anemia and RBCs Flashcards
What is anemia
Decreased circulating red cell mass
Leads to decreased Hemoglobin concentration of blood
leads to ddecreased O2 carrying capacity of blood
Leads to decreased O2 delivery to tissues (final physiologic consequence)
Compensatory mechanisms in anemia
increased red cell production
Increased 2,3 DPG, shunting of blood from non-vital to vital areas, increased CO, increased pulmonary Function
SIgns and symptoms of anemia
Tissue hypoxia–> weakness, malaise, easy fatigability
Increased RBC production–> marrow expansion with potential bony abnormalities
Shunting of blood to vital organs–> pallor
Increased CO–> tachycardia, cardiac ischemia in severity
Increased pulmonary function–> dyspnea on exertion
funtional classification of anemia
blood loss, decreased production, accelerated destruction
Morphologic classification of anemia
microcytic:
Normochromic- irond deficiecy early, thalesemia trait, anemia of chronic disease, some hemoglobinopathies
Hypochromic- iron deficiency, thalassemia trait, sideroblastic anemia, anemia of chronic disease
Normochromic/normocytic:
Anemia of chronic diseasea, anemia of renal failure, marrow infiltrative, aplastic anemoa, blood loss hemolysis
Macrocytic:
B12/folate deficiency, liver disease, myelodysplastic syndromes, blood loss, hemolysis, some drugs
investigation of anemia
clinical history, physical exam, CBC, Reticulocyte count, peripheral blood smeat diagnostic tests
CBC
Hb concentration (HB, g/dl, g/l): hemoglobin in a lysed sample with reagents, complexes are measured spectraphotometrically, MOST IMPORTANT PARAMETER FOR ASSESSMENT OF O2 CARRYING CAPACITY OF BLOOD
Hematocrit (Hct,%): packed cell colume (percentage of blood volume comprised of RBCs, centrifucation or calculated as MCV x RBC, USUALLY 3 TIMES HB DOES NOT ADD INDEPENDENT INFORMATION
RBC count: (direct number / volume, generally correlates well with Hb and Hct, adds little)
Mean cellular/coruscular voluem (MCV fL), measured directly based on either electricla impedence or light scatter, verry useful in differential of anemia (micor-normor, macro cytic anemia)
Mean corpuscular hemoglobin (MCH pg), calculated as Hb/RBC, measure of amount of hemoglobin/RBC, high correlation with MCV
Mean corpuscular hemoglobin concentration (MCHC)measure of chromacity of RBCs, Calculated as Hb/
(MCV x RBC), decreased in hypochromic anemias, increased ina few hyper chromic states- spherocyteosis, hemoglobin CC disease
Red cell distribution width- variation of red cell columes
Microcytic anemia differential diagnosis
Iron deficiency, thalassemia, anemia of chronic disease
Macrocytic anemia differential diagnosis
megaloblastic (impaired DNA dyntheis (B12 and folate deficiency, some drugs, myelodysplastic syndromes
Non megaloblastic- reticulocytosis, liver disease, hypothryoidism, some drugs
abnormal RBC shape
poikilocytosis Sphericytes- balls Target cells- targets Ellipocyteis-ovalocyted teardrop cells Sickle cells schistocyted- fragmented Bite cells- bites of spleen
REd cell size variabily,
average red cell size
Abnormal variablity- anisocytosis
Small average cell- micro, large-macrocytodis
hemoglobinization
Hypochromia, normochromia look at central pallor
Polychromasia- reticulocytes- wierd color (blue)
Red cell inclusions
Howell jolly bodies (nuclear fragments)- splenectomy megalo- little blue dots
Pappenheimer- iron dots
Basophillic stippling- little blue dots all over rBC
HbC crysitals- large bars
red cell arrangements
rouleaux- chains of RBC
Agglutination- globs of RBC (IgM ntibodie)
anemia of blood loss- acute
initially no anemia by CBC parameters despite decrease in blood volume
Ademia develops as tissue fluid enters vascular space to restore blood volume, producing dilution of cellular elements
Reticulocyte count will increase after 2-3 days and peaks after 7-10 days
anemia of blood loss- chronic
no anemia initially because marrow is able to compensate
Slight reticulocytosis
Eventual development of iron deficiency with resultant iron deficiency anemia
RBC production
Sites of RBC production- embryo (tolk sac) fetus (liver), bone marrow thru adults
Regulation: decreased o2–> kidney make more EPO, EPO causes prolifertion and differentiation of committed progenitor cells
normoblastic maturation
normoblasts (nucleated RBC precursors) obtain iron from plasma transferrin for hemoglobin syntheis
Up to 16 retivulocytes produced from each pronormoblast (earliest morphologically recognizable erythroid precursor)
Roughly equal numbers of reticulocytes and normoblasts in marrow
blue- mRNA, red Hb
Reticulocytes
earliest a nucleat erythroid form, a little larger than mature RBCs, contains residual TNA gives the cytoplasm a blue tinge on routinely stained blood smears (polychromasia)
Stai in marrow for a day or two making Hb, before being released into circulation
Normally continue as reticulocyte for a day in circulation before losing ribosomes, mitchondria, other organelles to become mature erythrocytes
1% of peripheral eirthorocytes
RNA stains, used as a measure of marrow RBC production (percent varies depending on total RBC) theres a corrected percentage and absolute RC
Anemia due to decreased RBC production: Innefective erythropoiesis
decreased RBC production despite increased RBC precursors in marrow
Characterized by defects in maturation
iron deficiency (cytoplasmic maturation defect), megaloblastic anemia (nuclear maturation defect), MDS.
Prominent morphologic abnormalities of erythrocytes due to disordered maturation, dysmaturation of of erythroid precursors in marrow, decreased reticulocyte count despite increased erythroid mass in marrow
Decreased RBC production: decreased RBC precursors aka marrow failure
proliferaton defect
Absolute decrease in the marrow mass of erythroid precusors
(decreased erythroid progenitors available for RBC production, decreased proliferation capacity of numerically adequate erythroid progenitor)
Normochromic/normocytic, usually little anisopoikilocytosis , decreased reticulocyte counts
Stem cell defects with adequate erythropoietin
Marrow replacement, decreased erythropoeietin
decreased RBC production due to anemia of chronic disease aka anemia of inflammation
inflammatory block in erythropoiesis, IL1 TNF alpha and IFN gamma mediated,
Accelerated destruction anemia
biconcave RBC, durability , flexibily and tensile strength
spectrin bound by ankyrin
Hemolysis, should live for 120 days, increased destruction results in marrow production (8x normal if needed, with enough iron folate and health)
when destruction>BM compensation, anemia develops
intavascular, extravascular or in combination
Extravascular hemolysis
most common form of hemolytic anemia
Final common pathway- decreased RBC deformability
Rigid cells cant get in narrow spaces between splenic cords and sinusoids, cells are damaged further with prolonged exposure to cordal envolvement, damaged cells phagocytized by cordal macrophages
fate of hemoglobin
could go to free haptoglobin in the liver where its dead
or splenic macrophage breaks it up into lipid, protein and heme–metabolized to bilirubin
