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
what are the treatments for thalassaemias
- transfusions
- iron chelation
- folic acid immunisation
what is hereditary spherocytosis
an inherited red cell membrane problem so they become sphere shaped (spherocytes) so no longer fit through capillaries
give examples of acquired RBc membrane problems
this is where there is mechanical damage to RBCs due to
- heart valves
- vessels
- burns
- drowning
what defects in rbc metabolism can lead to anaemia
G6P dehydrogenase deficiency
pyruvate kinase deficiency
how may blood be lost to cause anaemia
- stab wounds
- gastric ulceration
- gastric/colon cancer
outline how the RES can cause anaemia
haemoylytic anaemia occurs where theres increased RBC destruction
- this can occur in vessels (intravascular) or outside (extravascular)
- autoimmune where antibodies (IgG and IgM) bind to RBC membranes
what is myelofibrosis
there is decreased erythropoiesis as the fat cells in bone marrow are replaced by fibrous tissue so theres less room for RBC production
what are reticulocytes
immature RBCs
what are myeloproliferative disorders
where theres an overproduction of RBCs, WBCs and platelets
- causes thrombosis
- result in extramedullary haematopoiesis
- causes leukaemia
what is polycythaemia vera
where there are too many RBCs giving a high haematocrit
this makes the blood more sticky and prone to thrombosis
requires venesection, aspirin and rugs to reduce overproduction
what is polycythaemia
a group of disorders where there is an increase in circulations RBCs with a persistently raised haematocrit
what is erythrocytosis
an increase in the concentration of RBCs due to either a decrease in plasma vol, increase in RBC mass
- primary = polycythaemia vera
- secondary = driven by EPO production
what causes secondary erythrocytosis
- physiological = hypoxia
- pathological = cancers
