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| destruction of RBCs w/in phagocytes cuz RBC is less deformable -> anemia, splenomegaly and jaundice | Extravasc hemolysis
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| caused by mechanical injury (cardiac valves, bongo drumming), complement fixation, intracell parasites -> anemia, hemoglobinemia, hemoglobinuria, hemosiderinuria, and jaundice. Red-brown pee. Increased reticulocytes | Intravasc hemolysis
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| inherited disorder caused by insufficient membrane skeletal components (ankyrin, band 3, spectrin, band 4.2) that produce small, spheroid hyperchromic RBCs lacking central palor and high Hgb conc, sequestered/destroyed. Parvo->aplastic, Mono->hemolytic | Hereditary Spherocytosis
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| High Reticu count. Abnormalities in hexose monophosphate shunt or glutathione metab reduce ability of RBCs to protect against ROS. see Heinz bodies, RBCs with bites taken out of them. Contras: antimalarials, sulfonamides, nitrofurantoin, fava beans | G6PD deficiency
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| mutation of beta-globin (glutamate replaced by valine) -> HbS, which undergo polymerization when deoxygenated-> distorted sickle shaped RBCs -> chronic hemolysis, microvasc occlusions, tissue damage. Occlusive crises, most common cause of morbid/mortality | Sickle Cell
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| beta0=no beta-globin synth, beta+=reduced beta-globin synth. Def HbA synth makes hypochromic microcytic RBCs (def in oxygen transport capacity). Unpaired alpha chains become inclusions -> membrane damage. Crew-cut skull | Beta Thalassemias
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| delete 1 alpha gene: silent carrier delete 2: trait, mild microcytic hypochrom anemia delete 3: microcytic hypochromic anemia with target cells and Heinz bodies (precipitated HbH), splenomegaly delete all 4: Hydrops Fetalis, Hemoglobin Barts (4gammas) | Alpha Thalassemias
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| mutations in PIGA (essential for synth of cell surface prots). The only hemolytic anemia caused by an acquired genetic defect. Lysis by complement (intravasc hemolysis). | Paroxysmal Noturnal Hemoglobinuria
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| most common form of immunohemolytic anemia. IgG. Extravasc hemolysis. Spherocytes removed by spleen. Penicillins, cephalosporins, and alpha-methyldopa can induce. | Warm Antibody
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| IgM. Appear following infections (Myco. pneumoniae, Epstein-Barr, CMV, HIV) | Cold Agglutinin
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| paroxysmal cold hemoglobinuria. IgG bind P blood group. Child after viral infect | Cold Hemolysin
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| most from cardiac valve prostheses and microangiopathic disorders (DIC). Damage leads to schistocytes, burr cells, helmet cells, and triangle cell. | Trauma
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| autoimmune gastritis and failure of intrinsic factor->vit B12 def->FH4 def->impaired DNA synth. Lack of folate. Old Scandinavians. Atrophy of fundic glands, atrophic glossitis, demyelination of dorsal/lat spinal tracts | Pernicious anemia
- a megaloblastic anemia
- transcobalamin II delivers Vit B12 to liver etc.
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| most common nutritional disorder in the world. Hypochromic microcytic anemia. in adult men and postmenopausal women is GI blood loss (colon CA) until proven otherwise. Pencil cells. May cause pica. | Iron deficiency anemia
-Serum iron and ferritin are low, total plasma iron-binding capacity (transferrin) is high
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| esophageal webs, atrophic glossitis, and microcytic hypochromic anemia. association w Iron def anemia | Plummer-Vinson Synd
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| Microcytic d/t microbial infect (osteomyelitis, endocarditis, lung abscess); immune disorders (RA, regional enteritis); neoplasms (lung/breast carcinomas, Hodgkin lymphoma). systemic inflamm. IL-6 stimulates increased hepcidin ->suppress erythropoiesis | Anemia of Chronic Disease
- low serum iron, low iron-binding capacity, abundant stored iron in macrophages.
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| chronic primary hematopoietic failure and attendant pancytopenia. Most cases of known etiology are chemical or drug exposure related. Fanconi = defects in DNA repair-> weird thumbs/radii. Dry tap from marrow biopsies. Reticulocytopenia. | Aplastic Anemia
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| high RBC count w increase in Hgb. Relative w dec plasma vol, Absolute w inc total RBC mass. primary w/ low erythropoietin, secondary w/ high erythropoietin. | Polycythemia
- Most common cause of polycythemia is polycythemia vera (myeloproliferative disorder w/ mutations that lead to erythropoietin-independent growth of red cell progenitors).
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| purpuric rash on LEs, colicky ab pain, polyarthralgia, acute glomnephritis | Henoch-Schoenlein purpura
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| autosomal dominant. abnormal blood vessel formation(dilated, tortuous)in the skin, mucous membranes, and often in organs such as the lungs, liver and brain. freq epistaxis. most common cause of arteriovenous malformations | Osler-Weber-Rendu
- aka: hereditary hemorrhagic telangectasias
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| caused by autoantibods (IgGs) to platelets. Adult women. Pinpoint hemorrhages. | Chronic Immune Thrombocytopenic Purpura
- Acute is in children following viral illness and is self limited
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| defective platelet adhesion to subendothel matrix | Bernard-Soulier
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| defective platelet aggregation (IIb-IIIa def.). | Glanzmann Throbasthenia
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| most common inherited bleeding disorder | Von Willebrand disease
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| most common hereditary disease associated w/ life threatening bleeding. Mutant Coag factor VIII | Hemophilia A
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| Mutant Coag factor IX | Hemophilia B
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| High Reticu Count. Thrombohemorrhagic disorder characterized by excessive activation of coag -> thrombi in microvasc. Triggered by release of tissue factor or thromboplastic substances into circ or widespread endothel injury (TNF) | Disseminated Intravascular Coagulation
- Acute: Bleeding
- Chronic: Thrombotic complications
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