lecture 12 fuda
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| definition of anemia | defined as a decrease in RBC mass resulting in decreased capacity to deliver O2 to tissues
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| 3 basic pathophysiologic processes leading to anemia | 1) blood loss // 2) decreased RBC production // 3)increased RBC consumption/destruction
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| 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
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| normoblasts | the nucleated RBC precursors
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| gold standard lab test(s) for diagnosing anemias effectively | CBC with retic count and peripheral blood smear
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| low Hgb essentially = anemia | Hgb is more important than Hct
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| MCV | mean corpuscular volume, describes the size of each RBC
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| MCHC | mean corpuscular hemoglobin conc'n, describes the amt of Hgb per RBC
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| signs and sx of anemia | pallor, weakness, dizziness, palpitations, dyspnea
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| RDW | red cell distribution weight, describes the variation of RBC volume within blood. Higher RDW = greater variation in RBC size
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| increased RDW implies what conditon? | Fe deficiency
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| 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%
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| poikilocytosis | means there are a variety of RBC shapes seen on smear
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| 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
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| nl retic count seen after 2-3 days of anemia | 10-15%, usually peaks thought @ 7-10 days
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| iron deficiency in an elderly individual --> think what? | R sided colon ca until proven otherwise
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| anemia of chronic blood loss is actually anemia of Fe deficiency | continued blood loss over time cuases imbalance btwn iron loss and iron intake
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| anemia of decreased RBC production shows what on labs? | decreased retic count (abs decrease in marrow mass of erythroid precursors), normocytic and normochromatic anemia
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| how long do reticulocytes take to mature after being released from bone marrow? | 1-2 days in the periphery before they are mature RBCs
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| pathologic states that are associated with decreased RBC precursors (proliferation defects) | renal failure, aplastic anemia, myelophthisic anemia
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| renal failure | kidneys don't make enough erythropoietin to sustain nl amt of RBC production
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| 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
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| myelophthisic anemia | bone marrow is replaced by nonhematopoietic tissue
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| 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
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| dacrocytes | teardrop shaped cells usually seen in peripheral blood with myelophthisic anemia
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| 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
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| conditions causing ineffective erythropoiesis | iron, cobalamin (B12), folate deficiencies or myelodysplastic disorders (neoplasia of myeloid cells)
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| without erythropoietin working effectively, one doesn't see what in bone marrow? | pronormoblasts, not even 1st recognizable stage of maturing RBCs
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| 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
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| iron depletion phase (not yet detectable anemia) | plasma ferritin decreases as storage iron is mobilized, iron absorption increases
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| 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)
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| 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
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| high RDW is known as what? | anisocytosis, high degree of size variation among RBCs; seen with iron-deficiency anemias
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| bone marrow aspirate findings in a pt with iron-deficiency anemia | Prussian blue staining shows decreased/absent sideroblastic and histiocyte iron stores
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| 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
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| 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
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| 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]
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| B12 deficiency causes what dangerous sx | demyelination, neurologic defects that may be irreversible
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| serum methylmalonic acid is only elevated in which type of vitamin deficiency | vitamin B12 or cobalamin deficiency
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| bone marrow aspirate shows what in megaloblastic anemia? | hypercellularity and shift toward immature cells ("left shift")
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| distinguishing features of megaloblastic anemia as compared to myelodysplastic syndromes | hypersegmented (not hypo) neutrophils, giant metamyelocytes and giant band neutrophils
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| 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
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| 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
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| 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
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| nl circulation time of RBC | 120 days
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| 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
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| 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
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| 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
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| 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)
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| thalassemia | group of blood disorders characterized by decreased production of structurally normal globin chains - either alpha or beta, that make up normal HbA tetramers
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| 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
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| 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
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| 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
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| 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
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| 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
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| 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
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| hallmark of microangiopathic or traumatic anemias | increased amts of RBC fragments in blood aka schistocytes and/or triangulocytes
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| most common microangiopathic hemolyses | TTP, HUS and DIC
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