10 - Body Defense Mechanism

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Body Defense Mechanisms
 The body is constantly in contact with pathogens (bacteria, fungi, viruses)

 It has two defense systems for foreign materials:
1. Nonspecific defense system

 Mechanisms protect against a variety of invaders
 Responds immediately to protect body from foreign materials
 Nonspecific Body Defenses
1. Body surface coverings
 Intact skin
 Mucous membranes
2. Specialized human cells
3. Chemicals produced by the body
2. Specific defense system

 Specific defense is required for each type of invader
 Also known as the immune system
3 Lines of Defense
A. First Line of Defense: Surface Membrane Barriers

1. The skin
 Physical barrier to foreign materials
 pH of the skin is acidic to inhibit bacterial growth
 Sebum is toxic to bacteria
 Vaginal secretions are very acidic
2. Stomach mucosa
 Secretes hydrochloric acid
 Has protein-digesting enzymes
3. Saliva and lacrimal fluid contain lysozyme
4. Mucus traps microorganisms in digestive and respiratory pathways
5. Cilia sweep away pathogens.
B. Second Line of Defense: Inflammatory Response

 Triggered when body tissues are injured
 Produces five cardinal signs
 Redness (rubor)
 Heat (calor)
 Swelling (tumor)
 Pain (dolor)
 Deranged function (functio laesa)
 Results in a chain of events leading to protection and healing
Functions of the Inflammatory Response

 Prevents spread of damaging agents
 Disposes of cell debris and pathogens
 Sets the stage for repair
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C. Third Line of Defense: The Immune System

 Specific defense
 Antigen specific – recognizes and acts against particular foreign substances
 Systemic – not restricted to the initial infection site
 Has memory – recognizes and mounts a stronger attack on previously encountered pathogens
INFLAMMATION
 A defensive response of vascularized living tissue to cellular injury caused by endogenous or exogenous agents
 The body's reaction to invasion by an infectious agent, antigen challenge or physical, chemical or traumatic
damage
 Involves vascular and cellular responses working together in a coordinated manner to destroy substances
recognized as being foreign to the body
 True inflammation does not occur in avascular tissues (example: normal cornea).
 Most common causes:

o infection – from microorganisms in tissues
o physical trauma
o chemical, irradiation, mechanical or thermal injury
o immune reactions
 Common initiator: wound

 Intensity of inflammation is proportional to the degree of tissue injury
 Nonspecific: the pattern of events is similar regardless of the stimulus
 Acute Inflammation
o immediate or early response to an injurious agent
 Chronic Inflammation
o longer duration
o follows a persistent, self-perpetuating course with the source of the inflammation being unresolved
o may result in healing or develop into granulomatous inflammation
 Process of repair (Healing)
o closely intertwined with inflammatory response
o involves the return of tissue to its previous state
Acute Inflammation
 short duration
 lasting from minutes to several days
 Exudation
 process wherein fluids, proteins, and WBCs from the vascular system arrive into the interstitial
tissue because of vascular and cellular alterations
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Physiology of Acute Inflammation
INJURY
1. Release of chemical mediators
2. Vasodilation 3. Increased Capillary 4. Cellular influx

Permeability by chemotaxis
(phagocytes)
5. Increased blood flow 6. Extravasation of fluid

(hyperemia)
7. Elevated
cellular metabolism
CALOR RUBOR TUMOR DOLOR

(5, 7) (5) (4, 6) (1, 4, 6)
A. Vascular Phase
 follows within seconds of the tissue injury
 lasts for several minutes
 transient vasoconstriction (initial response by neural reflex)
Vasodilation and Increased Capillary Permeability
 hyperemic response
 arterioles in the injured area dilate
leads to increased blood flow to injured tissues
 Brings phagocytic cells, oxygen, and nutrients to injured area

 Plasma proteins leak into tissues
 pulls water from plasma into injured area
 RBC concentration inside the blood vessel increases
 viscosity of blood increases
 circulation slows down
 stasis
 cellular phase
B. Cellular Phase
 Usually occurs when there has been sufficient damage to tissues, or when infection has occurred
 takes place over the next few hours
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Hallmark:
appearance of granulocytes, particularly neutrophils, in the tissues
Neutrophils
 highly mobile
 arrive first at the site of injury
 begin phagocytosis
 release inflammatory mediators
 Movement of neutrophils:
Extravasation
 movement of WBCs from the blood vessel into the injured tissue
 accomplished through several processes:
margination emigration
pavementing chemotaxis
1. Margination
 granulocytes and monocytes move toward the endothelial lining of blood vessel
2. Pavementing
 adhesion of leukocytes to the vascular endothelium
3. Emigration
 leukocytes migrate by active amoeboid movement (diapedesis) through the walls of
venules and small veins
4. Chemotaxis
 movement of additional leukocytes to an area of inflammation in response to release of
chemical mediators by neutrophils, monocytes, and injured tissue
Phagocytosis
 Phagocytes
 neutrophils, eosinophils, monocytes and macrophages
 engulf foreign material into a vacuole
 enzymes from lysosomes digest the material
Chemical Mediators
1. Vasoactive Amines
a. Histamine
 found in basophils, mast cells and platelets
 causes dilatation of arterioles
 increases vascular permeability of venules
 constricts large arteries
 release is stimulated by mast cell and IgE reactions, C3 and C5a fragments, trauma, heat, and
lysosomes of neutrophils
b. Serotonin
 present in platelets
 powerful vasoconstrictor
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2. Complement System
 A group of at least 20 plasma proteins
 Activated when they encounter and attach to cells (complement fixation)
 Damage foreign cell surfaces
 Has vasodilators, chemotaxis, and opsonization actions
 Inflammatory process is greatly diminished in the absence of complement enzymes
Most important
 C3 and C5a
 increase vascular permeability
 cause vasodilatation
 C3 – assists in phagocytosis
 C5a – powerful chemotactic agent for neutrophils, monocytes, eosinophils and basophils
3. Arachidonic Acid Metabolites (Autocoids)
 Prostaglandins, thromboxanes, leukotrienes
 local, short-range hormones
 exert their effects locally
 then either decay spontaneously or destroyed enzymatically
 synthesized by most connective tissue, blood and parenchymal cells
a. Prostaglandins
 have histamine-like effects
 involved in fever and transmission of pain impulses
b. Thromboxanes
 involved in the platelet response to blood vessel injury
c. Leukotrienes
 causes vasodilatation and increased permeability
4. Kinins and Coagulation System

 Kinin System
 activated by Factor XII (Hageman factor) which is part of the coagulation system
 Bradykinin
 mediates vasodilatation, increased vascular permeability, contraction of smooth
muscle, and pain sensation
5. Lymphokines
 released from helper T lymphocytes during immunologic reactions
 induces chemotaxis for neutrophils and macrophages
6. Neutrophil Mediators
 lysosomes of neutrophils
 contain potent protein and proteases  chemotaxis and vasodilatation
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Exudate
 fluid or matter collecting in a cavity or tissue space
1. Serous exudates
 protein-rich fluid that escapes into the tissues in the early stages of inflammation
 because of high protein content  draws water  responsible for the edema at the site of inflammatory
reaction
2. Purulent exudates
 contain pus  a combination of phagocytic neutrophils and “pus-producing” organisms  localize or
contain organisms to prevent infection from spreading
CHRONIC INFLAMMATION
 persistence of the inflammatory process

 follow a less predictable course than acute inflammation
 chronically inflamed area:
 usually infiltrated by mononuclear leukocytes (macrophages and lymphocytes)
 sometimes (osteomyelitis) contain neutrophils
 Chronic inflammation results in

 infiltration of the site with fibroblasts
 increased amount of collagen deposits
 varying amounts of scar tissue formation
Cells of Chronic Inflammation

 Mononuclear phagocytic system (MPS)
 Monocyte
 emigrates to site during acute inflammation
 but not the primary cell type until about 48 hours after the injury
 becomes a macrophage when it reaches extravascular tissue
 Macrophage
 phagocytic
 unique capability: increase in cell size, increase levels of lysosomal enzymes, become
metabolically active
 disappear in acute inflammation but continue to accumulate in chronic inflammation
Granulomatous Inflammation
 type of chronic inflammation
 characterized by: accumulation of modified macrophages
 initiated by infectious or noninfectious agents
 example: tuberculosis

10 - Body Defense Mechanism

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1

Body Defense Mechanisms

 The body is constantly in contact with pathogens (bacteria, fungi, viruses)

1. Nonspecific defense system

2. Specific defense system

A. First Line of Defense: Surface Membrane Barriers

B. Second Line of Defense: Inflammatory Response

Functions of the Inflammatory Response

C. Third Line of Defense: The Immune System

 Most common causes:

 Common initiator: wound

 Nonspecific: the pattern of events is similar regardless of the stimulus

Physiology of Acute Inflammation

1. Release of chemical mediators

2. Vasodilation 3. Increased Capillary 4. Cellular influx

5. Increased blood flow 6. Extravasation of fluid

CALOR RUBOR TUMOR DOLOR

 Brings phagocytic cells, oxygen, and nutrients to injured area

4. Kinins and Coagulation System

 persistence of the inflammatory process

 Chronic inflammation results in

Cells of Chronic Inflammation

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