Haematinics Flashcards
microcytic anaemia
MCV<80fL iron deficiency anaemia of chronic disease copper deficiency acquired sideroblastic anaemia lead poisoning
normocytic anaemia
MCV 80-100fL acute haemorrhage or haemolysis renal failure anaemia of chronic disease combined nutritional deficiencies marrow disorders malignancy
microcytic anaemia
MCV>100fL hypothyroidism B12/folate deficiency liver disease ETOH compensated haemolysis/haemorrhage marrow disorder pregnancy drugs
treatment for iron deficiency
iron, oral or parenteral
treatment for renal failure
erythropoetin
B12/folate deficiency treatment
B12, folate
iron form more well absorbed
Fe2+ not Fe3+
acidic pH of stomach
reductive, maintains Fe2+
Fe in many foods is not absorbable because
it is complexed with phytates or phosphates
Fe replacement
oral
antacids
cause oxifation to Fe3+ making it not absorbable
iron preparations are best taken
on an empty stomach
antibiotics that complex with iron
tetracycline, and fluoquinolones
adverse effects of Fe
gastrointestinal intolerance
hypersensitivity
overdose of iron
serious, early GI irritation, later multi system failure and death
megaloblastic anaemias
folic acid deficiency (usually dietary)
vit B12 deficiency (usually malabsorption, EG pernicious anaemia)
dihydropholate reductase
turns folic and into dihydrofolic acid and then into tertahydrofolate
C1 metabolism
picks up singe carbon groups from tetrahydrofolate
single carbon groups are important for
making purines and thymidines
replacing folic acid
oral folic acid daily
no adverse effects
especially important in pregnancy
methotrexate
close analog of folic acid
dihydrofolic reductase works on it as well
rapidly dividing cells can’t work because methotrexate toxicity stops production of single carbon groups
vit B12 is needed for
turning 5-methyltetrahydrofolate into tetrahydrofolate
vit B12 deficiency is bad because
there’s too much 5-methyltatrahydrofolate ‘blocked hydrofolate’
replacing vit B12
hydroxocobalamine
intramuscular injection
weekly x4 to replenish stores
no adverse effects
Epo
encourages erythroid progenitor cells into red blood cells
agent encouraging production of platelets from megakaryocytic
Tpo
agent responsible for encouraging neutrophil progenitor cell into neutrophils
G-CSF
EPO comes from
kidney
EPO is deficient in chronic renal failure
times when recombinant G-CSF might be needed
- suppressed myeloid cell growth during cancer chemotherapy
- rebuilding leukocyte populations after bone marrow transplant
thombopoetin-mimetic
romiplostim
binds and activates thrombopoeitin receptor of megakaryocyte
clinical uses of thombopoetin mimetics
idiopathic thrombocytopaenic pursuer
rebuilding platelet population after bone marrow transplant
some other conditions where bone marrow fails to produce enough platelets
