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Session 3 CM- Hem-2

CM- Hem-2- Blood properties and disorders

what make up the formed elements proteins- albumin, antibodies, clotting factors, cells
How are RBC different than any other cell They don't have a nucleus
What role does RBC play in the body transport oxygen from lungs to tissue and CO2 from tissue back to lungs
How long does typical RBC last 120 Days
What organ removes defective RBC's Spleen
what protein transports iron from intestines to bone marrow to be stored as ferritin Transferrin
What protein is reflected in total iron binding capacity transferrin
What happens to Hgb when a RBC is destroyed it is metabolized the porphyrin ring is opened to form bilirubin
what is the process of making RBCs called Erythropoiesis
what is an immature RBC called and how many of them should you find in the blood stream reticulocyte .5-1.5%
How can reticulocytes be distinguished from mature RBCs reticulocytes will have fragmented nucleus RBC have no nucleus
What cell type in the blood is crucial to body's defense system against disease and actually can be split into several different types Whit Blood Cells or leukocytes
What are the 2 main divisions of WBCs Granulocytes (lobed nuclei and stain with wright stain) and Agranulocytes
Name the granulocyte cells in blood Neutrophil, Basophil, Eosinophil, monocytes
Name the agranulocytes T- lymphocytes (defend agains exogenous antigens) -cd4 (antibodies) helper cells and suppressor cells cd8 (cytotoxic); B cells (plasma cells) produce antibodies; Natural killer cells
What does the fab region of an antibody do binds the antigen it is made of both light and heavy chains pitchfork side of Ab
What is the most abundant antibody in serum and major antibody initiating an immune response IgG
Antibody also called secretory antibody found in saliva and tears blocks adherence of pathogens to tissue IgA
Ab that forms a penatmer in serum first antibody to respond to antigen but has a short half life used to diagnose recent illness IgM
Ab that has a delta type heavy chain and is a primitve antigen receptor on lymphoid B Cells IgD
Ab responsible for hypersensitivity rxns heavy chain is epsilon type and has high affinity for mast cells, basophils to cause release of heparin and histamine IgE
What is the complement cascade and what two main ways are there to activate it it is 9 serum proteins and regulatory factors that can be activated via the classical pathway or the alternate pathway
What is the classical complement cascade IgG and IgM bind C1, C1 cleaves and activates C2 and C4 which combine as C2+C4 complex and activate C3 which activates C5-C6-C7-C8-C9 membrane attacking complex to kill invading cell
What is the alternate complement cascade direct Activation of C3 by factor B stimulated by gram + or - cell walls. C3 activates C5-6-7-8-9 memrane attack complex
Patient presents with severe angioedema they also have laryngeal obstruction, abdominal cramping, nausea, and vomiting. You determine they have a C1INH hereditary complement deficiency what would you treat them with Fresh Frozen Plasma as patient won't respond to epinephrine
if your patient has a C1, C2 and C4 complement deficiency what recurrent problem are they likely to have recurrent sinopulmonary infections
if patient has C3 complement deficiency what are they likely to suffer from severe bacterial infections
Patient has a c5-9 complement deficiency what are they likely going to suffer from increased neisseria meningococcal/gonorrhea infections
These are fragments of megakaryocytes and are essential for clotting age quickly and degenerate in 10 days Platelets/thrombocytes
What is a normal platelet count? between 30,000-100,000 count falls below 10,000 there is a serious risk of bleeding
How is hemostasis maintained 4 phse reaction 1-vascular phase, 2-platelet phase, 3-coagulation phase, 4- fibriolytic phase
what is the vascualr phase of hemostasis marked by endothelial injury causes immediate vasoconstriction to decrease blood flow to injured area. Injured enodthelium releases von willebrand's factor 8 (VWF-VIII)
What is the platelet phase of hemostasis marked by? platelets form temp clot binding von willebrands factor 8 released in vascular phase then bind collagen exposed at injury site. Then release thromboxane A2 (txa2) causing vasoconstriction. Fibrinogen makes platelets sticky connecting IIa and IIb receptors
What will you measure to get direct indication of how platelets are functioning Bleeding Time is should be less than 7min
What is the autosomal dominanat disease where patient lacks VWF-VIII, von willebrand's antigen and coag factor VIII leading to increased bleed time, increased PTT, and normal PT Von willebrands disease - responsible for 10% of cases of menorrhagia
How do aspirin and NSAIDS cause clotting problems block cyclooxygenase decreasing available thromboxane A2 decreasing platelet aggregation increasing Bleed Time, PTT will be normal as well as PT
What will the lab values show in thrombocytopenia caused by DIC, TTP or ITP increased Bleeding Time, Normal PTT and PT
What is thrombocytopenia number of circulating platelets is decreased causing spontaneous bleeding from small vessels all over the body
What are the s/sx of thrombocytopenia small purplish blotches, petechiae
What are the causes of thrombocytopenia Production defect (bone marrow defect), hypersplenism (removes to many platelets), Survival defect (DIC, TTP, ITP or heparin induced thrombocytopenia
What is caused by an autoimmune IgG against platelets initiated 30% by drugs, 30% by lupus, 30% idiopathic and 10% HIV Idiopathic Thrombocytopenic Purpura
Your patient is suffering from idiopathic thrombocytopenic purpura what is the tx Give them corticosteroids or splenectomy but do not give platelet transfusion as the problem is an autoimmune IgG response against platelets and transfusion just fuels the fire
Patient has excessive amounts of Von Willebrands VIII in circulation causing pathogenic platelet aggregation what are they suffering from Thrombotic Thrombocytopenic purpura marked by CRAFT, CNS confusion, Renal Failure, Anemia (hemolytic with shistocytes), Fever, thrombocytopenia with petechiae
What is the tx for thrombotic thrombocytopenic purpura plasma exchange w/ fresh frozen plasma
Patient presents with hemolytic anemia w/ shitstocytes, RBC fragments, palpable purpura in lower extremities, renal failure w/ hematuria and oliguria Hemolytic Uremic Syndrome- similar to TTP but only affects afferent arterioles and glomeruli of the kidneys
What are the two coagulation pathways intrinsic and extrinsic pathway
What clotting pathway does heparin block intrinsic pathway
what test is used to gauge intrinisc pathway function PTT-partial thrombin time normal is 25-36 seconds
What test is used to test the extrinisic pathways funciton PT-prothrombin time normal 11-14 seconds
What is the fibrinolytic phase prevents excess clot formation by breaking down clots through fibrinolysis.
What is the signal that endothelium releases to inhibit further platelet aggregation once a clot has been formed Prostacyclin (PGI 2) blocks thromboxane A 2
What are tissue basophils called mast cells
What doe C3a and C5a do in complement stimulate neutrophils and monocytes to phagocytize they are anaphylatoxins
What does heparin sulfate do in fibrinolytic phase activates antithrombin III binding and deactivating factors 2,9,10,11,12. Also inhibits thrombin so no more clot is formed
If you have a deficiency in antithrombin III what state would your pt be in hypercoagulable state, since it is responsible for deactivting clotting factors and thrombin
What does thrombomodulin do in body activates protein C & S with deacivate coag factors V and VIII
If you have a deficiency in C&S proteins in the body what state is the pt in a hypercoaguable state
What does Tissue Plasminogen activator do? activates plasmin which increases fibrinolysis
What deficiency do you have in hemophilia A deficiency in factor VIII, increased PTT, normal PT and BT
If you have a deficiency in factor VII what will you see on labs PTT & BT normal, PT time increased
What will you see on labs in heparin therapy increased PTT, normal PT and BT it inhibits factors 2,9,10,11 and 12
What will you see on labs in coumadin therapy increased PT and PTT with a normal BT takes out factors 2,7,9,10 by taking out vitamin K
What will you see on labs in a platelet disorder normal PTT and PT but increased BT
if you have a deficiency in factors VIII, IX, Xi or XIII what will you see on your labs increased PTT normal PT and BT
If you add plasma to a patient with a bleeding disorder and PTT does not return to normal what are they likely suffering from an antibody against coagulation factors called inhibitor syndrome
What is a myeloproliferative syndrome stem cell disorder in bone marrow where you get proliferation of one or more cell type. Marked by splenomegally and basophilia
What is polycythemia increased red cell mass measured by increaed Hgb concentration. Also common high platelet count and impaired platelet fucntion.
What should you look at in evaluating polycythemia Look at Hgb level is it related to a decrease in plasma volume
This disease is an acquired stem cell disorder of bone marrow where you have an incerase in RBC produciton despite low plasma erythropoietin level. Polycythemia Vera
What s/sx would you expect in a pt suffering from polycythemia vera pruritis- especially after bathing in warm water, Plethoric reddish skin, clubbing distal digits, gout from over production of uric acid, splenomegally, bleedin from platelet dysfunction and angina from thrombosis
What will your lab values show in polycythemia vera for; erythropoietin, RBC mass, uric acid, Hct, BT, decreased erythropoietin, increased RBC mass, increased uric acid from hemolysis, HCT > 54%, BT > 7min, LAP values may be elevated too
Pt with polycythemia vera starts showin teardrop shaped RBC's on peripheral smear what might have happened to their bone marrow it may be burned out w/ myelofibrosis
What is tx for polycythemia vera blood letting (plasmapharesis) until hct is lowerd below 45% w/ maintenace phelbotomy monthly. Hydroxyurea may be needed as well if thrombocythemia is prevalent as well
What is relative polycythemia decrease in plasma volume can be from dehydration, increased catecholamine release, protein loss.
What is secondary polycythemia tissue oxygen supply is decreased (tissue hypoxia) causing erythropoieten production making more RBC to increase oxygen carrying capacity (can be caused by smoking , high altitude, congenital heart disease
What is the secondary polycthemia cause that is caused by tumors erythropoitin like hormone is produced by tumors and stimulates RBC production in bone marrow by mimicking erythropoitin
How can you tell primary polycythemia vera from secondary polycythemia erythropoitin is low in primary and high in secondary
What is agnogenic myeloid metaplasia or myelofibrosis fibrosis of bone marrow when stem cells migrate and make extramedullary erythropoiesis
what are the s/sx of myelofibrosis splenomegally, hemolytic anemia, thrombocytopenia and hepatomegally
what is the tx for myeloproliferative disease splenectomy if the spleen is enlarged and painful, transfusion with packed RBC's, oxymetholone for severe anemia, allopurinol for decreased uric acid levels
if patint has an increased platelet production and excess platelets what disorder are they suffering from Essential Thrombocytosis alos called primary thrombocythemia, makred by weakness, headache and bleeding, thrombosis, splenomegally
What is the tx for a pt suffering from primary thrombocythemia (essential thrombocytosis) Hydroxyurea, radioactive phosphorus, or plateletphoresis
What will you see in lab evaluation of pt suffering from primary thrombocythemia elevated platelet counts to 750,000 - 1,000,000 peripheral smear will have 6-10 giant platelets along with megakaryoctye fragments, normal RBC mass
Created by: smaxsmith



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