Macrocytosis and Macrocytic anaemia Flashcards
what is a macrocytic anaemia
anaemia where the red cells have a larger than normal volume
what are the units for MCV
femolitres
what will MCV be like in macrocytic anaemia
high
what will FBC be like in macrocytosis
MCV raised
Hb and RBC normal
how is MCV measured
light scatter properties of red cells
when is a red cell macrocytic
> 100fl
what are erythroblasts/ normoblasts
red cell precursors
have a nucleus and are usually marrow based
what triggers developing erythroblasts to stop dividing and loss their nucleus (enucleation)
when Hb accumulates to a certain level
what is a megoblast
an abnormally large nucleated red cell precursor with an immature nucleus
what are megablastic anaemia characterised by
lack of red cells due to predominant defects in DNA synthesis and nuclear maturation
(RNA and Hb synthesis are preserved)
(proerythroblasts expand but in maturing erythroblasts division is reduced and apoptosis increases)
what happens to cytoplasmic development and Hb accumulation in megablostic anaemias
normal - why the precursor cell is bigger (as has immature nucleus that isnt dividing= a megaloblast)
how is a macrocyte formed
when megaloblast (abnormally large precursor cell with immature nucleus) reaches specific level of Hb then nucleus is extruded leaving behind abnormally large red cell
are there more or less red cell in a macrocytic anaemia
less they are just bigger
less as reduced cell division and apoptosis
when is a cell macrocytic
when >100fl
what is a macrocyte
abnormally large mature red cell
why are cells large in megaloblatic anaemia
not because cell getting bigger but not able to become smaller during cell divisions
what does megaloblastic anaemia result in
larger precursor cells with immature nuclei leading to a macrocytic anaemia
what causes megaloblastic anaemia
B12 deficiency
folate deficiency
drugs
rare inherited abnormalities
why are B12 and folate important
essential co factors in:
- DNA synthesis and nuclear maturation (blood cell effect)
- DNA modification and gene activity (nerve system)
how is B12 absorbed
when first consumed binds to R-binder to prevent it getting broken down with food in the stomach
in response to food being in the stomach parietal cells secrete intrinsic factor which binds to B12 and releases it from food
pancreatic secretion raise the pH in the fluid in the small intestine to further separate it
IS ABSORBED IN THE ILEUM
taken into cells bound to transcobalamin
where is iron and calcium absorbed
proximal gut (duodenum- affected by crohns)
what can cause B12 deficiency
diet (vegans)
stomach:
- pernicious anaemia
- atrophic gastritis
- PPIs/H2-receptor antagonists
- gastrectomy/ by-pass
pancreas:
- chronic pancreatitis
small bowel:
- jejunum: bacterial overgrowth, coeliac disease
- Duodenum: resection, crohns disease
cubulin receptors: inherited deficiency
what is pernicious anaemia
autoimmune condition with resulting destruction of gastric parietal cells
results in intrinsic factor deficiency= B12 malabsorption and deficiency
what is pernicious anaemia associated with
atrophic gastritis
personal/ FHx of other autoimmune disorders (hypothyroidism, vitiligo, addisons)
