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Path 14 RBCs
Path
| Question | Answer |
|---|---|
| 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
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