Chapter 5: Inflammation and healing

First line of defense:

Nonspecific/Mechanical barrier/Skin and mucous membrane/Secretions such as tears, saliva, or gastric secretions contain enzymes to destroy damaging material

Second line of defense:

Nonspecific/Phagocytosis/Inflammation

Define interferons:

Nonspecific agents that protect uninfected cells from viruses

Third line of defense:

Specific defense/Production of antibodies or sensitized lymphocytes following exposure to specific substances

Physiology of inflammation:

Protective mechanism and important basic concept of in pathophysiology, s/s serve as warning for a problem, problems may be hidden within the body, infection is one cause of inflammation

Causes of inflammation:

Direct physical damage, caustic chemicals, infection, ischemia, allergic response, foreign body, and extreme of heat or cold

Acute inflammation:

Timing varies with sepcific cause

Chemical mediators affect blood vessels and nerves in damaged area: vasodilation, hyperemia, increase permeability, and chemotaxis to attract cells of the immune system

Histamine action:

Immediate vasodilation and increase capillary permeability to form exudate

Exudate:

Fluids, cells, and other substances move from blood vessels towards tissues

Chemotactic factor:

Attract netrophils to site

Platelet-activating factor:

Activate neutrophil platelet aggregation

Cytokines:

Increase plasma proteins, induce fever, chemotaxis, and leukocytosis

Chemotaxis:

The movement of organism toward a negative stimulus

Leukotrienes:

Later respone, vasodilation, and increase capillary permeability

Prostaglandins:

Vaodilation, fever, pain, and increase capillary permeability

Kinins:

Vasodilation, increase permeability, and pain

Complement system:

vasodilation and increase capillary permeability, chemotaxis, and increased histamine response

Function of cellular elemets in the inflammatory:

Neutrophils:

Phagocytosis of microorganism

Basophils:

Release of histaime leading to inflammation

Eosinophils:

Numbers are increased in allergic reactions

T-lymphocytes:

activated in cell mediated immune response

B-lymphocytes:

Produce antibodies

Function of monocytes:

Phagocytosis

Macrophages:

Active in phagocytosis, mature monocytes that have migrated into tissue from blood

Local effects of inflammation:

Redness and warmth, swelling, pain, and loss of function

Types of exudate:

Serous:

Watery, consist of fluids, some protein, and WBC’s

Fibrinous:

Thick,sticky, high cell and fibrin count

Purulent:

Thick, yellow-green, contains more leukocytes and microorganism

Abcess:

Localized pocket of purulent exudate in solid tissue

Heorrohagic exudate:

Present when blood vessels are damaged

systemic effects of inflammation:

Fatigued, anorexia, malaise, headache, and mild fever (common if inflammation is extensive, and release of pyrogens)

Changes in blood with inflammation:

Leukocytosis: Increased number of WBC’s, especially neutrophils

Differential count: Proportion of each WBC is altered, depending on cause

Plasma proteins: Increased fibrinogen and thrombin

C-reactive protein:Protein not found in blood, appears with acute inflammation and necrosis within 24-48hr

Increase erthrocyte sedimentation rate: Elevated plasma proteins increase rate at RBC settle in sample

Cell enzymes: Released from necrotic cells and enter tissue fluids and blood; may indicate site of inflammation

Complications may be local or systemic with inflammation on infections:

• Microorganism can more easily penetrate when skin or mucosa is damaged and blood spupply is impaired

• Some microbes resist phagocytosis

• Inflammatory exudate provides an excellent medium for microorgansim to reproduce and colonize

Complications may be local or systemic with inflammation from skeletal muscle spasms:

• Intiate inflammation by musculoskeletal injuries

• Spasma likely to force bone or spasm out of normal alignment, causing additional pressure on nerves, increase pain

Chronic inflammation:

• Follows acute episodes of inflammation

• Less swelling and exudate

• Presence of more lymphocytes, macrophages, and fibroblast

• More tissue destruction

• More collagen produce, resulting in more fibrous scar tissue

• Granuloma may develop around foreign object

Periodic exacerbation of acute inflammation:

Deep ulcers may result from severe or prolonged inflammation

What causes deep ulcers from prolonged inflammation? Complications that it can lead to:

Cell necrosis and lack of cell regeneration that causes erosion of tissue. Peroforation of viscera and extensive scar tissue formation

Types of healing: resolution

• Minimum tissue damage

• Damage cells recover, and tissue returns to normal within short period

• Ex: Mild sunburn

Types of healing: Regeneration

• Occurs in damaged tissue in which cells are capable of mitosis

• Damaged tissue is replaced with identical tissue by proliferation of nearby cells

Types of healing: Replacement

• Functional tissue replaced by scar tissue

• Extensive tissue damage of cells unable to undergo mitosis in brain and myocardium

• Damaged tissue is replaced by connective tissue (scar, and fibrous tissue)

Wound healing: First intention occurs when:

• Wound is clean, free of foreign material

• No necrotic tissue is present

• Edges are held close together

• Ex: Surgical incision

Wound healing: Second intention

• Occurs with larger breaks in tissue

• Results in: More inflammation, longer healing period, and formation of more scar (fibrous) tissue

Definition of collagen:

Protein that is the basic component of scar tissue and provides strength for new repair

Factors that promote healing:

No further trauma to site, absence of infection, clean and undisturbed wound, adequate hemoglobin, effective circulation, youth, and nutrition (protein, Vitamins A and C)

Factors that delay healing:

Advanced age, poor nutrition, dehydration, anemia, circulatory problems, certain chronic disease, irritation and bleeding, infection, radiation, chemotherapy, and prolonged use of glucorticoids

Complications of scar formation:

Loss of normal cells and specialized structures: hair follicles, receptors, and nerves

Contractions and obstructions of scar formation:

Scar tissue is nonelastic, and can restrict range of movement

Hypertrophic scar tissue with that involves comlications of scar formation:

Lead to hard ridges of scar tissue and keloid formation

When ulceration occur from complications of scar formation, what happens to blood?

Blood supply may be impaired around scar, and results in further tissue breakdown