Check Point 1 Flashcards
Discuss the vascular and cellular changes in inflammation? (Knee Injury Casestudy)
Andy’s fall damages the tissue located around the right knee causing the mast cells and platelets to release chemical mediators including Kinins, Histamine, prostaglandins, cytokines, and leukotrines into the blood and interstitial fluid.
Identify the local effects of inflammation and explain a rationale for each. (Knee Injury Casestudy)
Redness - Caused by increased blood flow into the damaged area.
Heat - Caused by increased blood flow into the damaged area.
Swelling - Caused by the shift of protein and fluid into the interstitial space.
Pain - results from the increases pressure of fluid on the nerves especially in enclosed areas, and by the local irritation of nerves by chemical mediators such as bradykinins.
What clinical manifestations might Andy describe if the inflammatory process becomes systemic? (knee injury casestudy)
Fever and Fatigue - possible infection due to skin abrasion or break that bacteria could have possibly entered.
Fever - results from the release of pyrogens or fever producing substances from white blood cells or macrophages.
Nausea - is directly related to the pain you’re in
Malaise - overall immune response
headache - Irritation of nerve endings.
What are Andy’s Identifiable holistic factors. (Knee injury casestudy)
Unable to work
24 year old athletic male on bed rest
No money
all of the above can lead the pt to become depressed.
Explain the basic pathophysiology of this disease? (SLE caseStudy)
SLE is characterized by the presence of large numbers of circulating autoantibodies against DNA, platelets, erythrocytes, various nucleic acids, and other nuclear materials (antinuclear antibodies [ANAs])
Explain why SLE is considered an autoimmune disease? (SLE casestudy)
When self-tolerance is lost, the immune system is unable to differentiate self from foreign material. The autoantibodies then trigger an immune reaction leading to inflammation and necrosis of tissue. Some individuals may lose their immune tolerance following tissue destruction and subsequent formation of antibodies to the damaged cell components. Aging may lead to loss of tolerance to self-antigens. There also appears to be a genetic factor involved in autoimmune diseases, as evidenced by increased familial incidence.
Why does inflammation lead to necrosis?
When self-tolerance is lost, the immune system is unable to differentiate self from foreign material. The autoantibodies then trigger an immune reaction leading to inflammation which causes severe damage and therefore leads to necrosis of tissue. Some individuals may lose their immune tolerance following tissue destruction and subsequent formation of antibodies to the damaged cell components.
Describe three (3) common clinical manifestations of this disease and the rationale for this physiological change?
Polyarthritis, with swollen, painful joints, without damage; arthralgia
Pleurisy - inflammation of the pleural membranes, causing chest pain
Raynaud’s phenomenon - periodic vasospasm in fingers and toes, accompanied by pain.
Carditis - inflammation of any layer of the heart, commonly pericarditis.
Describe three (3) lab or diagnostic findings that would assist in making the diagnosis. Provide a rationale for a change in each.
The presence of numerous ANAs (anti-nuclear antibodies), especially anti-DNA, as well as other antibodies in the serum is indicative of SLE. Lupus erythematosus (LE) cells, mature neutrophils containing nuclear material in the blood are a positive sign.
Complement levels are typically low, and the erythrocyte sedimentation rate (ESR) is high, indicating the inflammatory response.
Frequently counts of erythrocytes, leukocytes, lymphocytes, and platelets are low.
Additional immunologic tests for various antibodies may be required to confirm the diagnosis.
also, all organs and systems need to be examined for inflammation and damage.
Explain why SLE may be difficult to diagnose and treat.
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease that affects a number of systems; therefore it can be difficult to diagnose and treat. Also, the specific cause has not been established. A single lupus gene has not been identified, but genes increasing susceptibility to autoimmune disorders have been identified.
What types of psychological needs would you anticipate for Ms. Monroe? What other assessment data would you need to provide for these needs?
Psychoses, depression, mood changes, seizures
Clinical manifestations diagnosis result in psychological issues.
Describe the process taking place in the burned area during the first hours after the injury.
Acute inflammatory response release chemical mediators resulting in major fluid shift, edema, and decrease blood volume.
Discuss how to determine the percentage of body surface area that is burned. Predict Andy’s percent of affected BSA using the given assessment data.
Torso – 18%
Arms – 18%
Face – 4.5%
Total surface area burned = 40.5% (Figure 2-12)
Describe clinical manifestations Andy might experience and related causes.
Inflammation – an acute response due to damage to the skin, pain, shock (complication) – is because of low blood pressure and low blood volume, edema fluid shifted into interstitial space, temporary loss of function due to swelling and inflammation, blistering of skin, dizziness and headache, irritable, seizure, altered mental status due to dehydration, hypothermia, and low blood pressure because of decreased blood volume.
How is this process of inflammation similar to and different from Andy’s previous knee injury?
They both became inflamed and caused the release of chemical mediators. The knee injury only affected that area, whereas the burn affected the whole body. The burn causes a high risk of infection because the skin is exposed/broken; the knee injury did not break the skin. His knee injury was more localized and the burn is more systemic.