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18 Cards in this Set
- Front
- Back
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Iron deficiency
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decreased serum iron
increased TIBC decreased ferritin |
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Microcytic, hypochromic anemia (MCV<80)
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iron deficiency
thalassemias lead poisoning sideroblastic anemias |
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Macrocytic anemia
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Megaloblastic (Vitamin B12 or folate deficiency)
Drugs that block DNA synthesis (sulf, phenytoin, AZT) Reticulocytosis |
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Normocytic, normochromic anemia
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Acute hemorrhage
Anzyme defects (G6PD, PK deficiencies) RBC membrane defects (hereditary spherocytosis) Bone marrow disorders (aplastic anemia, leukemia Hemoglobinopathies Autoimmune hemolytic anemia Anemia of chronic disease |
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aplastic anemia
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failure or destruction of multipotent myeloid stem cells
inadequate production or release of differentiated cell lines radiation, benzene, chloramphenicol alkylating agents, antimetabolites viral agents (parvovirus B19, EBV, HIV) Fanconi's anemia, idiopathic may follow acute hepatitis |
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Sickle cell anemia
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HbA mutation (glutamic acid to valine)
HbC defect gives milder disease Low oxygen or dehydration precipitates sickling |
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alpha thalassemia (including HbH and Hb Barts)
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alpha-globin chain underproduced (there are 4 chains in total)
no compensatory increase of other chains HbH - lacks 3 alpha chains HbBarts - lacks all 4 |
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beta-thalassemia (major and minor)
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minor - beta chain underproduced
major - beta chain absent in both fetal hemoglobin is produced but not enough to compensate |
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autoimmune anemia
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extravascular hemolysis
warm agllutinin (IgG) etiologies: SLE, CLL, drugs like methyldopa cold agglutinin (IgM): Mycoplasma, mono erythroblastosis fetalis |
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Erythroblastosis fetalis
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Rh or other blood antigen incompatibility between mother and fetus
leads to mother's antibodies attacking fetal RBCs |
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Hereditary spherocytosis
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intrinsic, extravascular hemolysis due to spectrin or ankyrin defect
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paroxysmal nocturnal hemoglobinuria
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impaired synthesis of GP I anchor in the RBC membrane, leading to
intrvascular hemolysis, leading to increased sensitivity of RBCs to the lytic activity of complement |
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microangiopathic anemia
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intravascular hemolysis (as in DIC, TTP/HUS, SLE, or malignant HTN)
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DIC
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sepsis (gram -),
trauma, obstetric complications, pancreatitis (acute), malignancy, nephrotic syndrome or transfusion (StOP Making New Thrombi), leading to activation of coagulation cascade leading to microthrombi and global consumption of platelets, fibrin, coagulation factors |
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Bernard-Soulier disease
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defect of platelet adhesion (decreased GP IIb-IIIa)
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Glanzmann's thrombasthenia
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defect of platelet aGGreGation (decreased GP IIb-IIIa)
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PT
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extrinsic factors II, V, VII and X
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PTT
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intrinsic - all factors except VII
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