A male client with type 1 diabetes mellitus (DM) develops a gangrenous toe and is admitted for possible amputation. Which pathophysiological consequence of DM has contributed to this client's complication?

A) Increased preload that results in generalized peripheral edema:

This statement is incorrect. Decreased blood volume due to hemorrhage leads to decreased preload, not increased preload. Generalized peripheral edema is more commonly associated with conditions such as heart failure or kidney disease, where fluid retention leads to increased preload.

B) The lowered blood pressure results in a reduction of the heart rate:

While it's true that a decrease in blood pressure can trigger compensatory mechanisms such as an increase in heart rate (tachycardia), the specific response mentioned in this option is not entirely accurate. The primary compensatory response to hemorrhage-induced hypotension is typically an increase in heart rate, not a reduction.

C) Decreased preload that can lead to decreased cardiac output:

Correct. With decreased blood volume (preload), there is less blood returning to the heart during diastole. This leads to decreased ventricular filling and subsequently decreased stroke volume and cardiac output. Decreased cardiac output can contribute to hypotension and inadequate tissue perfusion.

D) Increased peripheral resistance resulting from poor renal perfusion:

While poor renal perfusion can trigger mechanisms to increase peripheral resistance (such as activation of the renin-angiotensin-aldosterone system), this option does not directly address the primary effect of decreased preload on cardiac output. Increased peripheral resistance alone does not adequately compensate for decreased preload to maintain cardiac output.

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.