A client with a sudden onset of big toe joint pain and swelling is diagnosed with gout. Which pathophysiologic process is producing the symptoms of gout?

Deposition of crystals in the synovial space of the joints produces inflammation and irritation.

Chondrocyte injury destroys joint cartilage, producing osteophytes and joint inflammation.

An immune complex and autoantibody deposition in connective tissue results in inflammation.

An autoimmune inflammation involving IgG response to an antigen causes joint destruction.

Answer and Explanation

The Correct Answer is A

Gout is a type of inflammatory arthritis caused by the deposition of monosodium urate crystals in the joints and surrounding tissues. Here's an explanation of the pathophysiological process producing the symptoms of gout:

A) Deposition of crystals in the synovial space of the joints produces inflammation and irritation:

Correct. In gout, elevated levels of uric acid in the blood lead to the formation and deposition of monosodium urate crystals in the synovial fluid of joints, particularly in the big toe joint (first metatarsophalangeal joint) in many cases. These crystals trigger an inflammatory response, activating immune cells and causing swelling, redness, warmth, and severe pain in the affected joint. The inflammation and irritation result from the body's immune response to the presence of these crystals.

B) Chondrocyte injury destroys joint cartilage, producing osteophytes and joint inflammation:

This option describes a process more characteristic of osteoarthritis, where degeneration of joint cartilage leads to the formation of osteophytes (bone spurs) and joint inflammation. Gout involves the deposition of urate crystals rather than direct chondrocyte injury.

C) An immune complex and autoantibody deposition in connective tissue results in inflammation:

This process describes the pathophysiology of autoimmune diseases such as rheumatoid arthritis, where immune complexes and autoantibodies contribute to inflammation and tissue damage. In gout, the inflammation is primarily triggered by the deposition of urate crystals rather than immune complex deposition.

D) An autoimmune inflammation involving IgG response to an antigen causes joint destruction:

This option describes the autoimmune process seen in diseases like rheumatoid arthritis, where antibodies target specific antigens, leading to joint destruction. Gout is not an autoimmune disease, and joint destruction in gout is primarily due to inflammation caused by urate crystal deposition rather than autoimmune mechanisms.

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Correct Answer is A,D,C,E,B

Explanation

This sequence starts with an injury to the arterial endothelium, leading to inflammation. Macrophages then consume LDL, forming foam cells. These foam cells release growth factors that stimulate the growth of smooth muscle cells. The smooth muscle cells grow over the fatty streaks, creating fibrous plaques. Finally, as these plaques grow, they narrow the vessel, which can result in ischemia. This is a simplified explanation of a complex process that involves many other factors and steps. It’s also important to note that this process can take many years to develop.

A. Epidermal fragility and skin excoriation with serous drainage. B. Hypodermal fluid accumulation and blister formation. C. Necrotic tissue, purulent exudate and eschar formation. D. Ischemic inflammatory response marked by erythemic skin.

Correct Answer is D

Explanation

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.

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A client with a sudden onset of big toe joint pain and swelling is diagnosed with gout. Which pathophysiologic process is producing the symptoms of gout?

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Naxlex Comprehensive Predictor Exams

The development of atherosclerosis is a process of sequential events. Arrange the pathophysiological events in order of occurrence. Place the first event on top, and the last on the bottom.

Correct Answer is A,D,C,E,B

Explanation

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?

Correct Answer is D

Explanation

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