Macrocytic Anemia Flashcards
How do we define macrocytic anemia, what are the two most common causes, and what do we specifically call the anemia that is caused by these two causes?
MCV greater than 100.
Folate or b12 deficiency
Megaloblastic anemia
Explain the big picture idea of how a macrocytic anemia is caused? Why are the RBCs larger?
It’s the opposite of microcytic anemia. There is basically one less division in the process of making a RBC. The reason there is one less division is because we have a reduced number of DNA precursors due to folate or b12 being low so we can’t divide as much.
Explain the dynamic of folate and b12 allowing for synthesis of DNA precursors?
Folate circulates in the serum as methyl THF and can’t participate in synthesis of DNA precursors until the methyl group is removed. That’s where b12 comes into play. It takes the methyl from folate and then homocysteine takes the methyl from b12.
What are the two identifying features of megaloblastic anemia, meaning from folate or b12 deficiency, that distinguish it from macrocytic anemia?
Hypersegmented neutrophils (more than 5 lobes) and megaloblastic change in other tissues of the body. Other rapidly growing cells will be affected by the reduced DNA precursor synthesis like gut epi cells.
Wha are three other notable causes of macrocytic anemia?
Alcoholism, liver disease, and drugs.
Where is folate absorbed in the body, how long does it take to get a deficiency and why, and what are 3 common causes?
Jejunum
Months because the stores are low
Poor diet (alcohol and elderly), increased demand, and folate antagonists like methotrexate
What would be 1 unique clinical finding and 3 lab values for folate deficiency and why?
Glossitis
Low serum folate
Increased serum homocysteine (remember folate gives methyl to b12 which gives the methyl to which turns it into methionine. If we don’t have folate, we aren’t doing this).
Normal methylmalonic acid (this is important because it tells us the problem is not b12. B12 turns m acid into scoa. So if b12 is fine, m acid is fine).
How do we absorb b12? Go through the process until it is absorbed.
B12 comes from animal proteins. Saliva frees b12 and binds it to r binder protein. R binder protein takes b12 through the gut. IN the duodenum, pancreatic proteases cleave b12 from r binder and b12 can then hook up with intrinsic factor. The ileum will only absorb the vitamin B as a complex with intrinsic factor.
Is b12 more common or less common than folate and how long does it take to get a b12 deficiency and why?
Less common than folate
Years because the body stores a ton of b12 in the liver
What is the most common cause of b12 deficiency, explain the mechanism?
Pernicious anemia, which is autoimmune destruction of the parietal cells so no intrinsic factor.
What are three other causes of b12 deficiency and explain how they work to cause the deficiency?
Pancreatic insufficiency because you won’t have the proteases to cleave b12 from r binder.
Damage to the terminal ileum so no absorption, like Crohns
Diet not having it, but very rare. Think vegans.
2 clinical findings of b12 deficiency and explain the mechanism of the second one?
Glossitis
Subacute combined degeneration of spinal cord.
Need b12 to convert m acid to SCOA. When m acid builds up due to low b12, we have impaired myelinzation of the spinal cord.
Poor proprioception and spastic paresis.
3 lab values of b12 deficiency?
Low b12
High homocysteine
High m acid
