Microcytic Anemias
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| Three causes of IDA | Inadequate intake, increased need, chronic blood loss
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| Iron Storage molecules | ferritin & hemosiderin
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| MCV 79 | microcytic
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| MCHC 34 | normochromic
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| MCHC 31 | hypochromic
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| Inadequate iron stores | iron deficiency anemia
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| Impaired immobilization of iron | anemia of chronic inflammation
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| Intrinsic RBC defect prevents iron from being incorporated into heme | siderotic anemia
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| Most common cause of microlytic anemia | iron associated anemias
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| Hb lost through urine | intravascular hemolysis - IDA
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| Stage___ = No evidence of iron deficiency. Iron levels? RDW? Ferritin levels? | Stage 1. Iron normal. Rdw very slightly increased. Ferritin will be low.
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| Stage __ = Prussian blue stain of marrow shows no iron stores. TIBC? Ferritin levels?? Iron levels? | Stage 2. TIBC increased. Ferritin and iron levels are low.
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| Stage __ = patient exhibit symptoms of anemia. HnH? Iron levels? MCV? MCHC? | Stage 3. HnH low. Iron levels are depleted. MCV is low (microcytic) and MCHC is low (hypochromic).
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| How do you diagnose anemias? | Chemistry studies
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| Iron low, ferritin low, transferrin low, TIBC high, transferrin saturation low | Iron deficiency anemia
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| Borderline RBC & HnH. MCHC normal. MCV slightly low. Iron low. Ferritin normal or increased. TIBC low. | Anemia of chronic inflammation
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| Hallmark of sideroblastic anemias | ringed sideroblasts in bone marrow (nRBC with iron ring)
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| Treatment of ACI | therapeutic erythropoietin, remove underlying cause.
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| Caused by diseases that interfere with heme production | sideroblastic anemia
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| Where does iron deposit in sideroblasts? | around mitochondria
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| Symptoms of lead poisoning | peripheral neuropathy with cramps and vomiting or seizures.
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| What stain is used to identify sideroblastic anemia? | Prussian blue
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| What is harmful about lead poisioning? | It interferes with porphyrin synthesis by stopping the conversion of aminolevulinic acid to porphobilinogen.
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| How can you measure lead poisoning | Accumulation of aminolevulinic acid spills into the urine
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| What are two compounds that accumulate in the body during lead poisoning? | Aminolevulinic acid and protoporphyrin
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| What two inclusions are present during lead poisoning? | siderotic rings and basophilic stippling
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| How do you treat lead poisoning? | Lead chelation - binds to lead and excretes it in the urine. Also, remove source of poisoning.
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| What anemia causes impaired production of heme? | Porphyrias - type of siderotic anemia
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| What biological molecule is missing to cause Porphyrias? | an enzyme that catalyzes reactions. Instead, previous products build up.
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| What can deposits of heme metabolism in the tissue lead to? | Severe photosensitivity and fluorescence of teeth and bones
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| What disease is associated with iron overloading, and how does it come about? | Hereditary Hemochromatosis = absorption is too high.
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| Which mutation can lead to hereditary hemochromatosis? | Mutation of the HFE chromosome
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| What is the first reaction to excess iron? | Form hemosiderin
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| What four tissues are affected in HH? | skin = golden color liver = cirrhosis and cancer pancreas = diabetes mellitus heart = congestive heart failure
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| What is the mechanism of disease in HH? | When a cell runs out of storage, free ferrous iron accumulates intracellularly, where exposure to oxygen converts it to superoxide and other radicals that affects all cellular membranes. It causes cell death.
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| When is HH usually seen in regards to gender and age? | usually around 40 to 60 years old. It's later for women than men. Can also be seen in juveniles.
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| What mutation causes the juvenile form of HH? | mutation of hepcidin gene
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| Iron high. ferritin high. Transferrin saturation high. Serum transferrin normal. TIBC normal. | Hereditary Hemochromatosis
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| What disease can cause hyperpigmentation, diabetes, and heart problems? | Hereditary Hemochromatosis
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| What is the treatment for Hereditary Hemochromatosis? | Removal of blood by phlebotomy about every 3 months for life. Treat secondary tissue damage. Give iron-chelating drugs.
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| What disease is associated with globin chain disorders? | Thalassemia
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| Which diseases are associated with Alpha Thalassemia? | Barts Hydrops fetalis, Hemoglobin H disease, Alpha-thalassemia trait, silent carrier
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| Absence of all globin chains. | Barts Hydrops Fetalis
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| How is Barts Hydrops Fetalis detected? | There is edema in fetal subcutaneous tissue due to severe anemia. This can be detected on an ultrasound. Gamma chains can be detected via electrophoresis.
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| What globin chains make up Barts Hydrops Fetalis and why is it so fatal? | four gamma globin chains, which have a high affinity for oxygen.
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| What is the signs, symptoms, and outcome of Barts Hydrops Fetalis? | Gross hepatosplenomegaly and cardiomegaly. Severe microcytic, hypochromic anemia with nRBCs. Fetus survives until third trimester due to the presence of Hb Portland. Usually premature and stillborn.
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| What risk does it present to the mother? | Can cause toxemia and severe postpartum hemorrhage. (recommend early termination)
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| Besides Hg Bart, what other Hg are associated with Hydrops Fetalis? | Trace amounts of Gower I, II, Hg H, and Portland
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| What defines normal globin chains genes? | 2 genes from each parent totaling four alpha chain genes.
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| What disease is characterized by a genetic defect of only one gene producing an alpha chain? | Hemoglobin H
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| Accumulation of excess unpaired beta chains that form tetramers | Hemoglobin H
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| When does Hg H appear in the body? | After the gamma-beta switch, Hg H replaces Hg Bart
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| What Hgs are present after the gamma-beta switch for Hemoglobin H disease | 30-50% Hg H and trace amounts of Hg A2, Bart, and A
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| What are the some symptoms of Hemoglobin H disease? | Decreased RBC lifespan, erythroid hyperplasia, splenomegaly, teeth and jaw protusion, brittle bones.
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| How can Hemoglobin H disease be detected? | Infection, pregnancy, or oxidative drugs may cause hemolytic crisis, which leads to disease detection.
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| What is the RBC blood picture for HgH? | microcytic, hypochromic with marked poikilocytosis such as target cells and bizarre shapes
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| What does the term hemolytic mean? | The cell dies early
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| How does Hg H alter RBC shape? | It precipitates in vivo and forms Heinz-like bodies of denatured Hg that alter the cells. (golf ball like appearance)
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| What stain is used to identify abnormal RBC for Hemoglobin H? | Brilliant cresyl or new methylene blue
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| What disease is characterized by the presence of only two alpha globin chains? | Alpha thalassemia trait
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| What disease is characterized by the presence of three alpha globin chains? | The person is a silent carrier.
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| What is the CBC picture for a silent carrier of Alpha Thalassemia? | Normal
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| What is the RBC picture for a person with the alpha thalassemia trait? | Mild anemia with microcytic, hypochromic RBCs. At birth, they ahve 2-10% Hg Bart. As adults, the alpha and beta chains balance out.
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| What disease is characterized by little or no Beta globin chains? | Beta Thalassemia major
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| What disease is characterized by severe anemia deteched in early childhood during the gamma-beta switch? | Beta Thalassemia major
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| What are the symptoms of Beta Thalassemia major? | Hepatosplenomegaly jaundice marked bone changes due to extreme erythroid hyperplasia long bones with lacy appearance prominance of forehead, cheeks, and upper jaw delayed development
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| What is the usual range for transfusion to take place with Beta Thalassemia major? | 3-4 g/dL
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| What is the RBC picture for Beta Thalassemia major? | Hypochromic RBCs with extreme poikilocytosis. Presence of target cells, teardrop, elliptocytes, fragments, and microspherocytes Stippled and nRBCs. retic count 2-8%. Very low MCV
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| What can cause an extremely low MCV? | Beta Thalassemia Major
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| What treatment is available for Beta Thalassemia Major? | Transfusion started in first year of life to prevent anemia and maintain Hb between 9 and 11.5 g/dL, combined with iron chelation therapy.
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| What is low protocol transfusion? | only when the patient is symptomatic is treatment needed
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| What is high protocol transfusion? | Done every 2 to 5 weeks. This helps slow bone changes and mental delays.
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