adult 1 test 1 vocabulary

complement system

- major mediator of the inflammatory response that is triggered by antibodies (IgM, IgE) (the liver helps to synthesize and produce these proteins); series of chemical reactions activated by antibody-antigen interation - check liver in prep to make sure its adequate to produce the proteins that support healing - when activated, the components occur in sequential order (relay) involving 2 pathways - end result: bacteria dies -ex. fever production

infection

-Causes of infection: biologic agents; microorganisms, bacteria, viruses, fungi, protozoa; pneumonia microbe -anticipate M.D. orders to: 1. obtain a (wound or sputum) culture ex. urine sample; this identifies what is causing the infection 2. administer the antibiotic specific to target the identified microbe

inflammatory response

-redness, heat, pain, swelling -loss of function/ slowing down body functions: forces the body to rest the damaged area so that it can heal -increased WBC count with a shift to the left (new baby WBCs, aka bands, being created) -increased plasma proteins -fever is okay and normal with inflammatory response (up to 103 F, unless in older and younger pt.); only treat the fever if it is bothersome to the patient; more fluids and food during times of fever because the calorie demands increase...calorie need increases 7% q 1 degree>100) - nausea and anorexia -increased pulse and respiratory rate -malaise: general icky feeling -there are all normal after surgery!!!!

Monocytes/ Macrophages

-second type of phagocytic cells to migrate to site of injury from circulating blood -attracted to the site by chemotactic factors -arrive within 3-7 days after the onset of inflammation - on entering tissue spaces, monocytes transform into macrophages (meld together) -assist in phagocytosis of inflammatory debris -Macrophages have a long life span and can multiply -macrophages are important for cleaning the area before healing can occur -stay in damaged tissues for weeks -cells may fuse to for a multinucleated giant cell

inflammation

-sequential response to cell injury; mechanism is basically the same regardless of the injuring agent -neutralizes and dilutes the inflammatory agent -removes necrotic materials -always present with infection -infection is not always present with inflammation -inflammation is the first stage to wound healing -supports the immune system -begins intraop, defends, protects, and prepares for healing...establishes an environment for healing and repair -intensity relates to extent of injury and severity and reactive capacity of the injured person -Causes on inflammation: nutritional imbalances, trauma, dead cells, parasites, ischemia (low blood flow, ex. DVT), allergies (immune response), surgery, heat, chemicals, infection

Prevention and control of MRSA

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Prevention and control of VRSE

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types of inflammatory responses

1. Acute: indicates no post-op complications; full healing occurs in 2-3 weeks, usually leaving no residual damage; neutrophils are the predominant cell type at the site of the inflammation; normal and desired 2. subacute: usually leaves no residual damage; neutrophils are the predominant cell type at the site of inflammation; persists longer than acute inflammation (ex. weeks-months, endocarditis) 3. Chronic: may last for years; injurious agent persists or repeats injury to site (ex. Oral bacteria and gum disease; may result from changes in the immune system (ex. autoimmune diseases); predominant cell types involved are lymphocytes and macrophages; this type of inflammation relates to cancer and diabetes

clotting process

1. vessel injury/vessel spasm 2. platelet aggregation (stimulated by serotonin) 3. platelet plug formed 4. clotting cascade: BLOOD CLOT is outcome -prothrombin to thrombin -fibrinogen to fibrin **Also clotting cascade (12 factors) - Factor XII-hageman factor activates kinin system and plasminogen-plasmin and activates complement cascade

Sequence of events for a macrophage attacking a virus

1. virus enters the body cells 2. macrophage engulfs the virus 3. macrophage has cytokine message release IL-1 which call over T helper cells 4. T-helper cell binds to macrophage and that stimulates the production of cytokines IL-1 and TNF by the macrophage and IL-2 and y-interferon by the T-cell 5. IL-2 instructs other T-helper cells and T cytotoxic cells to multiply: T helper cells release cytokines causing B cells to multiply and produce antibodies 6. t cytotoxic cells and natural killer cells destroy infected body cells 7. antibodies bind to the virus and mark it for macrophage destruction 8. Memory B and T cells remain behind to respond quickly if the same virus attacks again B cells are memory cells that remember the virus and release the antibodies for that specific virus; when the virus comes a second time the body is better able to fight it off bc the body remembers it

White Blood Cells

Differential Lab Data: -Normal WBC count: 5,000-10,000 - if increased= more WBC being put out because more are being used in order to maintain homeostasis -inflammation will NOT cause WBC to go higher than 10,000 but infection will -if it goes to 12,000 that is beyond normal range and due to infection -get baseline WBC count before surgery -band count exceeding 8% of total WBC then it is considered a shift to the left and indicates severe inflammation -increased neutrophils=acute inflammation -increased bands= prolonged acute inflammation -increased monocytes=chronic inflammation -increased eosinophils= destroy parasites, control effects of histamine and leukotrienes; respond to allergic reaction

cytokines

WBCs secrete to send messages to cause other cells to act to support the immune system; aka chemicals in the blood that cause cells to move or do something; keep the immune or inflammation process going the release of cytokines cause pain (specifically histamine, kinins, prostaglandins) they are WBCs and secretions of WBCs new cancer meds and RA meds are made from cytokines; interferon for HIV is made from cytokines Macrophages produce cytokines that support the inflammatory process IL-1, IL-6, Tumor necrosis factor- alpha stimulate the liver to produce acute phase proteins

anaplasia

Worst cell change! immature or embryonic form type of cancerous cell malignancy change in cell lack of differentiation between cells with a greater ability to multiply maladaptive response sublethal changes might reverse when stimulus is reversed but obviously not lethal injuries (you're already dead); ex. chronic inflammation can keep in place)

treatments for inflammation

antihistamines: interrupt histamine corticosteroids: (prednisone) interfere with lymphocytes and arachidonic acid non-steroidal antiinflammatory meds (NSAIDs): (aspirin, motrin, advil, naproxyn) to interrupt prostaglandin activity antibiotics: if the cause is microbial nutrition rest balanced with Turn, Cough, Deep Breathe (TCDB) plenty of fluids

Basophils

carry histamine and heparin in their granules that are released during inflammation have limited phagocytic capabilities

dysplasia

changes in size, shape, and appearance maladaptive response not always a bad thing but can turn cancerous if not attended to ex. looked at in pap smear- precancerous cell changes

atelectasis

collapsed alveoli...you should turn them on their side and support deep breathing can be related to blocking secretions lung congestion

atrophy

decrease in size of tissue or organ due to decreased number of cells ex. muscle size decreases with aging

immunosenescense

decreased immunity with age

evisceration

dehiscence plus protrusion of underlying organs to skin surface

Neutrophils

first leukocytes to arrive at site of injury (90mins to 6-12 hours) phagocytize bacteria, other foreign material, and damaged cells short life span of 24-48 hours body has a 6 day supply of mature neutrophils and when they are used up, they are replaced by bands Pus is composed of dead neutrophils at the site of injury, digested bacteria, and other cell debris bone marrow releases more neutrophils in response to infection resulting in EVELVATED WBC

autoimmunity

immune response against self mistake ex. Systemic lupus erythematosus, Rheumatoid arthritis, Diabetes mellitus 1, Inflammatory bowel disease, scleroderma, etc.

immunodeficiency

immune system does NOT provide adequate protection for the body impairment of phagocytosis, humoral response (b cells), cell mediated response (t-cells fungi, viruses, tumors), complement (antibodies cause bacteria death) corticosteroids cause immunodeficiency

hyperplasia

increase in # of cells ex. increased estrogen circulating in the blood to prepare pregnant women for lactation

hypertrophy

increase in size of cell positive ex. the uterus with pregnancy negative ex. after a heart attack, cardiac cells are hypertrophic because they are working harder -bigger is not always better, it mainly weakens

phlebitis

inflammation of a blood vessel

exudate

part of the inflammatory response consists of fluid and leukocytes that move from the circulation to the site of injury nature and quantity depend on the type and severity of the injury and the tissues involved serosanguinous: surgical drain, some redness, over time it'll become less red and more clear serous: blister, clear and watery infectious drainage: creamy colored, more profuse, it builds up over a period of days, does not go away, smells, is thicker, and cultures microbes

Eosinophils

released in large quantities during an ALLERGIC REACTION release of chemicals that act to control the effects of histamine and serotonin involved in phagocytosis of allengen-antibody complex

immunity

response to DEFEND and prevent infection promote HOMEOSTASIS (uniform and unchanged) SURVEILLANCE recognize and destroys forgeign cells

adhesion

scar tissue around between and around organs

metaplasia

transformation of one cell into another positive ex. monocyte (early WBC) that comes to the scene of a cell injury and becomes a macrophage (monocytes that link together to form multinucleated cell) negative ex. smoking over the years can lead to changing of cell shape and size that can cause bronchial metaplasia (can become cancerous)

dehiscense

unintended separation of wound edges

diapedesis

when blood vessels become more permeable and leak WBC to the tissue site of injury

pathophysiology of inflammatory response

2 pathways working together: the resolution is healing and with an infection, the process restarts; our immune system supports this sequence 1. Vascular response: - cell injury or death/ momentary vasoconstriction; inflammation response activated vvvv -release of chemical mediators (cytokines: histamine, kinins, prostaglandins) which send signals and cause pain vvvv -local vasodilation and hyperemia which results in redness and heat vvvv -increased capillary permeability causing local edema, aka diapedesis- this process leaks WBC to the tissue site of injury vvvv -leads to inflammatory fluid and cell exudates 2. Cellular Response - margination of leukocytes (moving to the inner walls of capillaries) vvvv -diapedesis of neutrophils and monocytes to the site of the cell injury vvvv -chemotaxis (cell transportation) occurs: directional migration of WBCs along concentration gradient of chemotactic factors vvvv -Neutrophils cause phagocytosis, monocytes turn into macrophages and cause phagocytosis, and lymphocytes produce the immune response, tissue macrophages cause phagocytosis vvvv -release inflammatory exudates: complements, lipids, platelets, coagulation-related chemokines inflammatory response can be divided into: - vascular response -celular response -formation of exudate -healing complement is the assortment proteins support this whole process: Complements C5a, C3a help with margination, diapedesis and chemotaxis you should start getting better in about 3 days and should be fully healed in 2-3 weeks

Post-op fever

Steps: (example of complement system) 1. monocytes and macrophages are activated by the immune system 2. trigger release of cytokines (IL-1, IL-6, and TNF: tumor necrosis factor) (interleukin means WBCs that go between) 3. these cytokines tell the anterior hypothalamus of the brain to produce prostaglandin E2 (PGE2) which raises the body temp; this leads to heat conservation and increased heat generation aka fever -up to 12 hours post surgery a temp of around 96.8 is normal because the anesthesia and surgical exposure puts the patient at risk for hypothermia -24-48 hours post surgery=100.4 F; this slightly elevated temperature is a response to surgical stress; however, if it is above 100.4 F then it could be an indicator of lung congestion, atelectasis, or something else adding to the surgical stimuli -on the 3rd day on, if the temperature is about 100 F then it signifies the presence of a urinary infection, respiratory infection of phlebitis -if the patient is not complaining, a temperature is helpful, especially with infection -nursing implications: patient needs to rest, get plenty of fluids and nutrition, medication, and keep the patient at a comfortable temperature beneficial aspects of fever: -increased killing of microorganisms -increased phagocytosis -increased proliferation of T lymphocytes -enhance activity of interferon (body's natural virus fighting substance)

lymphocytes

arrive later at the site -primary role of lymphocytes: 1. cell-mediated immunity (T-cell): cause cell death; recognition and destruction of cancer cells and viruses; provides protection from fungus, viruses (intracellular), chronic infectious agents, and tumor cells thymus secretes hormones (like thymosin) that stimulate maturation and differentiation of T lymphocytes; thymus size and activity declines with aging, and increases the risk for tumor and infection 2 types: -T cytotoxic cells (CD8) which are involved with attacking antigens and releasing cytolytic substances that kill the pathogen...in HIV/AIDS the T cell doesn't get turned off and the body keeps attacking its own cells -T Helper Cells (CD4) regulate cell mediated immunity and humoral antibody response; differentiate into 2 subsets that produce distinct types of cytokines (TH1 and TH2) 2. Humoral immunity (B cell): mediates allergic reactions, autoimmune disorders, and antibody deficiencies; causes antibody and immunoglobulin formation formation; provides protection against bacteria, viruses (extracellular), respiratory pathogens, and gastrointestinal pathogens

complement

assortment of proteins that assist the healing process plasma proteins are elevated during inflammation proteins mostly come from complement cascade check protein levels: 1. ESR or sed rate: erythrocyte sedimentation rate; blood cells are heavier due to higher protein level and they sink faster because of the increase in proteins; increased during chronic and acute inflammation(monocytes and lymphocytes); the more inflammation the faster the RBCs settle in tube of anti-coagulated blood 2. C-reactive protein: reaction of complement; means protein are surging in an elevated level in the blood; increased during acute inflammation (increased neutrophils)