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169 Cards in this Set
- Front
- Back
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Myeloid Products
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Erythrocyte
Granulocytes (Neutrophils, Eosinophils, Basophils, Monocytes/Macrophages) Platelets |
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Erythrocyte
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Life span: 120 days
Energy: 90% glucose, 10% HMP shunt Cl-HCO3 antiport |
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Anisocytosis
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Varying sizes
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Poikilocytosis
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Varying shapes
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Reticulocytosis
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Immature RBC
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Platelets
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Life span: 8-10 days
From megakaryocytes Primary hemostasis Dense granules (ADP, Ca2+) alpha-grandules (vWF, fibrinogen) 1/3 stored in spleen |
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Leukocyte
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Granulocytes (basophils, eosinophils, neutrophils), mononuclear cells (monocytes, lymphocytes)
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Basophil
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Found in blood
Mediates allergic reaction <1% of leukocytes Bilobate nucleus Basophilic granules (heparin, histamine, vasoactive amines, leukotrienes) |
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Mast Cell
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Found in tissue
Histamine, heparin, eosinophil chemotactic factors Binds IgE Type I hypersensitivity - Cromolyn sodium (prevents degranulation) |
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Eosinophil
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1-6% of leukocytes
Bilobate nucleus Fights: helminthic, protozoans Phagocytic for antigen-antibody complexes Histaminase and arylsulfatase (limit mast cells) |
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NAACP
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Eosinophilia
N = Neoplastic A = Asthma A = Allergic process C = Collagen vascular dz's P = Parasites (invasive) |
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Neutrophil
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Acute inflammatory response
40-75% of leukocytes Phagocytic Multi-lobed nucleus Hypersegmented = B12/folate deficiency |
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Monocyte
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2-10% of leukocytes
Kidney-shaped nucleus Frosted-glass cytoplasm Differentiates into macrophages |
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Macrophage
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Phagocytosis of bacteria, debris, senescent RBC's
Activated by gamma-interferon Can be APC via MHC II |
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Dendritic cells
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Professional APCs, express MHC II and Fc receptor on surface
Induces primary antibody response Dendritic cells = Langerhans cells (skin) |
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Lymphocyte
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Round, densely staining nucleus
B and T cells |
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B lymphocyte
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Humoral Immunity
Originiates in bone marrow Migrates to lymph nodes, white pulp of spleen Differentiates into plasma cells w/ antigenic stimuli Memory APC via MHC II |
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Plasma cell
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Produce antibodies (specific)
Off-center nucleus "Clock-face" chromatin Multiple myeloma - plasma cell neoplasm |
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T lymphocyte
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Cellular immune response
Originates in marrow Matures in thymus Differentiate into: cytotoxic T cells (MHC I, CD8), helper T cells (MHC II, CD4), suppressor T cells |
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Hemophilia A - Deficiency in...
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Factor VIII
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Hemophilia B - Deficiency in...
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Factor IX
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Vitamin K deficiency - decreased synthesis of...
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Factors II, VII, IX, X
Protein C & S |
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Antithrombin - Inhibits...
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Thrombin
IXa, Xa, XIa, XIIa (activated by heparin) |
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Bernard-Soulier
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GpIb deficiency
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Glanzman's
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GpIIb/IIIa deficiency
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Platelet Adhesion
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vWF links platelet's GpIb receptor to subendothelial collagen
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Platelet Aggregation
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- Thromboxane A2 released by platelets increases aggregation (Aspirin: COX inhibited by inhibiting TXA2)
- PGI2 and NO released by endothelium decreases aggregation |
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platelet plug Swelling
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Binding of ADP on platelet receptors leads to insertion of GpIIb/IIIa on platelet membrane = platelet cohesion (Ca2+ strengthens)
- Ticlopidine and clopidogrel inhibit ADP-induced expression of GpIIb/IIIa - Abciximab inhibits GpIIb/IIIa, directly |
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Vitamin K --> activated Vit K
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Epoxide reductase (inhibited by warfarin/coumadin)
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Vitamin K mediated
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Factors II, VII, IX, X, Protein C & S
(vWF carries/protects factor VIII) |
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Antithrombin inactivates...
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Factors II, VII, IX, X, XI
(Heparin activates antithrombin) |
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Protein C
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Protein S as a cofactor to activate (APC - active protein C)
Inactivates Va, VIIIa |
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Factor V Leiden
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Mutation produces factor V resistant to activated protein C
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tPA
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Converts plasminogen to plasmin = cleave fibrin
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Acanthocyte ("Spur Cell")
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Liver disease
Abetalipoproteinemia |
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Basophilic stippling
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Thalassemias, Anemia of chronic disease, Iron deficiency, Lead poisoning
"BASte the TAIL" |
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Bite Cell
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G6PD deficiency
(alpha-thalassemia) |
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Elliptocyte
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Hereditary elliptocytosis
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Macro-ovalocyte
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Megaloblastic anemia (also see: hypersegmented PMNs)
Marrow failure |
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Ringed Sideroblasts
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Sideroblastic anemia (microcytic)
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Schistocyte, helmet cell
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DIC
TTP/HUS Traumatic hemolysis |
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Spherocyte
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Hereditary spherocytosis
Autoimmune hemolysis |
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Dacrocyte (tear-drop cell)
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Bone marrow infiltration
Myelofibrosis |
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Target Cell
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HbC disease
Asplenia Liver disease Thalassemia "HALT" at the target |
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Heinz bodies
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alpha-thalassemia
G6PD deficiency Oxidation of iron from ferrous to ferric form leads to denatured Hgb precipitation and damage to RBC membrane (bite cells) |
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Howell-Jolly Bodies
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Functional hyposplenia (sickle cell anemia)
Asplenia Basophilic nuclear remnants found in RBCs |
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Microcytic anemia (MCV <80)
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Thalassemia (alpha, beta)
Anemia of chronic disease Iron deficiency Lead poisoning Sideroblastic anemia |
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Iron deficiency anemia
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Decreased Heme synthesis
Chronic bleed Malnutrition/malabsorption (Celiac, etc.) Increased demand (pregnancy) |
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Alpha-thalassemia
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Asia, Africa
Defect: alpha-globin gene (dec. synthesis) 4 gene deletion = no life; Hb Barts (4 gamma) = Hydrops fetalis 3 gene deletion = HbH disease (B4) 1-2 gene deletion = no anemia |
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Beta-thalassemia
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Mediterranean
Defect: point mutations in splicing sites and promoter sequences Increased HbF (a2g2) |
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B-thalassemia Minor
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Heterozygote
B-chain underproduced Usually asymptomatic Dx - increased HbA2 (>3.5%) |
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B-thalassemia Major
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B-chain absent = severe anemia requiring blood transfusion (secondary hemochromatosis)
Marrow expansion ("crew cut" on skull xray) = skeletal deformaties, chipmunk facies |
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HbS/B-thalassemia heterozygote
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Mild to moderate sickle cell disease depending on amount of B-globin production
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Lead poisoning
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Lead inhibits ferrochelatase and ALA dehydratase = decreased heme synthesis
inhibits RNA degradation = basophilic stippling |
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Sideroblastic anemia
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Defect in heme synthesis
Hereditary: X-linked Tx: pyridoxine (B6) therapy Reversible etiologies (EtOH, lead) Increased Iron, normal TIBC, Inc. ferritin - Ringed sideroblasts (iron-laden mitochondria) |
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Macrocytic anemia
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Impaired DNA synthesis = maturation of nucleus delayed relative to maturation of cytoplasm
Megaloblastic (folate, B12 deficiency) Non-megaloblastic |
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Non-megaloblastic macrocytic anemia
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Liver disease
Alcoholism (macrocytosis and bone marrow suppression in absence of folate/B12 deficiency) Reticulocytosis Metabolic disorder (congenital deficiencies of purine or pyrimidine synthesis) Drugs (5-FU, AZT, hydroxyuria, etc.) |
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Folate deficiency
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Megaloblastic macrocytic anemia
Hypersegmented PMNs, glossitis Increased homocysteine, normal MMA Causes: malnutrition (alcoholics), malabsorption, impaired metabolism (MTX, trimethoprim), Inc. requirement (hemolytic anemia, pregnancy) |
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B12 Deficiency
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Megaloblastic macrocytic anemia
Neurologic sx, Hypersegmented PMNs, glossitis Increased homocysteine, Inc. MMA Causes: malnutrition, malabsoprtion (crohn's), pernicious anemia, Diphyllobothrium (fish tapeworm) |
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Normocytic anemia (MCV 80-100)
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Hemolytic - intrinsic, extrinsic; intravascular, extravascular
Nonhemolytic |
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Nonhemolytic normocytic anemia
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Anemia of chronic disease
Aplastic Anemia Renal disease = AAR |
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Intrinsic hemolytic anemia
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Hereditary spherocytosis
G6PD deficiency pyruvate kinase deficiency sickle cell anemia HbC defect paroxysmal nocturnal hemoglobinuria |
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Extrinsic hemolytic
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Autoimmune, microangiopathic (DIC, TTP, HUS), infectious
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Intravascular hemolysis
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Paroxysmal nocturnal hemoglobinuria, autoimmune (cold agglutinins), mechanical destruction (Aortic stenosis, mechanical valves)
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Extravascular hemolysis
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Hereditary spherocytosis
G6PD deficiency pyruvate kinase deficiency sickle cell anemia HbC defect Autoimmune (warm agglutinins), microangiopathic (DIC, TTP/HUS) |
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Anemia of chronic disease
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Non-hemolytic normocytic anemia
Inflammation (cytokines) > Inc. hepcidin > dec. iron release from macrophages > dec. iron, TIBC, inc. ferritin Can become microcytic |
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Aplastic anemia
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Non-hemolytic normocytic anemia
Pancytopenia w/ severe anemia, neutropenia, & thrombocytopenia; Normal cell morphology Hypocellular marrow + fat infiltrate Sx - fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection Tx-withdraw source |
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Aplastic anemia causes
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Failure of destruction of myeloid stem cells due to:
1. Radiation and drugs (benzene, alkylating agents, antimetabolites, chloramphenicol) 2. Viral agents (parvovirus B19, EBV, HIV) 3. Fanconi's anemia (inherited defect in DNA repair) 4. idiopathic (immune mediated, primary stem cell defect); follow acute hepatitis |
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Kidney disease
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non-hemolytic normocytic anemia
Dec erythropoetin = Dec hematopoesis |
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Hereditary spherocytosis
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Defect in proteins interacting with RBC membrane skeleton and plasma membrane
Less membrane causes small and round RBCs with no central pallor (Inc. MCHC, inc. RDW) = premature removal of RBCs by spleen - splenomegaly, aplastic crisis (B19 infxn), Howell-Jolly bodies after splenomegaly + osmotic fragility test |
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G6PD deficiency
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X-linked
Defect in G6PD > Dec. glutathione > Inc. RBC susceptibility to oxidative stress - hemolytic anemia following oxidative stress (sulfa drugs, infxns, fava beans) Heinz bodies, bite cells |
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Pyruvate kinase deficiency
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Autosomal recessive
Defect in pyruvate kinase > Dec. ATP > rigid RBCs Hemolytic anemia in newborn |
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Sickle cell anemia
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Crescent shaped RBCs
"crew cut" on skull xray (marrow expansion from inc. erythropoesis; also thalassemias) Newborns Asx due to inc. HbF and Dec. HbS Tx - hydroxyurea (inc. HbF) and bone marrow transplant |
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sickle cell in African-Americans
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8% carry sickle cell (HbS) trait. = resistance to malaria
0.2% have disease |
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Sickle Cell mutation
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HbS mutation - single amino acid replacement in beta-chain (substitute glutamic acid with valine)
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Sickle cell pathogenesis
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deoxygenated HbS polymerizes
Low O2, dehydration precipitate sickling |
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Complications to sickle cell homozygotes (sickle cell disease)
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Aplastic crisis (parvovirus B19)
Autosplenectomy (infarctions > atrophy > inc. risk of infection from encapusulated organisms Salmonella osteomyelitis Painful crisis (vaso-occlusive) Renal papillary necrosis (low O2 in papilla) Splenic sequesteration crisis |
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HbC defect
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Different B-chain mutation
HbC or HbSC Milder disease than HbSS patients |
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Paroxysmal nocturnal hemoglobinuria
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intravascular hemolysis due to inc. complement-mediated RBC lysis
(Impaired synthesis of GPI anchor/decay-accelerating factor in RBC membrane) - inc. hemosiderin |
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Autoimmune hemolytic anemia
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Warm aglutinin (IgG) - chronic anemia seen in SLE, CLL, drugs (a-methyldopa)
Cold aglutinin (IgM) - acute anemia triggered by cold seen in mycoplasma pneumoniae, infectious mono Erythroblastosis fetalis - newborns; Rh or other antigen incompatibility (mother's antibodies attack fetal RBCs) |
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Direct Coombs test
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Anti-Ig antibodiy added to patient's RBCs agglutinate if RBCs are coated with Ig
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Indirect Coombs test
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normal RBCs added to patients serum agglutinate if serum has anti_RBC surface Ig
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Microangiopathic anemia
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RBCs damaged when passing through obstructed or narrowed vessels
DIC, TTP/HUS, SLE, malignant HTN Schistocytes, AS, mechanical valves |
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Infectious - extrinsic hemolytic normocytic anemia
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Increased destruction of RBCs (malaria, Babesia)
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Iron deficiency lab values
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Serum iron = low
Transferrin/TIBC = High Ferritin = Low % transferrin sat = Very low |
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Anemia of chronic disease lab values
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Serum Iron = low
Transferrin/TIBC = low (keep iron from pathogens) Ferritin = Increased (primary) |
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Hemochromatosis
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Serum iron = high
Transferrin/TIBC = Low Ferritin = high % transferrin sat = Very high |
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Pregnancy/OCP use
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Transferrin/TIBC = high (primary)
% transferrin sat = low |
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Ferritin
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Primary iron storage protein in body
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Transferrin
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transports iron in blood
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Porphyria
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Defective heme synthesis leads to accumulation of heme precursors
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Acute intermittent porphyria - effected enzyme and accumulated substance
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Affected enzyme - Porphobilinogen deaminase (aka: uroporphyrinogen I synthase)
Accumulations - Porphobilinogen, d-ALA, uroporphyrin (urine) |
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Acute intermittent porphyria - presentation & tx
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5 P's
Painful Abdomen Pink Urine Polyneuropathy Psychological disturbances Precipitated by drugs Tx - glucose, heme (inhibit ALA synthase) |
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Porphyria cutanea tarda - effected enzyme and accumulated substance
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Enzyme - Uroporphyrinogen decarboxylase
Substance - Uroporphyrin (tea colored urine) |
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Porphyria cutanea tarda - Presentation
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Blistering cutaneous photosensitivity. Most common porphyria
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Lead poisoning - affected enzyme and accumulated substance
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Enzyme - Ferrochelatase and ALA dehydratase
Substance - Protoporphyrin (blood) |
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Lead Poisoning - children, adults
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Microcytic anemia, GI and kidney disease
Children - exposure to lead paint = mental deterioration Adults - env. exposure (batteries, ammunition, radiator factory) = HA, memory loss, demyelination |
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Heme and ALA dehydratase activity
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Low heme = Inc. ALA dehydratase activity
Inc. heme = Dec. ALA dehydratase activity |
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Lead poisoning - presentation
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"LEAD"
Lines - Burton's lines Encephalopathy & Erythrocyte basophilic stippling Abdominal colic and sideroblastic Anemia Drops - wrist and foot, Dimercaprol, and eDta (1st line tx, succimer for kids) |
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Burton's lines
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Lead lines on gingivae
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Platelet disorders
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Defects in platelet plug formation = INC. bleeding time!
Microhemorrhage, mucous membrane bleeding, epistaxis, petechia, purpura, possible thrombocytopenia |
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Bernard-Soulier
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Defect in platelet plug formation
Platelet count = Dec Bleeding time = Inc Dec. GpIb = defect in platelet-collagen adhesion |
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Glanzmann's thrombasthenia
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Defect in platelet plug formation
PC = nml Bleeding time = Inc Dec. GpIIb/IIIa = defect in platelet-platelet aggregation (no clumping) |
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Idiopathic thrombocytopenic purpura (ITP)
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Dec. platelet survival
PC = Dec Bleeding time = Inc Anti GpIIb/IIIa antibodies = peripheral platelet destruction (Inc. megakaryocytes) |
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Thrombotic thrombocytopenic purpura
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Dec. platelet survival
PC = Dec, BT = Inc Deficiency of ADAMTS 13 (vWF metalloprotease) = Decreased degradation of vWF multimers |
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Thrombotic thrombocytopenic purpura - pathogenesis
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Inc. large vWF multimers > Inc. platelet aggregation > thrombosis
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TTP Smear and Symptoms
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Schistocytes, Inc. LDH
Pentad of neuro and renal symptoms, fever, thrombocytopenia, microangiopathic hemolytic anemia |
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PT
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Factors I, II, V, VII, X
= Extrinsic pathway |
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PTT
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All factors except VII, and XIII
= Intrinsic pathway |
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Hemophilia
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Intrinsic pathway coag defect (inc. PTT)
Hem. A - Deficiency in factor VIII Hem. B - Deficiency in factor IX = inc. PTT |
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Macrohemorrhage in hemophilia
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Hemarthroses, easy bruising, Inc. PT and/or PTT
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Vitammin K deficiency
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Inc. PT and PTT (extrinsic and intrinsic pathway)
General coag defect Dec. synthesis of factors II, VII, IX, X Protein C and S |
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von Willebrand's disease - labs
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PC, PT = normal
PTT = normal or inc BT = inc |
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von Willebrand's disease
(most common inherited bleeding disorder) |
Intrinsic pathway coag defect
= Dec. vWF (carry/protect factor VIII) > nml or inc. PTT Defect in platelet plug formation, dec vWF = defect in platelet-collagen adhesion |
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DIC - labs
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PC = Dec
BT = Inc PT = inc PTT = Inc Schistocytes, Inc. fibrin split products (D-dimer), Dec. fibrinogen, Dec. Factors V and VIII |
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DIC
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Widespread activation of clotting > deficiency in clotting factors = bleeding state
Causes: "STOP Making New Thrombi" Sepsis (gram -), Trauma, Obstetric complications, Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion |
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Factor V Leiden
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Production of mutant factor V - cannot be degraded by protein C.
Most common cause of inherited hypercoagulability |
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Prothrombin gene mutation
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Mutation in 3' untranslated region associated with venous clots
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ATIII deficiency
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Inherited deficiency of antithrombin III = reduced increase in PTT after administration of heparin
AT III normally inactivates factors II, VII, IX, X, XI |
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Protein C or S deficiency
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Dec. ability to inactivate factors V and VIII
Inc. risk of hemorrhagic skin necrosis following administration of warfarin |
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Multiple Myeloma = CRAB
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hyperCalcemia
Renal insufficiency Anemia Bone/Back pain |
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Multiple Myeloma - stats
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Monoclonal plasma cell = "fried egg" appearance
Cancer arising in marrow > produces IgG (55%) or IgA (25%). Most common primary tumor within bone in elderly (>40-50 y.o.) |
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Multiple Myeloma - presentations
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"CRAB"
Inc. susceptibility to infxn Associated w/ amyloidosis (AL) Punched out bone lesions (xray) |
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Multiple myeloma - path/present
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Monoclonal immunoglobin spike (M-protein) on serum protein electrophoresis and Bence jones protein in urine
Rouleaux RBCs |
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Bence Jones protein
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Ig light chains in urine
- Multiple myeloma |
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MGUS
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Monoclonal gammopathy of undetermined significance
= Asx multiple myeloma |
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Heparin
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Cofactor for activation of anti-thrombin
= Dec. thrombin and Xa = Follow PTT Does NOT cross placenta = OK to use in pregnancy Use - immediate anticoag for PE, stroke, ACS, MI, DVT |
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HIT - Heparin-induced thrombocytopenia
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Heparin binds to platelets, causing autoantibody production that destroys platelets and overactivates the remaining ones, resulting in thrombocytopenic hypercoagulable state
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LMWH
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Enoxaparin
Acts more on Xa, have better bioavailability and 2-4x longer t1/2. SubQ administration w/o lab monitoring |
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Heparin toxicity
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Bleeding, HIT, osteoporosis, drug-drug interactions
Reverse with protamine sulfate |
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Protamine sulfate
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Reverses heparinization
Positively-charged molecule that acts by binding negatively charged heparin |
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Lepirudin, bivalirudin
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Hirudin derivatives - directly inhibit thrombin
Used as alternative to heparin for anticoagulating patients with HIT |
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Warfarin (Coumadin) - Mechanism
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Interferes with normal synthesis and gamma-carboxylation of vit-K-dependent clotting factors (II, VII, IX, X, Protein C and S)
Extrinsic pathway = Inc. PT (long t1/2) |
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Warfarin (Coumadin)
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Metabolism - CYP-450 pathway
Use - Chronic anticoag (NOT pregnant women) Follow PT/INR values |
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Warfarin (Coumadin) - Toxicity
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Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions
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Thrombolytics
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Streptokinase, urokinase, tPA (alteplase), APSAC (anistreplase)
Directly or indirectly aid conversion of plasminogen to plasmin Increase PT and PTT, no change in PC Use - early MI, early ischemic stroke |
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Thrombolytics - toxicity
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Bleeding
Contraindicated in patients w/ active bleeding, Hx of intracranial bleed, recent surgery, known bleeding diarthresis, severe HTN Tx - aminocaproic acid (inhibitor of fibrinolysis) |
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Plasmin
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Cleaves thrombin and fibrin clots
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Aspirin - Mechanism
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Acetylates and IRREVERSIBLY inhibits COX 1 and 2 to prevent conversion of arachidonic acid to TXA2
BT = Inc; PT/PTT = no change |
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Aspirin - Use and toxicity
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Use - antipyretic, analgesic, anti-inflammatory, antiplatelet drug
Tox - Gastric ulceration, bleeding, hyperventilation, Reye's syndrome, tinnitus (CN VIII) |
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Clopidogrel, Ticlopidine - Mechanism
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Inhibit platelet aggregation by IRREVERSIBLY blocking ADP receptors
Inhibit fibrinogen binding by preventing GpIIb/IIIa expression |
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Clopidogrel, Ticlopidine - Use and toxicity
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Use - ACS, coronary stents, Dec. incidence of thrombotic stroke
Tox - neutropenia (ticlopidine) |
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Abciximab
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Monoclonal antibody - binds to GpIIb/IIIa on activated platelets, preventing aggregation
Use - ACS, perQ transluminal coronary angioplasty Tox - bleeding, thrombocytopenia |
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Hydroxyurea
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Inhibits Ribonucleotide Reductase
= Dec. DNA synthesis (S-phase specific) Use - Sickle Cell anemia (Inc. HbF), Melanoma, CML Tox - Bone marrow suppression, GI upset |
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Blastocyst
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Day 5
Endoderm Mesoderm = Hematopoetic progenitor cells Ectoderm |
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Rudimentary bone marrow
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Week 3
Yolk sac |
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Hematopoesis - timeline
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Yolk sac = 3 weeks (3-10 weeks)
Liver = 6 weeks (HbF) Spleen = 12 weeks Bone Marrow = 3rd Trimester |
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Hgb F
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alpha 2, gamma 2
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Bone Marrow Cellularity and Age
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Inversely proportional
20 y.o. = 80% cellular, 20% fat 70 y.o. = 30% cellular, 70% fat |
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Order of cells from Marrow out:
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Marrow > Sinusoids (release cells into blood stream) > Capillaries > Systemic
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Proerythroblast
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More immature cell (RBC)
Bigger and lighter colored, chromatin less condensed |
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Order to make erythroblast
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Erythroblast (normoblast) extrudes nucleus to become reticulocyte > erythrocyte
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Cellular Immunity
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T Cells
Viral, Fungal, mycobaterial infxns |
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Humoral Immunity
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B Cells, Plasma cells
- Antibodies Bacterial infxns |
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Primary Lymphoid Tissue
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Bone Marrow and Thymus
- Initial development of B and T cells - T cells mature in thymus (peaks at puberty, then involutes) |
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Secondary Lymphoid Tissue
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Spleen & Lymph nodes
- Maturation of immagure lymphocytes in response to antigen |
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Spleen = Odds
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1x3x5 inches
7 ounces 9-11 ribs |
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Splenomegaly
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Defective Bone Marrow -
CML, myelofibrosis, etc. Infiltration - Lymphocytosis (Reactive or malignant) |
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Thrombocytopenia
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Dec production
Inc destruction Dilution |
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Thrombocytopenia - Example causes
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Post-infxn (post-viral: Mumps, rubella, varicella, Hep C, Ebstein Barr)
Vit B12 or Folate deficiency ITP - autoimmune, post-infxn SLE Herbals - Garlic, St. Johns Wort Drugs - sulfa, AZT |
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Platelet Count (PC)
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Normal - 200-400k
Can have normal hemostasis at 50k Tx at 20k or less, or 50k + sx Wet purpura - 10k or less |
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Hematocrit (Hct)
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% of blood that is RBCs
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RDW
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Range of sizes of RBCs
High = Wide range of sizes in circulation - helpful in distinguishing IDA from thalassemia |
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MCV - Mean corpuscle volume
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Micro = <80 = TAILS
Normo = 80-100 = Acute hemorrhage, hemolysis, marrow dysfunction Macrocytic = >100 = B12, folate, drugs, liver dz, EtOHism, hypothyroid |
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Red Blood Cells
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Life span - 120 days
Components - Hgb, enzymes, membrane |
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RBC Disorders
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Erythrocytosis = too much
Anemia = too little - Do reticulocyte count! - High = good marrow response; RBCs destroyed in body and body is trying to make more |
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Platelets
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Life span = 8-10 days
Phospholipid membrane important for clot formation = primary hemostasis |
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Pseudothrombocytopenia
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EDTA-mediated clumping causes falsely low platelet levels
Use citrate and retest |
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Cytokines and hematopoesis
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Erythropoetin (kidney>>liver) = RBCs
THrombopoetin (liver) = Platelets (also requires IL-11) GM-CSF = monocyte/macrophages and neutrophils |
