A client is being treated for a gastric ulcer caused by Heliobacter pylori. The nurse should prepare the client for long term follow-up to which associated problem?

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.

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.