HEMA Flashcards
Most common anemia
Hypoproliferative
Normocytic and Normochromic RBC with inappropriately low retic response( <2 -2.5)
Hypoproliferative anemia
Most common Hypoproliferative anemia
early IDA
Mechanism Of Hypo proliferative anemia
- Abnormal iron metabolism: IDA, anemia of inflammation
2. Suboptimal erythropoietin response to anemia: renal disease, inflammation, cancer, hypometabolic states
Determines the turnover ra+e of transferrin iron
Plasma iron level and the activity of the erythroid marrow
Conditions associated with decreased clearance time of transferrin iron
(inc clearance /fast turnover)
Increased erythropoieSis
IDA
Average RBC lifespan
120 days
One ml Of RBC is equal to how many mg of Iron
One
Amount Of iron needed to replace the RBC lost through senescence
20 mg/ day
For pregnant women on their last- two trimesters, how much iron is required per day
increased to 5-6 mg /d
Primary location for iron absorption
proximal small intestine
principal iron regulator hormone
HepCidin
Increased iron absorption despite normal or inc iren stores with associated inappropriately Low hepcidin
Erythroid hyperplasia
Indicators Of decreased iron stores
Decreased Serum Ferritin
Decreased stainable iron on bone marrow aspirations
Represents the amount Of Circulating iron bound to transferrin
Serum iron ( NV: 50 to 150)
Indirect measure of circulating transferrin
TIBC (NV: 300 to 360)
TSAT in iron deficiency States
<18%
Test to estimate iron stores
Serum Ferritin level
Most common causes Of increased Red cell protoporphyrin levels
IDA, lead poisoning
Reflects the total erythroid mass and can distinguish between IDA and anemia of inflammation
transferrin Receptor protein
In absolute IDA TRP is
Elevated
Conditions that present with hypochromic microcystic anemia
Thalassemias
Anemia of inflammation with inadequate iron supply to the erythroid marrow
MDS
Max dose of elemental iron per day
200
Inhibits iron absorption and release from storage sites
Hepcidin
Known as Unpaired globin precipitates to form inclusions that damage the cell
Heinz bodies
When is reticulOcyte count expected to increase after iron therapy
4-7 dayswith peak rise 1-1.5 weeks
Most prominent SE of iron therapy
GI distress in 15-20% of Pxs
Categories in Hypoproliferative anemias with inadequate endogenous EPO production for the degree of anemia observed
l. Chronic inflammation/ infection
2. Renal disease
3. Endo and nutritional deficiencies
Goals for the tx of anemia
NO intervention until hgb <8(if wo serious underlying CV/ Pulmo disease
> 11g/dl if with physiologic compromise
AE Of Epo administration in cancer patients
Increased risk of thromboembolic complications and tumor progression
Mutation in the Beta- globin gene due to change of 6th aminoacid from glutamic acid to valine
sickle cell
