Pernicious anemia
***Introduction of disease
Originating from the Latin word “pernicies” or “perniciosus” meaning ruin or destructive. It is called pernicious anemia because the consequences of the disease was fatal before the availability of treatment and research efforts. It is less commonly known as Biermer’s anemia, Addison’s anemia, or Addison-Biermer anemia after British physician Thomas Addison and German physician Michael Anton Biermer. However, these names are rarely used nowadays. Anemia, itself, describes the condition of abnormally low levels of erythrocytes or hemoglobin in the blood resulting in lack of sufficient oxygen throughout the body.
***Etiology
The cause of pernicious anemia is a deficiency of vitamin B12 due to a variety of factors including a lack of intrinsic factor, unregulated pH of the small intestine, and an inability to absorb the B12 complexes within the terminal ileum due to surgical removal. Intrinsic factor is required in order for vitamin B12 to be absorbed into the body through the ileum. Another cause is also due to a lack of vitamin B12 in one’s diet. This is typically more common in strict vegetarians as vitamin B12 is common found in meat and dairy products.
If the cause is autoimmune, pernicious anemia is also a type of hypersensitivity reaction. More specifically, pernicious anemia is an antibody-mediated disease (Type 2). The type of injury caused is caused by anti-tissue antibodies that the body produces. These antibodies affect specific antigens, and therefore only affect a certain type of tissue. The parietal cells of the stomach are attacked by the immune system. This condition is known as atrophic gastritis. Intrinsic factor, produced by the parietal cells, play a key component in the absorption of vitamin B12. The neutralization of intrinsic factor causes decreased absorption of vitamin B12, resulting in a host of signs and symptoms that are life-threatening.
***Pathogenesis
The inadequacy of vitamin B12 from whatever the reason will result in cobalamin deficiency. Cobalamin is a type of organometallic substance that is responsible for thymidine production. Thymidine is a pyrimidine nucleoside made of the base thymine. In the case of pernicious anemia, the lack of cobalamin results in the lack of thymidine, a type of DNA precursor required for the synthesis of red blood cells. The effect is the “megaloblastic changes in all rapidly dividing cells because DNA synthesis is diminished.” In the case of erythrocyte production, macrocytosis and ineffective erythropoiesis is the end result vitamin B12 deficiency. Macrocytosis is the production of abnormally large cells, typically inefficient in nature. Erythropoiesis is the production of red blood cells, and thus when it is ineffective there are less able erythrocytes capable of effectively delivering oxygen throughout the body. One example is an immune mediated atrophic gastritis. This results in the destruction of parietal cells in the stomach. Consequently, there is a lower production of intrinsic factor, which is required to absorb vitamin B12. Without it, there is lower absorption of vitamin B12 in the ileum. The final result is the large and flimsy erythrocytes.
***Pathology
The examination of blood under a light microscope will reveal abnormally large, nucleated erythrocytes. This type of pathology is also called megaloblastosis, a condition that describes a shared common characteristic in the morphology of the cells: large cells with an arrest in nuclear maturation.
***Signs and Symptoms
The signs and symptoms of pernicious anemia can be divided into two subcategories of the signs and symptoms of anemia and the signs and symptoms of vitamin B12 deficiency. With regards to anemia, the most common sign is fatigue due to the lack of oxygen being delivered to the different parts of the body. Shortness of breath, dizziness, headaches, coldness within the extremities, or pale skin are also indications of anemia. With the lack of mature red blood cells, the heart needs to work harder in order to provide oxygen to the body, leading to possible arrhythmias, heart mummers, hypertrophy of the cardiac muscles, or possible heart failure.
In addition to conditions associated with anemia, the lack of vitamin B12 also contributes to more signs and symptoms. Vitamin B12 deficiency can lead to nerve damage, causing tingling and numbing sensations, muscle weaknesses, or weakened reflexes overall. Secondary conditions such as dementia, depression, and memory loss may result. Problems in the digestive tract may also occur, resulting in nausea, vomiting, heartburn, and other stomach-related symptoms.
The most telltale sign of vitamin B12 deficiency is a smooth, thick, red tongue. The lack of vitamin B12 causes depapillation of the tongue. The papillae is reduced, giving the smooth and red appearance. The alternate name for this may be called a “beefsteak” tongue, resembling a piece of raw steak.
***Diagnosis
A com