Inflammation
Learning Objectives:
1. Describe the definition and classification of
Inflammation.
2. Know the causes of inflammation
3. Understand the process of inflammations
4. Comprehend the etiopathogeneses of
granulomatous inflammations
5. Contrast the differences between acute and chronic
inflammations
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.
1. Acute inflammation
Macroscopic signs: classical
5 cardinal symptoms
1. heat
2. redness
3. swelling
4. pain & Tenderness
5. 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 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.
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; Microphages (small eaters)
2) Monocytes or histocytes: macrophages. (big eaters)
3) Lymphocytes: leukocyte of fundamental importance;
they determine the specificity of the immune response.
4) Plasma cells: A type of immune cell that makes large
amounts of a specific antibody, developed from
activated B cells.
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.
Phagocytosis
Steps of Phagocytosis
1. Recognition
2. Ingestion- pseudopods engulf microbe through endocytosis
3. Vacuole Formation- vacuole contains microbe
4. Digestion- merges with enzymes to destroy microbes
5. Exocytosis- microbial debris is released
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
Extensive watery low protein exudates
Serous
Mild inflammation in serous surface such as pleural cavity, joint cavity where no damage in
endothelium ex. Tuberculosis pleurisy and Common blisters
Fibrinous
Outpouring of exudates with high protein and less volume ex. in lobar pneumonia due to
Streptococcus pneumonia & pericardium inflammation
Membranous
Fibrinous inflammation in which network of fibrin entangling inflammatory cells and bacteria
forms pseudo-membrane. Example: Diphtheria , Bacillary dysentery.
Yellowish grey pseudo membrane rich in
fibrin , polymorphs & necrotic tissues
Hemorrhagic
In blood vessels e.g. in plague
Exudates rich RBCs
Acute appendicitis
Necrotic tissues resulting from thrombi or
emboli
Result to Ag – Ab reaction Hypersensitivity
Presence of edema &
increase in vascularity.
Exudates rich in fibrinogen
Gangrenous
Allergic
Caused by pyogenic bacteria and is characterized by pus formation Example: Abscess.
Suppurative
Large amount of Pus & Purulent exudates
produced
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.