HEMATOLOGY 311

FINALS WEEK 1: ANEMIA

• Sternal Tenderness
ANEMIA
• Lymphadenopathy
It is a manifestation of a certain disease associated with: • Cardiac murmurs
✓ Decreased in Red Blood Cells • Splenomegaly (enlargement of spleen)
✓ Decreased in Hematocrit • Hepatomegaly (enlargement of liver)
✓ Decreased in Hemoglobin • Vital Signs
-Temperature, Blood Pressure and Heart Rate
DEFINITION OF ANEMIA
FUNCTIONAL GENERAL CAUSES OF ANEMIA
• Decreased in the oxygen carrying capacity of the 1. Decreased Red Blood Cell Production
blood. ̵ Associated with Bone Marrow and Kidney
Problems
OPERATIONAL 2. Increased Red Blood Cell Destruction
• Reduction from the baseline value for the total ̵ Primary cause is Hemolysis (Hemolytic
number of RBCs, amount of circulating Anemia)
hemoglobin and RBC mass for a particular patient. 3. Blood Loss
̵ Accident
CONVENTIONAL ̵ Giving Birth
• Decrease in RBCs, hemoglobin and hematocrit
below the previously established reference for ANEMIA DUE TO DECREASE IN RBC PRODUCTION
healthy individuals of the same age, sex, and race, 1. Iron Deficiency Anemia (IDA): most common type
under similar environmental conditions. and easier to treat.
2. Anemia of Chronic Inflammation (ACI)
CLINICAL FINDINGS OF ANEMIA 3. Sideroblastic Anemia (SA)
1. History 4. Megaloblastic Anemia (MA)
2. Physical Examination 5. Aplastic Anemia (AA)
3. Signs and Symptoms Doctor 6. Thalassemia ( and )
4. Laboratory Procedures→ Medtech 7. Anemia due to Chronic Renal Failure
̵ CBC 8. Anemia due to Chronic Endocrine Disorder
̵ Iron Studies (Cushing Syndrome, Addison’s Disease)
̵ Hemoglobin Electrophoresis 9. Anemia due to Marrow Infiltration

Common Symptoms of Anemia ANEMIA DUE TO INCREASE DESTRUCTION OF RBC

o Shortness of Breath A. INTRACORPUSCULAR ABNORMALITY: defect in RBC
o Fatigue itself (shape)
1. MEMBRANE DEFECT: problem is the membrane
HISTORY OF PATIENT itself. Maybe it lacks protein, carbohydrate or
• Diet lipids.
• Bleeding History (Spectrin, Ankidin and Protein 4.1)
• Drug Ingestion a. Hereditary Spherocytosis
• Occupation b. Hereditary Elliptocytosis
• Exposure to chemicals c. Hereditary Pyropoikilocytosis: Abnormal
• Travels sensitivity to heat (severe Elliptocytosis).
• Previous Medications d. Hereditary Stomatocytosis
• Ethnic Groups e. Hereditary Acanthocytosis
• Family History of Disease f. Hereditary Rh Null Disease
• Hobbies
• Neurologic Symptoms 2. ENZYME DEFICIENCY
• G6PD Deficiency: Decrease in Hgb; eating of
Physical Examination beans, soya, Fava beans; check through
• Skin newborn screening
-Pallor (decrease of oxyhgb in skin and mucous • Pyruvate Kinase Deficiency: affects thesurvival
membrane), Jaundice (important in assessing of the RBC
anemia, may imply evidence of RBC destruction, • Porphyria: Heme synthesis
indicator of start hemolysis) and Petechiae (red
spots in the body caused by a minor hemorrhage, 3. PAROXYSMAL NOCTURNAL HEMOGLOBINURIA
breakage of the capillaries) (PNH)
• Eyes (Hemorrhage)
• Mouth (Mucosal Bleeding) 4. GLOBIN ABNORMALITY
Reference: Mrs. Agnes Guzman, RMT
 HEMATOLOGY 311
FINALS WEEK 1: ANEMIA
• Hemoglobinopathies 7. Urinalysis: check for bloody urine, hemoglobinuria
(Hb SS, CC, SC) or hematuria.
8. Fecalysis: for occult blood
B. EXTRACORPUSCULAR ABNORMALITY 9. Hematological Special Test Procedures: Hb
1. Mechanical electrophoresis
a. Microangiopathic Hemolytic Anemia (MAHA)
✓ Thrombotic Thrombocytopenic Purpura (TTP): MORPHOLOGICAL CLASSIFICATION OF ANEMIA
decreased in platelets. 1. Microcytic Hypochromic Anemia: RBC are small
✓ Hemolytic Uremic Syndrome (HUS): caused by compared to normal size and concentration is
0157H:7 serotype of E. coli; mainly in children decreased.
✓ Disseminated Intravascular Coagulation (DIC) 2. Macrocytic Normochromic Anemia: RBC are large
✓ HELLP Syndrome (Hemolysis; the H in the (<8)
acronym), elevated liver enzymes (EL), and low 3. Normocytic Normochromic Anemia: normal
platelet count (LP)

b. Traumatic Cardiac Hemolytic Anemia

2. Infection
• Hemolytic Anemia
1. Malaria
2. Babesia
3. Bartonella
4. Ehrlichia

3. Chemical and Physical Agents

- Caused by drugs, toxins, burns

4. Antibody – Mediated Anemia (AMA)

- Acquired Hemolytic Anemia

ANEMIA DUE TO BLOOD LOSS

✓ Acute Post Hemorrhagic Anemia
✓ Chronic Post Hemorrhagic Anemia

CLASSIFICATION OF ANEMIA BASED ON:

• Reticulocyte Count
• Mean Corpuscular Volume (MCV): most
important RBC indices
• Red Blood Cell Distribution Width (RDW) concentration of anemia.

LABORATORY TEST FOR ANEMIA ASSESSMENT I. MICROCYTIC HYPOCHROMIC ANEMIA

1. Complete Blood Count: very helpful for
determining the concentration of Hgb, number of
RBC and Hct.
2. Reticulocyte Count: helpful in assessing anemia
and will signify if our bone marrow is still capable
of producing RBC.
3. Peripheral Smear: important in evaluating
anemia. We will be able to check the size, shape, or
inclusion bodies whether it is from the RBC or WBC.
4. Bone Marrow Examination: when the cause is not
determined. used when the primary tests are
doubtful.
5. Iron Studies: Backbone test for Assessing Anemia;
Serum Iron, Serum Ferritin, Total Iron – Binding
Capacity (TIBC)
6. Blood Chemistry (Kidney Function Test, Liver
Function Test)
Reference: Mrs. Agnes Guzman, RMT
Read.
• Decrease of all erythrocyte indices: MCV (mean
corpuscular volume: pertains to the size of cell),
MCH (mean corpuscular hemoglobin) and MCHC
(mean corpuscular hemoglobin concentration)
• Found in Thalassemia and severe Iron deficiency
anemia (IDA)
IRON DEFICIENCY ANEMIA
-Most common cause of anemia.
Causes:
a. Inadequate Intake of Iron
̵ 1mg of iron cost every day.
b. Increased need of Iron
̵ Infancy, childhood, adolescence
 HEMATOLOGY 311
FINALS WEEK 1: ANEMIA
̵ Pregnancy (need to double the amount multiple morphologic changes: pencil cells, target cells,
of iron for the body to be able to supply teardrops, and rare fragments. Early iron deficiency may be
oxygen to the baby through the use of normocytic with no significant morphologic changes
iron)
c. Impaired Absorption IRON IS DISTRIBUTED AMONG 3 COMPARTMENTS
d. Chronic Blood Loss 1. Storage Compartment – principally as Ferritin in
̵ Heavy menstrual bleeding the bone marrow macrophages and liver cells.
̵ GI bleeding from ulcers or tumors 2. Transport Compartment of Serum Transferrin
̵ Urinary tract with kidney stones 3. Functional Compartment of Hemoglobin,
̵ Iatrogenic cause (iatrogenic anemia: lowered Myoglobin and Cytochrome
Hct and Hgb due to frequent removal of
sample) STAGES OF IRON DEFICIENCY
• Stage I: Iron Depletion
IRON DEFICIENCY ANEMIA BLOOD FEATURES: ̵ Normal Hgb
• Decrease to normal Reticulocyte count ̵ Normal Serum Iron
• Decrease Serum Iron ̵ Normal TIBC
• Decrease Serum Ferritin ̵ Decrease Ferritin
• Increase Total Iron – Binding Capacity (TIBC) • Stage II: Exhaustion
(Serum Transferrin) ̵ Normal Hgb
• Peripheral Blood Smear: ̵ Decrease Serum Iron
̵ Microcytic Hypochromic type ̵ Increase TIBC
̵ Anisocytosis (variation of size) ̵ Decrease Ferritin
/Poikilocytosis (variation of shape) • Stage III: Frank Anemia
• Decreased in Osmotic Fragility Test ̵ Decrease Hgb
*Taking Vitamin C will help ̵ Decrease Serum Iron
̵ Increase TIBC
NOTE: ̵ Decrease Ferritin
 Serum iron – measures the circulating iron that ̵
bound to transferritin TREATMENT
 Serum ferritin – protein that are used for storage • Oral Supplementation of Ferrous Sulfate
of iron
 Total Iron – Binding Capacity (TIBC) – measures Categories of Lab Diagnosis of Anemia
the capacity of iron to bind with transferritin 1. Screening – CBC, RBC indices
2. Diagnostic – Iron studies
CLINICAL FEATURES OF IRON DEFICIENCY: 3. Specialized – Hb electrophoresis
• Smooth Tongue: (TOP PANEL) Iron deficiency can
result in a painless, smooth, shiny and reddened
tongue. SIDEROBLASTIC ANEMIA
• Koilonychia: (BOTTOM PANEL) a condition also • Develop when the incorporation of iron into heme
referred to as “spoon – shaped nails” is associated is blocked (protoporphyrin pathway is blocked in
with iron deficiency in which the fingernails are thin, the heme synthesis that results to defective Hgb
brittle and concave with raise edges. synthesis and iron overload.)
• Pica: condition where in there’s craving for uncertain • Protoporphyrin pathway resulting in iron overload.
food (shortness of breath and fatigue) • Hallmark: (these 2 are produced instead of healthy
cell)
IRON DEFICIENCY BLOOD FILMS ̵ BM: Ringed Sideroblast
̵ PB: Pappenheimer Bodies

2 Types:
1. HEREDITARY SIDEROBLASTIC ANEMIA: due to a
congenital enzyme defect delta aminolevulinic acid
synthetase or heme synthetase.
2. Primary Acquired Sideroblastic ANEMIA: due to
somatic mutation of the erythroid progenitor cells that
cause either defect in heme synthesis or defects in
DNA synthesis.
• Primary is genetic.
TOP PANEL: This peripheral blood film demonstrates severe • Secondary caused by:
iron deficiency with microcytosis, hypochromasia, and ̵ Certain therapeutic drugs
Reference: Mrs. Agnes Guzman, RMT
 HEMATOLOGY 311
FINALS WEEK 1: ANEMIA
̵ Chronic transfusion (Aplastic) • Lead damage the activity of enzymes used for heme
̵ Alcoholism and Food pads synthesis (Basophilic Stippling)
• Diagnostic lab finding is ringed sideroblast in the • Also leads to sideroblastic anemia.
bone marrow and Pappenheimer bodies in the • Hallmark: Basophilic Stippling
peripheral blood.
• Increased Serum Iron CLINICAL FEATURES OF LEAD POISONING:
• Increased Ferritin level • TOP PANEL: Gums in lead poisoning. Lead lines are
• Normal TIBC shown in gums of the patient suffering from lead
• Decreased MCV poisoning.
• Stain: Perl’s Prussian Blue for Ringed Sideroblast

• BOTTOM PANEL: Peripheral blood film

demonstrating coarse basophilic stippling.
Normocytic or microcytic anemia may be present.
✓ Sideroblastic anemia.
✓ Peripheral blood film of dual population and
sideroblastic anemia.
✓ Normocytic cells are present, along with a minor
population of microcytic, hypochromic
erythrocytes possessing a thin rim of cytoplasm.
✓ Occasional teardrop cells are visible.
✓ Pappenheimer bodies, target cells, and basophilic
stippling occur in some cases.
TREATMENT: Chelators (salts of EDTA chelates the iron
that could be cast out on the urine)

HEME SYNTHESIS

PORPHYRIA
• Rare disease caused by accumulation of porphyrins in
developing RBCs.
-Impaired production of protoporphyrin.
✓ Sideroblastic anemia. • Characterized by dermal photosensitivity and rash
✓ Numerous ringed sideroblasts (blue ones) are seen caused by the sun.
in this marrow aspirate smear stained for iron.
✓ They are normoblasts with ≥10 iron containing CLINICAL FEATURES OF PORPHYRIA:
granules in the cytoplasm encircling at least one- • Neurologic Complications
third of the nucleus.
• Impaired Production of Heme
✓ Often, focusing up and down on the cell will more
-Porphyrin is the main precursor of heme so heme
clearly demonstrate the iron-containing granules.
is an essential constituent of Hgb.
• Skin Problems
LABORATORY FINDINGS:
• Abdominal pain
 Serum iron
• Photosensitivity
 Ferritin iron
• CNS disorder
 TIBC
TREATMENT
MICROCYTIC HYPOCHROMIC ANEMIA
• Pyridoxine – stimulate heme synthesis
• Second most common anemia
• Bone Marrow Transplant
• Anemia of Chronic Disease
• Decreased TIBC
LEAD POISONING
• Mild Anemia (7 – 11g/dL)
• Lead interferes with iron storage in the mitochondria.
• Increase WBC Count

Reference: Mrs. Agnes Guzman, RMT

 HEMATOLOGY 311
FINALS WEEK 1: ANEMIA
3. ANEMIA DUE TO CHRONIC INFLAMMATION BETA Other Names Description
• Is now called Anemia of Chronic disease THALASSEMIA
• Most common anemia among hospitalized
-Results when one
patients. Heterozygous
Thalassemia of the 2 genes that
• Anemia associated with systemic disease: Thalassemia
minor produce beta globin
a. Arthritis
is defective.
b. Tuberculosis Cooley’s trait
c. HIV
-Usually presents a
d. Malignancies: Leukemia, Lymphoma, Myeloma Rietti–Greppi –
Hgb: mild asymptomatic
Hallmark: Presence of sideropenia (decrease serum iron Micheli Disease
Male: 12.4- anemia
despite having an abundant iron source)
14.2g/dl
Female: 10.8 – -Normal or slightly
TREATMENT
12.8 mg/dL decrease RBCs
• Therapeutic Erythropoietin and Iron

ACUTE PHASE REACTANT IN RESPONSE TO ACI

1. Hepcidin: regulator of iron homeostasis. -More severe
2. Lactoferrin: iron – binding protein in the granules of Intermediate Thalassemia anemia than minor
neutrophils. - Intermedia  - Thalassemia but
3. Ferritin: Stores iron Thalassemia do not require
regular transfusion.
THALASSEMIA (chapter 28, p454, 5th ed.)
• Inherited disorders caused by genetic alterations that -Occasional
reduces of preclude the synthesis of the globin chains transfusions but do
Hgb: 7g/dL
of hemoglobin tetramer. not require them
-Its either alpha or beta globin chain problem. on a regular basis.
• Predominant in Mediterranean, African, and Asian -Decrease or
ancestry. Thalassemia Homozygous complete lack of
• First described by Cooley and Lee in 1925 major Thalassemia beta globin
-During their study they’ve seen a patient with production
hepatomegaly, splenomegaly and mongoloid facial Cooley’s anemia
features. -Death due to
-Thalassemia came from the word “thalassic” relating Hgb: Mediterranean circulating iron
to “sea” 3 – 4 g/dL anemia overload.
-RBC is weakened and destructed.
Target cell -Possible of
 Presence of anemia splenectomy
Hgb A
Laboratory -Diagnosed bet.
IDA ACI SA Thalassemia 6 months – 24
Test
Retics Count  N   moths of age
Serum
   N -Most severe form
Ferritin
and transfusion
Serum Iron    N
dependent anemia
Transferrin
   N (Monthly
Saturation
transfusion: if
TIBC    N untreated Hgb falls
FEP/ZPP    N within 3-4g/dl their
Prussian Blue No mcv is 50-70 only)
reaction (BM stainable /N  N
iron) iron -Slunted growth
Frontal Bossing

Reference: Mrs. Agnes Guzman, RMT

 HEMATOLOGY 311
FINALS WEEK 1: ANEMIA
4. Hemoglobin Lepore: rare class of anemia due to
ALPHA Hemoglobin crossing over of beta and delta.
Description
THALASSEMIA Present 5. Hemoglobinopathy + Thalassemia
Birth: 1% - 2% Hb ̵ Hemoglobin S – Thalassemia
Silent Carrier Deletion of one
Bart’s ̵ Hemoglobin C – Thalassemia
(-/)  globin gene
leaving 3 ̵ Hemoglobin E – Thalassemia
Adult: ̵
Can be mistaken functional 
Normal Hb A A. Hemoglobin S – Thalassemia
as IDA globin genes.
Normal Hb Bart ̵ Is a double heterozygous abnormality.
 - Thalassemia ̵ The abnormal genes for Hb S (Sickle cell) and
Trait/ thalassemia are co – inherited.
Deletion by the Birth: 2% - 10% Hb
Minor two  globin Bart’s Types:
Homozygous gene. 1. Hb S -  - Thalassemia
(-/-) Adult: 2. Hb SS -  - Thalassemia
Minor Asymptomatic Normal Hb A 3. Hb S -  - Thalassemia
Heterozygous
(--/) B. Hemoglobin C – Thalassemia
Birth: -  - Thalassemia with inherited Hb C.
- 10% - 40% Hb - Produces severe hemolysis and splenomegaly
Caused by the
Bart’s replaced and minimal or no beta chain production/
presence of only
by Hb H - Minimal amount or no .
one gene
Hemoglobin H
producing 
disease - 10% - 50% C. Hemoglobin E – Thalassemia
chain.
(--/-) remainderHb F, ̵ Co – inherited of hemoglobin E and 
Hb A2, Hb Bart’s Thalassemia that result to a marked reduction
Mild-moderate
and Hb A of  chain production.
anemia
̵ Similar to  - Thalassemia intermediate
Adult: 70% Hb A ̵ Common in Cambodia, Thailand and part of
Results in the India.
absence of all 
chains synthesis TREATMENT:
• Chelators (EDTA)
Incompatible
with life (leads LABORATORY FINDINGS OF THALASSEMIA
Birth:
to death)
HydropsFetalis - 80% - 90% Hb
(--/--) Bart’s 1. CBC
Hepatomegaly Hb and Hct
Counterpart:  -
Splenomegaly
- 5% - 20% Hb  / Normal RBC count
Thalassemia Portland RBC indices (MCV and MCHC)
Yellow color RDW – degree of anysocytosis
major
- Trace of Hb H
Patients: 2. Peripheral Smear
Neonates (After ̵ Microcytic hypochromic
delivery for ̵ Exhibits anisocytosis and Poikilocytosis (target
about hours/ cells and elliptocytes)
day only → ̵ Presence of NRBC (nucleated RBC)
death) ̵ Polychromasia and basophilic stippling

TYPES OF THALASSEMIA 3. Increased Reticulocyte Count

1. Beta () Thalassemia – Chromosome 11 - Indicates that the bone marrow is responding
-Alpha and beta chain carries the Hgb so its to hemolytic process.
important.
2. Alpha () Thalassemia – Chromosome 16 4. Bone Marrow Examination
-Predominated hemolysis - Shows hypercellular with extreme erythroid
3. Hereditary Persistence of Hb F (HPHF) hyperplasia.
-Thalassemia with increased levels of Hgb.
-Partial inactivation of delta/beta and Hbf 5. Decreased OFT (osmotic fragility test)
increased to compensate.
Reference: Mrs. Agnes Guzman, RMT
 HEMATOLOGY 311
FINALS WEEK 1: ANEMIA
6. Supravital stain - Shows Hb H inclusions ̵ Dietary deficiency
1. Inadequate Intake of VB12 of Folic acid
7. Electrophoresis • Sources of Folic Acid
̵ Differentiates hemoglobin variants. (Hb S, -Leafy green vegetables, dried beans, liver, beef
Hb C, Hb E) and some fruits.
̵ Best • Sources of Vitamin B12
-Meat, eggs and dairy products
8. Mass Spectrophotometry 2. Increased need
̵ Assess the difference in mass of the globin -During pregnancy, lactation and growth.
chains. 3. Impaired Absorption in the Intestine
̵ Detects single amino acid substitutions in 4. Impaired Use due to Drugs such as Antiepileptic
the globin chains. Drugs
5. Excessive Loss during Renal Dialysis
9. DNA Analysis
̵ Identify globin gene mutations. LABORATORY FINDINGS OF MEGALOBLASTIC ANEMIA
̵ Best 1. CBC
a. PCR a. Pancytopenia: decreased formed elements such
b. Single Amplification System as WBC, RBC and platelets
b. Hb and Hct: decreased
10. Increased Indirect Bilirubin c. MCV: increased (>120 fL)
d. MCH and RDW: increased
e. MCHC: normal
II. MACROCYTIC NORMOCHROMIC ANEMIA (chap 21, p.315)
2. Decreased in Absolute Reticulocyte Count
3. Peripheral Smear
1. MEGALOBLASTIC ANEMIA a. Oval macrocytes/megalocytes
• Disorder in the DNA synthesis of RBC. b. Poikilocytes
• The maturation of nucleus is delayed relative to ̵ Dacryocytes, fragments,
that of cytoplasm. microspherocytes
• RBCs are very fragile. The life span is shortened c. NRBCs
and may die in the bone marrow causing an d. Howell – Jolly bodies
increase LDH. e. Basophilic Stippling
Platelet is decreased bc of low production in the f. Cabot Rings
bone marrow. 4. Hypersegmented Neutrophils (5 or more lobes)
• Hallmark: Granulocytes are hypersegmented 5. Chemical Analysis
2 Types ̵ Decreased serum Folate level
a. PERNICIOUS ANEMIA ̵ Decreased serum Vitamin B12 level
̵ Vitamin B12 (cobalamin) deficiency. ̵ Increased Homocysteine – Folate Def. and
̵ Neurologic symptoms: Cardiovascular disorder
o Memory loss ̵ Increased Methylmalonic Acid – Vitamin B12
o Tingling in toes and fingers Def.
o Impairment of walking by loss ̵ Increased Lactate Dehydrogenase
̵ Increased total and indirect bilirubin
b. FOLIC ACID DEFICIENCY 6. Schilling Test
̵ Nutritional Megaloblastic anemia ̵ Used to distinguish malabsorption of Vitamin
̵ Neural defect→Spinal bifida B12 from other causes of malabsorption.
̵ Uses oral dose of radioactive Vitamin
Note: If either of the two is missing, there would be an B12.
impaired production of thymidine nucleotide which is very
important in DNA synthesis. Sequence of Megaloblastic Anemia:
1. Decreased vitamin levels (b12 or folic)
EFFECTS OF VITAMIN B12 AND FOLATE DEFICIENCY 2. Hypersegmented neutrophils
VITAMIN B12: 3. Oval macrocytes in peripheral blood smear
Neurologic symptoms: 4. Megaloblastosis in bone marrow
✓ Memory loss 5. Anemia
✓ Numbness
✓ Tingling in toes and fingers TREATMENT: Vitamin Therapy
✓ Impairment of walking by loss of vibratory sense. Vit
2. NON-MEGALOBLASTIC ANEMIA
CAUSES OF MEGALOBLASTIC ANEMIA
Reference: Mrs. Agnes Guzman, RMT
 HEMATOLOGY 311
FINALS WEEK 1: ANEMIA
• Lack of hypersegmented neutrophils, no oval ̵ A rare acute form of cold – generated
macrocytes and no megaloblastosis. hemolysis.
• Anemia caused by conditions such as: ̵ Hemolysis occurs when blood is warmed after
a. Alcoholism previous exposure to chilling.
b. Chronic Liver Disease ̵ Caused by an antibody (Donath – Landsteiner
c. Hypothyroidism - Myxedema Antibody) present in the plasma.
d. Myeloma ̵ Increased Retics
• No hypersegmentation. ̵ Increased Bilirubin
• No increased in MCV and decreased in 120 days of Primary Secondary
RBCs. Syphilis, Viral Respiratory
Idiopathic
Infection
III. NORMOCYTIC NORMOCHROMIC ANEMIA

A. EXTRINSIC HEMOLYTIC ANEMIA CHARACTERISTICS OF AUTOIMMUNE HEMOLYTIC ANEMIA

1. Antibody Mediated Anemia
2. Mechanical
3. Chemical and Physical Agents
4. Infection

ANTIBODY MEDIATED ANEMIA

Classifications:
1. Autoimmune Hemolytic Anemia (AIHA)
2. Drug – Induced Immune Hemolytic Anemia
3. Alloimmune Hemolytic Anemia

1. AUTOIMMUNE HEMOLYTIC ANEMIA

• Characterized by premature RBC destruction caused
by autoantibodies that bind the RBC surface.
• AIHA + Thrombocytopenia = Evan’s Syndrome 2. Drug-induced Immune Hemolytic Anemia

TYPES OF AUTOIMMUNE HEMOLYTIC ANEMIA ✓ Self – limiting, but severe even fatal following the
a. Warm – Reactive Autoimmune Hemolytic Anemia administration of drug that can cause immune
̵ Responsible for approximately 70% of immune hemolytic anemia.
hemolytic cases. ✓ Blood disorder that occurs when a medicine
̵ Most commonly encountered AIHA and DAT (direct triggers the body’s defense system to attack its
anti-globulin test) positive. own RBC (causes early breakdown of RBC).
̵ Mediated by antibody with maximum binding ✓ Stop the intake of drugs to prevent this.
affinity at 37oC. Examples of Drugs:
̵ Anisocytosis, Polychromasia, Spherocytosis, a. Penicillin
Macrocytosis, RBC, Increased Retics. b. Stibophen
c. Alpha Methyldopa
Primary Secondary
Idiopathic SLE, Viral Infection 3. Alloimmune Hemolytic Anemia
• Usually occurs in newborns following the
b. Cold – Reactive/Agglutinin Autoimmune transplacental passage of maternal anti-fetal red
Hemolytic Anemia cells antibody.
̵ Mediated by antibody with maximum binding 2 Causes:
affinity at 4oC or below 32oC. 1. Erythroblastosisfetalis
̵ Signs & symptoms: Fatigue, pallor, weakness. - Isoimmune HDN due to Rh incompatibility (the
̵ Commonly found in healthy individuals. HDN occurs when the IgG alloantibodies
̵ Mild anemia: 9-12g/dl of Hgb. If severe, it could crosses the placenta into the fetal circulation
lead to <5 Hgb and then it will bind to the fetal RBC that are
̵ IgM is responsible here (IgM binds to Hgb after positive).
exposure to cold) 2. Isoimmune HDN due to ABO Incompatibility
Primary Secondary
Accompanied with
Idiopathic
Mycoplasma pneumoniae

c. Paroxysmal Cold Hemoglobinuria (PCH)

Reference: Mrs. Agnes Guzman, RMT