NU 350 Non-malignant Blood Disorders
What are the characteristics of anemia?
Deficiency in the number of RBCs, quantity of hgb, volume RBCs.
How is anemia classified?
Morphologic - size, color, content of cells
Etiologic - Cause of the anemia. Goal is to correct the cause of the anemia.
Mild - Hgb 10 to 12, may exist w/o symptoms, might show in someone with other heart conditions or COPD
Moderate - Hgb 6-10, increased cardiopulmonary symptoms, experienced at rest or during activity, tachycardia, tachypnea, hypotension, short of breath, low activity tolerance (even talking).
Severe - Hgb less than 6. Involves multiple body systems. Jaundice, severe tachycardia, murmurs, bruits, thin blood, could lead to heart failure. Roaring in the ears, headache, confusion (especially in the elderly). Beefy red swollen tongue, distention from enlarged liver and spleen
What are the clinical manifestations of anemia?
Pallor, jaundice, tachycardia, tachypnea, diaphoresis, short of breath, low activity tolerance, hypotension. Symptoms even at rest.
How does anemia affect the older population?
Anemia is common in older adults due to chronic disease and nutritional deficiencies. HTN, diabetes, and lack of nutrition, especially lack of iron, will cause anemia.
S/s often go unnoticed or mistaken for normal aging changes.
What are the characteristics of iron-deficiency anemia?
One of the most common chronic hematologic disorders
Found in up to 30% of world population
Iron deficiency anemia develops from:
–Inadequate dietary intake (5-10%) of ingested iron is absorbed
–Blood loss (2 ml of blood contains mg of iron)
Nutrition is NOT usually the cause of deficiency. Some people have dumping syndrome where everything goes straight through you without being absorbed.
What are the clinical manifestations of iron-deficiency anemia?
General manifestations anemia, pallor most common, glossitis is 2nd, burning of the tongue.
What are some diagnostic tests used in diagnosis of anemia?
Labs: Hgb, Hct, MCV, MCHC, reticulocytes, serum iron, TIBC, bilirubin, platelets.
Stool guaiac test - like a hemoccult test
Endoscopy and Colonoscopy if there is GI bleeding.
What are the goals of treatment and how do we accomplish these goals?
Goal: Treat the underlying disease.
Possible underlying causes are malnutrition or alcoholism.
Increase intake of iron, nutritional therapy, oral iron (absorbed with vit C, not absorbed with milk, will stain the teeth) or occasional parenteral iron supplements, transfusion of packed RBCs.
What education should be considered with oral iron?
Enteric-coated or sustained-release capsules are counterproductive (released far down GI tract)
Best absorbed as ferrous sulfate in an acidic environment-take with Vitamin C to enhance absorption
Liquid iron should be diluted and ingested through a straw
Side effects-heartburn, constipation, diarrhea
What interventions should a nurse implement with a patient with iron-deficiency anemia?
Identify at-risk groups - very young, those on poor diets, women of child-bearing age.
Supplemental iron - best is ferrous sulfate
Discuss diagnostic studies
Must follow iron therapy for 2 to 3 months after hemoglobin levels return to normal.
What is the etiology of thalassemia?
An autosomal recessive genetic disorder of inadequate production of normal hemoglobin. It's gonna come from the parents. Most of the time they get one gene from mom, one from dad.
Causes decreased erythrocyte production.
Hemolysis also occurs
Problem with globulin protein
–Abnormal Hb synthesis
One thalassemic gene
Two thalassemic genes
What are the clinical manifestations of Thalassemia minor and thalassemia major?
T minor: Frequently asymptomatic, mild ot moderate anemia
Physical and mental growth often delayed
Symptoms develop in childhood by age 2
Splenomegaly from continuous removal of damaged RBCs
Hepatomegaly from build up of iron
Jaundice from hemolysis
Chronic bone marrow hyperplasia
- Expansion of bone marrow space
Bones look really big, face is square looking, joints look expanded.
What is the treatment for thalassemia?
No specific diet or drug is effective.
T minor: Body adapts to decreased hgb.
T major: Blood transfusions with IV deferoxamine. It's a chelating agent that binds to the iron.
May have spleen removed to treat that.
What is megaloblastic anemia? What are the two types of megaloblastic anemias?
Group of disorder caused by impaired DNA synthesis.
Characterized by presence of large RBCs
Majority result from deficiency in cobalamin and folic acid
What is the etiology of cobalamin deficiency? What is this caused by?
In cobalamin deficiency, intrinsic factor (IF), a protein secreted by the parietal cells of the stomach, is not produced. IF is required for cobalamin absorption in the small intestine.
Pernicious anemia (most common) -
Gastritis and Gastrectomy
What are clinical manifestations of cobalamin deficiency?
- General symptoms of anemia
- Sore, shiny tongue
- Abdominal pain
- Weakness-general and muscle
- Paresthesias of the feet and hands
- Muscle weakness
- Impaired thought processes
What are the diagnostic findings apparent in cobalamin deficiency?
- RBCs appear large
- Abnormal shapes
- Decreased serum cobalamin levels
- Normal serum folate levels and decreased cobalamin levels suggest megaloblastic anemia due to cobalamin deficiency
- Schilling test – determines if the body absorbs B12 normally. Radioactive agent is ingested. If passed through the body into the urine, the body is not absorbing the vitamin. Don't think they're using this anymore.
What nursing care is indicated in the management of cobalamin deficiency?
Parenteral or intranasal administration of cobalamin. Daily for the first 2 weeks, weekly for the next 4 weeks, then once a month for maintenance.
Increase in dietary cobalamin does not correct the anemia
Still important to emphasize adequate dietary intake
Ensure that injuries are not sustained because of the patient’s diminished sensations to heat and pain
Ensure patient compliance with treatment
Evaluate patient for gastric carcinoma frequently
What are clinical manifestations of folic acid deficiency?
- Clinical manifestations are similar to those of cobalamin deficiency
- Insidious onset
- Absence of neurologic problems
How do we treat folic acid deficiency?
Replace the folic acid. Eat green,leafy vegetables, whole grains, fish, liver, orange juice.
What are the causes of anemia of chronic disease? Why does it occur?
–End-stage renal disease
–Chronic liver disease
–Chronic endocrine diseases like thyroid problems or diabetes
Why? Underproduction of RBCs and shortened lifespan of RBCs.
Iron moves from circulation to storage sites.
What are some diagnostic findings in anemia of chronic disease? How do we treat it?
↑ Serum ferritin
↑ Iron stores
Normal folate and cobalamin levels
Mild anemia in most cases.
- Treating underlying cause is best
- Rarely blood transfusions
- Erythropoietin therapy to increase RBCs in the blood
What are the characteristics of aplastic anemia?
Pt has pancytopenia and hypocellular bone marrow. Small bones.
Low incidence, managed with Epogen or blood transfusion.
Can be critical condition in the case of hemorrhage or sepsis.
What are the different types of aplastic anemia?
Congenital: From chromosomal alterations
Acquired: Results from exposure to ionizing radiation, chemo drugs like dilantin or phenobarbital, chemical agents, viral and bacterial infections, and prescribed medications
Most with acquired have an autoimmune disorder
What are clinical manifestations of aplastic anemia?
Can present abruptly or insidiously
General manifestations of anemia. Fatigue, dyspnea, tachycardia, murmur, ankle edema, hypotension, headache, confusion.
What diagnostic studies are used to confirm aplastic anemia?
Hgb, WBC, and platelets are usually decreased along with reticulocyte count.
Bleeding time prolonged.
What are the goals, prognosis, and treatment options for aplastic anemia?
Goal: Prevent complications from infection and hemorrhage
Prognosis: 75% fatal
Treatment options: Bone marrow transplant or immunosupressive therapy