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49 Cards in this Set
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an anemic state characterized by the presence of abnormally large RBCs in the peripheral blood.
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Macrocytic anemia
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refers to a blood condition in which red blood cells (RBC) are larger than normal.
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macrocytosis
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Macrocytic anemia can usually be divided into two categories:
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megaloblastic
nonmegaloblastic |
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Differentiation of megaloblastic and nonmegaloblastic macrocytic anemias is based on the:
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The examination of the bone marrow
The peripheral blood smear |
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What are the common pathologic causes of macrocytosis?
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Drugs
Alcoholism Reticulocytosis Nonalcoholic and alcoholic liver disease Hypothyroidism VITAMIN B12 DEFICIENCY FOLATE DEFICIENCY Multiple myeloma Myelodysplastic syndromes APLASTIC ANEMIA Acute leukemia |
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Macrocytic anemies are?
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Normochromic, macrocytic anemias
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Macrocytic anemias have?
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Normal MCHC
High MCV |
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is the average concentration of hemoglobin per red blood cell and is calculated by dividing the hemoglobin by the hematocrit
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Normal MCHC (Mean Corpuscular Hemoglobin Concentration)
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is the average size of a red blood cell and is calculated by dividing the hematocrit (Hct) by the red blood cell count
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High MCV (Mean Corpuscular Value)
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What are two examples of macrocytic megaloblastic anemia
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Vitamin B12 deficiency
Folate deficiency |
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B12 binds with intrinsic factor (IF), absorbed in terminal ileum
Decreased B12 (cobalamin) Decrease or absent IF (intrinsic factor) Generally there is a 7-12 year supply of B12 therefore This may not present quickly Folate deficiency - Folate is not stored in body. This presents sooner |
Megaloblastic anemia
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The minimum daily requirement is about 2.5 μg.
2 mg is stored in the liver 2 mg is stored elsewhere in the body |
Cobalamin
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What are the causes of vitamin B12 deficiency?
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Dietary deficiency (rare)
Decreased production of intrinsic factor -pernicious anemia -gastrectomy Helicobactor pylori infection Competition for vitamin B12 in gut -Bind loop syndrome -Fish tapeworm (rare) Pancreatic insufficiency Decreaesd ileal absoprtion of Vitamin B12 -Surgical resection -Crohn's disease Transcobalamin II deficiency (rare) |
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a chronic illness caused by impaired absorption of vitamin B-12 because of a lack of intrinsic factor (IF) in gastric secretions.
defined as a severe lack of Intrinsic Factor (IF) due to gastric atrophy. |
Pernicious anemia
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Autoimmune attack on gastric intrinsic factor (IF)
Chronic atrophic gastritis which leads to a decline in IF production Autoantibodies directed against the gastricparietal cells (which produce IF) Increases the risk of intestinal-type gastric cancer and gastric carcinoid tumors |
Pernicious anemia pathophysiology
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What are five causes of B12 deficiency?
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Total or partial gastrectomy
Celiac disease Crohn's disease Infections of the gastrointestinal tract Poor nutrition |
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There is a high (approx 40%) prevalence of B12 deficiency in these patients?
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Hypothyroid patients
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General findings:
Weight loss of 10-15 pounds -50% - anorexia Low-grade fever -1/3 newly diagnosed patients Clinical Findings: pallor mildly icteric Changes in mucosal cells, leading to: Glossitis Anorexia Diarrhea |
Vitamin B12 Deficiency
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A red beefy tongue can be seen in what type of anemia?
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pernicious anemia
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The following are seen with what?
Severe Anemia (HCT as low as 10-15%) Leukopenia Thrombocytopenia Neurologic examination: Decreased vibration and position sense secondary to the demyelination in the CNS |
Advanced cases of B12 deficiency
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Clinical findings:
Complex neurologic syndrome Peripheral nerves affected with paresthesias Difficulty with balance Advanced cases: Cerebral function may be altered Dementia and other neuropsychiatric changes may precede hematologic changes |
Vitamin B12 Deficiency
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Reversible B12 deficiency manifestation:
Patients who are older and have Vit B12 deficiency may present with? |
symptoms suggesting senile dementia or Alzheimer disease:
memory loss irritability personality changes |
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Reversible B12 deficiency manifestation:
is less common and can be manifested by: delusions hallucinations outbursts paranoid schizophrenic ideation |
Megaloblastic madness
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Vitamin B12 deficiency may look like what other things?
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Anemia, iron deficiency anemia, aplastic anemia, folic acid deficiency, hemolytic anemia
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The presence of macro-ovalocytes
having an MCV >115 fl anisocytosis, poikilocytosis and hypersegmented neutrophils suggest a megaloblastic disorder |
Megaloblastic Anemia (B12 deficiency)– Lab Findings
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1. Give “flushing” dose of intramuscular B12 .
2. Give small oral dose of radioactive B12. • Healthy patients will excrete radioactive B12 in urine. • Patients who can’t absorb via gut will not excrete radioactive B12 in urine. 3. If urine has low radioactivity, give another oral dose of radioactiveB12 with intrinsic factor. • If patient now excretes radioactive B12, patient lacks intrinsic factor. • If patient still doesn’t excrete radioactive B12, the defect is not in intrinsic factor (probably, something else is wrong with absorption.) |
Shilling test
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How do you tx pernicious anemia?
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IM B12 injections of cyanocobalamin 1000 ug daily x 1 week, then weekly x 4 weeks, then monthly
Alternate: 1000 ug po daily ** Alternatively, hydroxocobalamin given in the same dose every 1-3 months intramuscularly is also effective therapy. |
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These types of patients need to be screened for what?:
Patients who have undergone gastric reduction for control of obesity Patients who are receiving long-term treatment with proton pump inhibitors |
B12 Deficiency
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This is necessary for red blood cell production and neural tube formation?
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Folic Acid
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This is the common name for pteroylmonoglutamic acid.
Many different plants and bacteria synthesize it. Fruits and vegetables form the primary dietary source of the compound but prolonged cooking destroys it. The minimum daily requirement is about 50 μg may be increased significantly during times of increased metabolic demand such as pregnancy or in hemolytic anemias. |
Folic Acid
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Is readily absorbed in the duodenum and proximal jejunum?
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Folic Acid
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What are the sources of folic acid?
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Liver, yeast, nuts, dried beans, whole grains, spinach and other leafy greens, oranges, avacados
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What are the causes of folate deficiency?
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Dietary deficiency
Decreased absorption Tropical sprue Drugs: phenytoin, sulfasalazine, trimethoprim-sulfamethoxazole Increased requirement Chronic hemolytic anemia Pregnancy Exfoliative skin disease Loss: dialysis Inhibition of reduction to active form methotrexate |
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What are the essentials of diagnosis for a folic acid deficiency?
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· Macrocytic anemia
· Macro-ovalocytes and hypersegmented neutrophils on peripheral blood smear · Normal serum vitamin B12 levels · Reduced folate levels in red blood cells or serum |
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Folic acid deficiency results in anemia and intestinal manifestations but not ?
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Neurological symptoms
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What is the differentiation between folate and B12 deficiency?
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Serum vitamin B12 level is normal.
The RBC folate level of less than 150 ng/mL is diagnostic of folate deficiency. Also no neurological deficits as in B12 deficiency |
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What is the tx of folic acid deficiency?
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Treated with folic acid, 1 mg/d orally
Response: Rapid improvement and a sense of well-being reticulocytosis in 5-7 days total correction of hematologic abnormalities within 2 months and treatment is generally continued for 4 months. |
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What do you have to do before large doses of folate are given?
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Exclude cobalamin deficiency (& if present. . .)
Correct cobalamin deficiency or cobalamin neuropathy may develop Even though the anemia appears to be corrected with folate treatment. |
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In any patient receiving long-term folic acid therapy:
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Measure the serum cobalamin level at regular (e.g., once yearly) intervals
Excludes missing the development of cobalamin deficiency. |
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is a severe, life threatening syndrome in which production of erythrocytes, WBCs, and platlets has failed.
The disease is characterized by peripheral pancytopenia (disappearance of rbc precursors from the marrow) and accompanied by a hypocellular bone marrow. |
Aplastic anemia
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Bone marrow failure: decreased RBC, WBC, platelets
Marrow replaced with fat Causes: idiopathic Viral infections stem cell damage from radiation Exposure to chemicals Certain antibiotics (chloramphenicol) Chemotherapeutic drugs |
Aplastic anemia
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Poorer prognosis in aplastic anemia is related to?
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Poorer prognosis is related to:
Neutropenia < 0.5 G/L Thrombocytopenia < 20 G/L Reticulocytes < 20 G/L |
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Just read this for reference:
Etiology Acquired Most cases of aplastic anemia are idiopathic and there is no history of exposure to substances known to be causative agents of the disease Exposure to ionizing radiation – hematopoietic cells are especially susceptible to ionizing radiation. Whole body radiation of 300-500 rads can completely wipe out the bone marrow. With sublethal doses, the bone marrow eventually recovers. Chemical agents – include chemical agents with a benzene ring, chemotherapeutic agents, and certain insecticides. Idiosyncratic reactions to some commonly used drugs such as chloramphenicol or quinacrine. |
Just read this for reference:
Etiology Acquired Most cases of aplastic anemia are idiopathic and there is no history of exposure to substances known to be causative agents of the disease Exposure to ionizing radiation – hematopoietic cells are especially susceptible to ionizing radiation. Whole body radiation of 300-500 rads can completely wipe out the bone marrow. With sublethal doses, the bone marrow eventually recovers. Chemical agents – include chemical agents with a benzene ring, chemotherapeutic agents, and certain insecticides. Idiosyncratic reactions to some commonly used drugs such as chloramphenicol or quinacrine. |
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Just read this for reference:
Etiology of aplastic anemia cont. Infections – viral and bacterial infections such as infectious mononucleosis, infectious hepatitis, cytomegalovirus infections, and miliary tuberculosis occasionally lead to aplastic anemia Pregnancy (rare) Paroxysmal nocturnal hemoglobinuria – this is a stem cell disease in which the membranes of RBCs, WBCs and platlets have an abnormality making them susceptible to complement mediated lysis. Other diseases – preleukemia and carcinoma |
Just read this for reference:
Etiology of aplastic anemia cont. Infections – viral and bacterial infections such as infectious mononucleosis, infectious hepatitis, cytomegalovirus infections, and miliary tuberculosis occasionally lead to aplastic anemia Pregnancy (rare) Paroxysmal nocturnal hemoglobinuria – this is a stem cell disease in which the membranes of RBCs, WBCs and platlets have an abnormality making them susceptible to complement mediated lysis. Other diseases – preleukemia and carcinoma |
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Congenital disorder associated with aplastic anemia:
the disorder usually becomes symptomatic ~ 5 years of age and is associated with progressive bone marrow hypoplasia. Congenital defects such as skin hyperpigmentation and small stature are also seen in affected individuals. |
Fanconi's Anemia
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Congenital disorder associated with aplastic anemia:
a subset of Fanconi’s anemia in which the congenital defects are absent. |
Familial aplastic anemia
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What are the clinical manifestations of aplastic anemia?
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Clinical Manifestations: vary with onset and severity of pancytopenia
Pallor, fatigue, headache, exertional dyspnea, tachycardia, heart failure Bleeding due to low platelet levels Fever, increased infection risk due to low WBC Diagnostics: bone marrow exam |
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What are the lab findings with aplastic anemia?
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Severe pancytopenia with relative lymphocytosis (lymphocytes live a long time)
Normochromic, normocytic RBCs (may be slightly macrocytic) Mild to moderate anisocytosis and poikilocytosis Decreased reticulocyte count Hypocellular bone marrow with > 70% yellow marrow |
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What are the three main interventions in treating aplastic anemia?
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Interventions:
Removal of causative agent Blood transfusions Bone marrow transplant |
