An adult client with extreme fatigue, weight gain, cold intolerance, and bradycardia is diagnosed with hypothyroidism. Which laboratory findings is this client likely to exhibit?

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) Deficiency of factors VIII or IX.

Hemophilia is a genetic disorder characterized by deficient or defective clotting factors, specifically factors VIII (hemophilia A) or IX (hemophilia B). These clotting factors are essential for the formation of stable blood clots. Therefore, if hemophilia is present, the deficiency of factors VIII or IX can lead to impaired clot formation and prolonged bleeding.

B) Diminished amount of vitamin K:

Vitamin K deficiency can lead to impaired blood clotting due to inadequate synthesis of clotting factors in the liver. However, hemophilia is specifically associated with deficiencies in factors VIII or IX, not vitamin K.

C) Decreased amount of platelets:

Platelets play a crucial role in primary hemostasis and initial platelet plug formation at the site of vascular injury. While decreased platelet count or dysfunction can lead to bleeding disorders such as thrombocytopenia or platelet function disorders, hemophilia specifically involves deficiencies in clotting factors, not platelets.

D) Missing factors V and VII:

Factor V and VII are other clotting factors involved in the coagulation cascade, but they are not deficient in hemophilia. Hemophilia is specifically characterized by deficiencies in factors VIII (hemophilia A) or IX (hemophilia B).