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53 Cards in this Set
- Front
- Back
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Erythrocyte (RBC) characteristics
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RBC:
• Non-nucleated • WNL = 4.2-6.2 • Gas transport to & from tissues/lungs • Life span 120 days |
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Leukocyte (WBC) characteristics
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WBC characteristics:
• Nucleated cell • WNL = 5,000-10,000 • Body defense mechanism |
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2 Kinds of Leukocytes = WBC
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2 kinds of WBCs:
1) Granulocytes 2) Agranulocytes |
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Granulocytes list
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Granulocytes:
1) Eosinophil 2) Neutrophil 3) Basophil |
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Agranulocytes list
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Agranulocytes:
1) Macrocytes 2) Lymphocytes |
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Lymphocyte
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Lymphocyte:
• Mononuclear immunocyte • 25-33% of WBC differential • Lives days to years, depending on type |
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Monocyte/Macrophage
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Monocyte/Macrophage:
• Large mononuclear phagocyte • 3-7% of WBC differential • Lives months or years |
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Eosinophil
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Eosinophil:
• Segmented polymorphonuclear phagocyte • 1-4% of WBC differential • Antibody-mediated defense against parasites • Allergic rxns • Associated with Hodgkin dz |
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Neutrophil
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Neutrophil:
• Segmented polymorphonuclear phagocyte • 57-67% of WBC differential • Phagocytosis, esp early stages of inflammation • Life span = 4 days |
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Basophil
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Basophil:
• Segmented polymophonuclear • 0-0.75% WBC differentials • Secretes chemicals for chemotaxis • Associated with allergic & mechanical irritation |
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Platelet
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Platelet
• Not a cell • An irregularly shaped cytoplasmic fragment • WNL = 140,000 – 340,000 • Hemostasis following vasc injury • Normal coag & clotting • Life span = 8-11 days |
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What Iron Deficiency Can Cause
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Iron deficiency can cause:
• Brittle nails • Cheilosis (fissures @ corners of mouth) • Smooth tongue • Formation of esophageal webs |
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Later Fe Deficiency Blood Smear
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Later iron deficiency blood smear may show –
Hypochromic RBC Microcytic RBC Anisocytosis (RBCs are all different sizes) Poikilocytosis (RBCs are oddly shaped) |
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Severe Fe Deficiency Causes Cells to Look Like This
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Severe iron deficiency will cause –
• Severely hypochromic cells • Target cells • Nucleated RBC (have been sent into the circulation at too young of an age) |
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Ferritin
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Ferritin
Tissues store iron in this form, esp in recticuloendothelial cells of liver, spleen, & bone marrow. (When you check the ferritin level, you are trying to ferret out how good the iron stores are. Alternately, you can buy a ferret at the store.) |
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How long to continue Fe tx for anemia
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Although hct will be normal in 2 months, tx should be continued > 6 months to replenish iron stores.
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Microcytic hypochromic anemias
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Microcytic hypochromic anemias:
1) Anemia of chronic disease 2) Iron deficiency anemia 3) Thalassemia 4) Sideroblastic anemia 5) Copper deficiency, maybe |
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Never
Let Monkeys Eat Bananas |
Neutrophils 60%
Lymphocytes 30% Monocytes/Macrophages 6% Eosinophils 3% Basophils 1% |
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Normocytic/normochromic anemias
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Normocytic/normochromic anemias:
1) Anemia of chronic disease 2) Hemolytic anemia 3) Aplastic anemia 4) Acute/chronic blood loss |
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Macrocytic/normochromic anemias
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Macrocytic/normochromic anemias
1) B12 deficiency 2) Folate deficiency |
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Macrocytic/hyperchromic anemia
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Macrocytic/hyperchromic anemia:
1) Hereditary spherocytosis |
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Hemoglobinopathies
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Hemoglobinopathies:
1) Sickle cell disease 2) Thalassemia |
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Thalassemia syndromes
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Thalassemia syndromes:
Hereditary anemias in which synthesis of alpha or beta-globin chains is reduced → defective hemoglobinization of RBCs |
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Thalassemia heredity
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Thalassemia heredity:
Alpha thalassemia – Southeast Asian/Chinese (mild or no sx) Beta thalassemia – Mediterranean (usually dx ages 4-6 months when switching from HgbF (fetal hgb) to adult hgb. |
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Most prominent sign of thalassemia
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Most prominent sign of thalassemia:
Microcytosis out of proportion to the degree of anemia (VERY small RBCs) that does not respond to iron tx |
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Problems 2° Beta Thalassemia
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Different cells seen with thalssemia:
Target cells Acanthocytes (all different sizes) Poikilocytes (odd shapes) Basophilic stippling Nucleated RBCs |
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Do you give iron for thalassemia?
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You do not give iron for thalassemia because
1) It will not help 2) You risk iron overload (hemosiderosis, heart failure, cirrhosis, endocrinopathies) |
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Beta-thalassemia treatment
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Beta-thalassemia treatment:
• transfusions to keep hgb at least 12 (but watch out for iron overload) • Allogeneic bone transplant |
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Sideroblastic anemia
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Sideroblastic anemia
• microcytic/hypochromic • an acquired disorder with ↓ hgb synthesis → • iron accumulation, esp in mitochondria • Prussian blue stain of bone marrow cells shows ringed sideroblasts |
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What is a sideroblast & why do they stain with Prussian blue?
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• A sideroblast is a nucleated erythrocyte containing iron granules in its cytoplasm.
• The positive Prussian-blue reaction indicates that the iron is ionized & not bound to the heme protein. |
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Causes of sideroblastic anemia
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Causes of sideroblastic anemia:
• Chronic alcoholism • Lead poisoning • Myelodysplasia (one of a group of dz in which there is an inadequate production of normal blood cells in the bone marrow. Sometimes they evolve into leukemia.) |
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Sideroblastic anemia lab findings
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Sideroblastic anemia lab findings:
• Hct 20-30% • MCV varies • Peripheral blood smear = normal & hypochromic RBCs • Basophilic stippling of RBCs if lead poisoning • But to diagnose, need bone marrow evaluation |
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Sideroblastic anemia tx
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Sideroblastic anemia treatment:
• Treat the underlying cause • Transfusion, maybe • Erythropoietin will NOT work |
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Normocytic normochromic anemias are caused by 1 of 3 things -
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Normochromic normocytic anemias are caused by 1 of 2 things:
1) Organ failure (kidney, endocrine, thyroid, liver. Anemia of renal dz is more severe) 2) Impaired marrow function that is 2° systemic dz 3) Acute or chronic blood loss |
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Impaired marrow fxn causing anemia is 2° -
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Impaired marrow function causing anemia is 2° to –
• Chronic infection • Aplastic anemia • Infiltrative marrow disease • Pure red cell aplasia |
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Aplastic Anemia can be 2° -
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Aplastic anemia can be 2° -
• T-cell-mediated autoimmune suppression of hematopoiesis (most common) • Chloramphenicol • Chemo/radiation • Toxins • SLE |
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Anemia of chronic disease
• Iron stores • Serum ferritin • Transferrin saturation • Serum iron • TIBC • RBC morphology & reticulocyte count • Serum iron & transferrin saturation |
Anemia of chronic dz:
• Bone marrow iron stores are high or normal • Serum ferritin is high or normal • Transferrin saturation may be very low • Serum iron may be very low • TIBC is low or normal • RBC morphology is & retic count are pretty nml |
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What is transferrin?
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Transferrin is a globulin that binds & transports iron.
What is a globulin? A plasma protein similar to albumin in that it controls colloidal osmotic (oncotic) pressure within capillaries. |
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Anemia of Chronic Disease Tx
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ACD tx:
1) Treat underlying disease 2) Erythropoietin, if RF, Ca, or inflmmtory disorder 3) RBC & platelet transfusion if mild 4) Bone marrow transplant or immunosuppression if severe |
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Causes of Folic Acid Deficiency Anemia
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Folic acid deficiency anemia
1) Common in ETOH abuse, anorexia 2) Folate requirements are ↑ by pregnancy , exfoliative skin dz, hemolytic anemias |
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Folic Acid Anemia Symptoms
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Folic Acid Anemia Symptoms:
• Glossitis (sore tongue) • Vague GI sx • NO neuro sx (as opposed to B12 deficiency) |
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Folic Acid Anemia Signs
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Folic acid anemia signs:
• Macro-ovalocytes • Hypersegmented PMNs • Howell-Jolly bodies • Normal serum B12 • Low RBC folate level |
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Causes of B12 deficiency
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Causes of B12 deficiency:
• Pernicious anemia → atrophic gastritis & increase risk of gastric Ca • Another autoimmune dz may co-exist • Strict vegan diet • Gastric surgery • Crohn’s dz Pernicious anemia = autoimmune dz. Parietal cells of stomach do not secrete enough intrinsic factor. Achlorhydria (↓HCL in stomach) 2° atrophy of stomach mucosa Northern Europeans ages 40-80. |
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Signs of B12 deficiency
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Signs of B12 deficiency
Glossitis & vague GI sx, maybe Neuro sx: o Stocking-glove paresthesias o Loss of position, fine touch, & vibrat. Sensation o Clumsiness o Dementia o Ataxia |
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Labs in B12 Deficiency Lab
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Labs in B12 deficiency
Severe anemia, maybe with ↑ MCV Anisocytosis, poikilocytosis, macro-ovalocytosis, hypersegmented PMNs ↓ reticulocyte count ↑ LDH & indirect bili ↓ serum B12 |
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Sickle Cell Anemia
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Sickle cell anemia:
• Autosomal recessive hemolytic anemia • Hgb is mostly hgb S & deoxygenated • Sx in infancy when hgbF (fetal hgb) levels fall • “Sickle cell crises” starting in childhood/teens |
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Labs in Sickle Cell Anemia
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Labs in sickle cell anemia:
• Hgb S in RBCs • 5-50% RBCs are sickled • Target cells, Howell-Jolly bodies • Nucleated RBCs, ↑ reticulocyte count • Elevated WBC, maybe thrombocytosis • Elevated indirect bili, maybe |
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Sickle Cell Anemia Tx
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Sickle Cell Anemia Tx
• Analgesics, fluids, O2 • Transfusion for vaso-occlusive crises • Routine folate supps for all sickle cell pts |
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G6PD Deficiency
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G6PD deficiency:
• An x-linked recessive disorder • Commonly seen in black males (10-15%) & some Mediterranean populations • Episodic hemolysis is caused by: o Oxidant drugs (dapsone, primaquine, quinidine, sulfonamides, nitrofurantoin) o Infection |
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G6PD Deficiency Clinical Features
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G6PD Deficiency Clinical Features:
• Usually healthy people • No splenomegaly • Female carriers are rarely affected |
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G6PD Deficiency Labs
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G6PD Deficiency Labs:
• ↑ reticulocytes & serum indirect bili during hemolytic episodes • Peripheral smear – bite cells & Heinz bodies • G6PD levels are low between hemolytic episodes |
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G6PD Deficiency Treatment
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G6PD Deficiency Treatment:
• Hemolytic episodes are self-limited as RBCs are replaced (in most cases) • Avoidance of oxidative drugs |
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Most common causes of adult anemia
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Most common causes of adult anemia:
• GI bleed • NSAIDS use |
