Clinical Hematology Anemia Due To Blood Loss and Nutrient Deficiencies


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Acute Blood Loss:
Due to sudden blood loss (accident)
Acute Blood Loss blood picture:
No poik
Once bleeding stops it takes 4-6 weeks for RBCs to return to normal, only a few days for WBCs and platelets return to normal
Chronic Blood Loss:
Slow loss of blood (erythropoietin not secreted)
Chronic Blood Loss blood picture:
Normocytic/Normochromic, unless iron stores become depleted then Micro/Hypo.
No significant increase in Poly
Chronic Blood Loss normally seen in:
Bleeding peptic ulcers
heavy menstrual periods
Iron Deficiency Anemia (IDA)
State in which body iron stores are depeted
Lab findings for IDA:
Hb and Hct decreased
Poik: Elliptocytes, Target cells, Pencil cells, Teardrops
Deceased serum iron
Increased total iron binding capacity (TIBC)
Symptoms of IDA:
Fatigue, lethargy, dizziness, shortness of breath, soresin mouth, spoon shaped convexed finger nails, and pica (craving strange things)
Macrocytic anemia/ non-megaloblastic are seen in:
Liver disease, hypothyroidism, increased poly
Megaloblastic anemia is seen in:
Vitamin B-12 deficiency and folic acid deficiency
Other causes of Megaloblastic anemia:
Myeloidysplastic syndromes and erythroleukemia
Lab findings for Megaloblastic anemia:
CBC: pancytopenia, MCV greater than 100 and normal MCHC.
Blood Smear: Oval Macrocytes and teardrops, HJ bodies and Cabot Rings, Hypersegmented neutrophils present.
Chemistry Tests: Increased LD and normal iron and TBIC
Bone Marrow: Hypercellular; megaloblastic RBCs
Vitamin B-12 Deficiency is caused by:
Dietary intake (meats, eggs, liver, dairy products)
Mal-absorption: Patients with resection of the small intestine, gastrectomy, tropical and nontropical sprue, chronic wasting disorder, fish tapeworm, bacteria in the blind loop, defective production of the intrinsic factor.
Clinical symptoms of B-12 Deficiency:
Pallor, weakness, shortness of breath, slight jaundice due to bilirubin increased, neurological malfunctions.
Folic Acid Deficiency causes:
Leading cause is dietary intake, liver disease due to alcoholism, elderly
Folic Acid Deficiency malabsorption :
Patients with gastrectomy or resection of the intestine, bacteria that competes for folic acid in the intestine
Folic Acid Deficiency increased utilization:
Infancy, pregnancy, hemolytic anemia
Folic Acid Deficiency inadequate utilization:
Impairment of the metabolism of folic acid: chemotherapy, malignancy, anticonvulsive drugs
Anemia of Chronic Disorders:
Anemia usually signals the production of erythropoietin, but in Anemia of Chronic Disease, the stimulus is absent and there is nothing wrong with the kidney. Iron can not be transported from the bone marrow so eventually a Micro/Hypo blood picture occurs.
Anemia of Chronic Disorders most striking feature:
Decreased serum iron and decreased TIBC in the face of increased storage iron in the tissues.
Anemia of Chronic Disorders blood picture:
Mild to moderate anemia in the first few weeks of illness, Normocytic/Normochromic, decreased Retic count, increased WBC, increased Sed Rate. Later becomes Micro/Hypo, increased storage iron in the bone marrow.
Treatment of Anemia of Chronic Disorders:
Only treatment of illness can reverse the anemia.
Anemia of Chronic Renal Disease:
Decreased erythropoietin level. May move into megaloblastic or IDA.
Anemia of Chronic Renal Disease blood picture:
Usually normocytic/normochromic, decreased Hb, Burr cells
Anemia of Liver Disease:
Variable blood pictures:
N/N with burr cells
Macro/N with target cells
Macro/N or N/N with acanthocytes
Macro/N with oval macrocytes and teardrop cells
* Only with lover disease will the target cells be macro
Anemia associated with malignancies blood findings:
Leukoerthroblastosis (NRBCs, myelocytic cells, teardrops, decreased platelets)
Bone marrow becomes fibrotic
Aplastic Anemia:
Primary defect is reduction or depletion of hematopoietic precursor cells with decreased production of RBCs, EBCs, and platelets
Aplastic Anemia etiology:
Acquired due to exposure to radiation, chemical agents, drugs, and infections. It can be idiopathic. It can also be congenital (Fanconi's anemia)
Aplastic Anemia symptoms:
Bleeding- ecchymosis, purpura, petechiae
Susceptible to infection
Aplastic Anemia treatment:
Blood transfusion, immunosuppressive drugs, hormones to stimulate the bone marrow, reverse isolation, bone marrow transplant (<40 yrs)-usually reject it.
Prognosis is poor: few months to 5 years.
Aplastic Anemia Lab findings:
N/N anemia, decreased platelets and WBC count, No significant poik, no Poly
Aplastic Anemia Diagnosis:
A least two of the flowing must be present:
Platelet count less than 20,000
Absolute Neutrophil less than 500
Retic count less than 1%
Bone marrow shows dry tap
Acquired Aplastic Anemia
Acute, sudden onset that usually results in death
Causes of Acquired Aplastic Anemia
Radiation, Benzene, Trinitrotoulene (TNT), Insecticides, Weed Killer, Mustard Gas, Arsenic, Drugs that affect hypersensitive people, hair dyes, DDT
Infections associated with Acquired Aplastic Anemia:
Hep B and C
Epstein-Barr Virus (EBV)
Cytomeglo Virus (CMV)
Miliary TB
Dengue fever
Familial Aplastic Anemia (Fanconi's)
Autosomal recessive, develop kidney and heart problems, die at an early age (< 20 yrs), bone marrow transplant has been successful.
Familial Aplastic Anemia (Fanconi's) physical abnormalities:
Skin hyperpigmentation, aplasia or hypoplasia of thumb, short stature, mental retardation.
Pure Red Cell Anemia:
Just the RBCs are aplastic, bone marrow shows normal cellularity with absence of RBC precursors, serum erythropoietin is increased.
Pure Red Cell Anemia causes:
Acquired or hereditary, Thymoma (tumor of the thymus), Congenital (Blackfin and Diamond), associated with hemolytic anemia
Sideroblasic Anemia:
Group of anemias characterized by erythroid hyperplasia of the bone marrow in which there is a defect of hemoglobin synthesis.
Hallmark of Sideroblastic Anemia:
The presence of Ringed Sideroblasts. Unable to utilize iron which becomes trapped in the mitochondira of the developing RBCs, results in a ring or halo around the nucleus
Classification of Sideroblastic Anemia:
Acquired: Primary Sideroblastic, Secondary Sideroblastic, Drug induced.
Hereditary X-linked
Pyridoxine responsive
Causes of Sideroblastic Anemia:
Drugs, lead poisoning, alcoholism, non-hematologic disorders: infection, uremia, porphyria, hypothyroidism, carinmatosis. Hematologic disorders: Hemolytic anemia, thalassemia, multiple myeloma, megaloblastic anemia, leukemias
Symptoms of Sideroblastic Anemia:
Paleness, weakness, loss of breath on exertion, angina on effort, mild enlargement of the spleen. Normally seen in elderly > 50 years, both women and men.
Sideroblastic Anemia peripheral blood:
Mild to moderate anemia, possible decreased WBC, Dimorphic RBCs, N/N, poik: oval macros and teardrops, Inclusions: pappenheimer Bodies
Sideroblastic Anemia Chemistries:
Increased serum iron, normal to increased TIBC, Increased % saturation, Increased tissue iron stores, Increased serum Ferritin.
Sideroblastic Anemia Bone Marrow:
Erthryoid hyperplasia, megaloblastiod, ringed sideroblasts (>25%), increased storage iron, increased MAST cells
Prognosis of Sideroblastic Anemia:
Mean survival > 8.5 years
Pre-leukemic signs Anemia:
Macrocytic with oval macrocytes, microcytic/hypochromic with iron loading, dimorphic anemia with macrocytes
Pre-Leukemic signs WBCs:
Neutrophils with increased monocytes, defective or absent neutrophilic granules.
Pre-Leukemic signs Platelets:
Abnormal shape and size, Defective and abnormal granulation, decreased or increased platelet count
Pre-Leukemic signs other:
b-12 deficiency, folate deficiency, sideroblastic anemia, side effects of drugs, refractory anemias, aplastic anemia, PNH
Type II or HEMPAS:`
Hereditary erythroblast mutinuclearity with positive acidified serum test. Positive Hamm's for PNH. Negative sucrose hemolysis for PNH.