anaemia, vitamin B12, folate and polycythaemia Flashcards
why might anaemia develop
- reduced erythropoiesis or dyserythropoiesis
- problems with haemoglobin synthesis
- problems with RBC structure or metabolism
- problems with the reticuloendotheial system
what is dyserythropoesis
where faulty RBCs are produced
what causes reduced erythropoiesis
- chronic kidney disease so EPO isn’t being made
- empty bone marrow which cant respond to EPO e.g. from chemotherapy or parvovirus
- bone marrow infiltrated by cancer cells or fibrotic tissue
what is anaemia of chronic disease
when iron stored in macrophages isn’t released meaning circulating RBC have a lower life span with a lack of response to erythropoietin.
often theres an increase in CRP and ferritin due to infection
there is no iron deficiency just lack of functional iron
seen in rheumatoid arthritis, IBD, TB
what is myelodysplastic syndromes
where theres a production of abnormal clones of marrow stem cells
the RBC produced are defective and large (macrocytic)
RBc prematurely destroyed
treated with transfusions
what types of haemoglobin synthesis abnormalities are there
- ones that give a lack of iron
- DNA synthesis errors
- mutations in genes coding for production
what are vitamin B12 and folate needed for
nuclear division and maturation so if deficient lead to large red cell precursors which large nuclei and open chromatin
what is megaloblastic anaemia
When DNA synthesis is impaired, the cell cycle cannot progress. This leads to continuing cell growth without division, which presents as macrocytosis.
due to folate or vit b12 deficiency
how is vitamin B12 obtained and transferred to tissues
- its combined with the glycoprotein intrinsic factor produced by parietal cells
- the IF-B12 complex binds in the ileum allows absorption of B12 and destruction of IF
- B12 is transported by being bound to the plasma protein transcobalamin
how results in a vitamin b12 deficiency
- dietary deficiency
- Intrinsic factor problems e.g. from autoimmune diseases attacking parietal cells
- if the IF-B12 complex cant bind to ileum e.g. in Crohn’s
- transobalamin problems
how is folate obtained and transferred
absorbed in duodenum and jejunum
- dietary folates converted into methylTHF
- this circulates and is need for DNS synthesis
- deficiencies occur due to diet, bowel diseases, drugs, alcoholism
what is a pancytopenia
when theres low platelets and neutrophils
outline sickle cell anaemia
- inherit sickle cell gene which is a mutation substituting valine for glutamic acid
- can be co inherited
- capillaries become occluded by misshapen RBC which get stuck
- in deoxygenated areas the chains polymerise
- made worse by cold, infection and stress
- gives decreased haemoglobin synthesis
outline thalassaemia
reduced rate of synthesis of normal globin chains
- leads to excess of other chain which causes RBC to be defective so they are destroyed
what is extramedullary haempoiesis
a compensation of thalassaemia attempt where the spleen and liver try to make more RBCs,so it becomes enlarged (splenomegaly and hepatomegaly) which causes skeletal abnormalities
- therefore EPO is stimulated to make more RBc resulting in iron overload
