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