INFLAMMATION &

HEALING
Kuntarti
DKKD Department
2017
 INFLAMMATION
The purpose of inflammation
The Cardinal signs of acute inflammation &
describe the mechanisms involved in
production of these signs
The comparison of hemodynamic & cellular
phases of the inflammatory response
The difference of acute & chronic
inflammation
The types of inflammatory exudates
 What is Inflammation?

the reaction of vascularized tissue to local

injury
a series of changes in terminal vascular
bed, in blood, in connective tissues to
eliminate the offending irritant and repair the
damaged tissue
involves cellular, humoral, chemical &
tissue participations
 What is Inflammation?

one of the most important & useful defense

mechanisms

Without an adequate inflammatory response none of us

would be living; wound would not heal, minor infection
would become overwhelmed
AGENT CAUSING INFLAMMATION
 THE ROLES/PURPOSES OF
INFLAMMATION

1. To neutralize & destroy invading &

harmful agents
2. To limit the spread of harmful agents
to other tissue
3. To prepare any damaged tissue for
repair
SIGNS OF INFLAMMATION
 LEWIS EXPERIMENT
-TRIPLE RESPONS/ RED LINE RESPONS-
 Vascular Response
Immediately after injury
Vasoconstriction vasodilation of arterioles & venules that
supply area
Hyperemic response: congested, redness (erythema) &
warmth
Increased capillary permeability, allows fluid escape into the
tissueswelling (edema)
Pain and impaired function is as a result of swelling & release
of chemical mediators
Benefits: dilute toxic&irritating agents and localizing the
spread of infectious agents
Fluid exudate

Normally the walls of small blood vessels are freely

permeable to water and crystalloids but relatively
impermeable to plasma proteins.
The formation of protein-rich fluid exudates is facilitated
by separation of the intercellular junction of the
endothelium.
 The fluid exude carries into the inflamed
area the following important constituents:

Serum bactericidal factors

a. Antibodies which act by opsonising bacteria prior

to phagocytosis and by neutralizing exotoxins

b. Components of the complement system

 Interferon: a non-specific antiviral agent
Fibrinogen which is converted to fibrin. Fibrin is
important in providing:
a. Cement substance uniting severed tissues
b. Scaffold for repair processes
c. Barrier to the spread of organisms
d. Surface against which phagocytosis of adherent
organisms is enhanced

Therapeutic agents-antibiotics, anti-

inflammatory drugs, etc.
Leukocyte exudates and
phagocytosis

Leukocytic margination,rolling

Adhesion: by the binding of adhesion molectures

(selections, immunoglobulins, intergrins, mucin like
glycoproteins)
 Emigrating

It refers to the process by which motile white cells

migrate out of blood vessels.

emigration is an active, energy-dependent process

red blood cell out of blood vessels, called diapedesis

 White cell migration
It is include following handings:
WBC margination

WBC adhesion with endothelial
surface adhesion molecule

WBC transmigration
2-12 minute EM: White cell migration
 Chemotaxis

Following extravasations, leukocytes

emigrate in tissues toward the site of
injury by a process called chemotaxis.
 Phagocytosis

Recognition and attachment of the

particle to the surface of the
phagocyte engulfment killing
and degradation
Types of leukocyte (inflammatory cells)

Leukocytes are out of blood vessels that are known

as inflammatory cells.
a. Neutrophils:
Small phagocytic cell
Commonly seen in early stage of inflammation, and
acute inflammation, and purulent inflammation.
b. Macrophages:

Tissue macrophages are derived from blood

monocytes that emigrate from blood vessels under
influence of chemotactic factors.

Commonly seen in later stage of inflammation,

chronic inflammation, non-purulent inflammation,
and viral, or protozoal, or fungal infections. And
macrophages are also related to specific immune
response.
c. Eosinophilia
Commonly seen in hypersensitivity reaction and
human parasitological infections.

d. Lymphocytes and plasma cells

Commonly seen in virus infection and chronic
inflammation.

e. Basophilic and mast cell

Proliferation

Proliferate constitution:
Endothelium, macrophages, and
fibroblasts commonly seen in later
stage of inflammation
MacrM
 Main mediators function
Function Types of mediator
Vasodilation Histamine, Bradykinin, Nitric oxide,
Prostaglandins PGE2, PGD2,PGF2, PGI2
Vascular Histamine, Bradykinin, C3a, C5a, PAF, active oxygen
Leakage metabolic products, Leukotrienes C4, D4, E4
Substance P
Chemotaxis C5a, LTB4, bacterial products, IL-8, TNF.
Fever IL-1, IL-6, TNF, PG.
Pain PGE2, Bradykinin
Tissue Neutrophil and macrophage lysosomal enzymes
damage Oxygen metabolites, Nitric oxide
 TYPE OF INFLAMMATION
Depending upon the defense capacity of the host & duration
of respons:
Acute inflammation Chronic Inflammation
- Short duration (< 2 weeks) - Longer duration;
- Main features: # the causative agent of acute
1. Accumulation of fluid & plasma at the inflammation persist for a long time
affected site; #
2. Intravascular activation of platelets - Main features:
3. Polymorphonuclear (PMN) neutrophil 1. Monocuclear (MN) lymphocites;
- Systemic effect: Fever; leucocytosis plasma cells & macrophages
(Bacteria: neutrophilia; virus: 2. Tissue destruction or necrosis
lymphocytosis; parasit: eosinophilia); 3. Proliferation changes: granulation tissue
lymphangitis-lympadenitis; shock formation
- Systemic effect: Fever, anaemia;
leucocytosis; ESR; Amyloidosis
REGENERATION
 CELLS
GROUP
REPAIR
GRANULATION TISSUE FORMATION
 WOUND CONTRACTION
Wound starts contracting 2-3 days & process completed by
the 14th day.
Wound is reduced by approximately 80%
Mechanism:
1. Dehydration as a result of removal of fluid by drying of
wound
2. Contraction of collagen, when the collagen content of
granulation tissue
3. Discovery of myofibroblast, appearing in active
granulation has resolved
WOUND HEALING
Type of wound healing

(1) Healing by fist intention

A clean wound with a minimum

of space between the margins.
healing by first intention
(2) Healing by second intention

Healing by second intention differs from healing by first

intention in:
Greater tissue loss
More inflammatory exudates and necrotic material to
remove
More granulation tissue therefore a bigger scar
Wound contraction necessary
Slower process
Increased liability to infection
healing by second intention
 FACTORS INFLUENCING HEALING
LOCAL FACTORS SYSTEMIC FACTORS
1. Infection 1. Age
2. Poor blood supply 2. Nutrition
3. Foreign bodies 3. Systemic infection
4. Movement 4. Administration of
glucocorticoids
5. Exposure to ionising 5. Uncontrolled diabetics
radiation
6. Exposure to ultraviolet light 6. Heamatologic abnormalitis
7. Type, size, & location
HAEMODINAMIC
DISORDER
Kuntarti
DKKD Department
2017
 Hyperemia and Thrombosis vs postmortem clots
congestion *disseminated intravascular
Edema coagulation (DIC)
Embolism
Transudat-eksudat
Ischemia
Aterosklerosis Infarction
Perdarahan Dehidration
(Hemorrhage) Shock
 HYPEREMA AND CONGESTON

Increased volume of blood in an affected tissue or

part
Hyperemia (active hyperemia): Arterial and
arteriolar dilatation produces an increased flow of
blood into capillary beds
Congestion (passive congestion or venous
congestion): Impaired venous drainage
 ACTVE HYPEREMA

Too much arterial blood is brought to an organ or

tissue by dilated arterioles and capillaries
Sympathetic neurogenic mechanisms or
The release of vasoactive substances
Inflammatory reaction
Heat applied locally to a part
Increased physiological activity
Hyperemia of the capillaries
Left: normal
Right: hyperemia of the interalveolar capillaries and edema in
alveoli
 PASSVE CONGESTON

Blood leaving an organ or part is impeded

(impaired venous drainage)
Grossly, the involved tissues appear bluish-
red because of the poorly oxygenated
venous blood
Microscopically, congestion is similar to
hyperemia (capillaries and veins are dilated
and filled with blood)
 TYPES OF PASSVE CONGESTON

Localized passive congestion

Generalized passive congestion
Chronic generalized passive congestion of the
lungs: Reduced left ventricular output (left-sided
heart failure).
Chronic passive congestion of the liver: Right-
sided heart failure (rarely from obstruction of the
posterior vena cava).
 EDEMA

Abnormal accumulation of fluid (water) in the

intercellular tissue spaces or body cavities
Localized (e.g. obstruction of venous outflow
from the leg)
Generalized in distribution (e.g. in chronic
congestive heart failure)
 EDEMA S CAUSED BY

(1) Decreased plasma osmotic pressure

(2) Increased hydrostatic pressure
(3) Increased permeability of vascular
endothelium
(4) Lymphatic obstruction
 DECREASED PLASMA OSMOTC
PRESSURE

Deficiency of blood proteins

(hypoproteinemia)
Decreased formation or excessive loss
Albumin
More fluid is pushed into the intercellular
spaces. Also, the force available to pull fluid
into the bloodstream at the venous end of the
capillary is reduced
 DECREASED PLASMA OSMOTC
PRESSURE-I

Malnutrition (starvation, emaciation)

Severe or advanced liver diseases
(cirrhosis, etc.)
The loss of plasma proteins (intestine and
kidneys)
 DECREASED PLASMA OSMOTC
PRESSURE-II
In the intestine, blood protein loss is usually
the result of hemorrhage over a long
period of time (stomach worms in sheep
and cattle, slowly bleeding stomach
ulcers in pigs and dogs, etc.)
In the kidneys, renal amyloidosis is the only
frequently encountered condition in
animals in which large volumes of blood
protein are lost through the urine
 INCREASED HYDROSTATC PRESSURE

Venous stasis
Subsequent to venous stasis, the capillaries
become more permeable to large molecules
(albumin and globulin), since they are deprived
of their normal supply of oxygen and other
nutrients
 INCREASED PERMEABLTY OF
CAPLLARY ENDOTHELUM

Occurs subsequent to venous stasis (resulting in

increased hydrostatic pressure), as well as from
direct damage, as in inflammation. Increased
vascular permeability is the most important
mechanism in the formation of inflammatory
edema (exudate)
 LYMPHATC OBSTRUCTON

Occurs when any lesion impedes normal

lymphatic drainage by pressure or
obstruction. Under normal conditions, the
lymphatics constantly drain small amounts of
fluid from the intercellular spaces. Thus, in the
absence of lymphatic drainage from a area,
fluid accumulates
 NOMENCLATURE

Anasarca: Generalized edema in which fluid in

subcutaneous tissues is especially prominent
Ascites: Collection of edematous fluid in the
peritoneal cavity
Hydrothorax: Collection of edematous fluid in the
thoracic cavity
Hydropericardium or Pericardial Effusion:
Collection of edematous fluid in the pericardial
sac
 TRANSUDATE-EXUDATE

Inflammatory edema is referred to as an

exudate and it is associated with an
inflammatory reaction
Non-inflammatory edema is referred to
as a transudate
 70

Atherosclerosis
(pengerasan arteri)
dpt menyebabkan
hipertensi.
Terjadi krn akumulasi
lemak/ kolesterol
(LDL) pd dinding
pembuluh darah.
Faal_KV/ikun/2006
 HEMORRHAGE

The presence of erythrocytes outside the blood

vessels
The vessel may be physically damaged so that
erythrocytes flow out through a break in the wall
(hemorrhage by rhexis) or
The erythrocytes may pass through an intact
vascular wall by a process called diapedesis
(hemorrhage by diapedesis)
 NAMNG HEMORRHAGE-1

Petechiae
Ecchymoses
Purpura
Agonal hemorrhages
Linear hemorrhages
Paint-brush hemorrhages
Hemothorax
Hemopericardium
 NAMNG HEMORRHAGE-2

Epistaxis
Hemoptysis
Enterorrhagia
Metorrhagia
Hematuria
Hematemesis
Melena
 THE SGNFCANCE OF
HEMORRHAGE DEPENDS ON:
(1) The volume of blood loss
(2) The rate of blood loss, and
(3) The site of hemorrhage
 THROMBOSS

Formation of a clot from elements of the

circulating blood within the vascular system during
life
May decrease or obstruct vascular flow causing
ischemic/hypoxic injury to cells, tissues and organs
May become dislodged or fragmented to create
emboli (an embolus is an intravascular mass
carried in the bloodstream to some site remote
from its origin)
 FACTORS EFFECTVE N THROMBOSS
(TRIAD VIRCHOW)

(1) Injury to vascular endothelium

(2) Alterations in normal blood flow
(3) Alterations in the blood
(hypercoagulability)
 ARTERAL VS VENOUS THROMBUS

Grossly: Thrombi are friable, a mixture of red and

gray in irregular layers, dull, and attached to the
endothelium
Arterial thrombus: Dry, friable gray masses
composed of almost regularly arranged layers of
platelets and fibrin, irregularly mixed with small
amounts of darker red coagulated blood
(White or conglutination thrombus)
Venous thrombus: Red, gelatinous
(Stasis or red coagulation thrombus)
 NOMENCLATURE OF THROMB-I
Mural thrombi - are attached to the wall of the
heart or blood vessel
Occluding thrombi - are attached to the entire
circumference of the vessel
Valvular thrombi - are attached to the heart
valves
Canalized thrombi - occur when new blood
channels form in an organized thrombus
 NOMENCLATURE OF THROMB-II

Saddle thrombi - straddle the bifurcation of

blood vessels
Septic thrombi - are those which contain
bacteria
Aseptic thrombi - are those that do not
contain bacteria, etc.
 THE THROMBUS MAY

(1) increase in size and, by its enlargement,

eventually cause obstruction of some
critical vessel
(2) give rise to emboli
(3) be removed by fibrinolytic action or
(4) become organized
 DSSEMNATED INTRAVASCULAR
COAGULATON (DIC)
Widespread microthrombi formation in capillaries,
arterioles and venules
Composed largely of fibrin and aggregated
platelets
A complication of a diverse group of clinical
diseases in which there is activation of the
intrinsic pathway of blood clotting
 EMBOLSM

Process of a foreign body moving through the

circulatory system and becoming lodged in a
vessel causing obstruction
An embolus (plural, emboli) is a detached
intravascular solid, liquid or gaseous mass that
is carried by the blood to a site distant from its
point of origin
Thromboembolism: pulmonary embolus
 INFARCTON

A localized area of ischemic necrosis in an

organ or tissue resulting from occlusion of
either its arterial supply or venous drainage
Usually caused by thrombosis and/or
embolism of the arterial blood supply
More rarely, external compression of vessels
by expanding tumors, etc.
Ischemia

Local anemia or a deficiency of arterial

blood to a portion of an organ or part.
The chief causes of ischemia are:
(1) External pressure upon an artery
(2) Narrowing of the lumen of an artery
(3) A thrombus or embolus
Effects of Ischemia
The organ involved
The size of the vessel
The degree of occlusion
The degree of collateral circulation

End artery (as in kidneys): Acute necrosis

Gradual obstruction: Atrophy
 Shock
Peripheral circulatory failure with pooling
of the blood in the terminal circulatory
beds (small capillaries)
The fundamental disturbance is that
blood volume is too small to fill the
vascular system, resulting in a fall of blood
pressure and cell damage due to anoxia
Hypovolemic, vasogenic, cardiogenic
and neurogenic
 Clinical Signs of Shock

Inconsistent and vary with the precipitating cause

Animals are usually inactive and unresponsive to
external stimuli
Muscle weakness is prominent and there is pallor
and coolness of the skin
Body temperature is subnormal and the heart rate
is increased in most types of shock (but it may be
slow and irregular). Depression of renal function
and urine production often occur
Shock

Hypovolemic shock: Due to loss of blood

volume (hemorrhage, trauma, loss of fluids
in burns, etc.)
Septic shock: Septicemia or an
overwhelming infection with gram-
negative (endotoxic shock) or gram-
positive (exotoxic shock) organisms.
Peripheral dilatation of the capillary beds
which subsequently lead to shock
Shock

Cardiogenic (Cardiac) shock: Pump

failure." Subsequent to the sudden
decrease in cardiac output
Neurogenic shock: A shock state
mediated by the nervous system which
induces peripheral dilatation (dilatation
of the capillary bed). It occurs in animals
with severe fright, pain and trauma
(without hemorrhage)
SELAMAT
BELAJAR