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) 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.

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.