Chapter 13 Flashcards
Anemia
- a deficit of red cells
- can be relative or absolute
Relative Anemia
- normal total red cell mass with disturbances in regulation of plasma volume
Absolute Anemia
- actual decrease in numbers of red cells
- decreased production
- increased destruction
Aplastic Anemia
- Body stops making enough new blood cells
- insidious onset of symptoms
- late symptoms include weakness, fatigue, lethargy, pallor (paleness), dyspnea, palpitations, transient murmurs and tachycardia related to low RBCs
- thrombocytopenia
- neutropenia
- fatal unless successful bone marrow transplant
Treatment of Aplastic Anemia
- Identify and avoid further toxic exposure
- type HLA and ABO to identify serologically defined loci and potential donors
- maintain minimally essential levels of hemoglobin and platelets
- prevent and manage infection
- determine efficacy of bone marrow transplantation
- administer immunosuppressive therapy
Anemia of Chronic Renal Failure
- failure of the renal endocrine function impairs erythropoietin production and bone marrow compensation
- decreased RBC count with low hematocrit and hemoglobin level
- 95% respond to erythropoietin therapy
Treatment of Anemia of Chronic Renal Failure
- dialysis
- administration of erythropoietin
- Replacement of iron, folate, and B12
Anemia Related to Vitamin B12 or Folate Deficiency (pernicious anemia)
- pernicious anemia due to lack of intrinsic factor leading to vitamin B12 deficiency
- Folate deficiencies from dietary deficiencies, alcoholism, cirrhosis, pregnancy, or infancy
- disruption in DNA synthesis of blast cells produces megaloblasts due to deficiencies
Clinical Manifestations of Pernicious Anemia
- low RBC (properly functioning), WBC, and platelet counts with increased MCV (Mean Corpuscular Volume); megaloblastic dysplasia
- peripheral nerve degeneration
- shillings test indicates low B12
- gastric analysis reveals achlordydria
- megoblastic madness
(MVC = Blood cell volume; Megaloblast = abnormally big RBC, doesnt function properly)
Treatment of Pernicious Anemia
- recognize that megaloblastic anemia is present
- ascertain if vitamin B12 folate or a combined deficiency is the cause
- diagnose underlying disease and mechanism responsible
- for B12 administer B12 parenterally or orally and K supplements
- For folate administer folic acid
Iron Deficiency Anemai
- most common nutritional deficiency in the world
- insufficient iron for hemoglobin synthesis
- hypochromic, microcytic RBCs; Low MCV, MCH, and MCHC
- Serum ferritin level decreased; serum iron level decreased; total iron binding capacity (TIBC) increased
- excellent prognosis
(MCH = Mean corpuscular Hemoglobin; MCHC = mean corpuscular hematocrit)
Symptoms of Iron Deficiency Anemia
- pica (craving for non food substances)
- Koilonychias (spoon shaped nails)
- Blue sclerae
Treatmen of Iron Deficiency Anemia
- oral administration of ferrous sulfate or intravenous ferric gluconate (only in severe cases)
Thalassemia
- increased RBC destruction (hemolysis) resulting in decreased RBC survival rates
- associated with mutant genes that auppress the rate of globin chain synthesis
- classified by the polypeptide chains with deficient synthesis (alpha and beta thalassemia)
- most clinically severe form: thalassemia major
- prognosis depends on type
Symptoms of Thalassemia
- Hypochromic, microcytic RBCs
- MCV, MCH, and MCHC are low
- Erythroblastic hyperplasia (bone marrow)
Treatment of Thalassemia
- blood transfusions
- splenectomy
- chelation therapy
- bone marrow transplantation
- genetic counseling
Sickle Cell Anemia
- genetically determined defect of hemoglobin synthesis resulting in hemoglobin instability and insolubility
- sickled cells cause vascular occulsion
- severe anemia, RBCs of different shapes and sizes, recurrent painful episodes
Treatment and Prognosis of SIckle cell Anemia
- treatment: stem cell transplant
- Prognosis: death if no/unsuccessful transplant
Glucose 6 Phosphate Dehydrogenase Deficiency
- genetic disorder resulting in RBC membrane destruction; most common
- Do not have hemolytic anemia unless challenged by drugs, infection
Treatment and Prognosis of Glucose 6 Phosphate Dehydrogenase Deficiency
Treatment is preventive: avoidance of drugs that trigger hemolytic episodes
Prognosis: good unless has fava bean susceptibility
Hemolytic Disease of the Newborn
- Fetal RBCs cross the placenta, stimulate production of maternal antibodies against antigen on fetal RBC not inherited from mother
- Maternal antibodies cross into the fetal circulation causing destruction of fetal cells
Treatment and Prognosis of Hemolytic Disease of the Newborn
Treatment: standard dose of anti-Rh immune globulin (RhoGAM) is given to the mother before or after delivery . In sever cases, in utero blood transfusion and early delivery
Prognosis: Death, possible retardation, or barely perceptible hemolytic process
Antibody Mediated Drug Reactions
- exposure to a drug causes destruction and lysis of the sensitized person’s own RBCs
- Mechanisms include: hapten mechanisms, neoantigen formation, membrane modification, and autoantibody induction
- May have schisocytes
Treatment and Prognosis of Antibody Mediated Drug Reactions
Treatment: Recognize and discontinue offending medications, sometimes steroids given
Prognosis: good unless severe hemolysis