front 1 First line of defense | back 1 Physical and chemical barriers such as skin mucous membranes tears saliva and gastric acid |
front 2 Second line of defense | back 2 Nonspecific inflammatory response phagocytosis and interferons |
front 3 Third line of defense | back 3 Specific immune response involving antibodies and sensitized lymphocytes |
front 4 Inflammation | back 4 Body's nonspecific response to tissue injury producing redness swelling warmth pain and possible loss of function |
front 5 Common causes of inflammation | back 5 Infection, physical injury, chemicals, ischemia, allergic reaction, extreme temperatures, foreign bodies |
front 6 Bradykinin | back 6 Chemical released from injured cells that activates pain receptors |
front 7 Histamine | back 7 Released from mast cells causing vasodilation and increased capillary permeability |
front 8 Basic steps of inflammatory process | back 8 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 |
front 9 Normal capillary exchange | back 9 Hydrostatic pressure pushes fluid out at arterial end and osmotic pressure pulls fluid back at venous end |
front 10 Capillary change in inflammation | back 10 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 |
front 11 What are the four physiologies of inflammation and local effects? | back 11 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) |
front 12 Exudate | back 12 Fluid rich in protein cells and electrolytes that accumulates in inflamed tissue |
front 13 Chemotaxis | back 13 Attraction of white blood cells to the site of injury |
front 14 Diapedesis | back 14 Movement of leukocytes through capillary walls into tissue |
front 15 Hyperemia | back 15 Increased blood flow to inflamed tissue causing redness and warmth |
front 16 Cardinal signs of inflammation | back 16 Redness, heat, swelling, pain, and sometimes loss of function |
front 17 Serous exudate | back 17 Watery fluid with protein and white blood cells |
front 18 Fibrinous exudate | back 18 Thick sticky exudate with fibrin that increases scar risk |
front 19 Purulent exudate | back 19 Pus containing leukocytes microbes and debris usually from bacterial infection |
front 20 Abscess | back 20 Localized pocket of purulent exudate in solid tissue |
front 21 Hemorrhagic exudate | back 21 Exudate containing blood due to vessel damage |
front 22 Systemic effects of inflammation | back 22 Fever (pyrexia), fatigue, malaise (feeling unwell), headache, anorexia (loss of appetite) |
front 23 Cause of fever in inflammation | back 23 Pyrogens released by macrophages reset hypothalamic temperature control |
front 24 Leukocytosis | back 24 Increased white blood cell count during inflammation |
front 25 C reactive protein | back 25 Protein appearing in blood during acute inflammation and necrosis |
front 26 Erythrocyte sedimentation rate | back 26 Lab test elevated in inflammation due to increased plasma proteins |
front 27 Chronic inflammation | back 27 Long term inflammation with more macrophages, lymphocytes, fibroblasts, tissue destruction, and scarring |
front 28 Granuloma | back 28 Mass of necrotic tissue surrounded by connective tissue in chronic inflammation |
front 29 Complications of chronic inflammation | back 29 Ulcers, local complications of specific site of inflammation, Infections, Skeletal Muscle spasms |
front 30 Aspirin | back 30 Decreases prostaglandin synthesis at the site of inflammation (anti-inflammatory) and reduces pain (analgesic) and reduces fever (antipyretic) |
front 31 NSAIDs | back 31 Anti inflammatory drugs that reduce prostaglandin synthesis and relieve pain fever and inflammation. Same thing as aspirin |
front 32 Acetaminophen | back 32 Analgesic and antipyretic drug but not anti inflammatory |
front 33 NSAID COX-2 inhibitor | back 33 Anti-inflammatory and analgesic drug |
front 34 Corticosteroids | back 34 Strong anti inflammatory drugs that decrease permeability and suppress immune response |
front 35 Side effects of corticosteroids | back 35 Delayed healing, high blood glucose, fluid retention, tissue atrophy, adrenal suppression |
front 36 RICE therapy | back 36 Rest ice compression elevation used to reduce swelling and pain |
front 37 Resolution healing | back 37 Minimal tissue damage with complete return to normal structure |
front 38 Regeneration healing | back 38 Replacement of damaged tissue with identical new cells through mitosis |
front 39 Replacement healing | back 39 Extensive damage repaired by connective tissue forming scar |
front 40 Healing by first intention | back 40 Clean wound with edges close together minimal inflammation and small scar |
front 41 Healing by second intention | back 41 Large wound with more inflammation slower healing and greater scar formation |
front 42 Healing process | back 42 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 |
front 43 Granulation tissue | back 43 Fragile vascular connective tissue that fills wound during healing |
front 44 Role of fibroblasts in healing | back 44 Produce collagen that strengthens repaired tissue |
front 45 Scar tissue characteristics | back 45 Nonfunctional fibrous tissue lacking specialized structures |
front 46 Factors that promote healing | back 46 Youth, good nutrition, adequate hemoglobin, effective circulation, clean wound, absence of infection |
front 47 Example good nutrition factor | back 47 Protein and vitamins A and C support collagen formation and tissue repair |
front 48 Factors delaying healing | back 48 Old age, poor nutrition, anemia, diabetes, infection, radiation, chemotherapy, prolonged steroid use |
front 49 Contracture | back 49 Shrinking nonelastic scar tissue causing joint deformity or restricted movement |
front 50 Stenosis | back 50 Narrowing of tubes or ducts caused by scar tissue |
front 51 Adhesions | back 51 Bands of scar tissue joining surfaces that normally move freely |
front 52 Hypertrophic scar | back 52 Excess collagen forming raised thick scar |
front 53 Keloid | back 53 Excessive overgrowth of scar tissue beyond wound margins |
front 54 Ulceration | back 54 Impaired blood supply around scar area |
front 55 Burn | back 55 Thermal electrical or chemical injury causing acute inflammation and tissue destruction |
front 56 First degree burn | back 56 Superficial burn affecting epidermis only and healing without scar |
front 57 Second degree burn | back 57 Partial thickness burn affecting epidermis and part of dermis causing blisters pain and possible scarring |
front 58 Third degree burn | back 58 Full thickness burn destroying all skin layers often charred and requiring grafting |
front 59 Rule of nines | back 59 Method estimating percent body surface area burned |
front 60 Eschar | back 60 Dead coagulated tissue forming hard crust over full thickness burn |
front 61 Escharotomy | back 61 Surgical incision through eschar (damaged tissue) to relieve pressure and restore circulation |
front 62 Major burn complication hypovolemic shock | back 62 Loss of fluid and protein from bloodstream decreases blood volume and pressure |
front 63 Major burn complication infection | back 63 Loss of skin barrier increases risk of bacterial invasion |
front 64 Burn hypermetabolism | back 64 Increased metabolic demand requiring more protein and calories |
front 65 Reason burn healing difficult fluid loss | back 65 Massive fluid and protein leakage causes shock and tissue damage |
front 66 Reason burn healing difficult tissue destruction | back 66 Extensive loss of regenerative structures requires grafting and prolonged repair |
front 67 Skin graft | back 67 Transplantation of skin to cover large burn wounds and promote healing |
front 68 Compression garments | back 68 Used after burns to reduce hypertrophic scar formation |