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<ul><li> Slide 1 </li> <li> HEMATOLOGY; ALTERATIONS OF BLOOD CELL AND LYMPHOID FUNCTION </li> <li> Slide 2 </li> <li> Blood Plasma Complex, aqueous Organic, inorganic molecules Plasma proteins Greatest weight in total plasma Important plasma proteins: Albumins Globulins Clotting factors </li> <li> Slide 3 </li> <li> Blood contd Other components Formed elements (blood cells) Erythrocytes (= red blood cells = rbcs) Leukocytes (= white blood cells = wbcs) Lymphocytes (= B and T cells) Thrombocytes (= platelets) Development (= hematopoiesis) Common stem cell Mitosis signaled by biochems released from the body Differentiate needed blood cell Hematopoiesis/cell breakdown continuous </li> <li> Slide 4 </li> <li> Slide 5 </li> <li> Erythrocytes (= Red Blood Cells = RBCs) Development = erythropoiesis Erythropoietin Renal hormone Reld when kidney senses decrd blood oxygen red bone marrow Signals differentiation of common stem cell rbcs </li> <li> Slide 6 </li> <li> RBCs contd Rbc cytoplasm contains Hemoglobin Other proteins, electrolytes Not many (if any) organelles No nucleus Doesnt replicate on own in bloodstream Where do more rbcs come from? </li> <li> Slide 7 </li> <li> RBCs contd Hemoglobin (Hb) carries O 2 and CO 2 within rbcs Composition Four protein chains (= globin) Complex organic molecule embedded in each globin chain (= heme) Iron (Fe) atom held in globin Binds oxygen Bodys synth of Hb requires Sufficient Fe and amino acids Vitamins folate (or folic acid) and B12 </li> <li> Slide 8 </li> <li> Slide 9 </li> <li> RBCs contd Hb contd Rbc/Hb breakdown Healthy rbcs live 120 days Approx. 174 million rbcs break down per minute In liver and spleen Hb released, broken down following rbc breakdown Globin amino acids; recycled new proteins Fe stored or recycled Heme converted bilirubin Bilirubin either stored or recycled, or Further converted in liver to bile </li> <li> Slide 10 </li> <li> Abnormalities of RBCs Anemias Clinical symptoms: Fatigue Dyspnea Syncope Angina Tachycardia Organ dysfunctions </li> <li> Slide 11 </li> <li> Anemias contd Macrocytic/megaloblastic large rbcs Commonly due to deficiency of Vit B12 or folate Pernicious anemia - typical Possible causes Congenital deficiency in protein nec to absorb B12 from small intestine Adult onset one example: autoimmune dysfunction destruction of gastric mucosa Develops slowly Fatal if untreated </li> <li> Slide 12 </li> <li> Slide 13 </li> <li> Anemias contd Microcytic abnormally small rbcs w/ decrd Hb Possible causes: disorders of Fe metabolism Globin synthesis Heme synthesis </li> <li> Slide 14 </li> <li> Anemias contd Microcytic contd Iron deficiency anemia typical Common causes Insufficient Fe intake Chronic blood loss (even 2-4 mL/day) Men gastrointestinal bleeding Women profuse menstruation, pregnancy Other causes Drugs gastrointestinal bleeding Eating disorders insufficient Fe </li> <li> Slide 15 </li> <li> Slide 16 </li> <li> Anemias contd Microcytic contd Treatment Eliminate blood loss Replace Fe Normocytic Aplastic anemia - typical Bone marrow dysfunction underdeveloped, defective, absent marrow or stem cells </li> <li> Slide 17 </li> <li> Anemias contd Normocytic contd Aplastic anemia contd Possible causes of bone marrow dysfunction: Cancer cells in marrow Autoimmune response Renal failure Exposure to radiation, drugs, toxins harming bone marrow Clinical symptoms those typical of anemias Treatment Treat underlying disorder Blood transfusions to increase [Hb] Bone marrow transplant </li> <li> Slide 18 </li> <li> Abnormalities of RBCs contd Myeloproliferative disorders Polycythemia = excessive proliferation of rbcs Secondary is most common Physiological response to hypoxia Seen in Smokers Those w/ congestive heart failure Those w/ cardiopulmonary diseases </li> <li> Slide 19 </li> <li> Polycythemia contd Leads to Incrd blood volume, viscosity Congestion of liver, spleen Clotting; thrombus formation Clinical Headache, dizziness, weakness Increased blood pressure Itching/sweating Treatment Reduce blood volume (= phlebotomy) to reduce rbc # Control symptoms Prevent thrombosis </li> <li> Slide 20 </li> <li> Sickle Cell RBCs </li> <li> Slide 21 </li> <li> Leukocytes (= White Blood Cells = wbcs) Granulocytes granules in cytoplasm Granules contain Enzymes to kill invading cells, break down cell debris Other biochems that signal, mediate inflammatory response Cell types (mostly phagocytic) Neutrophils Eosinophils Basophils </li> <li> Slide 22 </li> <li> Slide 23 </li> <li> Leukocytes (= White Blood Cells = wbcs) Agranulocytes no granules in cytoplasm Also impt phagocytes, release biochem signals Cell types Monocytes Macrophages </li> <li> Slide 24 </li> <li> Slide 25 </li> <li> Leukocytes (= White Blood Cells = wbcs) Origination Same red bone marrow stem cells as rbcs (and platelets and lymphocytes) Granulocytes mature in marrow Lifetime hours to days Agranulocytes mature in blood Live about 2-3 months </li> <li> Slide 26 </li> <li> Leukocytes (= White Blood Cells = wbcs) Production incrs when Infection Presence of steroids Decrd reserve leukocyte pool in bone marrow </li> <li> Slide 27 </li> <li> Leukocytes (= White Blood Cells = wbcs) Abnormalities Leukocytosis = incrd # wbcs May be a normal response When?? OR may signify a disease state When?? Leukopenia = decrd # wbcs Always pathological </li> <li> Slide 28 </li> <li> Leukemias -- malignant disorders of blood cells Single cell may undergo transformation to dysfunctional cell, then proliferates to dysfunctional clones Not nec faster prolifn, but do displace normal cells Result: dysfunctl cells accumulate, compete w/ proliferation of normal blood cells within bone marrow Overcrowding of bone marrow decrd production of normal, functioning blood cells </li> <li> Slide 29 </li> <li> Leukemias -- contd Probably risk env. factors + genetic predisposition Risk factors Some disorders of bone marrow, other organs; can progress to acute leukemias Some viruses Ionizing radiation in large doses Drugs Genetic - sibling occurrence </li> <li> Slide 30 </li> <li> Leukemias -- contd Classified as acute/chronic; myeloid/lymphoid Acute leukemias Characteristics Abrupt onset Rapid progression Severe symptoms Histology: incrd # immature blood cells Survival rate </li> <li> Slide 31 </li> <li> Leukemias -- contd Acute leukemias contd Clinical Signs/symptoms related to bone marrow depression Fatigue Bleeding Fever Anorexia/weight loss Enlargement of liver/spleen </li> <li> Slide 32 </li> <li> Leukemias -- contd Acute leukemias contd Clinical contd Neurologic effects (headache, vomiting, facial palsy, blurred vision Early detection difficult Treatment Chemotherapy Immunotherapy Marrow transplants </li> <li> Slide 33 </li> <li> Leukemias -- contd Chronic leukemias Characteristics Predominant cell mature but abnormal function Gradual onset Relatively longer survival time Chronic lymphocytic one example B cells fail to mature to active plasma cells Igs not produced, plasma cell # decrd Most signification Incrd infections Incrd autoimmune response </li> <li> Slide 34 </li> <li> Chronic lymphocytic leukemia (CLL) Lymphocyte (small, mature-looking) Acute lymphocytic leukemia (ALL) Two lymphoblasts, one neutrophil </li> <li> Slide 35 </li> <li> Lymphomas Often in secondary lymph tissue Lymph nodes, spleen, tonsils, intestinal lymphatic tissue Not in blood-borne cells, so solid tumor Hodgkins - distinctive abnormal chromosomes Cause unknown. May be Genetic Transmissible agent Other (strange) risk factors include: tonsillectomy/appendectomy; wood working (?) </li> <li> Slide 36 </li> <li> Lymphomas contd Hodgkins contd Clinical Painless swelling or lump in neck Intermittent fever Weakness, weight loss Obstruction/pressure can lead to secondary involvement of Lung Spinal cord/neurons Skin </li> <li> Slide 37 </li> <li> Lymphomas contd Hodgkins contd Early detection difficult Treatment Chemotherapy Radiation Prognosis good with early treatment </li> <li> Slide 38 </li> <li> Lymphomas contd Non-Hodgkins Cause unknown See B-cell and T-cell abnormalities Clinical Lymph node enlargement (gradual, painless) Extra-nodal areas can be affected Treatment Bone marrow transplant Prognosis good if growth is restricted to lymph node </li> <li> Slide 39 </li> <li> Thrombocytes = Platelets Characteristics Prodd by fragmentation of megakaryocyte Life span ~ 3 days Many held in spleen Coagulation (= hemostasis): Converts fluid blood to a nonflowing gel Long protein threads (fibrin) formed, come together to form blood clot </li> <li> Slide 40 </li> <li> Slide 41 </li> <li> Thrombocytes contd Coagulation contd Many proteins/enzymes/factors nec for clotting cascade Platelets bind at site of clot then activated Nec biochem changes at clot site successful clot formed Disorders of platelets Thrombocytopenia Decrd # platelets, due to Decrd prodn platelets, seen w/ Tumors Drugs/toxins Other </li> <li> Slide 42 </li> <li> Thrombocytes contd Thrombocytopenia causes contd OR incrd clearance of platelets, seen with Splenomegaly Tumors Infections Immune disorders Clotting factor disorders Clotting factors cant work to make a successful clot May be Genetic Hemophilia VonWillebrands disease </li> <li> Slide 43 </li> <li> Thrombocytes contd Clotting factor disorders contd May be Acquired Liver disease (where some clotting factors prodd) Drugs/toxins Inappropriate clotting Body has anticlotting mechanism (also necessary) Keeps clots from being too large, blocking vessel Keeps unneeded clots from forming Important in vascular disorders </li> </ul>