A male client with a massive pulmonary embolus is tachycardic, hypotensive, and has audible bilateral pulmonary crackles. His arterial blood gas (ABG) results are: pH 7.0: PaCO, 66 mm Fig; HCO3- 24 mEq/L (24 mmol/L); PaO, 60 mm Hg. Based on these findings, this client is at greatest risk for which pathophysiological condition?

Reference Ranges:

pH [7.35 to 7.45] PaCO, [35 to 45 mm Hg]

HCO3- [21 to 28 mEq/L (21 to 28 mmol/L)]

PaO, [80 to 100 mm Hg]

Gout is a form of inflammatory arthritis characterized by sudden, severe attacks of pain, redness, and swelling in the joints, commonly affecting the big toe joint (first metatarsophalangeal joint). The primary pathophysiological process underlying gout involves the deposition of monosodium urate crystals in the joints and surrounding tissues. Here's an explanation of why option A is the correct answer:

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

Correct. Elevated levels of uric acid in the blood can lead to the formation of monosodium urate crystals, which then accumulate in the synovial fluid of joints, particularly in the big toe 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 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 inflammation and the formation of osteophytes (bone spurs). Gout does not directly involve 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.

A) Sensory neuropathy:

Sensory neuropathy, while common in diabetes mellitus, primarily affects sensation in the extremities and can lead to reduced pain perception and protective sensation. While sensory neuropathy can contribute to the development of foot ulcers by reducing the ability to detect trauma or pressure, it is not the primary factor influencing the ability of the ulcer to heal.

B) Hyperlipidemia:

Hyperlipidemia, characterized by elevated levels of lipids (cholesterol and triglycerides) in the blood, is a common comorbidity in diabetes mellitus. It can contribute to the development of atherosclerosis and macrovascular complications such as coronary artery disease and peripheral arterial disease. While macrovascular disease can impair wound healing by reducing blood flow to the affected area, it is not the primary contributing factor to the ability of the ulcer to heal.

C) Ketoacidosis:

Ketoacidosis, a serious complication of uncontrolled diabetes mellitus, results from the accumulation of ketones in the blood, leading to metabolic acidosis. While ketoacidosis can have systemic effects and impair overall health, it is not directly related to the ability of a foot ulcer to heal.

D) Microvascular changes:

Correct. Microvascular changes, such as thickening of the capillary basement membrane and endothelial dysfunction, are hallmark features of diabetes mellitus. These changes lead to impaired microcirculation, reduced oxygen delivery, and compromised nutrient supply to tissues, including the skin and soft tissues of the foot. Poor microvascular perfusion contributes to delayed wound healing and an increased risk of infection in individuals with diabetes mellitus. Addressing microvascular changes is essential for promoting wound healing in diabetic foot ulcers, making it the primary contributing factor to the ability of the ulcer to heal.