First line of defense
Physical and chemical barriers such as skin mucous membranes tears saliva and gastric acid
Second line of defense
Nonspecific inflammatory response phagocytosis and interferons
Third line of defense
Specific immune response involving antibodies and sensitized lymphocytes
Inflammation
Body's nonspecific response to tissue injury producing redness swelling warmth pain and possible loss of function
Common causes of inflammation
Infection, physical injury, chemicals, ischemia, allergic reaction, extreme temperatures, foreign bodies
Bradykinin
Chemical released from injured cells that activates pain receptors
Histamine
Released from mast cells causing vasodilation and increased capillary permeability
Basic steps of inflammatory process
1. Injury 2. Bradykinin released from injured cells that activates pain receptors 3. Pain stimulates mast cells and basophils to release histamine 4. Bradykinin and histamine cause capillary dilation, increase blood flow and capillary permeability. 5. Break in skin allows bacteria to enter tissue; neutrophils and monocytes migrate to injury site 6. Neutrophils and macrophages phagocytize bacteria
Normal capillary exchange
Hydrostatic pressure pushes fluid out at arterial end and osmotic pressure pulls fluid back at venous end
Capillary change in inflammation
Injured cells release chemical mediators that cause vasodilation and increase permeability to allow proteins, fluid, and leukocytes to leave capillaries to form exudate and move towards site of injury to phagocytize foreign material
What are the four physiologies of inflammation and local effects?
1. Vascular Response (Causes local vasodilation and increased capillary permeability) 2. Cellular Response (WBC attracted by chemotaxis) 3. Excess fluid can collect in interstitial space (Exudate) 4. Inactivation of chemical mediators begins resolution of inflammation (Resolvins/metabolites of omega-3 fatty acids and lipoxins/derived from arachidonic acid)
Exudate
Fluid rich in protein cells and electrolytes that accumulates in inflamed tissue
Chemotaxis
Attraction of white blood cells to the site of injury
Diapedesis
Movement of leukocytes through capillary walls into tissue
Hyperemia
Increased blood flow to inflamed tissue causing redness and warmth
Cardinal signs of inflammation
Redness, heat, swelling, pain, and sometimes loss of function
Serous exudate
Watery fluid with protein and white blood cells
Fibrinous exudate
Thick sticky exudate with fibrin that increases scar risk
Purulent exudate
Pus containing leukocytes microbes and debris usually from bacterial infection
Abscess
Localized pocket of purulent exudate in solid tissue
Hemorrhagic exudate
Exudate containing blood due to vessel damage
Systemic effects of inflammation
Fever (pyrexia), fatigue, malaise (feeling unwell), headache, anorexia (loss of appetite)
Cause of fever in inflammation
Pyrogens released by macrophages reset hypothalamic temperature control
Leukocytosis
Increased white blood cell count during inflammation
C reactive protein
Protein appearing in blood during acute inflammation and necrosis
Erythrocyte sedimentation rate
Lab test elevated in inflammation due to increased plasma proteins
Chronic inflammation
Long term inflammation with more macrophages, lymphocytes, fibroblasts, tissue destruction, and scarring
Granuloma
Mass of necrotic tissue surrounded by connective tissue in chronic inflammation
Complications of chronic inflammation
Ulcers, local complications of specific site of inflammation, Infections, Skeletal Muscle spasms
Aspirin
Decreases prostaglandin synthesis at the site of inflammation (anti-inflammatory) and reduces pain (analgesic) and reduces fever (antipyretic)
NSAIDs
Anti inflammatory drugs that reduce prostaglandin synthesis and relieve pain fever and inflammation. Same thing as aspirin
Acetaminophen
Analgesic and antipyretic drug but not anti inflammatory
NSAID COX-2 inhibitor
Anti-inflammatory and analgesic drug
Corticosteroids
Strong anti inflammatory drugs that decrease permeability and suppress immune response
Side effects of corticosteroids
Delayed healing, high blood glucose, fluid retention, tissue atrophy, adrenal suppression
RICE therapy
Rest ice compression elevation used to reduce swelling and pain
Resolution healing
Minimal tissue damage with complete return to normal structure
Regeneration healing
Replacement of damaged tissue with identical new cells through mitosis
Replacement healing
Extensive damage repaired by connective tissue forming scar
Healing by first intention
Clean wound with edges close together minimal inflammation and small scar
Healing by second intention
Large wound with more inflammation slower healing and greater scar formation
Healing process
1. Injury 2. Blood clot forms and seals area 3. Inflammation develops in surrounding area 4. Granulation tissue grows into gap 5. Epithelial cells undergo mitosis, closing wound while granulation tissue forms 6. Fibroblasts and connective tissue cells enter area, producing collagen 7. Scar tissue remains, non-functional with no specialized structures
Granulation tissue
Fragile vascular connective tissue that fills wound during healing
Role of fibroblasts in healing
Produce collagen that strengthens repaired tissue
Scar tissue characteristics
Nonfunctional fibrous tissue lacking specialized structures
Factors that promote healing
Youth, good nutrition, adequate hemoglobin, effective circulation, clean wound, absence of infection
Example good nutrition factor
Protein and vitamins A and C support collagen formation and tissue repair
Factors delaying healing
Old age, poor nutrition, anemia, diabetes, infection, radiation, chemotherapy, prolonged steroid use
Contracture
Shrinking nonelastic scar tissue causing joint deformity or restricted movement
Stenosis
Narrowing of tubes or ducts caused by scar tissue
Adhesions
Bands of scar tissue joining surfaces that normally move freely
Hypertrophic scar
Excess collagen forming raised thick scar
Keloid
Excessive overgrowth of scar tissue beyond wound margins
Ulceration
Impaired blood supply around scar area
Burn
Thermal electrical or chemical injury causing acute inflammation and tissue destruction
First degree burn
Superficial burn affecting epidermis only and healing without scar
Second degree burn
Partial thickness burn affecting epidermis and part of dermis causing blisters pain and possible scarring
Third degree burn
Full thickness burn destroying all skin layers often charred and requiring grafting
Rule of nines
Method estimating percent body surface area burned
Eschar
Dead coagulated tissue forming hard crust over full thickness burn
Escharotomy
Surgical incision through eschar (damaged tissue) to relieve pressure and restore circulation
Major burn complication hypovolemic shock
Loss of fluid and protein from bloodstream decreases blood volume and pressure
Major burn complication infection
Loss of skin barrier increases risk of bacterial invasion
Burn hypermetabolism
Increased metabolic demand requiring more protein and calories
Reason burn healing difficult fluid loss
Massive fluid and protein leakage causes shock and tissue damage
Reason burn healing difficult tissue destruction
Extensive loss of regenerative structures requires grafting and prolonged repair
Skin graft
Transplantation of skin to cover large burn wounds and promote healing
Compression garments
Used after burns to reduce hypertrophic scar formation