Anemia




Microcytic Anemia
Microcytic Anemia Labs: MCV is decreased
Iron Deficiency Anemia – MC form of anemia
o Etiologies: chronic occult bleeding or menses
o Clinical picture

S/S

Pica and nail spooning

Restless leg syndrome, leg cramps, cold intolerance

Weakness, fatigue, exertional SOB, lightheadedness

Pallor in conjunctiva and mucous membrane

Labs

Iron studies
o Serum Iron: ↓
o Ferritin: ↓
o TIBC: ↑
o Transferrin: ↑

Peripheral smear: lack of target cells
o Treatment: Ferrous sulfate, 325 mg (65 mg of elemental iron)

Takes 6 weeks to correct and 6 months to replace iron stores

If Hgb < 8, packed RBC
Beta Thalassemia – genetic defect resulting in decrease production of beta chains
o Types

Minor (trait): mild disease

Cooley’s anemia – severe, hemolytic anemia that presents months after
birth
o Clinical picture

S/S: hepatosplenomegaly, jaundice, and growth retardation

Labs

CBC: RBC counts are higher than normal

Peripheral smear: target cells and dacrocytes
o Treatment: blood transfusions and iron chelation
Alpha Thalassemia – genetic defect resulting in decrease in production of alpha globin
chains
o MC in Chinese and SE Asian pts
o Types

Minima – a silent carrier

Minor/trait – minimal anemia

Hemoglobin H – shows Heinz bodies on peripheral smear

Fetal hydrops – fatal in utero
o Clinical picture

S/S: jaundice and palpable splenomegaly

Labs: Heinz bodies




Normocytic Anemia
Normocytic Anemia Labs: MCV is normal to low (> 75)
Anemia of Chronic Disease – occurs in any inflammatory, infectious, or malignant
disease of long-standing nature
o Clinical Picture

Labs

Iron studies
o Serum Iron: ↓
o Ferritin: ↑
o TIBC: ↔↓
o Transferrin: ↔↓

↑ Hepcidin (due to inflammatory disease)
Aplastic Anemia – anemia with pancytopenia
o The only type of anemia with decreased platelets, WBC, and RBC

Due to loss of blood cell precuroses leading to hypoplasia of the bone
marrow
o Etiologies

Chemicals, medications (ACEi, sulfonamides, phenytoin), and radiation
o Dx: bone marrow bx shows hypocellular tissue
o Treatment: stop causative agent and RBC transfusion
Other Normocytic Anemias
o Acute blood loss

H&H may be more concentrated and falsely elvated until equilbrilation
takes place
o Anemia due to multiple myeloma – immunoglobin causes rouleaux formation
o Anemia of CKD – 2/2 to los of EPO production by the disease kidney in pts with
stage IIIb CKD

Treatment: Epoetin alfa or Darbepoetin alfa titrated to keep Hgb between
10-12

Hgb > 12 increases risk of cardiovascular events
o Myelophthisic anemia – caused by disorders that infiltrate the bone marrow and
crowd out normal cellular precursors
o Myelofibrosis – fibrosis of the bone marrow
o Pure red cell aplasia (Diamond-Blackfan syndrome if congenital) – anemia with
low RBC

Need to assess pts for thymoma
Anemia



Macrocytic Anemia
Macrocytic Anemia Labs: MCV is elevated (> 100)
B-12 Deficiency – megaloblastic anemia with hypersegmented neutrophils
o Etiologies (malabsorption or dietary deficiency)

Bacterial overgrowth or IBD limiting absorption of cobalamin (B12)

Poor dietary intake
o Pernicious anemia – occurs due to atrophic gastritis and lack of parietal cells to
make intrinsic factor

Assess with Schilling test
o Clinical Picture

S/S

Symmetrical LE paresthesia and loss of vibratory/proprioception

Ataxia

CNS symptoms (dementia, irritability, and memory loss)

Atrophic glossitis and flattening of intestinal villi
o Diagnosis

1st vitamin B12 levels (diagnostic if < 200)

2nd: Methylmalonic acid levels
o Treatment: vitamin B12 IM injections, 1000 mcg
Folate Deficiency – megaloblastic anemia
o Etiologies

Alcoholism, nutritional deficiencies, pregnancy
o Diagnosis

Peripheral smear: hypersegmented polymorphonuclear leukocytes

RBC folate levels
o Treatment: Folate, 1 mg daily





Hemolytic Anemia
Hemolytic Anemia Labs
o LDH: ↑
o Indirect (unconjugated) bilirubin: ↑
o Haptoglobin: ↓
o Reticulocyte count: ↑
o Peripheral smears

Sphereocytes = extravascular hemolysis

Schistocytes = intravascular hemolysis
G6PD Deficiency –x-linked disorder that causes hemolysis occurs during episodes of
oxidative stress
o Flare triggers: Fava beans, antimalarials, sulfonamides
o Diagnosis: G6PD activity assay shows reduced levels

Peripheral smear shows Heinz bodies and Bite cells
Sickle Cell Disease – Hgb S causes RBCs to deform into a sickle shape at sites of low PO2
o The sickle shape causes vaso-oclusion in the capillaries, leading to inflammation
and thromboses
o Clinical Picture

S/S

Severe pain in bones from infraction and ischemia of the bones,
spleen, lungs, or kidneys

Jaundice, splenomegaly, priapism, pain/swelling in hands and feet

Acute chest syndrome – vaso-occlusive crisis of the lungs;
characterized by fever, chest pain, and pulmonary infiltrates
o Diagnosis: hemoglobin electrophoresis
o Treatment: Hydroxyurea
Other Hemolytic Anemias
o Autoimmune hemolytic anemia

Diagnosis: direct Coombs test

Treatment: corticosteroids
o Hereditary Spherocytosis

Diagnosis: osmotic fragility test

Treatment: total or partial splenectomy
o Alpha and beta thalassemia
Extrinsic vs Intrinsic Hemolysis
o Extrinsic – hemolysis occurs due to the environment

Auto-immune hemolysis

Drug induced
o Intrinsic – hemolysis occurs due to the RBC itself

Sickle cell disease and thalassemias

Spherocytosis

G6PD deficiency