Common Anemias

Common Anemias

Common microcytic, macrocytic, & normocytic anemias

  • Common anemias are:Pernicious anemia, folate deficiency, Iron deficiency anemia (IDA),thalassemia, & anemia of chronic disease
  • Anemia is a reduction in erythrocytes in the circulating blood or in the quality or quantity of hemoglobin
  • Blood loss is most common cause
  • There are 2 groups of people that look different when assessing for anemia: elderly patients & COPDers
  • Elderly tend to have lower H&H & up to 20% can have idiopathic anemia of aging
  • COPDers, smokers & people that live in high altitudes generally have a higher H&H (polycythemia & smoker’s polycythemia)
  • Every anemia is characterized by: RBC size (cytic) & RBC color (chromic)
  • Morphology: Cytic= size. Identified by Macrocytic (large), Microcytic (small) or Normocytic (normal)
  • The laboratory test that describes the size of a patient’s RBC is the Mean Corpuscular Volume (MCV)
  • Hemoglobin content: (Chromic=hemoglobin content) (Normochromic =normal) (hypochromic= small)
  • The laboratory test that describes the hemoglobin content of a patient’s RBC is the Mean Corpuscular Hemoglobin (MCH)
  • Red Cell Distribution Width (RDW) indicates the degree of variation in RBC size
  • Other terms: Anisocytosis= red blood cells that have various sizes
  • Poikilocytosis=red blood cells present in various shapes

General Clinical Manifestations of Anemia

The symptoms vary based on the body’s ability to compensate and the severity of the anemia

  • Fatigue
  • weakness
  • dyspnea & pallor

Macrocytic-Normochromic Anemia

Vitamin B12 = Pernicious Anemia (PA) & Folate Deficiency Anemia

  • The Megaloblastic Anemias
  • Folic acid & vitamin B12 are cofactors for pyrimidine synthesis of DNA
  • Pernicious anemia is the most common cause of vitamin B12 deficiency
  • PA is an autoimmune disease characterized by production of autoantibodies to gastric parietal cells & their secretory product, intrinsic factor (necessary for vitamin B12 absorption in the terminal ileum)
  • Defective DNA synthesis is due to Vitamin B12 or Folate deficiencies
  • Deficiency results in unequal growth of the nucleus & cytoplasm
  • Pernicious Anemia causes nerve demyelination
  • Inadequate intake of folate is the most common cause of deficiency in folate deficiency anemia
  • Etiologies: ETOH abuse, malabsorption (celiac disease, IBD), medications (methotrexate, trimethoprim, phenytoin), myelodysplastic syndromes (malignant hematopoietic stem cell disorders), pregnancy (usually a vitamin deficiency), bariatric surgery patients

Clinical Manifestations of Pernicious Anemia (PA)

  • Patient may be asymptomatic (most common)
  • Loss of appetite
  • Abdominal pain
  • Beefy red tongue
  • Atrophic glossitis
  • Jaundice & splenic enlargement
  • Paresthesias
  • weakness
  • Elderly may have cognitive changes

Diagnosis of B12 & Folate Deficiency

  • Serum B12 level (common method for establishing B12 deficiency)
  • Shilling test (confirms vitamin B12 deficiency is from intestinal malabsorption)
  • Methylmalonic acid (MMA) & homocysteine (HC) levels (sensitive measure of B12 deficiency)
  • MMA & HC are metabolic intermediaries & need B12 for metabolism
  • Serum folate levels for diagnosis of folate deficiency (not as sensitive)
  • RBC folate levels (a more sensitive test)

Differential Diagnosis for B12 & Folate Deficiency

  • Many causes of anemia should be first grouped according to the red cell indices: microcytic, normochromic-normocytic, & macrocytic
  • Once the patient is determined to have macrocytosis, the primary differential approach is the identification of vitamin B12 or folate deficiency

Treatment of Pernicious Anemia

  • Parenteral or high doses of Vitamin B12 (cobalamin) IM administered Q day x 1 week, then weekly for 1 month, then monthly for life
  • Intranasal forms available
  • Neurologic deficits of B12 deficiency usually reversible & improvement of symptoms usually takes 5-10 days
  • Reticulocyte count rapidly increases 7-10 days after treatment

Clinical Manifestations of Folate Deficiency Anemia
Folate Deficiency Anemia is lack of Folate absorption due to poor Folate intake in the diet

  • similar to Pernicious Anemia except neurologic manifestations are usually not seen

Treatment of Folate Deficiency Anemia

  • Folate deficiency: initiate treatment 1-2 mg of folic acid daily for 4-5 weeks
  • Maintenance therapy is not indicated for folate deficiency if the deficiency can be reversed after oral therapy
  • Treat folate deficiency for 1-4 months or until hematologic recovery


Microcytic-Hypochromic Anemia

Iron Deficiency Anemia (IDA) 

  • Iron deficiency anemia is the most common type of anemia
  • Iron deficiency is a nutritional Iron deficiency
  • Iron loss exceeds intake so that iron storage is progressively depleted
  • In adults, iron deficiency usually occurs from bleeding (GI bleeding)
  • In childhood & adolescence, poor dietary intake & increased iron demands are the most common cause
  • Children < 24 months, especially those between 9-18 months, are at highest risk for IDA 
  • Population at risk for IDA: pregnant women, elderly. ETOH abusers, NSAID users, females with heavy menses, vegetarians
  • IDA, the RDW is ↑, serum Fe ↓, TIBC ↑, & serum ferritin is ↓

Clinical Manifestations of Iron deficiency anemia

  • Most people are asymptomatic
  • Weakness/Fatigue
  • Pallor (may see in conjunctiva)
  • Cheilitis
  • Koilonychia
  • Headache
  • Irritability
  • Exercise intolerance
  • spoon shaped nails
  • red,sore,painful tongue (will not have red beefy tongue like PA)
  • brittle hair
  • poor attention span
  • shortness of breath
  • Palpitations
  • Elderly may present with angina or dementia


Do complete history & physical exam

  • MCV ↓
  • Serum ferritin ↓  ♦The single most important test for the diagnosis of IDA♦
  • Serum iron ↓
  • TIBC ↑
  • CBC= ↓H&H
  • A hemoglobin response ≥ 1g/dL over a 4 week period confirms the diagnosis of IDA

Differential diagnosis

  • Any condition that can cause acute or chronic blood loss
  • Thalassemia trait (no response to iron therapy)
  • Lead poisoning
  • Chronic infection
  • Chronic disease 
  • Hemolytic disease (Sickle cell)

Treatment of Iron deficiency anemia

Replacement is 150-200 mg daily of elemental iron

  • Ferrous fumarate 325 mg: 106 mg elemental iron
  • Ferrous sulfate 325 mg: 65 mg elemental iron ♦Recommended oral iron agent, inexpensive, well absorbed, & well tolerated ♦
  • Ferrous gluconate 325 mg: 28-36 mg elemental iron
  • Infants & children < 5 years of age: 3mg/kg/day of elemental iron TID
  • Children ages 5-12 years of age: One 60mg elemental iron daily (One 300 mg Ferrous Sulfate tablet= 60mg elemental iron
  • Adolescent males ages 12-18 years of age: Two tabs of 60mg elemental iron daily
  • Adolescent females ages 12-18 years of age: One to two tabs of 60mg elemental iron daily
  • Iron should be taken between meals for better absorption
  • May take with Vit C= will boot absorption
  • Liquid iron medication should be place in back of mouth to prevent staining of teeth
  • Keep iron out of reach form children to prevent accidental poisoning
  • Replace for 4-6 months
  • After 1 month, HCT should ↑by 3% & HGB ↑ by 1 point
  • Instruct on foods rich in iron: organ meats, red meat, dried peas & beans, dark, green, leafy vegetables, whole grains

Microcytic-Hypochromic Anemia


  • Thalassemia is the most common genetic disorder in the world
  • α-thalassemia is more common in Asians, people of Mediterranean origin (almost never in African Americans)
  • α-thalassemias often goes undetected
  • Thalassemia disorder affects the synthesis of hemoglobin causing an overproduction of unaffected hemoglobin chains
  • Many types of thalassemia: α & β (α-thalassemia needs no therapy)
  • Alpha minima & minor need no therapy
  • Avoid inappropriate exposure to iron in a patient with thalassemia
  • In thalassemia the RDW is normal, serum Fe is normal, TIBC is normal & serum ferritin is normal

Clinical Manifestations of Thalassemia

  • Weakness/Fatigue
  • Pallor (may see in conjunctiva)
  • Headache
  • Irritability
  • Exercise intolerance
  • Shortness of breath
  • Palpatations
  • Anorexia


  • CBC (essential for the diagnosis microcytic anemia)
  • Hub electrophoresis (↑ hemoglobin A2 level in β-thalassemia)
  • MCV ↓
  • Normal serum iron
  • Poikilocytosis, anisocytosis in β-thalassemia

Differential Diagnosis

Must be differentiated from other types of anemia: IDA, α-thalassemia, β-thalassemia, & sideroblastic anemia

Treatment of Thalassemia

  • Thalassemia often require no treatment other than vigilance by the health care provider concerning hematological markers 
  • Patients with severe anemia (associated with β-thalassemia major & hemoglobin H disease) require regular transfuson with RBC’s folate supplementation, & possibly oral iron chelation to prevent hemosiderosis & hemochromatosis (hemosiderosis of chronic standing may require referral for a splenectomy)
  • May require referral to hematologist

Normocytic-Normochromic Anemia 

Anemia of Chronic Disease (ACD)

  • Red blood cells that are normal in size and hemoglobin content but insufficient in number
  • Associated with chronic diseases: infections, inflammatory & malignant disease
  • RBC life span is shortened from the normal 100-120 days to 60-90 days
  • Aplastic Anemia: Pancytopenia= low in RBC’s, WBC’s & PLT’s
  • Pure Red Cell Aplasia= low in RBC’s only
  • Fanconi Anemia= very rare. Defects in DNA repair
  • Posthemorrhagic Anemia: acute blood loss
  • Hemolytic Anemia: accelerated destruction or red blood cells
  • Sickle Cell Anemia: An inherited form of anemia (Autosomal recessive). The red blood cells only last 8-20 days.

Clinical Manifestations of ACD

  • Clinical presentation is similar to IDA, but physical findings depend more on the nature of the underlying disease than on the anemia


  • Do complete history & physical
  • Always obtain stool for occult blood
  • The peripheral blood smear usually shows a normochromic, normocytic picture but in advanced stages, it may show hypo chromic & microcytic (not as severe as IDA)
  • Serum iron ↓
  • TIBC ↓ ♦ ↓TIBC helps to differentiate ACD from IDA♦
  • Serum ferritin is normal or ↑ ♦ ↑ serum ferritin helps to differentiate ACD from IDA♦

Differential Diagnosis

  • Must be differentiated from other types of anemia: IDA, α-thalassemia, β-thalassemia, & sideroblastic anemia
  • Many underlying causes: chronic infection, inflammatory processes, & malignant neoplasms


  • Treatment is aimed at control of underlying disease or diagnosing the occult disease or illness
  • Consult specialist for consideration of erythropoietin (EPO) use
  • RBC transfusion is effective but should be limited



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 Nursing. Philadelphia, PA. F.A. Davis. 

Uphold, C.R., & Graham, M.V. (2013). Clinical guidelines in family practice. (5th ed.)    Gainesville, Fl.:                    

            Barmarrae Books, Inc.