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| release histamine in response to allergy, thermal or light stimulation |
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| work in defense system, eat viral/bacterial/waste |
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| Potassium hydroxide exam with fungal culture |
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| scrapings taken for a sample |
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| surgically cutting out a portion of the questionable mass |
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| moisturize, sunscreen, protect from irritants |
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| emollients after baths, mild soaps |
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| harsh chemicals, soaps and dryer sheets |
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| apply after bathing, use fragrence free, hyopallergenic |
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| anything that causes sensitive individuals to have a reaction, pollen, bee sting, fragrences |
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| substance which is harsh to the skin, i.e. lye, bleach. surface related |
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| eczema predisposition to being itchy |
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| protitic, red, weeping crusted lesions. associated with rhinitis and asthma |
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| chronic, superficial, inflammatory usually onset in infancy. Triggers, food allergies, irritants, stress |
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| dry skin leads to crack/fissure/loss of barrier function |
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| focus on education, emotional support, impaired tissue integrity, sleep deprivation r/t physical discomfort, risk for infection |
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| no cure, hydrate, lubricate, reduce itching, inflammation, infection |
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| simple chronic itching. atopic patients or familial contact dermatitis. remove irritants and topical steroids to improve s/s |
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| contact dermatitis irritants |
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| allergens, harsh chemicals, metals, mechanical irritations, body substances |
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| Stevens- Johnson Syndrome |
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| severe expression of erythema multiformi basically loses all protection without eschar. |
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| small as possible, systemic, chills, fever, malaise, cause unknown. severe reactions to penicillin may be causative. can be fata. |
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| scales, plaque or small lesions |
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| chronic, noninfectious disease, 1-3% of population. mild 3-10$ severe >10% |
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| otc saliculic acid, coal tar. phototherapy, steroids less potent on head, these people go to tanning beads |
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| moderate to severe psoraisis treatements |
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| phototherapy, systemics (cyclosporin, methotrexate, acitretrin, off label systemics (accutane, etc) biologics (TNF, T-Cells) over proliferation of t-cells one atop the other |
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| pressure (bedsores or decubitus |
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| friction, shear, dampness ulcers or pressure |
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| ususally peripheral, pvd, huge issues. |
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| nonblanchin, intact skin with erythema (redness) in darker skin, discoloration of the skin, warmth, edema, notable. |
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| partial thickness, not through the skin yet. ulcer is superficial, abrasion, rash, etc. |
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| full thickness not through underlying fascia |
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| Wound VAC, closed to air, gause with antibiotics inserted then covered with a cover. |
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| frequent position change, meet nutritional needs, frequent skin assessments |
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| network of cells, tissues, organs, to defent against antigens. |
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| normal immune system function |
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| neutralize, eliminate or destroy threats to the body. |
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| developing the pediatric immunity |
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| children need to be exposed to allergens, viruses, etc. |
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| hives, resulting from allergens |
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| 1st inflammatory response |
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| leukocytes go to the site of invasion where organizms or cellular debris is engulfed by phagocytosis |
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| a specific response that causes a protective reaction to a foreign protein |
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| 1st immune response trigger |
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| intensity response depends on type/severity of type of invasion. |
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| Nonspecific activation of immune response |
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| systemic response to trigger |
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| short term, 1-2 weeks injurious agent removed healing occurs with tissue repair/scarring |
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| slower onset months-years, can be debilitating with severe tissue damage i.e. arthritis |
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| baso/platelets release histamine, serrotonin, prostaglandin, leukotrienes |
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| hyperemia (vasodialation) redness, warmth, swelling (edema |
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| leukocytes swarm to site (chemotaxis) to phagocytosis of offending agent and it's debris by neutrophils and monocytes |
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| hyperemia - redness/warmth, protein shift causes edema, increased pressure of fluid on the nerves, i.e. pain, loss of function may develop if cells lack nutrients or if swelling interferes with tissue mechanics |
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| systemic inflammation effects |
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| malaise, fatigue, headache, anorexia, fever common from pyrogens from WBC/macrophages. infection can cause severe fever. |
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| ASA, decreases prostaglandin synthesis at site, reduces fever, pain. inexpensive, anti-platelet effects, prolongs clotting time, can cause ulcers. |
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| nsaids block prostaglandin synthesis to stop inflammation, analgesic/antipyretic effect, similar to ASA |
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| immune-modulators, similar to natural steroids. |
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| decrease immune response, must wean off steroids, block prostaglandin response. long term use associated with multiple effects. long term therapy leads to long term effects. |
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| immune compromised, mucus ulcers, growth retardation, retention of sodium and water. |
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| alternative inflammation therapy |
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| RICE, analgesics, antibiotics, physiotherapy. |
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phases - inflammatory phase, reconstruction phase
requirements - adequate nutriion, blood supply, o2 |
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