THE UNIVERSITY OF JORDAN FACULTY OF MEDICINE DEPARTMENT OF PATHOLOGY

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1 THE UNIVERSITY OF JORDAN FACULTY OF MEDICINE DEPARTMENT OF PATHOLOGY INTRODUCTION TO ANEMIA Third year medical students First semester 2018/2019 Dr.

2 RBC DISORDERS Lecturer: Dr. Tariq Al-Adaily Office: JUH- outpatient building 3 rd floor, Hematology Lab Office hours: Wed 12-1 Reference: Robbins Basic Pathology, 10 th edition

3 Definition Reduction of oxygen transport capacity of blood, secondary to decrease in RBC mass to below average levels Leads to tissue hypoxia Practically, measure by Hemoglobin concentration, and Hematocrit (ratio of packed RBCs to total blood volume)

4 Adaptive changes Generalized tissue hypoxia leads to Increased cardiac output Increased respiratory rate Increased red cell 2,3-diphosphoglycerate (DPG) Increased erythropoietin level (except in renal failure, anemia of chronic disease)

5 General Symptoms Pallor Dizziness Headache Fatigue Hypotension Tachypnea Tachycardia

6 Symptoms in special types Jaundice (hemolytic anemias) Pigmented gall bladder stones Growth retardation Skeletal deformity Secondary hemosiderosis, causing heart, renal & endocrine failure

7 Classification according to cause 1) Blood loss 2) Diminished RBC production Iron deficiency anemia Megaloblastic anemia Aplastic anemia Pure red cell aplasia Myelophthisic anemia Myelodysplastic syndrome 3) Increased destruction (hemolytic anemia) Extrinsic factors (infection, antibody, mechanical) Intrinsic RBC abnormalities: 1) Hereditary (membrane, enzyme, Hg abnormalities) 2) Acquired (Paroxysmal nocturnal hematuria)

8 Classification according to morphology Blood film Size: normo, micro, macrocytic Color: normo, hypochromic Shape: anisopoikelocytosis (spherocytes, sickle, schistiocytes) Hypochromic microcytic anemia usually reflects impaired Hg synthesis Macrocytic anemia reflects stem cell disease and maturation

9 RBC indices Slight variation is present between labs, geographic areas Sex, age, race status have effect Red cell distribution width (RDW): the coefficient of variation in red cell volume

10 Anemia of acute blood loss Symptoms are related to decreased intravascular volume, might cause Hypovlemic Shock and death Body responds by shifting fluid from interstitial to intravascular space, causing dilutional anemia and hypoxia Erythropoietin secretion is stimulated, activating BM erythropoiesis Mature RBCs & Reticulocytes appear in blood after 5 days In internal hemorrhage, iron is restored from extravasated RBCs and used again in erythropoiesis, while in external hemorrhage, iron is lost The anemia is normochromic normocytic, with reticulocytosis Leukocytosis (secondary to stress)

11 Anemia of chronic blood loss Occurs when the rate of RBC loss exceeds regeneration Commonly seen in GI diseases (hemorrhoids, peptic ulcer, colon cancer) & gynecologic diseases (menorrhagea) Mostly associated with iron deficiency Appears as normochromic normocytic, or hypochromic microcytic

12 Hemolytic Anemia Normally, RBCs age is around 120 days, aged RBCs are engulfed by macrophages in spleen, liver and BM In Hemolytic anemia; premature destruction of RBCs, internal or external factors Extravascular hemolysis: results in increased phagocytic activity Intravascular hemolysis: occurs inside blood vessels Accumulation of Hg degradation products Increased: erythropoietin, Faculty of serum Medicine lacate dehydrogenase (LDH), Retic count Secondary increased erythropoiesis

13 Extravascular Hemolysis Generally caused when the RBC has abnormal shape (less deformable) or coated with antibodies This prevents its normal movement in splenic sinusoids Prolonged time of RBCs passage attracts histiocytes to engulf them Free Hg from destructed RBCs binds Haptoglobin in serum, causing decreased level Hg within phagocytes is converted to bilirubin The triad of extravascular Faculty of HA Medicine is: Anemia, splenomegaly and jaundice

14 Intravascular Hemolysis Less common Caused by mechanical damage, microorganism, exogenous toxins Due to large amount of free Hg, haptoglobin is cleared from the serum free Hg in serum is oxidized to Methemoglobin (methg) Excess free Hg and met Hg are excreted in urine (hemoglobinuria) causing dark urine Renal hemosiderosis may occur

15 THE END