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patho RBC


Hematocrit lab value - normal 40-50 percent
hemoglobin normal lab value 13.5 - 18.0
RBC count normal 4.2 - 6.0 times 10 to the 6th/mcL
WBC count normal 5.0 - 10.0 times 10 to the 3rd/mcL
if WBC count < 1000 indicates risk of infection
if WBC count < 500 indicates risk of life-threatening infection
normal platelet count 140,000 - 340,000 per mm cubed
platelet count < 100,000 indicates thrombocytopenia
platelet count <50,000 indicates risk of increased beeding from minor trauma
platelet count > 400,000 indicates thrombocytosis
platelet count > 1 million indicates thrombosis
What is the most abundant granulocyte neutrophils
normal neutrophil lab value 2,500 - 7,500
neutrophil shift to left immature neutrophils being released by bone marrow - demand exceeds supply
neutrophil shift to right indicates inflammation or infection has subsided and supply now meeting lowered demands
neutrophils <100 indicates serious condition such as granulocytopenia, agranulocytosis or can be found in some chemo therapy
main causes of anemia impaired RBC production, bone loss, increased RBC destruction, any combination thereofe
In general, how will body compensate for anemia these sysetmes compensate: CV, resp, hematological
what happens with fluid compartments in anemia fluid moves from interstitum to vascular space --> diluted blood moves faster, more turbulently
if blood is 'thinned' by anemia (fluid into intravasculature), what manifestions might we see? ventricular dysfunction, cardiac dilation, valve insufficiency
what is the impact of anemia with respect to hypoxia manifestations hypoxia --> increased respirations/increased CO, may lead to RAA activation, may lead to CHF as heart over worked to meet oxygen demands
if anemia is due to Vit B12 deficiency, what other types of manifestions might we see neurological symptoms
name two types of macrocytic normochromic anemias pernicious anemia, folate-deficient anemia
what causes pernicious anemia defective intrinsic factor-->cant absorb Vit B12, which is needed for nuclear maturity/DNA synth --> delayed divsion/large cells
what causes the defective intrinsic factor in macrocytic normochromic pernicious anemia congenital IF defect, adult onset gastric mucousal atrophy, H. pylori, gastritis, gastrectomies
how do we treat pernicious anemia tx with Vit B12
what is MOA of folate-deficiency macrocytic normochromic anemia insufficient folate --> impaired RNA synth-->decreased RBC production, maturation
what causes the folate deficiency state in this anemia improper diet - alcoholics, malnourished
how do we treat folate-deficient anemia admin folate replacements
name 3 microcytic hypochromic anemias iron-deficiency, sideroblastic, thalassemia
Class of iron-deficiency anemia microcytic hypochromic
class of sideroblastic anemia microcytic hypochromic
class of thalassemia microcytic hypochromic
iron-deficiency anemia causes men: GI bleed women: profuse menstruation both: meds --> insufficient Fe absorbtion, pica
tx of iron-deficient anemia eliminate blood loss, iron replacement
causes of sideroblastic anemia mitochondrial congenital Fe metabolism, drug/toxin effects
tx of sideroblastic anemia admin Vit B6
cause of thalassemia anemia congenital defect in globin synthesis
name 5 types of normocytic-normochromic anemias aplastic, post-hemorrhagic, hemolytic, sickle cell, anemia of chronic inflammation
what class is anemia of chronic inflammation normocytic-normochromic
what class is sickle cell anemia normoctyic-normochromic
what class is hemolytic anemia normoctyic-normochromic
what class is post-hemorrhagic anemai normoctyic-normochromic
what class is aplastic anemia normoctyic-normochromic
what are 2 types of polycythemia absolute (overproduction of RBCs) or relative (decrease of plasma volume)
what is primary polycythemia due to factors intrinsic to red cell precursors
name a type of primary polycythemia polycythemia vera, a myeloproliferative disease
what is MOA of polycythemia vera it is a myeloproliferative disease where the pluripotent stem cell overproduces RBCs. may also overproduce WBCs and platelets
what is the definition of a secondary polycythemia caused by either natural or artificial increased production of EPA
what is MOA of secondary polycythemia physiological response to hypoxic conditions, such as high altitude, CHF, COPD where body compensates by increasing EPO
how does secondary polycythemia manifest clinically redness, enlarged spleen/liver, angina, thrombotic dx, cerebral insufficiency
what is a complication of secondary polycythemia bleeding may develop because clotting factors have been consumed
what are the symptoms of secondary polycythemia HA, visual disturbances, Dizz/weak, HTN, weakness
how do we tx secondary polycythemia phlebotomy, stop smoking, tx CHF/COPD
Created by: lorrelaws