Inflammation: Chapter 11
★ Definitions of Concepts Related to Inflammation
○ Inflammatory response: response to cell injury
■ The inflammatory response…
● Neutralizes and dilutes inflammatory agents
● Removes necrotic/dead material
● Establishes an environment suitable for healing
● Occurs w/ microbial invasion, heat, radiation, allergens, chemicals, or
autoimmune reactions.
■ 4 phases of the inflammatory response:
● Vascular response
1. Arterioles undergo brief vasoconstriction
2. Chemical mediators are released from injured cells
a. This causes increased capillary permeability and fluid
movement from capillaries→ tissue
b. First, exudate contains serous fluid
c. Later, exudate contains plasma proteins (mainly albumin)
3. Proteins exert oncotic pressure that further draws fluid from blood
vessels
4. Vasodilation and increased permeability causes redness, heat, and
swelling at site of injury
5. Fibrinogen leaves the blood and turns into fibrin
a. Fibrin strengthens blood clots formed by platelets
6. Blood clots trap bacteria
7. Platelets release growth factors that initiate the healing process
● Cellular response
○ Chemotaxis: migration of WBCs (neutrophils and monocytes) to injury
site
Neutrophils: Monocytes: pacman Lymphocytes:
- First leukocyte to arrive - Phagocytic cell that migrates to site - Arrive later
- Phagocytize bacteria, damaged of injury - Has to do w/ humoral and
cells, etc. - Monocytes → macrophages cell-mediated immunity
- Short life span - Phagocytize debris and cleanses - B and T cells
- Pus contains dead neutrophils, area for healing
digested bacteria, and cell debris - Long life span
- Bone marrow releases more - Multiply and stay in
neutrophils, resulting in high WBC damaged tissue for weeks
count - When particles are too large,
- Immature neutrophils= bands macrophages fuse to form a
- Increased # of bands → multinucleated giant cell
WBC count increases/ - Encapsulated by collagen
“shift to the left” leading to granuloma (small
- Common in patients with area of inflammation)
acute bacterial infections formation
- Mature neutrophils= segmented
neutrophils
● Formation of exudate
○ Consists of fluid and leukocytes that move from circulation to site of
injury
○ Types:
■ Serous: clear, thin, watery
● Indicates early inflammation (ex: skin blisters)
■ Serosanguinous: thin, watery, and pale red to pink in color
(contain RBCs)
■ Fibrinous:thick, sticky, high cell and fibrin content
, ■Hemorrhagic: results from rupture or necrosis of blood vessel
walls
■Purulent: fluid rich in protein from WBCs, microbial organisms,
and cellular debris
■ Catarrhal: Thick mucous exudate (ex: runny nose)
● Healing: final phase
○ Regeneration: replacement of lost cells and tissues w/ cells of the same
type
○ Repair: most common phase
■ Connective tissue replaces lost cells and results in scar
formation
■ Occurs by primary, secondary, or tertiary intention
■ Chemical response
● Chemical mediators:
Histamine: Serotonin: Kinins: Complement Prostaglandins: Thromboxane Leukotrienes Cytokines
System:
Causes Causes Ex: Stimulates Cause vasodilation Powerful Stimulates They
vasodilation vasodilation bradykinins histamine leading to vasoconstrictor chemotaxis instruct
and and release and increased blood cells to
increased increased causes chemotaxis flow and edema Platelet Slow reacting alter their
capillary capillary vasodilation formation, aggregating substance of proliferati
permeability permeability and Enzyme proinflammatory agent anaphylaxis on,
contraction cascade (promotes clot differentia
Stimulates of smooth consisting of Results in pain and formation) Causes tion,
smooth muscle pathways to fever bronchoconstri secretion,
muscle mediate ction (airway or
contraction Results in inflammation Inhibits platelet and narrowing) activity.
pain/stimulat and destroy neutrophil
es pain pathogens aggregation Increased Causes
receptors capillary fever
Functions: permeability
Enhanced (results in
phagocytosis airway edema)
Increased
vascular
permeability
Chemotaxis
(migration)
Cellular lysis
(cell death)
■ Signs and symptoms of infection:
● Local manifestations: Redness, heat, swelling, pain, loss of function
● Systemic manifestations: increased WBC count (shift to the left), malaise,
nausea, anorexia, increased pulse, increased respiratory rate, fever
● Fever: triggered by release of cytokines (especially PGs)
○ Initiates changes in temp (raise thermostatic set point)
○ Body increases heat production and conservation to reach a new set
point
○ Body is hot, yet person feels chills until set point is reached (set point
can fluctuate)
○ Fever can be a defense mechanism:
■ Increased killing of microorganisms
■ Increased phagocytosis
■ Increased proliferation of T cells
■ Increased interferon activity
★ Types of inflammation:
○ Acute inflammation:
■ Lasts 2-3 weeks with usually no residual damage after healing
★ Definitions of Concepts Related to Inflammation
○ Inflammatory response: response to cell injury
■ The inflammatory response…
● Neutralizes and dilutes inflammatory agents
● Removes necrotic/dead material
● Establishes an environment suitable for healing
● Occurs w/ microbial invasion, heat, radiation, allergens, chemicals, or
autoimmune reactions.
■ 4 phases of the inflammatory response:
● Vascular response
1. Arterioles undergo brief vasoconstriction
2. Chemical mediators are released from injured cells
a. This causes increased capillary permeability and fluid
movement from capillaries→ tissue
b. First, exudate contains serous fluid
c. Later, exudate contains plasma proteins (mainly albumin)
3. Proteins exert oncotic pressure that further draws fluid from blood
vessels
4. Vasodilation and increased permeability causes redness, heat, and
swelling at site of injury
5. Fibrinogen leaves the blood and turns into fibrin
a. Fibrin strengthens blood clots formed by platelets
6. Blood clots trap bacteria
7. Platelets release growth factors that initiate the healing process
● Cellular response
○ Chemotaxis: migration of WBCs (neutrophils and monocytes) to injury
site
Neutrophils: Monocytes: pacman Lymphocytes:
- First leukocyte to arrive - Phagocytic cell that migrates to site - Arrive later
- Phagocytize bacteria, damaged of injury - Has to do w/ humoral and
cells, etc. - Monocytes → macrophages cell-mediated immunity
- Short life span - Phagocytize debris and cleanses - B and T cells
- Pus contains dead neutrophils, area for healing
digested bacteria, and cell debris - Long life span
- Bone marrow releases more - Multiply and stay in
neutrophils, resulting in high WBC damaged tissue for weeks
count - When particles are too large,
- Immature neutrophils= bands macrophages fuse to form a
- Increased # of bands → multinucleated giant cell
WBC count increases/ - Encapsulated by collagen
“shift to the left” leading to granuloma (small
- Common in patients with area of inflammation)
acute bacterial infections formation
- Mature neutrophils= segmented
neutrophils
● Formation of exudate
○ Consists of fluid and leukocytes that move from circulation to site of
injury
○ Types:
■ Serous: clear, thin, watery
● Indicates early inflammation (ex: skin blisters)
■ Serosanguinous: thin, watery, and pale red to pink in color
(contain RBCs)
■ Fibrinous:thick, sticky, high cell and fibrin content
, ■Hemorrhagic: results from rupture or necrosis of blood vessel
walls
■Purulent: fluid rich in protein from WBCs, microbial organisms,
and cellular debris
■ Catarrhal: Thick mucous exudate (ex: runny nose)
● Healing: final phase
○ Regeneration: replacement of lost cells and tissues w/ cells of the same
type
○ Repair: most common phase
■ Connective tissue replaces lost cells and results in scar
formation
■ Occurs by primary, secondary, or tertiary intention
■ Chemical response
● Chemical mediators:
Histamine: Serotonin: Kinins: Complement Prostaglandins: Thromboxane Leukotrienes Cytokines
System:
Causes Causes Ex: Stimulates Cause vasodilation Powerful Stimulates They
vasodilation vasodilation bradykinins histamine leading to vasoconstrictor chemotaxis instruct
and and release and increased blood cells to
increased increased causes chemotaxis flow and edema Platelet Slow reacting alter their
capillary capillary vasodilation formation, aggregating substance of proliferati
permeability permeability and Enzyme proinflammatory agent anaphylaxis on,
contraction cascade (promotes clot differentia
Stimulates of smooth consisting of Results in pain and formation) Causes tion,
smooth muscle pathways to fever bronchoconstri secretion,
muscle mediate ction (airway or
contraction Results in inflammation Inhibits platelet and narrowing) activity.
pain/stimulat and destroy neutrophil
es pain pathogens aggregation Increased Causes
receptors capillary fever
Functions: permeability
Enhanced (results in
phagocytosis airway edema)
Increased
vascular
permeability
Chemotaxis
(migration)
Cellular lysis
(cell death)
■ Signs and symptoms of infection:
● Local manifestations: Redness, heat, swelling, pain, loss of function
● Systemic manifestations: increased WBC count (shift to the left), malaise,
nausea, anorexia, increased pulse, increased respiratory rate, fever
● Fever: triggered by release of cytokines (especially PGs)
○ Initiates changes in temp (raise thermostatic set point)
○ Body increases heat production and conservation to reach a new set
point
○ Body is hot, yet person feels chills until set point is reached (set point
can fluctuate)
○ Fever can be a defense mechanism:
■ Increased killing of microorganisms
■ Increased phagocytosis
■ Increased proliferation of T cells
■ Increased interferon activity
★ Types of inflammation:
○ Acute inflammation:
■ Lasts 2-3 weeks with usually no residual damage after healing
