Inflammation
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| Injurious agents Physical | mechanical objects causing trauma, excessive heat or cold, radiation
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| Injurious agents Chemical internal irritants | (substances manufactured in body; ex: hydrochloric acid in stomach, as in GERD)
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| Injurious agents Chemical external irritants | strong acids , alkalis, poisons, irritating gases
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| bacteria | Microorganisms
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| viruses | Microorganisms
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| fungi | Microorganisms
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| parasites | Microorganisms
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| Function of inflammation | allows repair of injured area to proceed at faster pace
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| --Contains injury --Destroys microorganisms | Inflammaiton
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| also can occur in absence of infection. | Inflammation
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| Always present with infection | Inflammation
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| chronic Inflammation | Tissue is repeatedly destroyed & repaired, impairing healing.
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| autoimmune diseases | Disproportionate response to the irritating stimulus or against inappropriate target,
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| IBD—Crohn’s disease or ulcerative colitis | autoimmune diseases
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| Brings fluid, dissolved substances, blood cells to tissues where invasion or damage occurred | Adaptive response to injury or illness
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| Invader neutralized, eliminated, destroyed tissue removed healing initiated | Adaptive response to injury or illness
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| debrides, allows healing | Adaptive response to injury or illness Phagocytosis
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| same events occur regardless of cause | Adaptive response to injury or illness Nonspecific
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| Pain | 1 of the 5 signs of inflammation
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| Swelling | 1 of the 5 signs of inflammation
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| Redness | 1 of the 5 signs of inflammation
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| Heat | 1 of the 5 signs of inflammation
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| Impaired Function of Part, if injury severe | 1 of the 5 signs of inflammation
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| inflammation sufix | "-itis"
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| Margination | leukocytes line up inside vessel walls near injured area
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| emigration | occurs, when they move through the vessel wall into the tissue spaces.
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| Hyperemia | causes redness and heat characteristic of inflammation. Blood flow slows in dilated areas.
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| leukocytosis | leukocyte leakage into tissue
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| leukocytosis | The bone marrow produces more WBC’s in response to
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| organ function | Increased fluid in pleural or pericardial cavity can seriously affect
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| Inflammation can raise WBC’s from | 4500-11,000 to over 20,000 when inflammation occurs.
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| Joint mobility may be | impaired as well.
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| Pain is from | accumulating fluid putting pressure on nerve endings and effects of irritating chemical mediators
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| histamine | irritating chemical mediators
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| kinins | irritating chemical mediators
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| prostaglandins | irritating chemical mediators
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| 1st stage in inflammation | Vascular and Cellular Responses
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| Blood vessels constrict at site of injury | Vascular and Cellular Responses step 1
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| Rapidly followed by vasodilation caused by histamine release from injured tissues, increasing blood flow to area | Vascular and Cellular Responses step 2
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| Vascular permeability increases | Vascular and Cellular Responses step 3
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| Leukocytes leak into interstitial spaces; bone marrow makes more leukocytes and WBC count ↑’s in response to inflammation (leukocytosis— to 20,000 +) | Vascular and Cellular Responses step 4
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| Swelling and pain appear | Vascular and Cellular Responses step 5
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| Hemorrhagic | blood from ruptured blood vessels, red and thick
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| Purulent | pus; usually opaque, milky; normally indicates presence of infection, contains large # of cells & necrotic debris
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| Serous | typically accompanies mild inflammation; clear or straw-colored, then watery
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| 2nd stage in inflammation | Exudate (“exude” or “ooze”) Production
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| Made of fluid that escapes from blood vessels, dead phagocytic cells, and dead tissue cells and products they release (serous, purulent, or hemorrhagic | Exudate (“exude” or “ooze”) Production step 1
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| Fibrinogen converts to fibrin in the tissues with thromboplastin and platelets to form interlacing wall to close off the area and prevent spread of injurious agent | Exudate (“exude” or “ooze”) Production step 2
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| Exudate clears away injurious agent by way of lymphatic drainage | Exudate (“exude” or “ooze”) Production step 3
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| nerves | Poor regenerative capacity tissues
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| muscles | Poor regenerative capacity tissues
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| elastic tissues. | Poor regenerative capacity tissues
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| Epithelial tissues of skin | good regenerative capacity
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| GI tract | good regenerative capacity
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| bone | good regenerative capacity
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| lymph | good regenerative capacity
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| bone marrow | good regenerative capacity
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| If regeneration is not possible | repair occurs by scar formation
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| scar formation, mainly made of | collagen
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| 3rd stage of inflammation | Reparative Phase
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| Granulation tissue | appears early in this phase; fragile, gelatinous, pink or red tissue (from newly formed capillaries)
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| Repair of injured tissues by regeneration or replacement with scar tissue; damaged tissues replaced with connective tissue | Reparative Phase step 1
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| Regeneration replaces destroyed tissue cells by cells that are identical or similar in structure and function | Reparative Phase step 2
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| Cells are organized so patterns of cells and function of tissue are restored | Reparative Phase step 3
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| Granulation tissue—appears early in this phase; fragile, gelatinous, pink or red tissue (from newly formed capillaries) | Reparative Phase step 4
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| Histamine | is Key chemical mediator of inflammation
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| Stored in mast cells in skin, bronchial tree, GI tract, blood vessels | Histamine
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| Directly stimulates pain receptors, ↑ capillary permeability | Histamine
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| Dilates nearby blood vessels | Histamine
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| Anaphylaxis (life-threatening allergic reaction)— | Histamine
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| Anaphylaxis | (life-threatening allergic reaction)—rapid, large scale, widespread release of chemical mediators of inflammation throughout body
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| H1 receptors | vascular system, bronchial tree
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| H2 receptors | primarily in stomach
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| Histamine receptors | H1 receptors: vascular system, bronchial tree H2 receptors: primarily in stomach
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| Benadryl (diphenhydramine), | block H1 receptors
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| Vistaril (hydroxyzine) | block H1 receptors
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| Zantac (ranitidine), | block H2 receptors
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| Tagamet (cimetidine) | block H2 receptors
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| Common diseases | Appendicitis Crohn’s disease Arthritis—most common inflammatory disorder and leading cause of disability in U.S. Nephritis Peptic ulcers SLE (lupus) RA (rheumatoid arthritis) Inflammatory bowel disease
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| Erythrocyte sedimentation rate normal male | 0–15 mm/h
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| Erythrocyte sedimentation rate normal female | 0–25 mm/h
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| WBC with differential | WBC 4,500-11,000
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| C-reactive protein (CRP) | people with high levels may have ↑ risk for heart disease from inflammatory arterial damage
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| ESR measures | how fast erythrocytes (RBCS) settle in tube over given period of time
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| ESR | Erythrocyte sedimentation rate
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| RICE | Rest Ice Compression Elevation
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| Ice | 20 min q 2-3 hrs
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| Compression | i.e. ace wrap--√ color, sensation, temp, extremity ROM, pulses
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| preventing further injury | minimize mobility & wt-bearing: splints, slings, wheelchairs, walkers, crutches
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| Especially during 1st 24-48 hrs after injury: | RICE
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| flaxseed oil | anti-inflammatory
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| fish oil | anti-inflammatory
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| walnut oil | anti-inflammatory
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| omega 3’s | flaxseed oil, fish oil, and walnut oil
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| vitamin C for cellular repair | nutrients to support healing
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| protein | nutrients to support healing
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| carbs | nutrients to support healing
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| NSAIDS--Nonsteroidal Anti-Inflammatory Drugs | Inhibit synthesis of prostaglandins, lipids in all tissues that promote inflammation
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| Analgesics | pain NSAIDS
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| antipyretics | fever NSAIDS
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| Ibuprofen (Motrin), | ↓’s pain & fever-NSAIDS
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| Naproxen (Aleve), | ↓’s pain & fever-NSAIDS
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| aspirin | ↓’s pain & fever-NSAIDS
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| Indomethacin (Indocin), | ↓’s pain & fever-NSAIDS
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| Celecoxib | ↓’s pain & fever-NSAIDS
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| Celebrex | Cox 2 inhibitor-↓’s pain & fever-
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| peptic ulcers | Avoid NSAIDS or use with caution in client
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| anticoagulants | Avoid NSAIDS or use with caution in client
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| ↓ liver or kidney function | Avoid NSAIDS or use with caution in client
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| Corticosteroids (Glucocorticoids) | Comes from the adrenal gland
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| Natural hormones, released by adrenal cortex--↓ swelling & pain | Corticosteroids (Glucocorticoids)
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| Potent anti-inflammatory agents | Corticosteroids (Glucocorticoids)
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| Generally for short-term treatment due to potentially serious side effects | Corticosteroids (Glucocorticoids)
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| Cortisone, Prednisone, Dexamethasone, Methylprednisolone | Corticosteroids (Glucocorticoids)
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| ↓Immune response, ↑blood glucose, ↑WBC, mood swings, fluid retention, GI ulcers | Corticosteroids (Glucocorticoids) Adverse effects
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| To treat pain associated with inflammation if NSAIDS alone insufficient | Analgesics
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| Morphine, Oxycodone (opioids) | Analgesics
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| Monitor respiratory rate | Analgesics
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| Monitor pain status | Analgesics
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| Sedation, ↓ LOC, CNS depression, nausea, vomiting, constipation | Analgesics
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| EPA and DHA | Fish Oils
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| Also lower triglycerides | Fish Oils
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| May interact with NSAIDS to increase susceptibility to bruising, nosebleeds, or other sources of bleeding | Fish Oils
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