substance called methionin. This
substance will make the body can make the protein more efficiently substances.
c. Vitamin
For example vit.C, is a very
useful substance for the formation of hialuron acid which is an adhesive
substance ang network is very important.
d. Hormone
For example
cortisone. Provision of cortisone on inflammation can cause interference
with the mechanism of changes in the blood vessels, causing the formation of
inflammatory exudate that little or obstructed.
2. Local
Factors
a. Blood
supply
Blood deficiency can also cause
the body lacks substance that is needed such as vitamins and oxygen. This
in itself will cause delays in the healing process.
b. Foreign
object
Because of this foreign body is a
stimulus to the fixed network will maintain an inflammation
c. Movement
network
Eg fractures. If the object
is still no movement, healing will be hampered.
d. The
amount of tissue damage
If there is a total of an organ
damage usually can not be repaired perfectly.
e. Type
of network
Damage to body tissues (cells
stable and unstable cells) will heal perfectly, but on a permanent cell healing
occurred otherwise.
Regeneration and Organizations
The healing process can take
place in regeneration and organization.Organization process in wounds, whether
caused by trauma, inflammation, or necrosis, or caused by a foreign body is
basically the same. The difference is only dependent on the size of the
tissue damage.
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