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2 Peds Anemia
| Question | Answer |
|---|---|
| ratio of volume of RBC to the volume of whole blood | Hct |
| Hct in relation to Hgb | approximately 3x Hgb value |
| mathematic equation of MCV= | Hct/RBC |
| measure of RBC size, more reliable than estimation from peripheral smear | MCV |
| central pallor of an RBC should be | 1/3 of the size. |
| life span of a RBC | 120 days |
| Younger, larger, RBC's that are more purplish | Reticulocytes. Will throw the MCV off |
| Decreased blood vol sx | pallor, postural, hypotension |
| Decreased Oxygen transport | fatigue, dyspnea, syncope |
| Increased cardiac output causes | congestive heart failure |
| At birth, a child is | polycythemic and macrocytic. Highest in the life. |
| Physiologic nadir of Hgb | occurs around 6-8 weeks (not a good time to do blood draws) |
| Most common anemia | iron deficiency anemia |
| Blood values | Hgb, Hct, MCV, RBC#, reticulocyte count, peripheral smear, UA, coombs test, stool guaiac |
| MCV in peds rule of thumb | age + 70 |
| Microcytic, hypochromic anemias | iron deficiency (#1), lead poisoning, thalassemias, others-chronic inflammation, sideroblastic anemia. (T.I.C.S.) |
| elemental iron for kids | niferex (6mg/kg/day). |
| tx of iron deficiency in kids | elemental iron (niferex), Reticulocytosis within 5-10 days. Hgb is 2/3 corrected after 1 month. Hct rises 1% per day in first week, if responds continue tx for 6 months to build storage |
| Ethnicities where Thalassemias are more likely | AA and mediterranean. Do a Hgb electrophoresis - elevated Hgb A2 |
| Beta Thalassemia on peripheral smear | anisocytosis, poikilocytosis |
| Which type presents as either microcytic or normocytic anemia | Chronic inflammation. Ex: JRA, lupus, etc |
| Type of macrocytic anemia that is nonmegaloblastic | Reticulocytosis. Also, liver dz, down's syndrome, normal newborn |
| Macrocytic Megaloblastic Anemia causes | folic acid deficiency, Vit B12 def |
| If B12 is low, do a _____ test | Schilling's test. Radioactive test to see if you have intrinsic factor (in the gastric and early bowel lining). Necessary for the absorption of B12 |
| most common cause of folic acid deficiency in adults | alcoholism |
| malabsorptive states can cause | Vit B12 deficiency. Only anemia that presents with neurologic findings. (ex: position sense) |
| Test of choice for spherocytosis | osmotic fragility |
| TIBC | total iron binding capacity |
| Hereditary Hemolytic Anemia on newborn screens that only affects males | G-6-PD deficiency. Common worldwide, gene is X-linked. G-6-PD protein helps to detox the blood. |
| Heinz bodies are formed in | G-6-PD deficiency |
| Clincal Presentation in Iron deficiency Anemia | Vary with severity of sx. Mild usually asx. In infants with more severe: pallor, fatigue, irritability, delayed motor development. Children whose def is due to drinking unfortified cows milk may be fat w/ poor muscle tone. Hx of pica common |
| Lab findings in Iron Deficiency Anemia | microcytic, hypochromic (low MCV, low MCH). abosolute reticulocyte count low. Decreasd serum ferritin, low serum iron,decreased transferrin sat. elevated TIBC and transferrin levels |
| Peripheral Blood smear in Iron Deficiency Anemia | microcytic, hypochromic RBCs with anisocytosis (varying size), occassional target, teardrop, elliptical and fragmented RBCs. Leukocytes are nl, very often plt count increased with nl morphology |
| Serum iron | a measurement of the quantity of iron bound to transferrin |
| Iron from the diet is absorbed in the small intestine and transported to the plasma. From there, it is picked up by a globulin protein called _____ and carried to the bone marrow for incorporation into hemoglobin | transferrin |
| Iron overload or poisoning is called | hemochromatosis or hemosiderosis. Excess iron is usually deposited in the brain, liver and heart and causes severe dysfunction of these organs. |
| Ferritin binds | stored iron |
| Transferrin in acute inflammatory rxns and chronic illnesses | b/c it is a negative acute-phase reactant protein, in these situations, transferrin levels diminish. Transferrin represents the largest quantity of iron-binding proteins, resulting in anemia. Also, anemia of chronic dz is caused by inhibited erythropoetin |
| Transferrin is produced by which organ? | the liver |
| Causes of Increased Serum Iron Levels | hemosiderosis or hemochromatosis, iron poisoning, hemolytic anemia (iron in the Hgb of hemolyzed RBCs leaks out into the bloodstream), Massive blood transfusions, Hepatitis or Hepatic necrosis, Lead toxicity (lead overload may displace iron stores) |
| Causes of decreased Serum iron levels include: insufficient dietary iron (all body iron is from dietary intake), Chronic blood loss (depletes body's iron b/c most of the iron in the body exists in the Hgb of RBCs), and | Inadequate intestinal absorption, Pregnancy (late: fetal requirements deplete the mother's store of iron), Iron-deficiency anemia, Neoplasia (iron levels depleted in these pts for several reasons) |
| Causes of Increased TIBC or Transferrin levels | Estrogen therapy, Pregnancy (late), Polycythemia vera, Iron-deficiency anemia |
| Causes of Decreased TIBC or Transferrin levels | Malnutrition, hypoproteinemia (transferrin is a protein), Inflammatory diseases (transferrin is a negative acute-phase reactant protein), Cirrhosis, Hemolytic anemia, Pernicious anemia, Sickle cell anemia. These anemias have high iron levels. |
| Causes of Increased Transferrin Saturation or TIBC saturation | Hemochromatosis or hemosiderosis (too much iron), Increased iron intake (oral or parenteral; increasd iron saturates the transferrin), Hemolytic anemias (serum iron levels are increased and saturate transferrin) |
| Causes of Decreased Transferrin Saturation or TIBC Saturation | Iron-deficiency anemia, Chronic illness (iron levels are low and transferrin levels are increased) |
| The most accurate indicator of iron deficiency | Ferritin. This is a measure of iron stores. |
| Tx of iron-deficiency anemia | oral dose of elemental iron: 6mg/kg/d in three divided daily doses (AKA 2mg/kg TID). Iron tx increases reticulocyte count w/in 5-10 days. Resolution of anemia w/in 4-6 wks, Tx for 6 months to replenish iron stores |
| Erythropoiesis: Renal interstitial peritubular cells detect low oxygen levels in the blood and secrete | Erythropoietin. EPO stimulates the proliferation and differentiation of erythroid progenitors into reticulocytes. Retics--> erythrocytes |
| Stages of Iron Deficiency | 1. Loss of storage Iron (decreased serum ferritin); 2. Loss of Circulating Iron (decreased serum iron). 3. Decreased Hgb production (decreased Hgb and MCV) |
| anemia results from inhibition of synthetic enzymes necessary for production of hemoglobin | lead poisoning. Lab findings: low MCV, basophilic stippling on smear, elevated FEP (?) |
| Tx for Lead poisoning anemia | Succimer 100mg/kg x14 days |
| Microcytic Anemias: TICS | Thalassemias, Iron deficiency, Anemia of Chronic Inflammation, Sideroblastic Anemia |
| Normocytic Anemias: NORMAL SIZE. N-Normal Pregnancy (result of a 30% plasma vol increase), O-Overhydration and expanded plasma volume, R-Chronic Renal Disease (from relative decrease in EPO production), M-Myelophthisic anemia (bone marrow invasion), | A-Acute blood loss, L-Leukemia and Liver disease (increase plasma volume and alter RBC survival), SI-Systemic inflammation (anemia of chronic inflammation), Z-zero production, E-Endocrine Disorders (hypo/hyperthyroidism, adrenal insufficiency, hypogonad) |
| Labs in Megaloblastic Anemias | Peripheral blood smear, B12 level (nl range 200-800pg/ml), Folate level (nl range 1.7-12.6mg/ml), Schillings test, Bone marrow |
| Tx of Folate insufficiency megaloblastic anemia | 1mg po daily of folic acid |
| Howell jowell bodies and paresthesias of extremities suggest which type of Anemia? | vitamin B12 deficiency megaloblastric anemia. High MCV and MCH. Tx:Parenteral Vit 12 (lifelong) |
| Clinical findings of Spherocytosis | Hemolytic anemia type. Splenomegaly, jaundice, pallor, fatigue, or malaise. Intermittent crisis: abdominal pain, fever, even CHF |
| Lab findings of Spherocytosis | Normocytic, hyperchromic, many pts have elevated MCHC. Peripheral smear: spherocytes and polychromasia |
| Which test confirms the diagnosis of Spherocytosis? | Osmotic fragility test (increased in spherocytosis) |
| US finding in adults with hereditary spherocytosis | Gallstones occur in 60-70% of Hereditary Spherocytosis adults who have not undergone splenectomy and may form as early as age5-10 years |
| Tx for Spherocytosis | Supportive measures: folic acid to prevent development of red cell hypoplasia due to folate deficiency. Splenectomy in many cases (note: splenectomy associated with bacterial infxns, particularly pneumococci). Gallstones too. |
| Hemolytic Anemias | Spherocytosis, thalassemias, sickle cell dz and trait, G6PD deficiency |
| Alpha Thalassemia | 1 gene deletion: silent carrier. 2 gene deletion: A thal trat.Asx,Hypochromic, microcytic anemia, Nl Hgb Electrophoresis. 3 gene deletion: Hemoglobin H, moderately severe hemolytic anemia. 4 gene deletion: Bart's of Hydrops Fetalis, incompatible with life |
| Hemoglobin H dz | Alpha thalassemia with 3 gene deletion. Children may have jaundice and splenomegaly. Key to diagnosis is decreased MCV and marked hypochromia. With the exception of B-thalassemia, most other hemolytic anemias have normal or elevated MCV and normochromic |
| Tx for alpha thalassemia trait: none. Tx for hemoglobin H disease | supplemental folic acid |
| B-Thalassemia minor | normal neonatal screening test, african, middle eastern or asian, mild microcytic, hypochromic anemia. No response to iron tx. Elevated levels of Hemoglobin A2. |
| B-Thalassemia Major/ Cooley's anemia: Iron overload, chronic problems | Neonatal screening shows hemoglobin F only. Mediterranean, Middle Eastern, or Asian. Severe microcytic, hypochromic anemia with marked hepatosplenomegaly. Tx: chronic transfusion with iron chelation and stem cell transplantation. |
| Down's syndrome is associated with which type of anemia? | Nonmegaloblastic macrocytic anemia |
| elevated MCHC is seen in | Spherocytosis: Hereditary Hemolytic Anemia |
| G-6-PD deficiency notes: | gene is X-linked, only males affected. Assay to determine. |
| Heinz bodies are found in | G-6-PD deficiency |
| SS tx in kids | are functionally asplenic. Must be on PCN prophylactic until age 5 to prevent sepsis from encapsulated organisms. Then Pneumovax |
| acute clinical manifestations of SS | Acute vasoocclusive episodes: pain crises, stroke, acute chest syndrome, priapism. Acute Anemic Episodes: splenic sequestration, hyperhemolytic episodes, aplastic crises. infxn |
| Normocytic anemia with low retic response: | inadequate marrow response/red cell aplasia, transient Erythroblastopenia of Childhood (TEC), Diamond Blackfan Anemia, Aplastic Crises (transient, usually due to viral insult) |
Created by:
ltm12