Blood and Electrolytes: Common Anemias PDF
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Uploaded by ResplendentFourier7024
University of Toronto
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This document provides information on common anemias, including their causes, symptoms, and treatment. It details factors influencing oxygen binding and the breakdown of red blood cells. The document is likely part of a broader medical study or textbook.
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BLOOD AND ELECTROLYTES Common Anemias Not reviewed yet: anemia flashcards - Normalhematocrit(H CT, volume to volume): 40-50%for males, 35-44% in females - ↑ hematocrit can be due to: decreased body water/dehydration, congenit...
BLOOD AND ELECTROLYTES Common Anemias Not reviewed yet: anemia flashcards - Normalhematocrit(H CT, volume to volume): 40-50%for males, 35-44% in females - ↑ hematocrit can be due to: decreased body water/dehydration, congenital heart disease, HF - Lifespan of RBCs ≈ 120 days - Structure of Hgb: - Two alpha subunits + two beta subunits, each with an associated heme group - Each heme group is a pophyrin ring, where 4 N’s are associated with an iron atom (Fe2+) - Iron binds O2 reversibly; oxygen binding has an allersteric effect (“cooperative binding”) - Factors that decrease oxygen binding/oxygen affinity: - ↑ temperature - ↑ blood CO2 - ↓ blood pH (↑ H+) = “Bohr effect” - *tissues have all these factors (compared to the lungs) to allow for O2 offloading - Myoglobin for muscle is a porphyrin monomer - Erythropoeisis: from stem cells to mature RBCs (takes≈ 1 week) - Kidneys produce erythropoetin in response to reduced O2 levels - Other requirements: iron, folate/folic acid, VB12 (both required for RNA and DNA synthesis) - Reticulocytes(immature RBCs, the last step beforematuration) are an important indicator of RBC production/erythropoesis - Reticulocyte count: % reticulocytes vs. erythrocytes in the blood - High reticulocyte count = bone marrow suppression (chronic anemia) - Low reticulocyte count = hemolytic anemia, acute blood loss - Breakdown of RBCs are mostly done by splenic macrophages into 3 components - Bilirubin (a heme byproduct): conjugated by liver - Globulin: recycled as amino acids - Fe2+: recycled for new heme synthesis - Anemia: ↓ capacity for carrying O2 = ↓ Hgb, ↓ RBCs,↓ HCT - WHO definition: ferrous sulfate (60mg > ferrous gluconate (35mg) - Other options: - eme iron polypeptide: 11mg per 11mg dose, 100% H - Polysaccharide iron complex (“FeraMax”): 150mg per 150mg dose, better tolerated but decreased efficacy compared to iron salts - Side effects: constipation, GI upset (can try with food or take HS), teeth staining from liquid formulations - Most patients will try oral therapy first for 1-3 months prior toIV iron therapy - Formulations: iron sucrose, sodium ferric gluconate, iron isomaltoside or derisomaltose (Monoferric) - Side effects: anaphylaxis, hypotension, dyspnea, dizziness, arthralgia, arthritis (highest incidence with iron dextran, which is no longer available; infuse slower to avoid and monitor patients for >30 minutes after completion) - Absolute contraindication: inflammatory disease of the liver - When and how to take iron: - Ideally on an empty stomach to increase absorption - With vitamin C (orange juice) to increase absorption (>200mg per 30mg of iron) - In CKD patients, use apple juice to create an acidic environment (avoid orange juice) - Separate from calcium, calcium-containing phosphate binders, antaids (Mg, Al), tetracyclines, and quinolones, PPIs and H2RAs, sodium bicarbonate, cholestyramine, levodopa, coffee and tea, by 2 hours - If the patient is not deficient in folate, VB12 or iron, starterythroposis stimulating agent (ESA) - Are glycoproteins that mimicc endogenous EPO, binding to the erythropoietin receptor - Criteria for starting: in non-dialysis patients, if Hb
