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) 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.

Acute leukemia, including acute myeloid leukemia (AML), involves the proliferation of abnormal myeloblasts (immature white blood cells) in the bone marrow, leading to decreased production of normal blood cells. Here's the breakdown of the pathophysiology contributing to bruising in acute leukemia:

A) Oxyhemoglobin provides less oxygen to tissues:

Oxyhemoglobin refers to hemoglobin bound to oxygen, and its role is in oxygen transport, not in the process of bruising. Therefore, this option is not directly related to the pathophysiology of bruising in acute leukemia.

B) Insufficient platelets delay the clotting process:

Correct. Thrombocytopenia, or low platelet count, is a common complication of acute leukemia due to the replacement of normal bone marrow cells with leukemia cells, leading to inadequate production of platelets. Platelets play a crucial role in hemostasis and clot formation. Insufficient platelets result in delayed clotting, leading to easy bruising and bleeding tendencies in patients with acute leukemia.

C) Phagocytic cells are inadequate in fighting infection:

Leukopenia, or low white blood cell count, can occur in acute leukemia due to suppression of normal hematopoiesis by leukemia cells in the bone marrow. While leukopenia predisposes patients to infections due to impaired immune function, it is not directly related to the pathophysiology of bruising.

D) Lack of iron causes hypochromic blood cells:

Iron deficiency anemia can result in hypochromic red blood cells, but this is not typically associated with the pathophysiology of bruising in acute leukemia. Anemia may contribute to other symptoms such as fatigue and pallor, but bruising primarily results from thrombocytopenia-induced clotting abnormalities.