Blood Can move. tentacles. 1. TYPES. Eosinophils (used. to be called

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1 Shuster s A&P Notes Series Blood 11 2) LEUKOCYTES (WBCs; leuko = white ). - Completee cells w/ nucleus, organelles. - < 1% of volume. - Involved in defense. Several types with different roles in immunity. - Can move out of capillaries into interstitial space using process called DIAPEDESIS ( leaping across ); inflammation & immune function. * Once in tissue, move tissue using AMOEBIC MOTION - extend cytoplasm like an octopus s tentacles. * CHEMOTAXIS: leave a trail of chemicals, attracting other WBCs to the site. This allows them to gather at a problem site. 1. TYPES - Several types, lumped into 2 main categories based on whether or not they appear grainy under the microscope. 2 Main categories: (i) GRANULOCYTE - Spherical, larger than RBCS, lobed nuclei, cytoplasmic granules, phagocytotic. - 3 kinds, named on how they react to different ph solutions: Neutrophils: prefer neutral environments Eosinophils (used to be called acidophils) : prefer acidic environments Basophil: prefer basic environments Related Clinical Terms - the condition of having more than we expect of one of these cells in a blood sample: Neutrophilia, Basophilia, and Eosinophilia

2 Shuster s A&P2 Note Series Blood 12 (a) NEUTROPHILS - > 1/2 (60-70%)) of all WBCs * Fine granules, 3-6 lobes per nucleus, ~ 2X size of RBC. * Granules contain hydrolytic enzymes = LYSOSOMES. * Chemically attracted to inflammation site= ACTIVE PHAGOCYTES. Especially attracted to bacterial & fungal infection - ingest & destroy. ** Respiratory Burst or Oxidative Burst - the rapid release of f reactive oxygen-containing compounds (superoxide radical and hydrogen peroxide) with bleach-like effects. Neutrophils releasee them as they come into contact with different bacteria or fungi. Chronic granulomatous disease (CGD): Several genetic mutation,, the person cannot make the oxygen compounds. Lots of infections as kids, pneumonia. (b) EOSINOPHILS * Only 1-4% of all WBCs. * 2 lobed nucleus (looks like an old-time phone receiver). Bluish in color. Also have granules w/ lysosomes. * However, less effective w/ bacteria; more effective against PARASITIC WORMS. Dump lysosome on outer surface. * Also, releasee chemicals that inactivate inflammationn chemicals = lessen allergic responses. ** Lots in blood of people undergoing allergic response = EOSINOPHILIA. (c) BASOPHILS - < 1 % of WBCs. Same size, little smaller. * Large granules; large, purple, obvious. U- or S- shaped nucleus.. * Granules contain several important chemicals for thee immune response, including these 2: HISTAMINE = inflammatory chemical (A VASODILATOR) = dilates blood vessels, theyy become more leaky, therefore, get more water in tissues. * MAST CELLS similar cell as basophil, by in tissues, not blood vessels. **ANTIHISTAMINE - any chemical that lessens the ability of histamine to function.

3 Shuster s A&P Notes Series Blood 13 HEPARIN an anticoagulant (see later section on Coagulation). (ii) AGRANULOCYTES - without grains - no visible granules. - 2 Types of agranulocytes: * * * * 25-33% of WBCs Large, dark purple nucleus that takes up most of cell s volume. Most often found in lymph tissue. Act against viruses and tumors. * 2 types of lymphocytes: (a) LYMPHOCYTES - 2nd most numerous cell. Lymph cells. 1. T-Lymphocytes -made in thyroid. Several different types, with different roles. More detail in i Immunity chapter. 2. B-Lymphocytes (Plasma cells) - made in bone; produce antibodies (see Blood Types section at the end of this chapter, and Immunity chapter). (b) MONOCYTES -largest; 2X size off RBC. U-shaped nuclei. * Active phagocytosis with CHRONIC infections (tuberculosis, etc.) & crucial in defense against bacteria. CHRONIC long-term An infection that will last more than 3 months under treatment (rule of thumb). ACUTE - short-term. An infection lasting less than 3 months under treatment. Enter tissue, become MACROPHAGES. * 3-8% of all WBCs Obli at en.wikipedia [CC-BY- SA-2.0 ( /licenses/by-sa/2.0)], from Wikimedia Commons

4 Shuster s A&P2 Note Series Blood PRODUCTION OF LEUKOCYTES - LEUKOPOIESIS. Very complicated. Involves, in some cases, cloning. More detail in Immunity chapter. - COLONY STIMULATING FACTORS (CSFs) - Several hormones that causes the stem cell (hemocytoblast) to turn into one of the WBC. *released to specific chemical signals. Complex set of pathways. - currently, injecting CSFs into cancer patients to stimulate the bone marrow of people s whose immune system has been lowered due to chemotherapy. - Pluripotent cell can become (we will not be covering all possible pathways or precursors): (i) Myeloblast, which becomes all of the granulocytes and the monocytes (eventually). (ii) Monoblast, which becomes a monocyte. (iii) Lymphoblast, which becomes any one of the lymphocytes. - Why this emphasis? proliferating. Because we name leukemias (see next section) based on which cell is

5 Shuster s A&P Notes Series Blood DISORDERS (i) LEUKOPENIA - low WBC count; often duee to drugs & anticancer agents. (ii)leukemias - ( white blood ) * Group of cancerous conditions * Cloning of a single cell into a large # of mitotic cells, which suppresses bone marrow function. Mitotic cells crowd out other cells inn marrow. Immune system is compromised; open to infections ( pneumonia, etc.). * Acute (fast advancing; childhood)) vs chronic (slow advancing): In chronic leukemia, the leukemia cells come from mature, abnormal cells. The cells thrive for too long and accumulate. The cells grow slowly. Acute leukemia, on the other hand, develop from early cells, called "blasts". - No need to know all the different types; I am just showing you how the nomenclature works: Four major kinds of leukemia Cell type Acute Lymphocytic leukemia (or "lymphoblastic") Acute lymphoblastic leukemia (ALL) Myelogenous leukemia Acute myelogenous leukemia (also "myeloid" or (AML) "nonlymphocytic") (or myeloblastic) Chronic Chronic lymphocytic leukemia (CLL) Chronic myelogenous leukemia (CML) *Among others! Monoblastic leukemia exists, but is rarer. (iii) INFECTIOUS MONONUCLE EOSIS - viral in origin * The virus infects and causes the appearance of many B-lymphocytes. * Tired, achy, no cure; ~ 4-5 weeks to run course 3) PLATELETS (THROMBOCYTES) - not cells, but fragments. - Have granules; contain several clotting chemicals (SEROTONIN, ADP, Ca++, etc.). See section on Hemostasis. -Literally just sacs of chemicals. Not living, so can t maintain themselves. Annucleate; age quickly. 1. Production - THROMBOPOIETIN - hormone that controls platelet production. - Precursor cell = MEGAKARYOCYTE.

6 Shuster s A&P2 Note Series Blood Function: HEMOSTASIS - stoppage of bleeding. SEE NEXT PAGE FOR REVIEW IMAGE - RECALL: the lining of the vessel is squamosal epithelial called endothelium. If it is broken or damaged, there is a series of reactions leading to a positive feedback loop: (i) VASCULAR SPASMS - constrict vessel. Smooth muscle around vessel contracts due to chemical released by damage to endothelium. (ii) PLATELETT PLUG FORMATION 1. Ruptured collagen fibers are exposed on damagedd endothelium. 2. Thrombocytes swell, become sticky, and attach to exposed fibers 3. DEGRANULATION occurs; several chemicals are released, including: (i) SEROTONIN N - increases vascular spasms. (ii) ADP - attractt others to thee spot Positive Feedback Loop (iii) Also releasee the Procoagulants ( iii) COAGULATION - change blood from a liquid to a gel throughh a series of steps we will call the CASCADE. The end result is the formation of fibrin threads, forming a clot, and continuing the positive feedback loop. STEP 1: an overview of the CASCADE: Liver makes prothrombin and fibrinogen, whichh are circulated in the blood stream Positive Feedback Loop

7 Shuster s A&P Notes Series Blood 17 RBCs Platelets Thrombus: a clot forms on the wall of a healthy vessel (a vessel without a break). Can stop/lower blood flow, killing tissue. Embolism: A thrombus that breaks off, floating around the bloodstream. It may get caught in a small vessel and stop blood flow, causing tissue death. See the Blood Vessel chapter for more details! Interesting Note: Aspirin is a blood thinner (i.e., it lowers the amount of coagulation that occur) becausee it lowers the stickiness of the platelets. It is VERY effective in lowering the risk of a heart attack! * STEP 2: a closer look at the procoagulants and thee NTRINSIC & EXTRINSIC PATHWAYS of Coagulation SEE IMAGE NEXT PAGE What the student needs to know: - There are 2 pathways to coagulation: 1. One is faster, but makes less thrombin (and therefore fibrin). This is the Extrinsic pathway, so- pathway, so-called becausee is started by platelets within the blood called becausee it begun by near-by damaged tissues.. 2. The other is slower, but makes a LOT of thrombin, and thereforee fibrin. This is the Intrinsic itself.

8 Shuster s A&P2 Note Series Blood Both pathways lead into the Common pathway, as they both form Factor X ( 10 ). In the common pathway, Prothrombin Activator catalyzes the formation of Thrombin, which in turn catalyzes the formation of fibrin, coagulating the blood. - The Extrinsic pathway starts as nearby tissuess release clotting factors, which combine to form Factor X. - The Intrinsic pathway starss as the platelets degranulate. Clotting factors are included, called procoagulants. 4. All 3 pathways need Ca+ ++. This is why we see bleeding problems if there is a problem with Ca+ ++ homeostasis. Also, some of the clotting factors need vitamin K (not shown here), which is made by the friendly bacteria living inside your gut. 5. Also, the common pathway needs one of the platelet factors (PF3). This is an antigen important in transfusion reactions (the rejection of tissues from the body; see the section called Blood Types ) ). - Factors limiting clotting: ANTICOAGULANTS - anything thatt lowers/stopss this process. Otherwise, your blood would clot in vessels as a response to an increase in friction of the walls over years, causing the formation of thrombi & emboli. * Basophils, mast cells make HEPARIN. - Clot retraction: platelets trapped in the fibrin mesh release chemicals that break down fibrin (fibrinolysis) and dissolve the clot. This takes a number of days. * Failure to retract might indicate thrombocytopenia (low # platelets; see Disorders section next).

9 Shuster s A&P Notes Series Blood DISORDERS (i) THROMBOCYTOPENIA - deficiency leading to spontaneous bleeding - Symptom: PETECHIAE purple patches (bleeding) from normal movements. - Some causes: * Bone marrow malignancy, radiation, some drugs. * Impaired liver function - lowers supply of procoagulants. * Vitamin K deficiency after systemic antibiotic treatment. Kills the good bacteria. * Ca++ deficiency. (ii) HEMOPHILIA - Genetic defect can t make one of the procoagulants, sex-linked (on the X chromosome, so males have it more often). * Treatment = transfusions. 4. TRANSFUSIONS - Loss of 15% blood volume leads to weakness; loss of > 30% leads to shock, possible death. - WHOLE BLOOD TRANSFUSION: with either a great loss of blood or thrombocytopenia. - PACKED RED BLOOD CELL: plasma is removed; treat any of the anemias. *mixed w/ anticoagulants.