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Path 14 RBCs


destruction of RBCs w/in phagocytes cuz RBC is less deformable -> anemia, splenomegaly and jaundice Extravasc hemolysis
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
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
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
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
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
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
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
most common form of immunohemolytic anemia. IgG. Extravasc hemolysis. Spherocytes removed by spleen. Penicillins, cephalosporins, and alpha-methyldopa can induce. Warm Antibody
IgM. Appear following infections (Myco. pneumoniae, Epstein-Barr, CMV, HIV) Cold Agglutinin
paroxysmal cold hemoglobinuria. IgG bind P blood group. Child after viral infect Cold Hemolysin
most from cardiac valve prostheses and microangiopathic disorders (DIC). Damage leads to schistocytes, burr cells, helmet cells, and triangle cell. Trauma
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.
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
esophageal webs, atrophic glossitis, and microcytic hypochromic anemia. association w Iron def anemia Plummer-Vinson Synd
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.
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
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).
purpuric rash on LEs, colicky ab pain, polyarthralgia, acute glomnephritis Henoch-Schoenlein purpura
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
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
defective platelet adhesion to subendothel matrix Bernard-Soulier
defective platelet aggregation (IIb-IIIa def.). Glanzmann Throbasthenia
most common inherited bleeding disorder Von Willebrand disease
most common hereditary disease associated w/ life threatening bleeding. Mutant Coag factor VIII Hemophilia A
Mutant Coag factor IX Hemophilia B
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
Created by: Jakphooey