EXTRACORPUSCULAR HEMOLYSIS Nonimmune

فهرست عناوین اصلی در این پاورپوینت

فهرست عناوین اصلی در این پاورپوینت

● HEMOLYTIC ANEMIAS
● HEMOLYTIC ANEMIA
● HEMOLYTIC ANEMIA
Testing
● HEMOLYTIC ANEMIA
Causes
● HEMOLYTIC ANEMIA
Membrane Defects
● RED CELL CYTOSKELETON
● HEREDITARY SPHEROCYTOSIS
● SPLENIC ARCHITECTURE
● HEREDITARY SPHEROCYTOSIS
Osmotic Fragility
● Paroxysmal Nocturnal Hemoglobinuria
● GPI BRIDGE
● Paroxysmal Nocturnal Hemoglobinuria
GPI Proteins
● HEMOLYTIC ANEMIA
Membrane abnormalities – Enzymopathies
● G6PD DEFICIENCY – Function of G6PD
● Glucose 6-Phosphate Dehydrogenase
Functions
● Glucose 6-Phosphate Dehydrogenase
Different Isozymes
● HEMOLYTIC ANEMIA
Causes
● EXTRACORPUSCULAR HEMOLYSIS
Nonimmune
● Microangiopathic Hemolytic Anemia
Causes
● Microangiopathic Hemolytic Anemia
Causes – #2
● IMMUNE HEMOLYTIC ANEMIA
General Principles
● IMMUNE HEMOLYTIC ANEMIA
General Principles – 2
● IMMUNE HEMOLYTIC ANEMIA
Coombs Test – Direct
● IMMUNE HEMOLYTIC ANEMIA
Coombs Test – Indirect
● HEMOLYTIC ANEMIA – IMMUNE
● IMMUNE HEMOLYSIS
Drug-Related
● DRUG-INDUCED HEMOLYSIS
Immune Complex Mechanism
● DRUG-INDUCED HEMOLYSIS
Haptenic Mechanism
● DRUG-INDUCED HEMOLYSIS
True Autoantibody Formation
● DRUG-INDUCED HEMOLYSIS – Mechanisms
● ALLOIMUNE HEMOLYSIS
Hemolytic Transfusion Reaction
● INCOMPATIBLE RBC TRANSFUSION
Rate of Hemolysis
● ALLOIMMUNE HEMOLYSIS
Testing Pre-transfusion
● ALLOIMMUNE HEMOLYSIS
Hemolytic Disease of the Newborn
● ALLOIMMUNE HEMOLYSIS
Hemolytic Disease of the Newborn – #2
● AUTOIMMUNE HEMOLYSIS
● AUTOIMMUNE HEMOLYSIS
Warm Type
● AUTOIMMUNE HEMOLYSIS
Cold Type
● HEMOLYTIC ANEMIA
Summary

نوع زبان: انگلیسی حجم: 3.24 مگا بایت
نوع فایل: اسلاید پاورپوینت تعداد اسلایدها: 44 صفحه
سطح مطلب: نامشخص پسوند فایل: ppt
گروه موضوعی: زمان استخراج مطلب: 2019/06/15 08:28:36

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عبارات مهم استفاده شده در این مطلب

عبارات مهم استفاده شده در این مطلب

hemolysis, cell, hemolytic, rbc, anemia, complement, immune, antibody, antigen, cause, drug, red,

توجه: این مطلب در تاریخ 2019/06/15 08:28:36 به صورت خودکار از فضای وب آشکار توسط موتور جستجوی پاورپوینت جمع آوری شده است و در صورت اعلام عدم رضایت تهیه کننده ی آن، طبق قوانین سایت از روی وب گاه حذف خواهد شد. این مطلب از وب سایت زیر استخراج شده است و مسئولیت انتشار آن با منبع اصلی است.

http://www.columbia.edu/itc/hs/medical/pathophys/hematology/2008/hemolytic.ppt

در صورتی که محتوای فایل ارائه شده با عنوان مطلب سازگار نبود یا مطلب مذکور خلاف قوانین کشور بود لطفا در بخش دیدگاه (در پایین صفحه) به ما اطلاع دهید تا بعد از بررسی در کوتاه ترین زمان نسبت به حدف با اصلاح آن اقدام نماییم. جهت جستجوی پاورپوینت های بیشتر بر روی اینجا کلیک کنید.

عبارات پرتکرار و مهم در این اسلاید عبارتند از: hemolysis, cell, hemolytic, rbc, anemia, complement, immune, antibody, antigen, cause, drug, red,

مشاهده محتوای متنیِ این اسلاید ppt

مشاهده محتوای متنیِ این اسلاید ppt

hemolytic anemias hemolytic anemia anemia of increased destruction normochromic normochromic anemia shortened rbc survival reticulocytosis response to increased rbc destruction increased indirect bilirubin increased ldh hemolytic anemia testing absent haptoglobin hemoglobinuria hemoglobinemia hemolytic anemia causes intracorpuscular hemolysis membrane abnormalities metabolic abnormalities hemoglobinopathies extracorpuscular hemolysis nonimmune immune hemolytic anemia membrane defects microskeletal defects hereditary spherocytosis membrane permeability defects hereditary stomatocytosis increased sensitivity to complement paroxysmal nocturnal hemoglobinuria red cell cytoskeleton ۱۷.bin hereditary spherocytosis defective or absent spectrin molecule leads to loss of rbc membrane leading to spherocytosis decreased deformability of cell increased osmotic fragility extravascular hemolysis in spleen splenic architecture ۱۹.bin hereditary spherocytosis osmotic fragility paroxysmal nocturnal hemoglobinuria clonal cell disorder ongoing intra extravascular hemolysis classically at night testing acid hemolysis ham test sucrose hemolysis cd ۵۹ cd ۵۵ negative acquired deficit of gpi associated proteins including decay activating factor gpi bridge paroxysmal nocturnal hemoglobinuria gpi proteins gpi links a series of proteins to outer leaf of cell membrane via phosphatidyl inositol bridge with membrane anchor via diacylglycerol bridge pig a gene on x chromosome codes for synthesis of this bridge multiple defects known to cause lack of this bridge absence of decay accelerating factor leads to failure to inactivate complement thereby to increased cell lysis hemolytic anemia membrane abnormalities enzymopathies deficiencies in hexose monophosphate shunt glucose ۶ phosphate dehydrogenase deficiency deficiencies in the em pathway pyruvate kinase deficiency g۶pd deficiency – function of g۶pd glucose ۶ phosphate dehydrogenase functions regenerates nadph allowing regeneration of glutathione protects against oxidative stress lack of g۶pd leads to hemolysis during oxidative stress infection medications fava beans oxidative stress leads to heinz body formation  extravascular hemolysis glucose ۶ phosphate dehydrogenase different isozymes level needed for protection vs ordinary oxidative stress hemolytic anemia causes intracorpuscular hemolysis membrane abnormalities metabolic abnormalities hemoglobinopathies extracorpuscular hemolysis nonimmune immune extracorpuscular hemolysis nonimmune mechanical infectious chemical thermal osmotic microangiopathic hemolytic anemia causes vascular abnormalities thrombotic thrombocytopenic purpura renal lesions malignant hypertension glomerulonephritis preeclampsia transplant rejection vasculitis polyarteritis nodosa rocky mountain spotted fever wegener’s granulomatosis scleroderma renal crisis microangiopathic hemolytic anemia causes ۲ vascular abnormalities av fistula cavernous hemangioma intravascular coagulation predominant abruptio placentae disseminated intravascular coagulation immune hemolytic anemia general principles all require antigen antibody reactions types of reactions dependent on class of antibody number spacing of antigenic sites on cell availability of complement environmental temperature functional status of reticuloendothelial system manifestations intravascular hemolysis extravascular hemolysis immune hemolytic anemia general principles ۲ antibodies combine with rbc either activate complement cascade or opsonize rbc for immune system if ۱ if all of complement cascade is fixed to red cell intravascular cell lysis occurs if ۲ or if complement is only partially fixed macrophages recognize fc receptor of ig or c۳b of complement phagocytize rbc causing extravascular rbc destruction immune hemolytic anemia coombs test direct looks for immunoglobulin or complement of surface of red blood cell normally neither found on rbc surface coombs reagent combination of anti human immunoglobulin anti human complement mixed with patient’s red cells if immunoglobulin or complement are on surface coombs reagent will link cells together and cause agglutination of rbcs immune hemolytic anemia coombs test indirect looks for anti red blood cell antibodies in the patient’s serum using a panel of red cells with known surface antigens combine patient’s serum with cells from a panel of rbc’s with known antigens add coombs’ reagent to this mixture if anti rbc antigens are in serum agglutination occurs hemolytic anemia immune drug related hemolysis alloimmune hemolysis hemolytic transfusion reaction hemolytic disease of the newborn autoimmune hemolysis warm autoimmune hemolysis cold autoimmune hemolysis immune hemolysis drug related immune complex mechanism quinidine quinine isoniazid haptenic immune mechanism penicillins cephalosporins true autoimmune mechanism methyldopa l dopa procaineamide ibuprofen drug induced hemolysis immune complex mechanism drug antibody bind in the plasma immune complexes either activate complement in the plasma or sit on red blood cell antigen antibody complex recognized by re system red cells lysed as innocent bystander of destruction of immune complex requires drug in system drug induced hemolysis haptenic mechanism drug binds to reacts with red cell surface proteins antibodies recognize altered protein ± drug as foreign antibodies bind to altered protein initiate process leading to hemolysis drug induced hemolysis true autoantibody formation certain drugs appear to cause antibodies that react with antigens normally found on rbc surface and do so even in the absence of the drug drug induced hemolysis mechanisms alloimune hemolysis hemolytic transfusion reaction caused by recognition of foreign antigens on transfused blood cells several types immediate intravascular hemolysis minutes due to preformed antibodies life threatening slow extravascular hemolysis days usually due to repeat exposure to a foreign antigen to which there was a previous exposure usually only mild symptoms delayed sensitization weeks usually due to ۱st exposure to foreign antigen asymptomatic incompatible rbc transfusion rate of hemolysis alloimmune hemolysis testing pre transfusion abo rh type of both donor recipient antibody screen of donor recipient including indirect coombs major cross match by same procedure recipient serum donor red cells alloimmune hemolysis hemolytic disease of the newborn due to incompatibility between mother negative for an antigen fetus father positive for that antigen. rh incompatibility abo incompatibility most common causes usually occurs with ۲nd or later pregnancies requires maternal igg antibodies vs. rbc antigens in fetus alloimmune hemolysis hemolytic disease of the newborn ۲ can cause severe anemia in fetus with erythroblastosis and heart failure hyperbilirubinemia can lead to severe brain damage kernicterus if not promptly treated hdn due to rh incompatibility can be almost totally prevented by administration of anti rh d to rh negative mothers after each pregnancy autoimmune hemolysis due to formation of autoantibodies that attack patient’s own rbc’s type characterized by ability of autoantibodies to fix complement site of rbc destruction often associated with either lymphoproliferative disease or collagen vascular disease autoimmune hemolysis warm type usually igg antibodies fix complement only to level of c۳ if at all immunoglobulin binding occurs at all temps fc receptors c۳b recognized by macrophages therefore hemolysis primarily extravascular ۷ associated with other illnesses responsive to steroids splenectomy autoimmune hemolysis cold type most commonly igm mediated antibodies bind best at ۳ º or lower fix entire complement cascade leads to formation of membrane attack complex which leads to rbc lysis in vasculature typically only complement found on cells ۹ associated with other illnesses poorly responsive to steroids splenectomy responsive to plasmapheresis hemolytic anemia summary myriad causes of increased rbc destruction marrow function usually normal often requires extra folic acid to maintain hematopoiesis anything that turns off the bone marrow can result in acute life threatening anemia ۲ ۴ ۶ ۸ ۱ .۳ .۴ .۵ .۶ nacl of normal saline hemolysis normalhs ۲ ۴ ۶ ۸ ۱ ۲ ۴ ۶ ۸ ۱ ۱۲ rbc age days g۶pd activity normal gdb black variant gda mediterranean gd med ۲ ۴ ۶ ۸ ۱ ۱۲۳۴۵۶۷ weeks post transfusion surviving cells normalimmediate intravascular hemolysis slow extravascular hemolysisdelayed extravascular hemolysis …

کلمات کلیدی پرکاربرد در این اسلاید پاورپوینت: hemolysis, cell, hemolytic, rbc, anemia, complement, immune, antibody, antigen, cause, drug, red,

این فایل پاورپوینت شامل 44 اسلاید و به زبان انگلیسی و حجم آن 3.24 مگا بایت است. نوع قالب فایل ppt بوده که با این لینک قابل دانلود است. این مطلب برگرفته از سایت زیر است و مسئولیت انتشار آن با منبع اصلی می باشد که در تاریخ 2019/06/15 08:28:36 استخراج شده است.

http://www.columbia.edu/itc/hs/medical/pathophys/hematology/2008/hemolytic.ppt

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