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41 pathoma.com 5 Red Blood Cell Disorders ANEMIA BASIC PRINCIPLES I. Reduction in circulating red blood cell (RBC) mass A. Presents with signs and symptoms of hypoxia B. Weakness, fatigue, and dyspnea 1. Pale conjunctiva and skin 2. Headache and lightheadedness 3. Angina, especially with preexisting coronary artery disease 4. Hemoglobin (Hb), hematocrit (Hct), and RBC count are used as surrogates for RBC C. mass, which is difficult to measure. Anemia is defined as Hb < 13.5 g/dL in males and < 12.5 g/dL in females (normal 1. Hb is 13.5–17.5 g/dL in males and 12.5–16.0 g/dL in females). Based on mean corpuscular volume (MCV), anemia can be classified as microcytic D. (MCV < 80 µm 3 ), normocytic (MCV = 80–100 µm 3 ), or macrocytic (MCV > 100 µm 3 ). MICROCYTIC ANEMIAS BASIC PRINCIPLES I. Anemia with MCV < 80 µm A. 3 Microcytic anemias are due to decreased production of hemoglobin. B. RBC progenitor cells in the bone marrow are large and normally divide multiple 1. times to produce smaller mature cells (MCV = 80–100 µm 3 ). Microcytosis is due to an “extra” division which occurs to maintain hemoglobin 2. concentration. Hemoglobin is made of heme and globin; heme is composed of iron and C. protoporphyrin. A decrease in any of these components leads to microcytic anemia. Microcytic anemias include (1) iron deficiency anemia, (2) anemia of chronic D. disease, (3) sideroblastic anemia, and (4) thalassemia. IRON DEFICIENCY ANEMIA II. Due to decreased levels of iron A. ↓ 1. iron → ↓ heme → ↓ hemoglobin → microcytic anemia Most common type of anemia B. Lack of iron is the most common nutritional deficiency in the world, affecting 1. roughly 1/3 of world’s population. Iron is consumed in heme (meat-derived) and non-heme (vegetable-derived) forms. C. Absorption occurs in the duodenum. Enterocytes have heme and non-heme 1. (DMT1) transporters; the heme form is more readily absorbed. Enterocytes transport iron across the cell membrane into blood via ferroportin. 2. Transferrin transports iron in the blood and delivers it to liver and bone marrow 3. macrophages for storage. Stored intracellular iron is bound to ferritin, which prevents iron from forming 4. free radicals via the Fenton reaction. Copyright Pathoma LLC. All Rights Reserved. Purchase online at www.pathoma.com

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Page 1: red Blood cell Disorders 5 - pathoma.com · 42 funDaMentals of PatHology fig. 5.1 Microcytic, hypochromic RBCs of iron deficiency anemia fig. 5.2 Ringed sideroblasts (Prussian blue

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5

Chapter 5.  Red Blood Cell Disorders

red Blood cell Disorders

aneMiaBasic PrinciPlesI.

Reduction in circulating red blood cell (RBC) massA. Presents with signs and symptoms of hypoxiaB.

Weakness, fatigue, and dyspnea1. Pale conjunctiva and skin2. Headache and lightheadedness3. Angina, especially with preexisting coronary artery disease4.

Hemoglobin (Hb), hematocrit (Hct), and RBC count are used as surrogates for RBC C. mass, which is difficult to measure.

Anemia is defined as Hb < 13.5 g/dL in males and < 12.5 g/dL in females (normal 1. Hb is 13.5–17.5 g/dL in males and 12.5–16.0 g/dL in females).

Based on mean corpuscular volume (MCV), anemia can be classified as microcytic D. (MCV < 80 µm3), normocytic (MCV = 80–100 µm3), or macrocytic (MCV > 100 µm3).

Microcytic aneMiasBasic PrinciPlesI.

Anemia with MCV < 80 µmA. 3

Microcytic anemias are due to decreased production of hemoglobin. B. RBC progenitor cells in the bone marrow are large and normally divide multiple 1. times to produce smaller mature cells (MCV = 80–100 µm3).Microcytosis is due to an “extra” division which occurs to maintain hemoglobin 2. concentration.

Hemoglobin is made of heme and globin; heme is composed of iron and C. protoporphyrin. A decrease in any of these components leads to microcytic anemia. Microcytic anemias include (1) iron deficiency anemia, (2) anemia of chronic D. disease, (3) sideroblastic anemia, and (4) thalassemia.

iron deficiency aneMiaII. Due to decreased levels of ironA.

↓1. iron → ↓ heme → ↓ hemoglobin → microcytic anemiaMost common type of anemiaB.

Lack of iron is the most common nutritional deficiency in the world, affecting 1. roughly 1/3 of world’s population.

Iron is consumed in heme (meat-derived) and non-heme (vegetable-derived) forms.C. Absorption occurs in the duodenum. Enterocytes have heme and non-heme 1. (DMT1) transporters; the heme form is more readily absorbed. Enterocytes transport iron across the cell membrane into blood via ferroportin.2. Transferrin transports iron in the blood and delivers it to liver and bone marrow 3. macrophages for storage.Stored intracellular iron is bound to ferritin, which prevents iron from forming 4. free radicals via the Fenton reaction.

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Page 2: red Blood cell Disorders 5 - pathoma.com · 42 funDaMentals of PatHology fig. 5.1 Microcytic, hypochromic RBCs of iron deficiency anemia fig. 5.2 Ringed sideroblasts (Prussian blue

42 funDaMentals of PatHology

fig. 5.1 Microcytic, hypochromic RBCs of iron deficiency anemia�

fig. 5.2 Ringed sideroblasts (Prussian blue stain)�

Laboratory measurements of iron statusD. Serum iron—measure of iron in the blood1. Total iron-binding capacity (TIBC)—measure of transferrin molecules in the 2. blood% saturation—percentage of transferrin molecules that are bound by iron 3. (normal is 33%) Serum ferritin—reflects iron stores in macrophages and the liver4.

Iron deficiency is usually caused by dietary lack or blood loss.E. Infants—breast-feeding (human milk is low in iron)1. Children—poor diet2. Adults (20–50 years)—peptic ulcer disease in males and menorrhagia or 3. pregnancy in femalesElderly—colon polyps/carcinoma in the Western world; hookworm 4. (Ancylostoma duodenale and Necator americanus) in the developing world Other causes include malnutrition, malabsorption, and gastrectomy (acid aids 5. iron absorption by maintaining the Fe2+ state, which is more readily absorbed than Fe3+).

Stages of iron deficiencyF. Storage iron is depleted—1. ↓ ferritin; ↑ TIBC Serum iron is depleted—2. ↓ serum iron; ↓ % saturation Normocytic anemia—Bone marrow makes fewer, but normal-sized, RBCs.3. Microcytic, hypochromic anemia—Bone marrow makes smaller and fewer 4. RBCs.

Clinical features of iron deficiency include anemia, koilonychia, and pica.G. Laboratory findings include H.

Microcytic, hypochromic RBCs with 1. ↑ red cell distribution width (RDW, Fig. 5.1)↓2. ferritin; ↑ TIBC; ↓ serum iron; ↓ % saturation↑3. Free erythrocyte protoporphyrin (FEP)

Treatment involves supplemental iron (ferrous sulfate).I. Plummer-Vinson syndrome is iron deficiency anemia with esophageal web and J. atrophic glossitis; presents with anemia, dysphagia, and beefy-red tongue

aneMia of cHronic diseaseIII. Anemia associated with chronic inflammation (e.g., endocarditis or autoimmune A. conditions) or cancer; most common type of anemia in hospitalized patientsChronic disease results in production of acute phase reactants from the liver, B. including hepcidin.

Hepcidin sequesters iron in storage sites by (1) limiting iron transfer from 1. macrophages to erythroid precursors and (2) suppressing erythropoietin (EPO)

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Page 3: red Blood cell Disorders 5 - pathoma.com · 42 funDaMentals of PatHology fig. 5.1 Microcytic, hypochromic RBCs of iron deficiency anemia fig. 5.2 Ringed sideroblasts (Prussian blue

PATHOMA.COMFundamentals of Pathology: Medical Course and Step 1 Review, First Edition

ISBN 978-0-9832246-0-0

Printed in the United States of America.

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All rights reserved. No part of this publication may be reproduced, distributed, or transmitted in any form, or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without prior permission in writing from the publisher (email: [email protected]).

Disclaimer Fundamentals of Pathology aims at providing general principles of pathology and its associated disciplines and is not intended as a working guide to patient care, drug administration or treatment. Medicine is a constantly evolving field and changes in practice regularly occur. It is the responsibility of the treating practitioner, relying on independent expertise and knowledge of the patient, to determine the best treatment and method of application for the patient. Neither the publisher nor the author assume any liability for any injury and/or damage to persons or property arising from or related to the material within this publication.

Furthermore, although care has been taken to ensure the accuracy of information present in this publication, the author and publisher make no representations or warranties whatsoever, express or implied, with respect to the completeness, accuracy or currency of the contents of this publication. This publication is not meant to be a substitute for the advice of a physician or other licensed and qualified medical professional. Information presented in this publication may refer to drugs, devices or techniques which are subject to government regulation, and it is the responsibility of the treating practitioner to comply with all applicable laws.

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