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lecture 12 fuda

definition of anemia defined as a decrease in RBC mass resulting in decreased capacity to deliver O2 to tissues
3 basic pathophysiologic processes leading to anemia 1) blood loss // 2) decreased RBC production // 3)increased RBC consumption/destruction
how the body tries to normally compensate for tissue hypoxia increasing RBC production through erythropoietin production, increasing oxygen delivery by shifting 2,3-DPG curve, increasing CO and shunting blood from non-vital to vital areas
normoblasts the nucleated RBC precursors
gold standard lab test(s) for diagnosing anemias effectively CBC with retic count and peripheral blood smear
low Hgb essentially = anemia Hgb is more important than Hct
MCV mean corpuscular volume, describes the size of each RBC
MCHC mean corpuscular hemoglobin conc'n, describes the amt of Hgb per RBC
signs and sx of anemia pallor, weakness, dizziness, palpitations, dyspnea
RDW red cell distribution weight, describes the variation of RBC volume within blood. Higher RDW = greater variation in RBC size
increased RDW implies what conditon? Fe deficiency
characteristics of reticulocytes and nl count anucleate red cell precursors seen at final stage of differentiation, have reticular basophilic matrix of rRNA, polychromasia seen by special staining, high # reticulocytes shows that body is making new RBCs (good for anemia), nl values 0.5%-1.5%
poikilocytosis means there are a variety of RBC shapes seen on smear
CBC will not recognize any abnormalities with acute blood loss only until body moves interstitial fluid out into IV space to compensate for fluid loss does one see dilution of blood components
nl retic count seen after 2-3 days of anemia 10-15%, usually peaks thought @ 7-10 days
iron deficiency in an elderly individual --> think what? R sided colon ca until proven otherwise
anemia of chronic blood loss is actually anemia of Fe deficiency continued blood loss over time cuases imbalance btwn iron loss and iron intake
anemia of decreased RBC production shows what on labs? decreased retic count (abs decrease in marrow mass of erythroid precursors), normocytic and normochromatic anemia
how long do reticulocytes take to mature after being released from bone marrow? 1-2 days in the periphery before they are mature RBCs
pathologic states that are associated with decreased RBC precursors (proliferation defects) renal failure, aplastic anemia, myelophthisic anemia
renal failure kidneys don't make enough erythropoietin to sustain nl amt of RBC production
aplastic anemia congenital or acquired stem cell defects lead to failure in production of ALL hematopoietic lineages; bone marrow is hypocellular and peripheral blood is pancytopenic
myelophthisic anemia bone marrow is replaced by nonhematopoietic tissue
sites of extramedullary hematopoiesis, would be stimulated with myelophthisic anemia spleen and liver; however since these sites doesn't have regulatory environments, immature granulocytes and RBCs are released into peripheral blood thus increased retic count
dacrocytes teardrop shaped cells usually seen in peripheral blood with myelophthisic anemia
ineffective erythropoiesis aka maturation defects bone marrow is hypercellular with increased RBC precursors, only a small percentage of the cells proceed to maturity thus few mature RBCs in periphery
conditions causing ineffective erythropoiesis iron, cobalamin (B12), folate deficiencies or myelodysplastic disorders (neoplasia of myeloid cells)
without erythropoietin working effectively, one doesn't see what in bone marrow? pronormoblasts, not even 1st recognizable stage of maturing RBCs
iron-deficiency anemia forms microcytic and hypochromic RBCs, due to increased iron loss compared to absorption. #s of RBCs and reticulocytes is low b/c all require Fe for existence
iron depletion phase (not yet detectable anemia) plasma ferritin decreases as storage iron is mobilized, iron absorption increases
iron deficiency phase (not yet detectable anemia) plasma Fe levels fall when iron stores are exhausted, transferrin and its soluble receptor increase (Fe-binding protein in plasma, most important Fe pool)
iron deficiency anemia develops when all iron stores have been exhausted; early stages: normocytic and normochromic BUT late stages without tx: microcytic and hypochromic, poikilocytosis and anisocytosis
high RDW is known as what? anisocytosis, high degree of size variation among RBCs; seen with iron-deficiency anemias
bone marrow aspirate findings in a pt with iron-deficiency anemia Prussian blue staining shows decreased/absent sideroblastic and histiocyte iron stores
type of anemia that's attributable to folate or cobalamin deficiency megaloblastic anemia - cells are very large b/c their nuclei can't mature or divide without being able to make dTMP, folate and vitamin B12 are necessary cofactors
CBC findings in megaloblastic anemia macrocytic index, decreased # of RBCs, very high RDW, low # of reticulocyte (relative to anemia), possible leuko and thrombocytopenia, nucleated RBCs with basophilic stippling, macro-ovalocytes and hypersegmented PMNs
5 lab tests that should be ordered when megaloblastic anemia is suspected serum cobalamin, serum and RBC folate, serum methylmalonic acid and serum homocysteine [serum bili and LD will also be elevated due to RBC death in medulla]
B12 deficiency causes what dangerous sx demyelination, neurologic defects that may be irreversible
serum methylmalonic acid is only elevated in which type of vitamin deficiency vitamin B12 or cobalamin deficiency
bone marrow aspirate shows what in megaloblastic anemia? hypercellularity and shift toward immature cells ("left shift")
distinguishing features of megaloblastic anemia as compared to myelodysplastic syndromes hypersegmented (not hypo) neutrophils, giant metamyelocytes and giant band neutrophils
anemia of chronic dz is associated with inflammatory states or malignancy due to what mechanism? release of different inflammatory cytokines decreased Fe absorption, induction of macrophage sequestration of Fe and lessened erythropoietin production
most anemias of chronic dz are normocytic and normochromic when Hgb is lower than 9 and microcytic/hypochromic RBCs are noted, could be either nl 20% population or OTHER ETIOLOGY
IL-6's action within context of anemia of chronic dz anemia increased hepcidin that blocks ferroportin from allowing release of Fe stores from within cells like duodenal enterocytes. iron gets stuck within macrophages and other storage sites
nl circulation time of RBC 120 days
CBC and other lab findings associated with hemolytic anemia increased LD, serum unconjugated (hasn't been through liver yet) bili and urobilinogen. decreased haptoglobin (binds bili breakdown products). erythroid hyperplasia, peripheral reticulocytosis
paroxysmal nocturnal hemolysis PIG-A gene mutated causing GPI anchors to be dysfunctional, various proteins like CD55 & CD59 which regulate complement lysis of RBCs are lost. this causes periodic hemolysis
manifestations of vaso-occlusive episodes in sickle cell pts pain crises, MS pain, acute chest syndrome, renal dysfunction, priapism and retinal pathology, functional asplenia by adulthood
sickle cell pts' blood smears show? normocytic and normochromic smear, marked anisopoikilocytosis, sickle cells, occasional spherocytes, hyposplenism (Howell-Jolly bodies, nucleated RBCs and pappenheimer bodies)
thalassemia group of blood disorders characterized by decreased production of structurally normal globin chains - either alpha or beta, that make up normal HbA tetramers
why thalassemia causes hemolytic anemia decreased production of one of the chains leads to excess in the others, this causes precipitation of chains within the RBC and subsequent hemolysis
the most clinically significant thalassemias which manifest as mod-severe anemia (microcytic and hypochromic) 3 or 4 deletion alpha-thalassemias OR compound heterozygous beta-thalassemias
hereditary spherocytosis and warm Ab type immunohemolytic anemias are similar in that both show predominant spherocytes and (+) osmotic fragility tests. what differentiates them? direct antiglobulin test or DAT - immune hemolysis test that will be (-) for hereditary spherocytosis but (+) for the warm Ab immunohemolytic anemias
hereditary spherocytosis is the most commonly inherited hemolytic anemia various mutations cause defective interactions btwn the RBC membrane and underlying cytoskeleton; vesiculation and fragility of the membrane make them take on spherical shape, they get caught in RES cords and removed in spleen
G6PD deficiency G6PD enzyme is defective within RBCs thus no glutathione can be made to protect against oxidative stress. thus when it does happens, Hgb denatures and precipitates forming Heinz bodies; splenic macrophages eat precipitates forming "bite & nibble" RBCs
immunohemolytic anemias DAT (+)/warm - IgG Abs cause opsonization and subsequent phagocytosis in the spleen or biting off small bits to make spherocytes that are then cleared // cold - IgM Abs with their pentamers aggregate RBCs
hallmark of microangiopathic or traumatic anemias increased amts of RBC fragments in blood aka schistocytes and/or triangulocytes
most common microangiopathic hemolyses TTP, HUS and DIC
Created by: sirprakes