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45 Cards in this Set
- Front
- Back
2 causes of anemia associated with iron metabolism
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1. faulty heme production
(lack of Fe, defective iron production, or defective PORPHYRIN production) 2. faulty globin synthesis (thalassemias) |
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Etiology of Iron deficiency anemia (IDA)
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1. poor diet
2. malabsorption 3. increased demand (pregnancy, etc) 4. blood loss (most common cause) |
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symptoms of decrease of hemoglobin in body
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weakness, fatigue, dizziness
shortness of breath palpitations skin pallor |
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symptoms of decrease of Fe-containing enzymes in tissues
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impaired neutrophil phagocytosis
impaired cell-mediated immunity splenomegaly inflammation koilonychia neurologic abnormalities |
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Stages of IDA
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1. iron depletion: Fe stores exhausted, normal peripheral blood values & morphology except for slight increase in RDW
2. Fe-deficient erythropoiesis: Fe levels drop, no sideroblasts in marrow Increased: FEP, TIBC Decreased: MCV 3. Fe deficiency anemia decrease in Hb, microcytic hypochromic RBCs |
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peripheral blood smear features of IDA
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Microcytosis, hypochromia, anisocytosis, poikilocytosis
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changes in bone marrow in IDA
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erythroid hyperplasia in bone marrow, abnormal erythroblasts, decreased hemosiderin, decreased sideroblasts
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lab findins of IDA
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DECREASED: Hb, Hct, RBC count, Retic count, Serum Fe, ferritin, transferrin saturation
INCREASED: TIBC |
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What is hemachromatosis?
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condition of Fe overload characterized by high Fe absorption rate
note: NOT assoc. w/ anemia! |
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Etiology of Hemachromatosis
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1. PRIMARY idiopathic (inherited)
2. Chronic transfusion therapy |
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Pathophysiology of hemachromatosis
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excess Fe deposits accumulate & interfere w/ normal cellular function
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Lab findings of hemachromatosis
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DECREASED: normal or low TIBC
INCREASED: Serum Fe, serum ferritin, transferrin saturation |
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what is sideroblastic anemia?
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group of disorders characterized by abnormalities of HEME metabolism
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Pathophysiology of sideroblastic anemia
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1. Fe absorption is normal but UTILIZATION is impaired
2. Fe present but not incorporated into hemoglobin 3. Positive Fe balance, yet anemia still exists |
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Unique characterics of sideroblastic anemia
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1. ringed sideroblasts in bone marrow
2. dimorphic peripheral blood picture |
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classifications of sideroblastic anemia
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1. Idiopathic (primary) - idiopathic refractory anemia w/ dyserythropoiesis, abnormal Fe utilization, PRE-Leukemia
2. secondary - disturbance in enzymes regulating heme synthesis (alcoholism, malignancies, etc) |
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visual characteristics of secondary sideroblastic anemia
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poikilocytosis, inclusions, basophilic stippling, dimorphism in peripheral blood
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lab findings in secondary sideroblastic anemia
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DECREASED: TIBC (can be normal too)
INCREASED: serum Fe, transferrin, FEP |
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what is anemia of chronic disease (AOD)/anemia of inflammation (AOI)
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anemia caused by a long term chronic disease, 2nd most common anemia in western world
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Pathophysiology of AOD/AOI
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caused by decrease of Fe flow to bone marrow (by blockage?)
erythropoietin not stimulated shortened RBC survival: changes to rbc surfaces, hyperactive macrophages, intramedullary destruction suppression of erythropoiesis: release of IL-1 |
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Effect of IL-1 on body in situation of AOD
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IL-1 inhibits erythroid stem cell proliferation. Activates neutrophilic response w/ release of lactoferrin. Aids release of tissue necrosis factor (TNF)
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Clinical findings of AOI/AOD
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1. general symptoms of anemia
2. generally present in mild form |
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Lab findings of AOD/AOI
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Polychromasia, Anisocytosis (P b4 A)
DECREASED: serum Fe, TIBC, transferrin saturation, sideroblasts in marrow INCREASED: serum ferritin |
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what is a megaloblastic anemia
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group of disorders which have characteristic of macrocytosis. Caused by impairment of DNA synthesis, resulting in abnormal erythrocyte, GRANULOCYTE, & MEGAKARYOCYTE maturation
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megaloblastic vs. non-megaloblastic macrocytosis
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nonmegaloblastic macrocytosis results if RBCs are released too early from marrow (acute blood loss, hemolysis, alcoholism)
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classification of megaloblastic anemia (3)
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1. due to folic acid deficiency
2. due to vitamin B12 deficiency 3. due to unresponsiveness to folic acid or B12 |
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Mechanism of megaloblastic transformation
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unbalanced growth of developing cells in bone marrow due to impaired DNA synthesis w/o assoc. impairment of RNA/protein synthesis. disparity between nucleus & cytoplasm called NUCLEAR-CYTOPLASMIC ASYNCHRONISM
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nutritional aspects of Folic Acid deficiency
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SOURCES: leafy veggies, liver, kidney, yeast, mushrooms, dairy, eggs
DAILY REQ: narrow margin between what is required and what is intaked BODY STORES: depleted within months if no new source INTESTINAL ABSORPTION: most in proximal jejunum |
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Etiology of folic acid deficiency
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1. inadequate dietary intake (folate is destroyed when heated during cooking)
2. increased requirements of Folic acid 3. impaired absorption 4. drug inhibition: alcoholism, oral contraceptives, anti-cancer drugs |
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Clinical features of folic acid deficiency
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1. general signs of anemia
2. glossitis 3. insidious onset 4. diarrhea/steatorrhea (fatty stool) 5. weight loss |
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visual findings of peripheral blood in folic acid deficiency
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MACROCYTIC, NORMOCHROMIC
hypersegmented neutrophils large, hypogranular bands decreased, enlarged platelets oval macrocytes poikilcytosis Howell-jolly bodies, baso. stip., cabot rings polychromatophilia, nucleated RBCs |
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lab findings in folic acid deficiency
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DECREASED: Hb, Hct, RBC count, retic count (RPI<2), pancytopenia
INCREASED: LDH, Bilirubin |
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Changes in bone marrow in folic acid deficiency
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hypercelluar
2. megaloblastic changes a. loose, open chromatin in RBC precursors b. Giant bands & metamyelocytes c. giant megakaryocytes |
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Specific features of folic acid deficiency
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decreased serum and red cell folate
NORMAL B12 levels treated w/ folic acid INCREASED FIGLU (intermed. in glutaminic acid synthesis) |
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nutritional aspects of Vitamin B12 deficiency (sources, daily req., body stores, absorption)
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SOURCES: liver, meat, milk, eggs, fish
Daily requirements: 3-5ug, plenty in all but vegan diets Body stores: enough for few years absorption: occurs in ileum and requires INTRISIC FACTOR (IF) & TRANSCOBALAMIN II (TC II) |
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etiology of B12 deficiency
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1. impaired absorption:
several problems, main is Pernicious anemia 2. microorganism competition: tapeworms, bacteria in blind loop syndrome 3. defects in transport proteins: hereditary deficiency of TCII abnormal TC II 4. dietary deficiency |
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What is Pernicious anemia?
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megaloblastic anemia caused by absence of IF secondary to gastric atrophy. B12 can't be absorbed w/o it. most common B12 deficiency
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Clinical features of B12 deficiency
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1. same as folic acid deficiency
2. addition of NEUROLOGIC abnormalities: parasthesias, gait abnormality, difficulty w/ fine motor coordination |
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Lab findings of B12 deficiency
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same as seen in folic acid deficiency and megaloblastic anemia in general.
SPECIFIC features: decreased serum B12 responsive to B12 therapy increased methylmalonic acid |
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causes of megaloblastic anemia to be unresponsive to B12 or folate therapy
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1 antimetabolic drugs
2. Congenital deficiencies a. hereditary orotic aciduria b. Leysch-Nyhan syndrome c. errors of folate metabolism 3. unexplained disorders a. myelodysplastic syndrome (preleukemia) b. erythroleukemia |
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causes of macrocytosis WITHOUT megaloblastic changes
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1. Alcoholism
2. liver disease some overlap, lipids build up on RBC surface w/ no way to metabolise them 3. reticulocytosis |
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Characteristics of macrocytosis
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1. ROUND, not oval macrocytes
2. less pronounced macrocytes 3. no super segs 4. no pancytopenia 5. absence of megaloblastic anemia signs: jaundice, glossitis, neuropathy |
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Etiology of macrocytosis
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there is an increase in membrane lipids
there is a delay in blast maturation |
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chemsitry tests useful in differential Dx of macrocytosis
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LDH, bilirubin, serum B12, serum and red cell folate levels, gastric analysis, SCHILLING TEST, BONE MARROW EXAMINATION
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what is Schilling test?
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differentiates B12 deficiency resulting from malabsorption, dietary inadequacy, or lack of IF.
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