StudyKraken Medicine
Print Сite this

Pathophysiology of the Body’s Response to Pernicious Anemia

Pernicious anemia is a condition that develops due to failure of gastric parietal cells to release sufficient amounts of IF (Intrinsic Factor). Intrinsic Factor is a gastric protein that is responsible for absorption of vitamin B12. Pernicious anemia can also be caused by lack of absorption adequate quantities of cobalamin.

Deficiency in cobalamin hinders thymidine synthase function and slows DNA function, leading to adverse megaloblastic changes in body cells. System degeneration occurs in cobalamin deficiency as a result of neurological impairment.

Typical neurological symptoms which are elicited in patients with pernicious anemia are paresthesias, extensor plantar response, distal sensory loss and unsteady gait. Hematological manifestations which might occur independently of the neurological symptoms include cytopenias and pseudothrombotic microangiopathy.

Paresthesia and ataxia in pernicious anemia patients

Like other types of anemia, individuals with pernicious anemia show nonspecific symptoms such as shortness of breath, fatigue and dizziness. However there are symptoms which are more specific to pernicious anemia which include glossitis (smooth and sore tongue), parathesia (numbness, tickling, pricking or burning sensation of skin) and ataxia (trouble with coordination and balance). Jackson & Snow (2014) explains that these neurological symptoms are as are caused by myelin degeneration and loss of nerve fibers in spinal cord and worsens in darkness as the patient is unable to rely upon vision due to loss of proprioception.

Therefore the reason Deb’s nurse practitioner is asking about the patient’s ataxia and paresthesia is because these are symptoms that are more specific to pernicious anemia as opposed to all other types of megaloblastic anemia.

Oral and Intramuscular Injection of Vitamin B12

In most cases vitamin B12 replacement is administered by intramuscular injection because absorption through the gastrointestinal tract is deficient for most of pernicious anemia patients. Thus, regular intramuscular injection of Vitamin B12 is recommended to rapidly replace body stores. The standard traditional vitamin B12 replacement for this type of anemia has been injection of cyanocobalamin (CN-Cbl) and hydroxocobalamin (OH-Cbl).

Though vitamin B12 is not absorbed well when taken orally, high doses can be effective in some cases. Mega doses of oral vitamin B12 medication can be used as a cost effective and comfortable alternative. However, oral doses can only be administered for patients showing some vitamin B12 absorption through the gastrointestinal tract.

Causes of pernicious anemia

Pernicious anemia (PA) is caused by impaired gastric absorption of vitamin B12. This impairment is usually caused by autoimmune destruction of gastric parietal cells. The destruction of these cells, which are seated in the atrophic gastritis, leads to autoantibody inactivation of intrinsic factor, a protein essential for absorption of vitamin B12 in the ileum.

PA can also be caused by the removal of a large part an individual’s stomach for medical reasons (gastrectomy). Gastrectomy can cause loss of gastric parietal cells which secretes intrinsic factor.

Block & Leeuw (2013) shows that other disorders that lead to interference of the absorption or metabolism of vitamin B12 can also cause this type of anemia. For example, autoimmune glandular deficiencies such as hypothyroidism and thyroiditis have long been associated with megaloblastic anemia.

Technical terms used to describe anemia with high MCV and normal MCH

Andres & Serra (2012) explains that pernicious anemia is suspected in a patient if the blood smear shows megaloblasts, which are large, fragile and immature erythrocytes. Blood smear from PA patient also shows hyper segmented neutrophils and ovalocytes, which are common feature of all types of megaloblastic anemia. A full blood count evaluates the mean corpuscular volume (MVC) as well as the mean corpuscular hemoglobin concentration (MCHC).

Normal MCV is called normocytic and when MCV is high the condition is called macrocytic. When the MCV is low, the condition is microcytic. On the other hand normal MCHC is referred to as normochromic, while abnormally high MCHC is called hyper chromic. Abnormally Low MCHC is called hypochromic. Pernicious anemia is diagnosed when blood smear shows a high MCV (macrocytic anemia) and a normal MCHC (normochromic anemia).


Andres, E., & Serra, K. (2012). Optimal Management of Pernicious Anemia. Journal of Blood Medicine, 76(1), 102.

Block, E., & Leeuw, H. (2013). Autoimmune Gastritis in Diabetes: A Clinical Oriented Review. The Journal of Clinical Endocrinology and Metabolism, 93 (2), 363.

Jackson, C., & Snow, F. (2014). Laboratory Diagnosis of Vitaminb12 and Folate Deficiency. Archives of Internal Medicine, 159(2), 192.

Cite this paper
Select style


StudyKraken. (2022, April 17). Pathophysiology of the Body’s Response to Pernicious Anemia. Retrieved from


StudyKraken. (2022, April 17). Pathophysiology of the Body’s Response to Pernicious Anemia.

Work Cited

"Pathophysiology of the Body’s Response to Pernicious Anemia." StudyKraken, 17 Apr. 2022,

1. StudyKraken. "Pathophysiology of the Body’s Response to Pernicious Anemia." April 17, 2022.


StudyKraken. "Pathophysiology of the Body’s Response to Pernicious Anemia." April 17, 2022.


StudyKraken. 2022. "Pathophysiology of the Body’s Response to Pernicious Anemia." April 17, 2022.


StudyKraken. (2022) 'Pathophysiology of the Body’s Response to Pernicious Anemia'. 17 April.

This paper was written and submitted to our database by a student to assist your with your own studies. You are free to use it to write your own assignment, however you must reference it properly.

If you are the original creator of this paper and no longer wish to have it published on StudyKraken, request the removal.