Anaemia Flashcards
Cell production and cell loss and survival
Any insult to bone marrow, it very quickly manifests in blood counts because it is highly active and dividing quickly.
Normal blood count-need healthy bone marrow and need components to make cells
Red blood cell production and survival:
Why is FBC so useful?
- Tissue easily obtained for monitoring disease
- Most organ systems are solid organs eg liver, heart, brain. But blood is a liquid tissue that is easy to sample and simple to analyse.
FBC normal range and key questions
- Look at info in groups so for red cells-hb, mcv and reticulocytes
- White cells-don’t just look at total WCC, look at each individual cell count eg check for neutropenia (could be due to gram neg speticaemia)
- Is this an isolated single lineage disorder or are multiple lineages affected. Eg if only platelets are affected not likely to be bone marrow issue but production issue eg platelets being destroyed. If bone marrow destruction all cell lines affected. Whereas peripheral destruction only targets a specific cell line.
- Vit B12 deficiency-very high MCV
- Auto immune haemolytic anaemia-modest MCV as release of reticulocytes released into peripheral blood pushes up mean
- Fe deficiency anaemia-very low MCV
Summary MCV and causes
Vegan, Indian and on NSAIDs
- Iron deficiency anaemia due to veganism
- Beta thalassaemia trait
- Anaemia of chronic disease
Further info:
What is the diagnosis?
= Anaemia of chronic disease
From history it could have been any of the 3 but from the tests it is anaemia of chronic disease because she has a low transferrin.
Low ferritin confirms iron deficiency, a normal or high ferritin doesn’t exclude iron deficiency because ferritin is an acute phase reactant so it can be increased in inflammation.
The key to distinguish the 2 is TRANSFERRIN! Low transferrin is anaemia of chronic disease. ie lots of iron but it’s not easily available. Think of transferrin as an indirect measure of TIBC.
Iron haemostasis:
Anaemia of chronic disease explained:
-Sequestering the iron away in chronic inflammation we keep it away from bacteria which would use it to proliferate so it is advantageous, but it also stops red blood cells from using iron so its bad.
Random iron deficiency anaemia explained:
Teaching points Different normal range for ESR for men and women
- Transferrin – transporter (also discuss transferrin sat) Ferritin –storage, ESR –
- Rouleaux: stacks of red cells•The resemble a pile of coins•They result from alterations in plasma proteins
- The high ferritin and low transferrin support a diagnosis of anaemia of chronic disease.
- Advise her to take folic acid
- She has beta thalassaemia trait as has modest suppression of Hb, she has very low MCV
- Not low ferritin so not likely iron deficiency
- But she has a raised HbA2, so not issue to her but may be issue to her kid so get her kid or partner screened to check to see if they have beta thalassaemia.
- Trait is diagnosed with raised HbA2 and normal ferritin and low MCV.
- Body has no way to excrete iron so quickly they can become iron overloaded and chelation is expensive and not very successful.
Can increase HbF and so cure it
Microcytic anaemia causes:
- Post menopausal women and men with low iron- GI malignancy causing occult blood loss until proven otherwise
=hypothyroidism, alcoholic liver disease, could be autoimmune haemolytic anaemia
Could have forgotten to take thyroid replacement meds or done previous damage to liver
=autoimmune haemolytic anaemia
Raised MCV, so not SCA, normal B12 and folate, raised bilirubin and moderately raised transaminase. She has reticulocytosis so bone marrow healthy and replacing lost cells. LDH is intracellular enzyme and so is released when cells are broken down eg rapidly dividing cancer cells or red blood cell breakdown (due to unconjugated bilirubin).
Haemolytic anaemias:
Haemolysis can be subdivided into inherited (defect of membrane etc) and acquired (in toxic environment eg autoimmune destruction or microangiopathic)
How to determine if haemolysis is inherited or acquired?
=Direct antiglobulin test aka coombs test
Spherocytes seen in hereditary spherocytosis or in haemolytic anaemia
-Wash away plasma, then resuspend in plasma. If ABs bound to RBCs and you put in antigens that bind you have autoimmune haemolytic anaemia
Autoimmune haemolytic anaemia
Acquired haemolytic anaemia:
=Folate deficiency
As she has coeliac disease (disease of prox small bowel and this is where folate is absorbed). B12 is absorbed in terminal ileum not affected by coeliac disease
Also get howell jolly bodies due to functional hyposplenism
Megaloblastic anaemia
b12 and folate:
Deficiency linked neurological disease
folate-neural tube defects eg spina bifida, hydrocephalus (why we supplement bread and flour
b12-peripheral neuropathy, subacute combined degeneration of the spine, dementia
Safe for child to undergo GA?
=Yes
Child has sickle cell trait. SCD has 70-90 Hb, theirs is too good so must be trait. SCD-musn’t have GA as hypoxia can be exacerbated and lead to stroke etc.
Child is AS so heterozygote so no risk to have GA.
=G6PD enzyme deficiency is very common
Inherited haemolytic anaemias, usually a single gene defect impacting on one of the three components of RBCs, (non-nucleated cells)
=Breast cancer metastasises to bone marrow
Not isolated anaemia, involves all lineages so something wrong with marrow. Normal b12 and folate so must be failure of BM with normal haematinics.
In blood film, see immature cells (can see nucleus in RBC) which should only be present in BM. Fits with BM failure and thsi is caused by cancer infiltrating
Bone marrow failure
=Severe Aplastic anaemia
Severe pancytopenia seen
Due to radiation poisoning, hepatitis, chloramphenicol antibiotic but none would cause helical nuclei so this was due to poisoning. Complete bone marrow failure. Could see this in acute leukaemia but would expect to see blasts in blood film in this case.
