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Hematology - Anemia1

Microcytic Anemias

Three causes of IDA Inadequate intake, increased need, chronic blood loss
Iron Storage molecules ferritin & hemosiderin
MCV 79 microcytic
MCHC 34 normochromic
MCHC 31 hypochromic
Inadequate iron stores iron deficiency anemia
Impaired immobilization of iron anemia of chronic inflammation
Intrinsic RBC defect prevents iron from being incorporated into heme siderotic anemia
Most common cause of microlytic anemia iron associated anemias
Hb lost through urine intravascular hemolysis - IDA
Stage___ = No evidence of iron deficiency. Iron levels? RDW? Ferritin levels? Stage 1. Iron normal. Rdw very slightly increased. Ferritin will be low.
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.
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).
How do you diagnose anemias? Chemistry studies
Iron low, ferritin low, transferrin low, TIBC high, transferrin saturation low Iron deficiency anemia
Borderline RBC & HnH. MCHC normal. MCV slightly low. Iron low. Ferritin normal or increased. TIBC low. Anemia of chronic inflammation
Hallmark of sideroblastic anemias ringed sideroblasts in bone marrow (nRBC with iron ring)
Treatment of ACI therapeutic erythropoietin, remove underlying cause.
Caused by diseases that interfere with heme production sideroblastic anemia
Where does iron deposit in sideroblasts? around mitochondria
Symptoms of lead poisoning peripheral neuropathy with cramps and vomiting or seizures.
What stain is used to identify sideroblastic anemia? Prussian blue
What is harmful about lead poisioning? It interferes with porphyrin synthesis by stopping the conversion of aminolevulinic acid to porphobilinogen.
How can you measure lead poisoning Accumulation of aminolevulinic acid spills into the urine
What are two compounds that accumulate in the body during lead poisoning? Aminolevulinic acid and protoporphyrin
What two inclusions are present during lead poisoning? siderotic rings and basophilic stippling
How do you treat lead poisoning? Lead chelation - binds to lead and excretes it in the urine. Also, remove source of poisoning.
What anemia causes impaired production of heme? Porphyrias - type of siderotic anemia
What biological molecule is missing to cause Porphyrias? an enzyme that catalyzes reactions. Instead, previous products build up.
What can deposits of heme metabolism in the tissue lead to? Severe photosensitivity and fluorescence of teeth and bones
What disease is associated with iron overloading, and how does it come about? Hereditary Hemochromatosis = absorption is too high.
Which mutation can lead to hereditary hemochromatosis? Mutation of the HFE chromosome
What is the first reaction to excess iron? Form hemosiderin
What four tissues are affected in HH? skin = golden color liver = cirrhosis and cancer pancreas = diabetes mellitus heart = congestive heart failure
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.
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.
What mutation causes the juvenile form of HH? mutation of hepcidin gene
Iron high. ferritin high. Transferrin saturation high. Serum transferrin normal. TIBC normal. Hereditary Hemochromatosis
What disease can cause hyperpigmentation, diabetes, and heart problems? Hereditary Hemochromatosis
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.
What disease is associated with globin chain disorders? Thalassemia
Which diseases are associated with Alpha Thalassemia? Barts Hydrops fetalis, Hemoglobin H disease, Alpha-thalassemia trait, silent carrier
Absence of all globin chains. Barts Hydrops Fetalis
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.
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.
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.
What risk does it present to the mother? Can cause toxemia and severe postpartum hemorrhage. (recommend early termination)
Besides Hg Bart, what other Hg are associated with Hydrops Fetalis? Trace amounts of Gower I, II, Hg H, and Portland
What defines normal globin chains genes? 2 genes from each parent totaling four alpha chain genes.
What disease is characterized by a genetic defect of only one gene producing an alpha chain? Hemoglobin H
Accumulation of excess unpaired beta chains that form tetramers Hemoglobin H
When does Hg H appear in the body? After the gamma-beta switch, Hg H replaces Hg Bart
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
What are the some symptoms of Hemoglobin H disease? Decreased RBC lifespan, erythroid hyperplasia, splenomegaly, teeth and jaw protusion, brittle bones.
How can Hemoglobin H disease be detected? Infection, pregnancy, or oxidative drugs may cause hemolytic crisis, which leads to disease detection.
What is the RBC blood picture for HgH? microcytic, hypochromic with marked poikilocytosis such as target cells and bizarre shapes
What does the term hemolytic mean? The cell dies early
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)
What stain is used to identify abnormal RBC for Hemoglobin H? Brilliant cresyl or new methylene blue
What disease is characterized by the presence of only two alpha globin chains? Alpha thalassemia trait
What disease is characterized by the presence of three alpha globin chains? The person is a silent carrier.
What is the CBC picture for a silent carrier of Alpha Thalassemia? Normal
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.
What disease is characterized by little or no Beta globin chains? Beta Thalassemia major
What disease is characterized by severe anemia deteched in early childhood during the gamma-beta switch? Beta Thalassemia major
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
What is the usual range for transfusion to take place with Beta Thalassemia major? 3-4 g/dL
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
What can cause an extremely low MCV? Beta Thalassemia Major
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.
What is low protocol transfusion? only when the patient is symptomatic is treatment needed
What is high protocol transfusion? Done every 2 to 5 weeks. This helps slow bone changes and mental delays.
Created by: annie.na.ch