A client with pernicious anemia asks why she must take vitamin B12 injections for the rest of her life. What is the nurse’s best response?
A. “The reason for your vitamin deficiency is an inability to absorb the vitamin because the stomach is not producing sufficient acid.”
B. “The reason for your vitamin deficiency is an inability to absorb the vitamin because the stomach is not producing sufficient intrinsic factor.”
C. “The reason for your vitamin deficiency is an excessive excretion of the vitamin because of kidney dysfunction.”
D. “The reason for your vitamin deficiency is an increased requirement for the vitamin because of rapid red blood cell production.”
Correct Answer: B. “The reason for your vitamin deficiency is an inability to absorb the vitamin because the stomach is not producing sufficient intrinsic factor.”
Most clients with pernicious anemia have deficient production of intrinsic factor in the stomach. Intrinsic factor attaches to the vitamin in the stomach and forms a complex that allows the vitamin to be absorbed in the small intestine. Intrinsic factor antibodies are immunoglobulin G isotype, and they can be either type 1 or type 2 antibodies. Type 1 operates against the cobalamin binding site, whereas type 2 directs its activity against the ileal mucosa receptor. B12 and intrinsic factor bind to receptors on the ileum, which allows for absorption.
Option A: Pernicious anemia (PA) is megaloblastic anemia resulting from a deficiency of cobalamin (vitamin B12), which in turn is caused by a lack of intrinsic factor (IF). Intrinsic factor is a glycoprotein that binds cobalamin and thereby enables its absorption in the terminal ileum. Autoimmune gastritis is characterized by the destruction of gastric parietal cells and the resulting lack of the glycoprotein intrinsic factor secreted by these cells. The antibodies identified with autoimmunity are intrinsic factor antibodies (IFA) and parietal cell antibodies (PCA).
Option C: Vitamin B12, once absorbed, is a cofactor for the enzyme methionine synthase, which takes part in the conversion of homocysteine to methionine. If this process cannot occur due to pernicious anemia, homocysteine levels accumulate, and pyrimidine bases cannot form, which interferes with DNA synthesis and causes megaloblastic anemia.
Option D: The stomach is producing enough acid, there is not an excessive excretion of the vitamin, and there is not a rapid production of RBCs in this condition. Vitamin B12 is also a cofactor for the enzyme methylmalonyl-CoA mutase, which converts methylmalonyl-CoA to succinyl-CoA. In patients with pernicious anemia, methylmalonic acid (MMA) levels accumulate. Elevated levels of MMA and homocysteine contribute to myelin damage, which causes neurologic deficits, such as neuropathy and ataxia.
No comments:
Post a Comment