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Faculty of Medicine Dr. Tariq Aladily

Faculty of Medicine Dr. Tariq Aladily

THE UNIVERSITY OF JORDAN

FACULTY OF MEDICINE

DEPARTMENT OF PATHOLOGY

INTRODUCTION TO ANEMIA

Third year medical students

First semester

2018/2019

Dr. Tariq Aladily

Faculty of Medicine Dr. Tariq Aladily

RBC DISORDERS Lecturer: Dr. Tariq Al-Adaily

Email: TNALADILY@ju.edu.jo

Office: JUH- outpatient building

3rd floor, Hematology Lab

Office hours: Wed 12-1

Reference: Robbins Basic Pathology, 10th edition

mailto:TNALADILY@ju.edu.jo

Faculty of Medicine Dr. Tariq Aladily

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)

Faculty of Medicine Dr. Tariq Aladily

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)

Faculty of Medicine Dr. Tariq Aladily

General Symptoms

Pallor

Dizziness

Headache

Fatigue

Hypotension

Tachypnea

Tachycardia

Faculty of Medicine Dr. Tariq Aladily

Symptoms in special types

Jaundice (hemolytic anemias)

Pigmented gall bladder stones

Growth retardation

Skeletal deformity

Secondary hemosiderosis, causing heart, renal & endocrine failure

Faculty of Medicine Dr. Tariq Aladily

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)

Faculty of Medicine Dr. Tariq Aladily

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

Faculty of Medicine Dr. Tariq Aladily

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

Faculty of Medicine Dr. Tariq Aladily

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)

Faculty of Medicine Dr. Tariq Aladily

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

Faculty of Medicine Dr. Tariq Aladily

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, serum lacate dehydrogenase (LDH), Retic count

Secondary increased erythropoiesis

Faculty of Medicine Dr. Tariq Aladily

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 HA is: Anemia, splenomegaly and jaundice

Faculty of Medicine Dr. Tariq Aladily

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

Faculty of Medicine Dr. Tariq Aladily

THE END