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
Diagnosis
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
- 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
Diagnosis
- 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
Diagnosis
- 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
- 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
References
Dunphy, L.M., Winland-Brown, J. E. (2011). Primary Care: The Art and Science of Advanced Practice
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.