1 N5315 Advanced Pathophysiology Disorders of Erythrocytes Please review these lab values on slides 2, 3, and 4. You will need to know the normal ranges for the WBC, Hgb, HCT, MCV and platelets for testing purposes. • Diagnostic Testing • Complete Blood Count (CBC) i. This is a series of blood tests that measures the amounts of various blood cells or blood cell shapes/sizes ii. Cells measured 1. White Blood Cells (WBC)- 5,000-10,000mm3 2. Red Blood Cells (RBC) a. Males: 4.7- 6.1 b. Females: 4.2-5.4 3. Hemoglobin (Hgb) a. Measures total hemoglobin in the blood and decreased levels indicate anemia. b. Men: 14-18 c. Females: 12-16 4. Hematocrit (HCT) a. Measures the percentage of total RBCs. Decreased levels means anemia. b. Men: 42%- 52% c. Females: 37%-47% 5. Mean Corpuscular Volume (MCV) 80-100mm3 a. Measures the average size of RBC, helps with the classification of anemia 6. Reticulocyte Count 0.5% - 2% a. Measure of immature RBCs and is an indicator of how the bone marrow is responding to anemia2 7. Neutrophils 55-70% a. Bands-immature neutrophils i. 0.2 mm3 is normal. An elevation indicates the presence of infection that has resulted in a need for increased neutrophils. Therefore, the bands are released to meet the demand. This is called a shift to the left. 8. Lymphocyte 20-40% 9. Monocytes 2-8% 10. Eosinophils 1-4% 11. Basophils 0.5- 1.0% 12. Platelets 150,000-450,000 mm3 Anemia Anemia is a broad, nonspecific term used to describe a decrease in the total number of red blood cells. This term is not an acceptable diagnosis and requires one to differentiate between the potential etiologies and determine the correct diagnosis. There are multiple causes of anemia and it can be easy to get lost in the possible causes. The causes include decreased production of RBC, hemolysis of RBC, acute or chronic blood loss or any combination of these factors. When you have identified an anemia, the first step in determining the cause is to review the mean corpuscular volume (MCV) on the CBC. The MCV identifies the size of the red blood cell (RBC). Anemias are most commonly classified based on the size of the red blood cell. The normal range of an MCV is 80-100. If the MCV is < 80 then the anemia is said to be a microcytic (small cell) anemia. If the MCV is 80-100 then the anemia is said to be a normocytic (normal cell) anemia. If the MCV is > 100 it is classified as a macrocytic (large cell) anemia. Anemias typically fit into one of the three aforementioned categories.3 As you will see some types of anemia can be in more than one category. One important point to note is that alcohol can cause a macrocytic anemia. You will see this in individuals who abuse alcohol. Some of these individuals will have an elevated MCV and not be anemic. Alcohol can cause a macrocytosis without causing an anemia. Beware that the elderly can have a slightly elevated MCV as well and this is considered normal for their age group. The main pathological effect of anemia is a reduced oxygen-carrying capability of the red blood cell. The low amount of total red blood cells lowers the blood volume and consistency. The body compensates for the low blood volume by shifting fluid from the interstitial space into the intravascular space thus expanding the intravascular volume. This decreases the blood viscosity. Because the blood is less viscous, it flows faster and is more turbulent in its flow. This causes a hyperdynamic circulatory state which increases stroke volume and heart rate. This hyperdynamic state may cause cardiac dilation and heart valve insufficiency if the anemia is not corrected. Reduced levels of oxygen in the blood is referred to as hypoxemia and it is associated with anemia. The hypoxemia can contribute to the cardiac dysfunction associated with anemia by causing arterial and venous vasodilation thus leading to a decreased vascular resistance and increased blood flow. This contributes to increasing the heart rate and stroke volume to help compensate. This may lead to heart failure. Tissue hypoxia caused by anemia increases respiratory rate in an attempt to increase tissue oxygen levels. In an attempt to compensate for the tissue hypoxia, more oxygen is released from hemoglobin. These compensatory mechanisms cause the clinical manifestations of dyspnea, rapid heart rate, palpitations, dizziness, fatigue, and chest pain. Anemia which is severe can lead to a heart attack particularly in individuals with CADS. Other manifestations of anemia include pale skin and mucous membranes, jaundice if the anemia is secondary to hemolysis, impaired healing, loss of tissue elasticity, thinning and graying of the hair. Decreased oxygen to the GI tract may lead to abdominal pain, nausea, vomiting and anorexia.4 An acute anemia will result initially in vasoconstriction to divert blood flow to the vital organs. The decreased blood flow is detected by the kidneys and they activate RAAS to increase blood volume. Severe blood loss may lead to renal injury. Macrocytic Anemias The two most common macrocytic anemias are pernicious anemia and folic acid anemia. Pernicious anemia is a reduction in the amount of RBCs caused by a vitamin B12 deficiency. The deficiency is caused by a lack of intrinsic factor which results in the malabsorption of B12. In normal physiology, intrinsic factor is secreted by parietal cells and binds with B12 in the small intestine. This complex then binds to the surface of cells in the ileum and is transported across the intestinal mucosa. Causes include vegan diets, gastrectomy, or atrophy of gastric mucosa due to autoimmune disease. Other causes include resected ileum, infestation with tapeworms, conditions which require increased levels of B12 such as pregnancy/hyperthyroidism/chronic infection/disseminated cancer. Alcohol abuse, hot tea ingestion and smoking can all lead to B12 deficiency. Proton pump inhibitors decrease cobalamin absorption and may contribute to a B12 deficiency. Autoimmune pernicious anemia is characterized by the presence of autoantibodies to the H+-K+ ATPase, which is the major protein in parietal cell membranes. Pernicious means highly destructive. It was named this because the condition used to be fatal. The disease usually manifests later in life, around age 60. This is because we store ten years of vitamin B12 and a person must deplete their stores prior to becoming symptomatic. Clinical manifestations
View Full Document
Unlocking...