The nurse is caring for an immobilized client who is at risk for breakdown in skin integrity. Which pathophysiological process should the nurse note early in the development of a pressure injury?
Epidermal fragility and skin excoriation with serous drainage.
Hypodermal fluid accumulation and blister formation.
Necrotic tissue, purulent exudate and eschar formation.
Ischemic inflammatory response marked by erythemic skin.
The Correct Answer is D
Pressure injuries, also known as pressure ulcers or bedsores, result from prolonged pressure on the skin, leading to tissue ischemia and damage. Early recognition of the pathophysiological processes involved in pressure injury development is crucial for prevention and timely intervention. Here's why option D is the correct choice:
A) Epidermal fragility and skin excoriation with serous drainage:
This description more closely aligns with the characteristics of a superficial wound or abrasion rather than the early stages of a pressure injury. In pressure injuries, epidermal breakdown may occur later in the process, after prolonged pressure and tissue ischemia.
B) Hypodermal fluid accumulation and blister formation:
While fluid accumulation and blister formation can occur in some types of wounds, such as friction blisters or burns, they are not typically characteristic of the early stages of pressure injury development. Pressure injuries primarily involve tissue ischemia and damage due to pressure and shear forces.
C) Necrotic tissue, purulent exudate, and eschar formation:
This description is more indicative of advanced or severe pressure injuries rather than the early stages. Necrotic tissue, purulent exudate, and eschar formation typically occur in pressure injuries that have progressed to deeper tissue involvement and infection.
D) Ischemic inflammatory response marked by erythemic skin:
Correct. In the early stages of pressure injury development, the affected area may exhibit signs of tissue ischemia and inflammation, which can manifest as erythema (redness) of the skin. This erythema is a result of the body's inflammatory response to tissue damage caused by pressure and may indicate the need for intervention to relieve pressure and prevent further injury.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Chronic osteoarthritis (OA) is a degenerative joint disease characterized by the breakdown of joint cartilage and underlying bone changes. The pathophysiological process of OA involves various factors contributing to joint pain and inflammation. Here's why option C is the correct choice:
A) Inflammation results from deposition of crystals in the synovial space of joints producing irritation:
This statement is more characteristic of crystal-induced arthritis, such as gout or pseudogout, where crystals (e.g., urate or calcium pyrophosphate crystals) deposit in the joints and cause acute inflammation and irritation. While inflammation may occur in OA, it is primarily a result of mechanical stress and cartilage degradation rather than crystal deposition.
B) Inflammation is caused by immune complex and autoantibody deposition in connective tissue:
This statement is more characteristic of autoimmune diseases such as rheumatoid arthritis (RA), where immune complex deposition and autoantibody production lead to chronic inflammation and joint damage. In OA, inflammation is not primarily mediated by immune complex deposition or autoantibodies.
C) Joint inflammation occurs when chondrocyte injury destroys joint cartilage, producing osteophytes:
Correct. In osteoarthritis, joint inflammation occurs as a result of chondrocyte injury and cartilage breakdown. Over time, the degenerative changes in the joint lead to the formation of osteophytes (bone spurs) at the joint margins. These changes can irritate surrounding tissues, including the synovium, ligaments, and tendons, contributing to joint pain and inflammation.
D) Joint destruction happens due to an autoimmune inflammation involving IgG response to an antigen:
This statement is more characteristic of autoimmune arthritis, such as rheumatoid arthritis (RA), where autoantibodies (e.g., rheumatoid factor, anti-citrullinated protein antibodies) target joint tissues, leading to chronic inflammation and joint destruction. In OA, joint destruction primarily results from mechanical stress and wear-and-tear on the joint structures rather than autoimmune mechanisms.
Correct Answer is C
Explanation
A) An increase in afterload results in decreased systolic pressure, which creates a decreased cardiac output:
This statement is incorrect. According to the Frank-Starling law, afterload refers to the resistance against which the heart must pump blood during systole. An increase in afterload typically results in increased systolic pressure, not decreased, as the heart works harder to overcome the increased resistance. However, increased afterload can lead to decreased cardiac output due to the increased work of the heart.
B) A decrease in afterload causes the cardiac muscles to hypertrophy, resulting in increased diastolic volume:
This statement is incorrect. A decrease in afterload typically reduces the workload on the heart, which may lead to reverse remodeling and a reduction in cardiac hypertrophy. Increased diastolic volume may occur due to reduced afterload, but it's not the direct result of hypertrophy.
C) An increase in preload results in greater shortening of myocardial fibers, thereby increasing contractility:
Correct. The Frank-Starling law states that an increase in preload (end-diastolic volume or stretch of myocardial fibers) leads to greater overlap of actin and myosin filaments within myocardial fibers during systole. This increased overlap results in stronger myocardial contraction (increased contractility), leading to an increased stroke volume and cardiac output.
D) A decrease in preload results in increasing diastolic muscle fiber length, which impedes contractility:
This statement is incorrect. Preload refers to the degree of stretch of the myocardial fibers at the end of diastole. A decrease in preload would lead to decreased stretch of the myocardial fibers, not increasing diastolic muscle fiber length. Decreased preload typically results in decreased contractility rather than an impediment to contractility due to reduced myocardial stretch.
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