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And immunological defense against tissue injury, infection, or allergy.
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135 inflammation
| Question | Answer |
|---|---|
| And immunological defense against tissue injury, infection, or allergy. | Inflammation |
| For potential outcomes of information | Acute inflammation followed by restitution, fibrous repair, chronic inflammation, death of tissue impossible host. |
| Signs of immune response | Calor, dolor, tumor, parlor |
| Categories of inflammation | Acute inflammation, chronic inflammation, reparative or restorative |
| Physiological effects of inflammation | Edema, fever, fatigue, distended belly, vomiting, pain, and diaphoresis |
| Negative consequences of inflammation | Overly severe response to stimuli such as anaphylaxis, SIRS, sepsis. Some patients have an adequate response such as patients who are neutropenic, immunocompromise or immuno suppressed |
| Fibrous repair where cells cannot be restored cause what | Scar tissue |
| The inflammatory process involves proinflammatory hormones and what | White blood cells; neutrophils, leukocytes |
| A series of cellular changes that signal the body’s response to injury or infection | The inflammatory process |
| Examples of inflammatory process causes | Physical agents such as excessive sunlight, sunburns, radiation. Chemical stimuli such as insect venom, other chemicals, bug bites, bug stings. Biological agents such as bacteria, or viruses. |
| Dilation of the capillary beds, increase blood flow to the area, warmth and brightness at the site of inflammation. | Hemodynamic changes |
| Leukocytes line small blood vessel walls near inflammatory site, cells inhabit inflamed area, then ingest and carry away bacteria & foreign substances, fluids flow through vessel walls and collect to become Swelling | Increase capillary permeability |
| Hemodynamic changes and vascular permeability occur with the help of several chemical mediators such as | Prostaglandins, histamine, leukotrienes, cytokines & eicosanoids |
| Chemical mediators that causes blood and blood vessel changes | Cytokines & eicosanoids |
| Massive release of histamine‘s and other substances that produce marked vasodilation, vascular permeability, and smooth muscle contraction | Immunologically mediated reactions involving antigen-antibody complexes |
| Cellular changes that produce classic signs of anaphylactic shock such as hypertension, swelling, and bronchoconstriction | Vasodilation, vascular permeability , and smooth muscle contraction |
| An anti-inflammatory substance that’s produced by the adrenal cortex that slows the release of histamine, stabilizes lysosomal membranes, and prevents the influx of leukocytes leukocytes | Cortisol |
| Cortisol impedes the inflammatory process and does what | Protects the body from excessive or prolonged inflammation |
| Vasodilation, swelling, increase vascular permeability, leakage of small plasma proteins, walling off, immune cells to side of injury, exudate formation, move glucose and oxygen to repair site, activated endothelial cells release chemical repair factors | Physiological process of an ACUTE inflammatory response |
| Macrophages released thromboplastin, which facilitate hemostasis and promotes fibroblast activity, removal of foreign pathogen and chronic tissue, healing interrupted by re-injury or renewed information and immune system activity | Chronic inflammation steps |
| Elevated C reactive proteins CRP, increased risk the site sedimentation rate ESR | Diagnostic/lab values for subclinical evidence |
| Local tissue damage from compression, development of chronic inflammation, or systemic pathology such as atherosclerosis, chronic renal disease, neurological disorders | Consequences of an excessive or ineffective inflammatory response |
| The very young, the very old, the uninsured or under insured | risk factors for severe or ineffective inflammatory response |
| Patients with autoimmune disease, allergies, history of ineffective inflammatory response, family history of ineffective inflammatory response, poor hygiene practices, exposed to environmental factors such as pollution, irritants or excessive sun exposure | Individual risk factors |
| History such as where they work, chronic diseases, pain, medication, family history. Or physical examination such as swelling, redness, increased temperature. | Assessment of increased inflammatory responses |
| Heat, swelling, redness, and pain which could result in loss of function | Local inflammation (at site of injury) |
| Fever, headache, muscle aches, chills, sweating, and increased leukocytes | Systemic inflammation (body wide) |
| CBC, WBC with differential, CRP, ESR, serological testing to detect specific antibodies or viruses | Common laboratory diagnostic test |
| MRI, CAT, PET scans, colonoscopy | Common radiographic diagnostic studies |
| Hand hygiene, falls prevention, reduce risk for injury and infection. Properly using safety equipment such as helmets. Properly storing and preparing food such as washing and cooking properly. | Primary prevention for increased inflammatory response |
| RICE | Rest, ice, compression, elevation |
| How long is RICE most beneficial for after injury | 24 to 48 hours after injury |
| Helps minimize swelling and pain | RICE, followed by compression and heat. |
| Steroids, NSAIDS, narcotics, recombinant DNA and monoclonal antibodies, antipyretics, analgesics, antimicrobials | Pharma logical agents for collaborative intervention of increased inflammatory response |
| Tissue repair and regeneration start at the beginning of the inflammatory process. Macrophage cells clean up inflammatory debris, fibroblast begin to repair by laying down elastin and collagen at the edges of the wound. Epithelial cells migrate over and u | Wound healing |
| Patient population at risk for delayed healing | The elderly, patients with impaired nutrition and a diabetic patient |
| Which blood cells are involved in the inflammatory response | WBC |
| Which of the white blood cells are most prominent in inflammatory response to viral antigens | Lymphocytes |
Created by:
Michelle McCourt
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