Journal of Clinical Research Update

Print ISSN 2304-3768

Rev.Act.Clin.Medv.43LaPazMay2014
ARTICLE

I INFLAMMATION
Ericka Herrera Villalba Wendie

SUMMARY
Inflammation is a natural physiological process of the body 's defense against
environmental assaults, showing signs such as pain, heat, redness and
edema, in addition to loss of functionality.
This process can occur in acute form with immediate reaction to theoffending agent,
which phagocytes, upon encountering an offending agent they try to destroy secrete
mediator substances that act on endothelial cells causing changes in vascular
permeability, allowing the migration of leukocytes the inflammatory focus for
phagocytosis of pathogens, returning to normal when the lesion is restored.
Similarly inflammation occurs with evolution result of persistent infections,
autoimmunity, or as a continuation of acute inflammation at the persistent offending
agent, leading to chronic inflammation. At this level of mononuclear cell infiltration,
tissue destruction and attempts at healing of damaged tissue by angiogenesis or
fibrosis it occurs.
The purpose of inflammation is to rid the body of the initial cause of cellular
aggression, however whatever the inflammatory, acute or chronic condition, you
should take appropriate measures to control the consequences of inflammation in the
body, without interfering pharmacological measures its beneficial effects.
KEYWORDS
Inflammation. Edema. Exudate. Transudate. Stasis. Suffusion. Hydrostatic
pressure. Osmotic pressure.Chemotaxis. Phagocytosis.

ABSTRACT
Inflammation is a physiological process naturally of the body's defense Assaults
Against environmental, presenting signs : such as pain, heat, redness and edema, in
Addition to loss of functionality.

This process can Occur acutely With immediate reaction to the stressor, in Which
phagocytes, upon encountering an offending agent secreting Mediators try to destroy
substances That act on endothelial cells Causing Changes in vascular permeability,
Allowing the migration of leukocytes the inflammatory focus for phagocytosis of
pathogens , returning to Normal When the injury was restored.
Likewise, the inflammation progresses to persistent infections, as a result of evolution
of autoimmunity; or a continuation of acute inflammation as the injurious agent
Persists, leading to chronic inflammation. At this level of mononuclear cell infiltration,
tissue destruction and Attempts at healing of damaged tissue by angiogenesis or
OCCURS fibrosis.
The purpose of inflammation is to rid the body of the initial cause of cell aggression,
however whatever the acute or chronic inflammatory condition, you Should Take
Appropriate Measures to Control the sequelae of inflammation in the body without
interfering With ITS beneficial pharmacological effects Measures.
KEY WORDS
Inflamation. Edema. Exudate. Trasudate. Stasis. Suffusion. Hydrostatic
pressure. Osmotic pressure. Chemotaxis.Phagocytosis.

INTRODUCTION
The human organism like all multicellular organisms, has defense mechanisms against
any aggression affecting their tissues. Thus endogenous or exogenous assaults
provoke a defensive cascade where innate immunity through the inflammatory process
succeeds in isolating the lesion destroys the pathogen and repairs tissue in order to
restore functionality and the affected organ. 1 , 3.5
Etymologically the word inflammation comes from the Latin inflammatio, which means
fire or a fire; so that this word was used in the medical literature to describe a bulky
body, with increased local heat, which compared with an internal combustion process,
resulting in what Celso first described the typical cardinal signs of inflammation such as
the redness, heat, and tumor pain. 1.7
Meanwhile John Hunter, the Scottish surgeon, in 1793 clarified that inflammation is not
a disease per se, but a specific response that has a salutary effect on the host. If not
for the inflammatory process infections could not be controlled, healing and wound
repair would be impossible and injured organs would not recover their
functionality. Anyway , the most representative problem caused by inflammation
triggered is that this process of defense is directed towards harmful agents as to those
who are not, so that it is dangerous to cause serious organ damage as hypersensitivity
reactions . 1

DEFINITION
Inflammation is a natural defense reaction or process the body 's immune system in
response to damage to your cells and tissues vascularized by harmful agents such as

microorganisms, trauma, necrosis, chemical or physical agents, or immune reactions

among others. Essentially, it is a protective response that emerges in order to isolate,
contain the damage, destroying the offending agent and subsequently prepare the
damaged for repair, a process that consists of mid vascular and cellular changes by
chemical factors clinically apparent tissue data Aulus Cornelius Celsus, a Roman
medical encyclopedist, described as cardinal signs that occur in all inflammatory
process: 1,2,3,5

CLINICAL SIGNS
The characteristic signs of inflammation are:
1) Heat: local or secondary temperature increase vasodilation, and increased local
consumption of oxygen.
2) Flush: produced by increasing irrigation in the affected area, by increasing blood
flow
3) Pain: caused by tissue distension and release of prostaglandins as chemical
mediators.
4) Edema resulting from increased capillary permeability and therefore suffusion of
fluid in the interstitial tissue.
These signs Rudolf Virchow, German physician, joined them a fifth clinical
sign, functiolaesa, which is the loss of functionality, resulting from the limitation to
conducting the conjugation of the four signs already mentioned.1,8,9

CLASSIFICATION
The classification of inflammation is done by taking into account the duration, nature of
exudate, etiology, morphologic characteristics and location:
1. For the duration may be:
. to Agudas: This type of inflammation is an immediate response to the offending
agent whose purpose is to release the body's defense mediators in the area of the
lesion whose onset is rapid and short duration courses.
b. Chronicles: It is a long process, existing at that time tissue destruction, active
inflammation and repetitive repair attempt.
2. By the nature of exudate can be:
to. Trasudado: characterized by the presence of extravascular fluid with low protein
content, theproduct of a slight change in vascular permeability.
b. Exudates: presence of inflammatory extravascular fluid with high protein content,
which denotes enough permeability in blood vessels.

3. etiology, can be:

to. Infectious: either by bacteria, viruses, parasites or microbial toxins
b. Traumatic and intense blows with immediate or delayed response, as with sprains or
hygroma.
c. Resulting from thermal, thermal burns or frostbite.
d. Irradiations.
and. Exposure to environmental chemicals.
F. Tissue necrosis.
g. Presence of foreign bodies such as chips.
h. Immune or hypersensitivity reactions to common allergens or colagenopticos
processes.
4. By its morphological characteristics, can be:
to. Serous: accumulation of tissue fluid by low protein content.
b. Fibrinous: with presence of large amounts of exudate with fibrinogen.
c. Suppurative or purulent: characterized by purulent exudate production consisting of
leukocytes and necrotic cells.
d. Abscesses: has purulent inflammatory tissue necrosis accompanied by liquefactive.
and. Ulcers: produced by sloughing of necrotic inflamed tissue.
5. Location: They are divided into:
to. Focal: produced in areas and specific organs, in which case the -itis suffix
is used, for example pharyngitis, otitis, laryngitis, conjunctivitis, peritonitis.
b. Diseminados. Result of the spread of persistent inflammatory processes either via
canalicular, fistula or metastasis 1,2,8

PHYSIOPATHOLOGY
Inflammation is a picture where the most outstanding pathophysiological changes are:
a) Vascular Change:
Inflammatory process in the blood vessels undergo important changes in flow and size
that enable and maximize the output of protein and plasma cells from the circulation
into the inflammatory focus. An early vascular changes is vasodilation induced by

histamine, produced by mast cells and nitric acid, which act on vascular smooth
muscle, expanding it , with the consequent increase in microvascular permeability,
resulting from the combination of increased hydrostatic pressure and lower osmotic
pressure, leading to fluid exit intravascular extravascular space with edema formation.
These changes have resulted in a decrease in blood velocity, which together with the
loss of intravascular fluid, red cell concentration and increased blood viscosity, results
in stasis, which is responsible for the exclusion of leukocytes, which normally circulate
in the center of the vessels. They occur simultaneously:
b) Changes Phones:
Leukocytes light must travel from the blood vessels to the site of the lesion and its
functions run defense there, ie engulf the pathogen. This process is called
extravasation and consists of three stages:
Marginalization, rolling and adhesion to endothelium.
diapedesis.
Migration to the interstitial tissues.
For leukocytes to migrate through the interendothelial junctions to the site of injury
follow the course of a chemical gradient oriented, that is chemotaxis
locomotion; leukocytes "know where to go" thanks to chemotactic agents, which in
turn cause leucocyte activation.
Already activated leukocytes fulfill their primary function, remove the offending agent
of the inflammatory focus by phagocytosis which will occur in three stages, the
recognition and binding of particles, internalisation with formation of phagocytic
vacuole, and death or degradation of pathogenic material ingested.
As this type of inflammation is indicated rapid reaction, so his resignation is also fast
when the offending agent is removed and anti - inflammatory mechanisms finalize the
process.
Inflammation can be restored to full normal status only if the causative agent is
removed completely absorbed exudate and destroyed tissues regenerate. This process
depends on the degree of response of each organism to chemical mediators, and may
show three possible outcomes of the same:
Complete resolution.
Healing replacement connective tissue (fibrosis).
progression to chronic inflammation.

1,4,6,8,9

The inflammatory process described corresponds mostly to an acute inflammation. In

chronic inflammation the most important features are:
cellular infiltrate composed of macrophages, lymphocytes and plasma cells.

 Important tissue destruction.

Formation of fibrous tissue and angiogenesis (proliferation of small blood vessels)
prevails over ooze fluid.
Macrophages are derived from monocytes from the blood stream, which, like
neutrophils in acute inflammation are induced to migrate from the vessel lumen to the
focus of inflammation, chemotactic factors action. Thesemacrophages are activated by
cytokines produced by T cells or by other factors nonimmune origin. This cell group will
be the most persistent accumulation in chronic inflammation.
Other cells that interfere in this inflammatory condition are lymphocytes and
eosinophils. Mast cells are distributed connective tissues and are present in both acute
inflammation and chronic.
A specific form of chronic inflammation is granulomatous inflammation, as distinct
inflammatory reaction, which involves the presence of granulomas. Granulomas are
microscopic foci which are characterized by the presence of aggregates of
macrophages transformed into epithelioid cells, reflected by cell flattening bulking
addition, and in turn these epithelioid cells are surrounded by a collar of mononuclear
leukocytes. Among the causes for this type of inflammation is triggered, we can
mention bacterial causes, as in the case of tuberculosis and leprosy, parasitic, fungal,
heavy metals, foreign bodies, and unknown causes. 1.10

NOTES
1

Univ. Third Year Faculty of Dentistry UMSA

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2016 Dra. Gladys Bustamante Cabrera