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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 |