anaemia Flashcards
what is anaemia
low hb in blood
what are the symptoms of anaemia
shortness of breath, tiredness, cardiac failure, palpitations and headache
what are signs of anaemia
allow, thrachycardia and hypotension
what is the life cycle of RBC
bone marrow (controlled by erythropoiesis and hb synthesis) RBC (controlled by structure and function) and removal (controlled by reticuloendothelial systems)
9 ways anaemia develops
- hormonal control of erythropoiesis
- dyserthyropoesis
- nutrient deficiency
- mutations in proteins encoding globin chains
- defects in membrane structure
- acquired defects in membrane structure
- defects in red cell metabolism
- removal of excess red cells by RES
- multifactoral
describe how it evolves by hormonal control
eryhtropoetin is a hormone which controls synthesis of RBC. when someone becomes anaemic its detected by kidney and more RBC produces. BUT in kidney disease erythropoietin production is reduced. if empty bone marrow after chemo then can’t respond to erythropoietin. if marrow infiltrated by cancer haemopoitic cells reduced and therefore reduced response to erythropoietin.
describe how it evolves by dyserythropoesis
this is the defective development of RBC. this could be due to;
iron not being related for use in hb (happens in inflammatory diseases e.g RA which make iron stay in macrophage)
can also lead to reduced life span because don’t have proper structure and removed by spleen
example- myelodysplastie syndrome where abnormal clone of marrow stem cells are produced so don’t develop properly and can’t enter circulation OR if they do they are removed by the spleen
describe how it evolves by nutrient deficiency
lack of iron means hb synthesis is deficient
describe how it evolves by mutations in proteins encoding global chains
e.g thalassaemia. can’t be made properly in RBC
describe how it evolves by defects in membrane structure (hereditary)
spherocytosis, eliptocytosis and pyropolikilocytosis. draw these. it means cells are flexible and break up easily or they are removed from circulation = haemolytic anaemias
describe how it evolves by acquire defects in membrane structure
mechanical defects e.g heart valves put in and RBC become sheered as they move through
heat - turn them to spherocytes
drowning
describe how it evolves by defects in red cells metabolism
glucose 6 phosphate dehydrogenase and pyruvate kinase deficients mean won’t be able to keep membrane in good condition and therefore RBC will be removed by spleen (upkeep of S-S bonds)
describe how it evolves by removal of excess RBC by RES
antibodies bid to RBC membrane and RES removes them from circulation = AUTOIMMUNE
describe how it evolves by multiple factors
example- myelofibrosis. fibrotic bone marrow= reduced response to erythropoietin. then RBC are enlarged and removed in excess by spleen
3 factors that we can use to evaluate anaemia
by mechanism, by size and by presence or absence of reticulocytes
what are microcytic cell causes in anaemia
TAILS - thalassaemia, aneamia of chronic disease, iron defiecney, lead poisoning and sideroblastic anaemia
what is sideroblastic anaemia
sideroachrestic anemia is a form of anemia in which the bone marrow produces ringed sideroblasts rather than healthy red blood cells
what are macrocytic cell causes in anaemia
vit B déficient, folate deficiency, liver disease, hypothyroidism and alcohol.
what could be the reason for normal cell size, normal reticulocyte number in anaemia
primary bone marrow failure or secondary bone marrow failure which is due to disease e.g HIV
what could be the cause of bleeding if there are reduced reticulocytes but no haemolysis
bleeding
what is the cause of anaemia if there are unusual numbers of reticulocytes and haemoylsis
could be mechanical acquired structural defect, hereditary defect in structure, enzyme defects meaning less stable membrane , increased splencic sequestration or immune mediated response (autoimmune)
building blocks of DNA
vit B12 and folate
how is visit B12 absorbed
parietal cells in stomach produce HCL and Intrinsic factor . the intrinsic factor binds to fit B12 and allows it to be absorbed in the last part of the ileum
causes of low B12
3-6 years worth of it stored up. if deficient occurs v slowly and causes cardiac problems because heart begins to compensate.
causes;
diet
lack of IF (intrinsic factor)
disease of ileum (e.g churns prevents absroption)
lack of Transcobalamin (congenital). This is a glycoprotein which serves to protect vit B12 from acid in stomach by forming a complex with it
causes of low folate
store lasts for about 3-4 months and absorption occurs in the duodenum and the jejunum
causes;
dietary
increased use (e.g pregnancy)
disease of duodenum and jejunum e.g in coeliac disease
lack of methyTHF - some drugs may inhibit the enzyme
what is the B12 folate link
if deficient of 1 then deficiency of thymidylate.
bad because uracil incorporated into DNA instead of thymine. this causes an error which is detected and then the DNA is destroyed
how does B12 or folate deficiency result in megalobalsic anaemia
error in DNA due to lack of thymine means DNA is being destroyed and doesnt fully mature leading to a large nuclei with open chromatin. also asynchronous maturation between cytoplasm and nuclei meting more cytoplasm. = larger cell than normal (microcytic)
megalobasltic cell features
microcytic, anidpoikilocytosis, hyper-segmented WBC and white cell precursors
what does B12 and folate deficiency lead to
neurological disease and lack of folate in pregnant women also to neural tube defects
megaloblastic anaemia signs
low hb,
high MCV
high bilirubin/LDH (due to hardworking bone marrow which isn’t properly producing any cells)
low B12 and folate serum levels in blood
how to treat low folate and B12
low folate= oral folic acid
low B12= intramuscular hydroxycobalmine if problem with absorption OR cyanacocobalamine if dirty problem BUT must be V careful of cardiac failure because heart is already compensating
