The nurse assesses the wound of a client who received sutures for a laceration of the hand two days ago. Which finding is a normal inflammatory response?

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.

A. Myocardial infarction one year ago:

A myocardial infarction (MI) that occurred one year ago is not directly related to the current acid-base imbalance described in the scenario. While a history of MI may have implications for the client's overall cardiovascular health and management, it is not the most likely cause of the acid-base imbalance indicated by the laboratory results.

B. Occasional use of antacids:

Occasional use of antacids is unlikely to cause the acid-base imbalance described in the scenario. Antacids primarily work by neutralizing gastric acid and are not typically associated with significant alterations in acid-base status, especially when used intermittently.

C. Chronic renal insufficiency:

Chronic renal insufficiency is the most likely cause of the acid-base imbalance indicated by the laboratory results. A low hemoglobin level suggests anemia, which can occur in chronic kidney disease due to decreased erythropoietin production. An elevated creatinine clearance indicates impaired kidney function, as the kidneys are clearing creatinine at a faster rate than normal. Decreased urine specific gravity suggests the kidneys' inability to concentrate urine properly, which is a common finding in renal insufficiency. Renal insufficiency can lead to metabolic acidosis due to the kidneys' decreased ability to excrete acid and regulate bicarbonate levels.

D. Shortness of breath with exertion:

Shortness of breath with exertion, a symptom commonly seen in COPD exacerbations, is unlikely to directly cause the acid-base imbalance described in the scenario. While respiratory distress can lead to respiratory acidosis, which is characterized by elevated carbon dioxide levels and decreased pH, the laboratory results indicate metabolic rather than respiratory acidosis.