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45 Cards in this Set
- Front
- Back
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What is another name for Polys PMNs, Polymorphonuclears and Segs?
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Neutrophils. They are first fighter in the immune response and less mature neutrophils are called bands or stabs indicating a left shift, when the body has to resort to less mature neutrophils because it is an ongoing infection and has to pull all its resources
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What are the critical values of WBC?
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Less than 2.5 WBC x 10 to the 3 /mm to the 3 or 2500 WBC/mm to the 3 or
Greater than 30 WBC x 10 to the 3/mm to the 3 or 30,000 WBC/mm to the 3. |
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What are 2 acquired disorders of the erythrocytes in children?
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Iron deficiency anemia and HDN
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Define anemia and What are the 3 main causes of anemia?
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Anemia is the overall decrease in rbc. The 3 causes of this condition are: decreased production (erythropoeisis) of erythrocytes; increased loss of erythrocytes (hemorrhage); or increased destruction of erythrocytes (hymolysis).
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What will the reticulocyte count show and will they be increased or decreased?
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Reticulocytes are immature rbc that will be decreased in diseases where there is less erythropoesis, but will be increased in diseases with hemorrhage, or in hemolytic anemias.
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What is MCH and MCV tests used for?
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MCV (Mean corpuscular volume) is a test that will differentiate between normocytic, macrocytic, and microcytic anemias; MCH (Mean Corpuscular Hemoglobin) is used to differentiate hypochromic and normochromic anemias.
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Name a macrocytic anemia; Name a microcytic anemia
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Macrocytic anemias are anemias that are making too large of blood cells, large stem cells from lack of B12 (pernicious) or Folate. Folate is needed for DNA synthesis, which doesn't happen, so the nucleus is small, but rna synthesis is happening and enlarges the cell; Microcytic anemia is iron deficient anemia, the most common anemia in the world, characterized by abnormally small erythocyte that contains abnormally reduced amounts of hemoglobin.
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What type of anemia presents koilonychia and hemoglobin that drops to 7 or 8 g/dl, sob, fatigue, weakness, and conjunctiva, all diagnostics will show a decrease, but TIBC will be increased.
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Iron Deficiency Anemia, which is a microcytic anemia that has a reduction in erythropeisis, low erythroctye count and low hemoglobin. TIBC is total iron binding capacity, there will be vacancies.
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What is the most common cause of acquired hemolytic anemia?
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Autoimmune reaction ABO blood, Rh and drug induced hemolysis.
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What is the composition breakdown of blood percentages?
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Starting with the body breakdown: 92% is other body fluids/ 8% is blood; Now break down blood: of the 8%Plasma is 55% and 45% is other formed elements; Now break down plasma: of the 55%- water is 92%, plasma proteins are 6%, and other solutes are 2%. Now break down the plasma proteins: of the 6% pp, albumin is 58%, globulins(think MegaD) are 38% and fibrinogen is 4%. Now break down the 2%solutes: they are ions,nutrients, regulatory subs,waste products and gases; Now let's break down the other formed elements (the other almost 1/2 (45% of blood) which are the platelets(aka Thrombocytes), @ 145,000-340,000, leukocytes @ 5-10,000 and erthrocytes @ 4.2-6.2 million. Now lets break down the leukocytes: There are the granulocytes: with neutrophils make up 54-67%, eosinophils @ 1-4%, basophils @ less than 1%, of volume; and the agranulocytes: the lymphocytes at 25-36% and the monoctyes @ 3-8%.
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What are some distinctive characteristics about the rbc erythrocytes that make it so unique?
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Well, it cannot replicate or go through mitosis, it only lasts 120 days, while others are being made in the bone marrow, it is the most abundant blood cell, it is responsible for tissue oxygenation, carries gases and electrolytes and regulates diffusion the the cell's membrane, it's unique size and shape help its function. It is biconcave disc, which provides more surface area /volume making it optimal for gas diffusion into and out of the cell, it circulates through splenic sinusoids, it can reverse its shape or become torpedolike to fit through microcirculation and then return to normal.
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What is the process and rbc goes through to be broken down?
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1) Healthy RBC’s live about 80- 120 days, Break down about 174 million per minute; 2) Removed from circulation by the liver & spleen
3) Broken down into heme and globin portions; 4) Globin is broken down into amino acids; 5) Iron is removed from heme and stored or recycled; 6) Heme is broken down into biliverdin ,then into bilirubin. |
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What do granules in granulocytes contain?
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Enzymes that Kill microorganisms,
Break down debris from phagocytosis,and also there are other biochemicals that serve as signals & mediators of the inflammatory response. |
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What are the agranulocytes and their characteristics?
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Agranulocytes have Granules too small to be visible; They are Monocytes, which are immature macrophages @ 5%, they circulate in bld about 3 days before enter tissue to become macrophages.
As Macrophages, they can live for months to years. They Migrate in & out of tissue; They are rore efficient phagocytes vs. neutrophils; and they are capable of cell division & proliferate at the site of inflammation; Then there are the other agranulocytes, theLymphocytes, their job is immune function, amount is 25-36%; They can live for years: Of the lymphocytes there are: NK cells – natural killer cells: they are Innate immune cells and Not antigen specific. Then there are the T cells, which mature in thymus: 1 of which has the CD 4 protein, called the T helper cells-they interact w/ antigens on surface of specialized antigen presenting cells. Then there's the CD 8 protein - Cytotoxic T cells, they carry out cell-mediated destruct of tumor cells or cells infected with virus. Then there are the B cells, which mature in bone marrow. They produce antibodies & respond to only 1 specific antigen. They require help from T helper cells. |
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Where do WBC originate and where do they mature?
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If you're talking about granulocytes: neutrophils, basophils, and eosinophils, they originate in the bone marrow and they also mature in the bone marrow before they are sent out into the blood and only live hours to days; Where as Agranulocytes, monocytes, and lymphocytes, originate in the bone marrow as well, but mature either in the blood or in other locations like the thymus...and live for days and months...
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In what instances will we see an increase in wbc?
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Infection, Presence of steroids and
Decreased reserve of leukocyte pool in bone marrow |
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Explain platelet degranulation or formation of a clot.
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Platelets normally circulate freely suspended in plasma when they are unactivated. It is the endothelial cells that line vessels that control platelet activation. Their products: nitric oxide (NO), and Prostaglandin I2 (PGI2) are what keep platelets in their inactive state. But when a blood vessel is damaged, platelets are activated in a 3 step process: adhesion, aggregation, and activation. In ADHESION: Platelets go from weakly adhering to the vessel wall to strong adherence (they do this with the help of the sticky glycoprotein VWF and collagen),with each other. This is called the Activation phase, because the platelets go through a conform-ational change, which makes platelets degranulate and become spikey (called platelt-release reaction), releasing 3 chemicals: lysosomes, dense bodies, and alpha granules. The dense bodies contain ADP, serotonin and calcium and the alpha granules contain clotting factors (fibrinogen, and factor V, as well as growth factors, and heparin-binding proteins). These all combine to promote and inhibit platelet activity so as not to go crazy either way, in the eventual process of clot formation.
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What is the process of lysis of blood clots?
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Lysis is carried out by the fibrinolytic system. Another plasma protein, plasminogen is converted to plasmin by several products of coagulation and inflammation. Plasmin is an enzyme that dissolves clots (called fibrinolysis), by degrading fibrin and fibrinogen into fibrin degradation products. The fibrinolytic system removes clotted blood from tissues and dissolves small clots (thrombi) in blood vessels. A balance between the amounts of thrombin and plasmin in circulation maintains normal coagulation and lysis.
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What stimulates the production of rbcs?
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The kidneys release increased
amounts of erythropoietin whenever the oxygen capacity of the blood is reduced. Erythropoietin stimulates the red bone marrow to speed up its production of red blood cells, which carry oxygen. Once the oxygen-carrying capacity of the blood is sufficient to support normal cellular activity, the kidneys cut back on their production of erythropoietin. |
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What is the structure of a hemglobin molecule?
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Made up of 2 pairs of globin & 4 hemes
Heme contains iron & carries 1 O2 molecule. |
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Explain hemoglobin synthesis
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Hgb is oxygen carrying protein, and
RBC normally contain up to 300 Hgb molecules. 1 hemoglobin molecule is made up of 2 pairs of globin & 4 hemes. A Heme group contains iron & carries 1 O2 molecule. Fe (diet) gets absorbed in the duodenum & jejunum and either goes to liver to be stored or is digested and broken down. When old RBC's are broken down into globins, heme (down to bilirubin and iron, the iron will be tranferred on transferrin (TIBC). Once all of the TBIC sites are full, then transferrin transports Fe to the bone marrow where RBC are made to be used for synthesis of of heme on rbcs. If Fe is not needed it is released & stored as ferritin in the liver or the spleen. Some of it will not be stored and will go out in the bile and out to digestion. |
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What are the nutritional needs for hemoglobin synthesis?
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Protein is needed for the structure of plasma membrane in hemoglobin;
Vit B12 – DNA synthesis, intrinsic factor required for Folate metabolism Folate is needed for DNA & RNA synthesis; Vit B6 is needed for Heme synthesis; Vit C is needed for Fe metabolism & maintain in ferrous form.; Vit E is needed in Heme synthesis as it protect agst oxidative damage.; Pantothenic acid needed for Heme synthesis too. |
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What are all the values that are considered in a CBC?
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White Blood Cell Count (WBC)
Red Blood Cell Count (RBC) Hemoglobin (Hgb) Hematocrit (Hct) WBC Differential (Diff) Platelet Count (Plt) RBC Indices (MCV, MCH, MCHC) Red Cell Distribution Width (RDW |
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What are the normal hemoglobin values for women, men and newborns?
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Normal values:
Adult Males: 13.5 – 17.5 g/dL Adult Females: 12.0 – 16.0 g/dL Newborns: 13.5 – 20.0 g/dL |
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What are the percentages and normal values for hematocrit?
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Percentage of red blood cells in a volume of whole blood; Values closely parallel values for hemoglobin
Hgb & HCT are best determinate of the degree of anemia orpolycythemia Normal values: Adult male: 40-55% Adult female: 38-48% Newborn: 50-65% |
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What are red cell indices?
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Calculations of average size, hemoglobin content and hemoglobin concentration of red cell
HCT, RBC ct, Hgb all used to determine RBC Indicies. Of value in classification of anemias there are 3 red cell indices: Mean corpuscular volume (MCV) Mean corpuscular hemoglobin (MCH); Mean corpuscular hemoglobin concentration (MCHC) |
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What is the red cell indices MCV used for?
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Mean Corpuscular Volume: HCT divided by total RBC count
Determine size of RBC’s Classification of anemias Normal values: Adult male & female – 85-95 fl Newborn – 95-115 fl < 85 fl = microcytic cells (small) > 95 fl = macrocytic cells (large) |
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What is mean corpuscular hemoglobin?
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Weight of Hgb in 1 RBC,
Divide Hgb by RBC count Normal value: 27-33 pg < 27 = hypochromic or microcytosis red cells; > 33 = macrocytosis |
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What does the red cell indices: MCHC mean?
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Mean Corpuscular Hemoglobin Concentration: Percentage of RBC saturated w/ Hgb; Divide Hgb by the HCT; Normal value:32-36% < 32 = hypochromia; > 36 = spherocytosis – abnormal shape of cell.
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What is red cell distribution width?
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Indicates degree of red cell size variation or how much difference exists between largest and smallest red cells;
Normal values: Adult: 11.5 – 14.5 % Newborn: 15 - 18 % >14.5 % corresponds with anisocytosis (variation in size of red cell) on the peripheral blood |
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What is the difference between relative and actual anemia?
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Relative
Normal RBC ct, disturbance in the regulation of plasma volume: maybe hyper volemic, it looks like the rbc are low against such a high volume. Absolute Actual decrease in RBC’s Decrease in production or an increase in destruction |
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What would be the causes of microcytic anemia, and what would be the causes of macrocytic anemia?
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In microcytic anemia: Inadequate diet, Blood loss (ulcers, cirrhosis, CA) chronic, increase req, (preg), CRI; In macrocytic anemia: Inadequate diet, lack of intrinsic factor for pernicious anemia, impaired absorption, poor diet low in veggies.
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What are the morphological characteristics,causes and the pathophysiology of the following types of anemia: aplastic, hemolytic, post hemorrhagic/acute hemorrhage?
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Aplastic: Normocytic, normochromic RBCs, depletion of leukocytes and platelets; Causes: drug toxicity, genetic failure, radiation, chemicals, infections; Pathophysiology: Damage of destroyed stem cells inhibit blood cell production.
Hemolytic: Morphological: Normocytic, normochromic, inc number of reticulocytes; Causes: Mechanical injury, RBC antigen-antibody reaction, chemical reactions; patho:Reduced RBC survival. Post hemorrhagic/acute hemorrhage: Morphological:Normocytic, normochromic, inc number of reticulocytes within 48-72 h; causes: Internal or external hemorrhage; Reduced circulating blood volume. |
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What are the hallmark characteristics of hemolytic anemia and what are the types?
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Hallmarks:Destruction of erythrochtes & acceleration of erythropoesis Type 1) Inherited
Abnormalities in the cell membranes Sperocytosis & elliptocytosis Abnormalities in enzymes in production of Hgb Glucose-6-phosphate dehydrogenase Type 2) Acquired Infection, chemical agents & abnormal immune response, Blood Transfusion |
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What is DIC, and what are its causes and pathophysiology? Part 1 of DIC card
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DIC is a Catastrophic bleeding disorder characterized by thrombus formation and hemorrhage secondary to overstimulation of the normal coagulation process, resulting in a decrease in clotting factors and platelets; Causes of DIC: Shock, Fat embolism; Sepsis Infection;Malignancy – Acute leukemia, Breast, Colon, pancreas, Prostate, Ovarian, Lung CA
Hematologic – Hemolytic transfusion rx, sickle cell, Anaphylaxis, Transplant rejection; Obstetric – amniotic fluid embolism, eclampsia, septic abortion, abruptio placentae. Pathophysiology: Release of Tissue Factor leading to damage to vascular endothelium; TF contributes to conversion of prothrombin to thrombin. Would not be surprised to see clot formation. Intravascular thrombin produced converts fibrinogen to a fibrin clot & platelet aggregation;Excessive blood coagulation leads to thrombi in the microvascular leading to ischemia |
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What would be the clinical manifestations if someone had microvascular thromboisis vs. hemorrhage.
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1) Microvascular Thrombosis: Neurologic: Multifocal, Delirium, Coma; Renal:Oliguria, Azetemia, Cortical Necrosis; GI: Paralytic Ileus; Integument: Facial Iscemia, Superficial Gangrene; Pulmonary: ARDS;
2) Hemorrhage: Neurologic: Intracerebral Bleeding; Renal: Hematuria; Mucous Membranes: Epitaxis, Gingival oozing; GI: Massive Bleeding; Pulmonary: Repiratory congestion, dyspnea, hemoptysis; Integument: Petichae, Echymosis, Venipuncture oozing. |
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What are the diagnostics for blood clots?
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Decreased platelet count – varying degrees: because they are eating the blood clots…?
Prolong bleeding times ( InR is not measured in time) PT, PTT Decreased fibrinogen levels Increased FSP Natural anticoagulants – reduced Protein C & S, Antithrombin III D Dimers – Fibrin Degradation Fragment Increased: |
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What are the lab values of concern in HELLP?
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AST value of >70, and a platelet value of <100,000.
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What are the clinical manifestations and potential complications in persons with HELLP?
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Clinical Manifestations: Decreased platelet count – varying degrees: because they are eating the blood clots…? Prolong bleeding times ( InR is not measured in time)
PT, PTT Decreased fibrinogen levels Increased FSP; Natural anticoagulants – reduced Protein C & S, Antithrombin III D Dimers – Fibrin Degradation Fragment Increased: Complications: Anemia Abruptio placenta Liver damage & potential failure Ischemia – CVA, ACS: acute coronary syndrome. , Renal Injury, Pulmonary DIC Fetal/mother demise |
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What drugs would inhibit folic acid absorption?
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oral contraceptives and anticonvulsants slow or prevent absorption of folic acid.
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What nutrient helps the rbc to mature?
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folic acid
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Part 2: of DIC Pathology continued...
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Natural anticoagulants are decreased; Antithrombin III, Protein C & S, expect them to be decreased with dic. Excessive aggregation leads to thrombocytopenia;
Excessive blood coagulation leads to depeletion of clotting factors , because they are being used up. – hemorrhage; Loss of Hgb & O2 carrying capacity; you would see ischemia because of the clots and hemorrhaging combined. Body will naturally try to break up the clots which adds to the bleeding Fibrinolysis causes destruction of clots & bleeding; Activation of plasminogen to plasmin causing clot lysis. Fibrinolysis leads to the production of fibrin split products or fibrin degradation products Split products act as anticoag & perpetuates bleeding; Coat platelets & interfere w/ platelet function Interfere w/ thrombin & disrupt coagulation; Attach to fibrinogen, interfering w/ process necessary to form a stable clot; Cascade of clotting leads to activation of inflammatory & complement systems Increase permeability of vascular bed leads to HOTN; Complement induces destruction of platelets. |
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What triggers platelet formation and where does it come from?
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Thrombopoeitin is released from the LIVER to trigger thrombopoiesis: megablast to megakaryoctye, to platelet or thrombocyte fragments that float around in the blood.
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What is thalassemia?
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chains of the globins are defected and so you can't make hemoglobin so you you have anemia.
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What is acute lymphoctyic leukemia?
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Making soooo many lymphocytes in the bone marrow so that there isn't any room to make other blood cells including the rbcs, so then the person has anemia. Therapy is to go in and kill the lymphocytes, but harvest some ahead of time and you kill the bone marrow, so you need a marrow transplant.
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