Inflammatory Response
A protective response that eliminates the initial cause of the injury as well as any necrotic cells that result from the injury.
Dilutes, destroys or neutralizes and sets the stage for healing
Cardinal Signs of Inflammation
Rubor - redness
Tumor - swelling
Calor - heat
Dolor - pain
Functio Laesa -Loss of Function
Rubor
Redness
Tumor
Swelling
Calor
Heat
Dolor
Pain
Functio Laesa
Loss of Function
Increased Capillary Permeability
Causes redness, warmth and pain felt. This localizes the infection and facilitates the movement of the WBCs coming into the area
Acute Inflammation
1.Vascular Stage
Response of Blood Vessels to Injury
2.Cellular Stage
Response of Immune Cells to Injury
Vascular Stage of Acute Inflammation
Response of Blood Vessels to Injury:First a momentary vasoconstriction of small vessels, followed by rapid dilation of arterioles and venules supplying the area. Redness, warmth and pain felt.
Cellular Stage of Acute Inflammation
Response of Immune Cells to Injury: Movement of White Blood Cells into area of injury:
1. Granulocytes ("granules")
2. Monocytes
Granulocytes ("granules")
Three different types of cells: Neutrophils, Basophils and Eosinophils
Neutrophils - Phagocytic cells
First responder
Generate Toxic free radicals
Life-span only 10 hours, must be replaced.
Basophils
Release cytokines and other Inflammatory Mediators
Eosi
Neutrophils
A type of Granulocyte. Phagocytic cells. First responder. Generate Toxic free radicals. Life-span only 10 hours, must be replaced. Visually identified by: PMN - polymorpho nuclear cell
Seg - segment
Basophils
A type of Granulocyte. Release cytokines and other Inflammatory Mediators
Eosinophils
A type of Granulocyte that "regulate inflammation" and are toxic to parasites.
Monocytes
Long-Lived White Blood Cells created in bone marrow. Migrate into tissues (24-48 Hours) and become Macrophages:
Large Phagocytic Cells
Migrate to local lymph nodes
The 4 Roles of WBC
1.Margination
2.Transmigration "Diapedesis"
3.Chemotaxis
4.Phagocytosis
Endothelial cells role in Inflammation
Adhesion molecules, cytokines, Eicosonoids, Chemokines and Oxygen radicals.
Neutrophils role in Inflammation
Aggregation Priming
Acute Phase Response
Fever, anorexia, hypertension, increased heart rate, corticoid steroid and ACTH release.
Mast Cells
Widely distributed in connective tissues throughout the body and found in the openings of the body. (i.e. mucus cells, lungs, etc.) Contain "granules with numerous Inflammatory Mediators (Histamine, Leukotrienes, Prostaglandins) that are released when tis
Major Effects of Histamine
Vasodilator
Bronchial spasms
Hypotension
Muscle contraction
Prostaglandins
Cause fever.
Arachidonic Acid Metabolites
A type of inflammatory mediator. Arachidonic Acid:
20 carbon fatty acid found in cell membranes
Released by cell injury or inflammation
Used to synthesize prostaglandins & leukotrienes
Tissue Repair
An Extension of the Inflammatory Response.
1. Regeneration (cardiac and nerve cells can't do this)
2. Scar Tissue Replacement
Regeneration
Occurs in "parenchymal" (FUNCTIONAL CELLS) that are capable of cell proliferation. Lost functional tissue is repaired with new functional tissue. No loss of function. Little or no evidence of injury
Labile Cells
Those that continue to divide throughout life.Skin, oral cavity, vagina & cervix, G.I. epithelium, urinary tract.
Stable Cells
Those that have stopped growing but can regenerate if needed. i.e. Hepatocytes - Liver cells. In order for stable cells to regenerate the "stroma" (connective tissues & blood vessels) must be in-tact!
Hepatocytes
Liver Cells
Cirrhosis
Scarring of the liver. Regeneration is disorganized because stroma is damaged. It starts with steatosis and that becomes hepatitis. The hepatitis inflammation persists so long that the liver tissue becomes destroyed.
Connective Tissue Replacement
When cells that can not divide are destroyed they are replaced with connective ("scar") tissue
Ex. "Permanent or Fixed Cells:
Cardiac Muscle
Skeletal Muscle
Nerve Cells
Inflammatory Phase of Skin Tissue Repair
In this stage Neutrophils are destroying bacteria.They are removing dead tissue.
Hemostasis
Vascular & Cellular Inflammatory Responses
24-48 hours
Proliferative Phase of Skin Tissue Repair
Begins in 2-3 days, may last 3 weeks. Macrophages help eat the pathogens. Granulation tissue is not fully repaired.
Lots of groundwork for a repair of tissue. (i.e. collagen fibers laid out, etc.)
Fibroblasts:
Produce collagen
Release growth factors
Proli
Fibroblasts
Produce collagen
Release growth factors
Proliferation of vascular endothelium
Angiogenesis
Proliferation of epithelial cells at edges
Maturational (remodeling) phase of Skin Tissue Repair
3 weeks-6 months post injury. Remodeling of repaired tissue to give maximal strength. Continued activity of fibroblasts & collagen deposition. 70-80% of tensile strength of unwounded skin at 3 months....
Primary Intention
Small wounds that repair quickly and completely.
Secondary Intention
Larger wounds that require longer to heal and often leave significant scar tissue.
Keloids
A type of abnormal healing. Abnormal formation of scar tissue during wound repair. Most Common in African-Americans. Most likely has a genetic basis. Abnormal proliferation, apoptosis, or expression of growth factors and extracellular matrix proteins by f
Proteins & Amino Acid's Contribution to Wound Repair
Collagen
Carbohydrates Contribution to Wound Repair
Energy for WBC's
Vitamins Contribution to Wound Repair
Important co-enzymes for many synthetic enzymes.
Diseases that Affect Nutrition in Wound Repair
Kawashikor, Cachexia, G.I. Disease
Blood Flow & Oxygen Delivery's Role in Wound Repair
Supply nutrients for repair
Remove debris
WBC's require oxygen to generate free radicals for destroying foreign organisms.
Hyeprbaric oxygen for wounds that won't heal.....
Diseases that Affect Blood Flow & Oxygen in Wound Repair
PVD, CHF, Anemia, Diabetes, Shock
Impaired Immune or Inflammatory Response
Inflammation and Infiltration by immune cells are vital for tissue repair.
HIV, Immunossupression, Diabetes, Genetic disorders of WBC's
Drugs??
Effects of Age in Wound Repair
Decreased skin thickness & elasticity
Decrease fibroblast activity & collagen synthesis
Decreases WBC activity & number?
Decreased re-epithlialization