Learning Objectives:
1. Define pathology and scope of human pathology.
2. Describe the definition and classification of
Inflammation.
3. Know the causes of inflammation
4. Understand the process of inflammations
5. Comprehend the etiopathogeneses of
granulomatous inflammations
6. Contrast the differences between acute and chronic
inflammations
Definition: Pathology is defined as the structural and
functional changes in the body caused by disease or
trauma. Diseases are the deviations from normal.
The Scope of Human Pathology
• Pathology deals with recognition of diseases,
their causes (aetiology), and their progression.
• Pathologists study structural changes (gross, or
microscopic), etiology and mechanisms of
diseases (pathogenesis)
• Most diseases can be placed in one of these
categories:
1. Inflammatory
2. Neoplastic
3. Degenerative conditions
4. Developmental conditions
Inflammation
Inflammation: Local defense and protective response
against cell injury or irritation or Local vascular and
cellular reaction, against an irritant.
Irritating or injurious agents (Irritant)
Living:
• Bacteria,
• Fungi,
• Virus,
• Parasite
• or their toxins
Non-Living:
• Chemical
• Physical
• Mechanical
Inflammation is designated by adding the suffix (itis) to the end
of the name of the inflamed organ or tissue.
Types of inflammation
1) Acute
inflammation
3) Chronic
inflammation
2) Sub acute
inflammation:
rarely occur.
1. Acute inflammation
Macroscopic signs: classical
5 cardinal symptoms (Celsus
1st c. B.C., Virchow 19th c.
A.D.)
1. calor - heat
2. rubor - redness
3. tumor - swelling
4. dolor – pain & Tenderness
5. functio laesa - loss (or
impairment) of function
Microscopic signs:
Inflammatory response
1. Local
vascular
change
2. Formation of
inflammatory
exudate
Inflammatory response: (microscopic signs)
First: Local vascular changes:
1. Initial temporary vasoconstriction for few seconds.
2. Active vasodilatation of arterioles and capillaries (by
chemical mediators: Histamine) and passive dilatation of
venules. Increase in capillary permeability (fluid exudate to
the extravascular tissue) thus concentration of blood cells,
slowing of blood flow (stasis)
3. Pavmentation: the margination of leukocytes.
Normal
Inflammation
Second: Formation of inflammatory exudates:
• Immigration or infiltration of the various leukocytes, fluid
and plasma proteins outside the blood vessels into the
surrounding tissue without injury of the blood vessels.
• Leukocytes seem to leave the smallest blood vessels by
inserting pseudopodia into the interendothelial junctions and
sliding through the wall by amoeboid movement.
• This is also due to the increased capillary permeability
caused by the high osmotic pressure of the surroundings.
• The early stages are marked by the predominance of
polymorphs especially neutrophils migration, particularly
when the inflammation is caused by pyogenic cocci, later on
monocytes infiltration occurs.
 ****In some cases RBCs may also pass (Diapedesis)
Function of inflammatory exudates
1-Dilute the invading microorganism and its
toxins.
2-Bring antibodies through the plasma to the
inflamed area.
3-Bring leukocytes that engulf the invading
microorganisms.
4-Bring fibrinogen through the plasma, which is
converted, to fibrin mesh, helping in trapping the
microorganism and localize the infection.
Blood stem cell
Cells of inflammatory response
1) Polymorphonuclear leukocytes: are basophils,
neutrophils and eosinophils; lobed nucleus and grainy
cytoplasm (granulocyte). Microphages (small eaters)
2) Monocytes or histocytes: macrophages. (big eaters)
3) Lymphocytes: leukocyte of fundamental importance;
they determine the specificity of the immune response
to infectious microorganisms and other foreign
substances.
4) Plasma cells: A type of immune cell that makes large
amounts of a specific antibody, developed from
activated B cells (Derived from lymphocytes originate
in the bone marrow). It is a type of WBCs and also
called plasmacyte.
Neutrophil
Lymphocyte
Eosinophil
Plasma cell
Basophil
Monocyte
Name
Neutrophil
Eosinophil
Basophil
Monocyte
Lymphocyte
Microphage
Acidophile
Basophil
Macrophage = >Polymorphs
Histocytes
and < RBCs
Plasmacyte
Shape
Pale pink to
blue,
Minimal
granulation.
Red with
eosin,
Coarse
granulation.
Blue with
eosin,
Coarse
granulation
1.5 to 2 times
larger,
Abundant fine
granulation
Agranular:
non-granulated,
Large round
nucleus
Basophilic,
Encentric
nucleus
% of
WBCs
60-70%
1-2% (50%
in allergy)
1%
4-6%
30%
Found in
tissue only
Functi
on
Phagositic
1st defense
Unknown
but could
neutralize
histamine,
serotonin
and other
kinins
Unknown
but contain
histamine
&heparin
Phagocytic
2nd defense
element
engulf
bacteria, dead
cells, debris &
dead
neutrophils
(pus cells)
Antibodies
production
Late stage of
the
inflammation
Primary
source of
specific
Antibodies
Monocytes
Plasma cell
Plasma
Plasmacell
cell
Phagocytosis
• Process by which Phagocytic cell (microphages and
macrophages) engulf and kill foreign particles (bacteria)
Two main types of phagocytes:
1- Motile phagocytes found in the blood stream and
migrate to the inflamed area (microphages)
2- Histocytes (macrophages) of the reticuloendothelial
system (RES) which remove bacteria that escapes from
the inflamed area.
Normal cell
Phagocytosis
Phagocytosis
Steps of Phagocytosis
1. Recognition
2. Ingestion- pseudopods engulf microbe through endocytosis
3. Vacuole Formation- vacuole contains microbe
4. Digestion- vacuole merges with enzymes to destroy microbes
5. Exocytosis- microbial debris is released
It occurs in two subsequent stages
1. Ingestion
of the m.o.
2. Intracellular killing of the m.o. (digestion):
• Increased glycolysis and the PH drop to 4 -4.5
• As a result, the proteolytic enzymes,
phagocytin, lysozyme and other hydrolytic
enzymes (lipase, esterase, nuclease … etc.) are
released
and
digest
the
ingested
microorganism.
Some species of bacteria e.g. tuberculosis are not
killed within the phagocyte and even multiply within it.
Methods of Intracellular killing of the m.o. (digestion)
I. Oxygen-dependent intracellular killing:
Production of a superoxide.
Use of the enzyme myeloperoxidase from neutrophil granules
II. Oxygen-independent intracellular:
1. electrically charged proteins
2. lysozymes
3. lactoferrins
4. proteases and hydrolytic
enzymes
Ingestion stage
Chemotaxis
• Positive directional response to chemical stimuli
(chemotactic subs)
• The migration of leukocytes (by amoeboid movement)
toward the injurious agent and the injured cells due to
chemical stimuli (chemotactic subs).
Chemotactic subs:
 Exogenous (Specific): Polysaccharide secreted by
m.o.
 Endogenous (General): Reaction product of the
antigen-antibody reaction .
Chemotaxis
Types of acute inflammation
(based on type of exudates)
1- Catarrhal inflammation:
2- Serous inflammation:
3- Fibrinous inflammation:
4- Membranous inflammation:
5- Hemorrhagic inflammation:
6- Gangrenous inflammation:
7- Allergic inflammation:
8- Suppurative or purulent
inflammation:
Name
Occur in
Characterized by
Exudates rich in mucous
Catarrhal
Mild inflammation in mucous membrane of
respiratory or alimentary tracts e.g. common cold
and catarrhal appendicitis
Serous
Mild inflammation in serous surface such as pleural
cavity, joint cavity where no damage in endothelium
ex. Tuberculosis pleurisy and Common blisters
Extensive watery low
protein exudates
Fibrinous
Outpouring of exudates with high protein and less
Exudates rich in fibrinogen
volume ex. in lobar pneumonia due to Streptococcus
pneumonia & pericardium inflammation
Fibrinous inflammation in which network of fibrin
entangling inflammatory cells and bacteria forms
Membranous
pseudo-membrane. Example: Diphtheria , Bacillary
dysentery.
Yellowish grey pseudo
membrane rich in fibrin ,
polymorphs & necrotic
tissues
In blood vessels e.g. in plague
Exudates rich RBCs
Acute appendicitis
Necrotic tissues resulting
from thrombi or emboli
Allergic
Result to Ag – Ab reaction Hypersensitivity
Presence of edema &
increase in vascularity.
Suppurative
Caused by pyogenic bacteria and is characterized
by pus formation Example: Abscess.
Large amount of Pus &
Purulent exudates produced
Hemorrhagic
Gangrenous
Lobar Pneumonia due to Streptococcus pneumonia is
associated with massive fibrinous exudates in the lung alveoli.
3. Fibrinous type:
4. Membranous type
Pseudomembranous inflammation in diphtheria showing network of fibrin entangling
inflammatory cells. Bacteria forming pseudo-membrane (left).
5. Suppurative or purulent
Pyemic abscess in myocardium. Abscess containing necrotic cell debris, colonies of
bacteria, and large number of neutrophils, many of them degenerate. Myocardium is
on the right.
Suppurative or purulent inflammation
Pus: thick fluid containing viable and necrotic polymorph and
necrotic tissue
1. Localized:
ex. Abscess:
Abscess is the localized collection of pus, commonly seen solid
block of tissue - Example: dermis, liver, kidney, brain etc. Pus
consists of partly or completely liquefied dead tissue mixed with
dead or dying neutrophils and living or dead bacteria, formed of
3 zones
1. Small abscess is called boil or furuncle
2. Large one carbuncle
3. Fistula
2. Diffused: Spreading of pus to adjacent areas e.g. cellulites
occurring in subcutaneous tissue . Usually caused by
streptococci.
Abscess:
Fate of acute inflammation
1- Resolution: exudates are reabsorbed
and tissue becomes normal again.
2- Healing: by repair and regeneration.
3- Spread: through lymphatics or blood
stream.
4- Chronicity
Chronic inflammation:
(granulomatous)
• Results from increased resistance of the causative agent
to phagocytosis or the body defense mechanism is
depressed.
• Shows lower vascular and exudative response
• The inflammatory cells are mainly macrophages,
plasma cells, giant cells, lymphocytes, fibroblasts.
• Occurs in the form of granuloma.
• Chronic
inflammation
usually
occur
with
granulomatous infections; e.g. leprosy, tuberculosis and
fungal infections.
Thanks