Patho week2 ch 9
Histamine and Bradykinin cause vasodilation and permeability of blood vessels, leading to fluid, WBCs, and platelets flooding to the site of injury.
Capillary permeability allows WBCs in the fluid from capillaries to consume foreign material through phagocytosis.
Vasodilation and permeability of blood vessels
Phagocytosis by WBCs
Microbial agents, endothelial cells, and WBCs attract platelets and other WBCs to the site of injury.
Margination forms a protective wall, and cytokine/interleukin is released, leading to leukocytosis.
Chemotaxis of WBCs
Leukocytosis
Cytokines are proteins from glial cells in the nervous system that act as signaling molecules, stimulating the liver to release CRP and increasing or decreasing reactions.
Interleukins are a subset of cytokines that moderate cellular behavior and act as messenger molecules between immune cells.
Signaling molecules
Moderation of cellular behavior
Neutrophils are the first line of defense, with a lifespan of 10 hours to 2 days, and start phagocytosis.
Monocytes are the largest WBCs that differentiate into macrophages and take over phagocytosis, indicating a more chronic process.
Phagocytosis
Chronic inflammation
Prostaglandins, leukotrienes, TNF alpha, interleukins, and pyrogens control the systemic response.
Prostaglandins are responsible for pain, leukotrienes help produce mucus, TNF alpha comes from monocytes, interleukins play a role in cell growth, and pyrogens act on the hypothalamus and activate heat, leading to fevers.
Systemic response
Acute inflammation is a process that occurs in response to injury or infection.
Stage 1 Vascular Permeability
Stage 2 Cellular Chemotaxis
Stage 3 Systemic Response
Tissue Healing
Histamine (Mast Cells) + Bradykinin = vasodilation and permeability of blood vessels
Fluids, WBCs, and platelets flood to the site of injury
Capillary permeability
WBC in the fluid that comes from capillaries consumes foreign material = phagocytosis
Microbial agents, endothelial cells, and WBCs attract platelets and other WBCs to the site of injury
Margination protective wall is formed
Cytokine/Interleukin gets released
Leukocytosis occurs
Neutrophils: first line defense, start phagocytosis
Monocytes: largest WBC, differentiate into macrophages, take over phagocytosis, indicates the more chronic process
Controlled by prostaglandins, leukotrienes, TNF alpha, interleukins, pyrogens
Prostaglandins: responsible for pain
Leukotrienes: helps produce mucus
TNF alpha: come from monocytes
Interleukins: play a role in cell growth
Pyrogens: act on hypothalamus and activate heat- leading to fevers
Stage 1: Inflammation occurs
Stage 2: Reconstructive/proliferation occurs
Fibroblasts synthesize collagen to make a foundation for scar tissue (granulation tissue)
Granulation tissue secretes cytokines and growth factors
Epithelial cells help make a new surface
Stage 3: Maturation/remodeling
Fibroblast/myofibroblasts refine scar tissue
3 stages of tissue healing: primary intention, secondary intention, tertiary intention
Healed primary intention scar ends up as a hairline scar
Healed secondary intention scar: epithelium grows over
Histamine and Bradykinin cause vasodilation and permeability of blood vessels, leading to fluid, WBCs, and platelets flooding to the site of injury.
Capillary permeability allows WBCs in the fluid from capillaries to consume foreign material through phagocytosis.
Vasodilation and permeability of blood vessels
Phagocytosis by WBCs
Microbial agents, endothelial cells, and WBCs attract platelets and other WBCs to the site of injury.
Margination forms a protective wall, and cytokine/interleukin is released, leading to leukocytosis.
Chemotaxis of WBCs
Leukocytosis
Cytokines are proteins from glial cells in the nervous system that act as signaling molecules, stimulating the liver to release CRP and increasing or decreasing reactions.
Interleukins are a subset of cytokines that moderate cellular behavior and act as messenger molecules between immune cells.
Signaling molecules
Moderation of cellular behavior
Neutrophils are the first line of defense, with a lifespan of 10 hours to 2 days, and start phagocytosis.
Monocytes are the largest WBCs that differentiate into macrophages and take over phagocytosis, indicating a more chronic process.
Phagocytosis
Chronic inflammation
Prostaglandins, leukotrienes, TNF alpha, interleukins, and pyrogens control the systemic response.
Prostaglandins are responsible for pain, leukotrienes help produce mucus, TNF alpha comes from monocytes, interleukins play a role in cell growth, and pyrogens act on the hypothalamus and activate heat, leading to fevers.
Systemic response
Acute inflammation is a process that occurs in response to injury or infection.
Stage 1 Vascular Permeability
Stage 2 Cellular Chemotaxis
Stage 3 Systemic Response
Tissue Healing
Histamine (Mast Cells) + Bradykinin = vasodilation and permeability of blood vessels
Fluids, WBCs, and platelets flood to the site of injury
Capillary permeability
WBC in the fluid that comes from capillaries consumes foreign material = phagocytosis
Microbial agents, endothelial cells, and WBCs attract platelets and other WBCs to the site of injury
Margination protective wall is formed
Cytokine/Interleukin gets released
Leukocytosis occurs
Neutrophils: first line defense, start phagocytosis
Monocytes: largest WBC, differentiate into macrophages, take over phagocytosis, indicates the more chronic process
Controlled by prostaglandins, leukotrienes, TNF alpha, interleukins, pyrogens
Prostaglandins: responsible for pain
Leukotrienes: helps produce mucus
TNF alpha: come from monocytes
Interleukins: play a role in cell growth
Pyrogens: act on hypothalamus and activate heat- leading to fevers
Stage 1: Inflammation occurs
Stage 2: Reconstructive/proliferation occurs
Fibroblasts synthesize collagen to make a foundation for scar tissue (granulation tissue)
Granulation tissue secretes cytokines and growth factors
Epithelial cells help make a new surface
Stage 3: Maturation/remodeling
Fibroblast/myofibroblasts refine scar tissue
3 stages of tissue healing: primary intention, secondary intention, tertiary intention
Healed primary intention scar ends up as a hairline scar
Healed secondary intention scar: epithelium grows over