Study Guide for Final Exam
Chapter 42 Care of Patients with Hematologic Problems
1. Identify the etiologies and clinical manifestations common to all types of anemia. (See Table 42-1 p 870 and Chart 42-1 p 871) Common Cause
Sickle cell disease: autosomal recessive inheritance of two defective gene alleles for hemoglobin synthesis Glucose-6-phosphate dehydrogenase (G6PD) deficiency anemia: X-linked recessive deficiency of enzyme G6PD Autoimmune hemolytic anemia: abnormal immune function in which a person’s immune reactive cells fail to recognize his or her own red blood cells as self cells Iron deficiency anemia: Inadequate iron intake caused by: iron deficient diet, chronic alcoholism, malabsorption syndromes and partial gastrecromy. Rapid metabolic (anabolic) activity caused by: pregnancy, adolescence and infection Vitamine B12 deficiency anemia: dietary deficiency, failure to absorb vitamin b12 from intestinal tract as a result of: partial gastrectomy, pernicious anemia, malabsorption syndromes Folic acide deficiency anemia: dietary deficiency, malabsorption sndromes Drugs: oral contraceptives, anticonvulsants, methotrexate Aplastic anemia: exposure to myelotoxic agents: radiation, benzene, chloramphenicol, alkylating agents, antimetabolites, sulfonamides and insecticides. Viral infection (unproven): Epstein-Barr virus, hepatitis B and cytomegalovirus. Manifestations:
-pallor, especially of the ears, the nail beds, the palmar creases, the conjunctivae, and around the Mouth
- Cool to the touch
- Intolerance of cold temperatures
- Nails become brittle and may lose the normal convex shape; over time, mails become concave and figures assume clublike appearance. Cardivascular manifestations:
- Tachycardia at basal activity levels, increasing with activity and during and immediately after meals - Murmurs and gallops heard on auscultation when anemia is severe - Orthostatic hyptension
- Dyspnea on exertion
- Decreased oxygen saturation levels
- Increased somnolence and fatigue
2. Describe the pathophysiology, etiology, clinical manifestations, and interventions for sickle cell anemia. pp 870 – 875
Pathophysiology: is a genetic disorder that results in chronic anemia, pain disability, organ damage, increased risk for infection and early death. The problem is the formation of abnormal hemoglobin chains. At least 40% of the total hemoglobin is composed of an abnormality of the beta chains, known as hemoglobin S (HbS). HbS is sensitive to changes in the O2 content of the RBC. When RBCs having large amounts of HbS are exposed to decreased O2 condition, the abnormal beta chains contract and pile together within the cell, distorting the shape of RBC. Etiology: sickle cell disease is a genetic disorder with an autosomal recessive pattern of inheritance. The formation of the beta chains of hemoglobin depends on a pair of gene alleles. A mutation in these alleles leads to the formation of HbS instead of HbA. Patient has two HbS genes alleles, one inherited from each parent, because both hemoglobin alleles are S, sickle cell disease is simtimes also abbreviated “SS”. Manifestations: Pain is the most common symptom of SCD crisis. Other manifestation vary with the site of tissue damage. Cardiovascular: high-output HF due to anemia, SOB, gatigue, murmurs at S3 heart sound, Increased jugular-venous pulsation or distention, low BP, slow capillary refill, reduced or absent pulse.
Skin: pallor, cyanosis, color changes at lips, tongue, nail bed, (all due to poor oxygenation from decreased perfusion and anemia), jaundice, sores or ulcers on the lower leg, Abdominal changes: damage to spleen and liver. Kidney and urinary...
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