Blood

Blood Artery White blood cells Platelets Red blood cells

Function Blood Deliver O2 Remove metabolic wastes Maintain temperature, pH, and fluid volume Protection from blood loss- platelets Prevent infection- antibodies and WBC Transport hormones

Blood Plasma-55% Buffy coat-<1% Formed elements-45%

Blood Plasma Components-55% 90% Water 8% Solutes: Proteins Albumin (60 %) Alpha and Beta Globulins Gamma Globulins fibrinogens Gas Electrolytes

Blood Plasma Components Organic Nutrients Carbohydrates Amino Acids Lipids Vitamins Hormones Metabolic waste CO2 Urea

Buffy Coat- <1% Leukocytes Platelets

Formed Elements of the Blood-45% Erythrocytes (red blood cells) Leukocytes (white blood cells) Platelets (thrombocytes)

Erythrocytes

Erythrocyte7.5m in dia ·   Anucleate- so can't reproduce; however, repro in red bone marrow ·   Hematopoiesis- production of RBC ·   Function- transport respiratory gases ·   Hemoglobin- quaternary structure, 2  chains and 2  chains ·   Lack mitochondria. Why? ·  1 RBC contains 280 million hemoglobin molecules ·   Men- 5 million cells/mm3 ·   Women- 4.5 million cells/mm3 ·   Life span 100-120 days and then destroyed in spleen (RBC graveyard)

Hemoglobin

Hematopoiesis Hematopoiesis (hemopoiesis): blood cell formation Occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur

Hematopoiesis Hemocytoblasts (hematopoietic stem cells) Give rise to all formed elements Hormones and growth factors push the cell toward a specific pathway of blood cell development New blood cells enter blood sinusoids

Erythropoiesis Erythropoiesis: red blood cell production A hemocytoblast is transformed into a proerythroblast Proerythroblasts develop into early erythroblasts

Erythropoiesis Phases in development Ribosome synthesis Hemoglobin accumulation Ejection of the nucleus and formation of reticulocytes Reticulocytes then become mature erythrocytes

Developmental pathway Stem cell Committed cell Developmental pathway Phase 1 Ribosome synthesis Phase 2 Hemoglobin accumulation Phase 3 Ejection of nucleus Proerythro- blast Early erythroblast Late erythroblast Reticulo- cyte Erythro- cyte Hemocytoblast Normoblast Figure 17.5

Regulation of Erythropoiesis Too few RBCs leads to tissue hypoxia Too many RBCs increases blood viscosity Balance between RBC production and destruction depends on Hormonal controls Adequate supplies of iron, amino acids, and B vitamins

Hormonal Control of Erythropoiesis Erythropoietin (EPO) Direct stimulus for erythropoiesis Released by the kidneys in response to hypoxia

Hormonal Control of Erythropoiesis Causes of hypoxia Hemorrhage or increased RBC destruction reduces RBC numbers Insufficient hemoglobin (e.g., iron deficiency) Reduced availability of O2 (e.g., high altitudes)

Hormonal Control of Erythropoiesis Effects of EPO More rapid maturation of committed bone marrow cells Increased circulating reticulocyte count in 1–2 days Testosterone also enhances EPO production, resulting in higher RBC counts in males

Formation & Destruction of RBCs

Blood Cell Production

RBC Diseases Anemia- when blood has low O2 carrying capacity; insufficient RBC or iron deficiency. Factors that can cause anemia- low iron, B12 deficiency

RBC Diseases Sickle-cell anemia- HbS results from a change in just one of the 287 amino acids in the  chain in the globin molecule. Found in 1 out of 400 African Americans. Homozygous for sickle-cell is deadly, but in malaria infested countries, the heterozygous condition is beneficial.

RBC Diseases Polycythemia- excess of erythrocytes,  viscosity of blood; 8-11 million cells/mm3 Usually caused by cancer; however, naturally occurs at high elevations Blood doping- in athletesremove blood 2 days before event and then replace it- banned by Olympics.

Types of Leukocytes (WBC) 4,000-11,000 cells/mm 3 Never let monkeys eat bananas Granulocytes Neutrophils- 40-70% Eosinophils- 1-4% Basophils- <1% Agranulocytes Monocytes- 4-8% Lymphocytes- 20-45%

Lymphocyte Eosinophil Basophil platelet Neutrophil Monocyte

ID WBC’s

White Blood Cells Protect body against microorganisms and remove dead cells and debris Movements Ameboid Diapedesis Chemotaxis Passive Immunity Active Immunity Antigen – Antibody

What do T- and B-cells do? T- and B-cells are highly specialized defender cells - different groups of cells are tailored to different germs. When your body is infected with a particular germ, only the T- and B-cells that recognize it will respond. These selected cells then quickly multiply, creating an army of identical cells to fight the infection. Special types of T- and B-cells 'remember' the invader, making you immune to a second attack. Above show T cells http://www.sciencemuseum.org.uk/whoami/findoutmore/yourbody/whatdoesyourimmunesystemdo/howdoesyourimmunesystemwork/whatdot-andb-cellsdo.aspx

Left shows T cells top and E-Coli below T- and B-cells recognize invaders by the shape of molecules - antigens - on their surfaces. Your immune system can produce a T- and B-cell to fit every possible shape. However, any T- or B-cell that recognized molecules found on your cells were destroyed while you were growing in the womb, to prevent them from attacking your own body. But you were left with millions of others, one for every foreign antigen you might ever encounter.

Left shows T cell (orange) attacking a cancer cell Having recognized the invader, different types of T-cell then have different jobs to do. Some send chemical instructions (cytokines) to the rest of the immune system. Your body can then produce the most effective weapons against the invaders, which may be bacteria, viruses or parasites. Other types of T-cells recognize and kill virus-infected cells directly. Some help B-cells to make antibodies, which circulate and bind to antigens. http://www.sciencemuseum.org.uk/whoami/findoutmore/yourbody/whatdoesyourimmunesystemdo/howdoesyourimmunesystemwork/whatdot-andb-cellsdo.aspx

Left shows the molecular structure of an antibody. With the help of T-cells, B-cells make special Y-shaped proteins called antibodies. Antibodies stick to antigens on the surface of germs, stopping them in their tracks, creating clumps that alert your body to the presence of intruders. Your body then starts to make toxic substances to fight them. Patrolling defender cells called phagocytes engulf and destroy antibody-covered intruders http://www.sciencemuseum.org.uk/whoami/findoutmore/yourbody/whatdoesyourimmunesystemdo/howdoesyourimmunesystemwork/whatdot-andb-cellsdo.aspx

Leukocyte Squeezing Through Capillary Wall Diapedesis Leukocyte Squeezing Through Capillary Wall WBCs Moving out of the blood stream

WBC Diseases Mononucleosis Leukopenia Leukemias Abnormally low WBC count—drug induced Leukemias Cancerous conditions involving WBCs Named according to the abnormal WBC clone involved Mononucleosis highly contagious viral disease caused by Epstein-Barr virus; excessive # of agranulocytes; fatigue, sore throat, recover in a few weeks

White Blood Cells Types Neutrophils: Most common; phagocytic cells destroy bacteria (60%) Eosinophils: Detoxify chemicals; reduce inflammation (4%) Basophils: Alergic reactions; Release histamine, heparin increase inflam. response (1%) Lymphocytes: Immunity 2 types; b & t Cell types. IgG-infection, IgM-microbes, IgA-Resp & GI, IgE- Alergy, IgD-immune response Monocytes: Become macrophages

Platelets Small fragments of megakaryocytes Formation is regulated by thrombopoietin Blue-staining outer region, purple granules Granules contain serotonin, Ca2+, enzymes, ADP, and platelet-derived growth factor (PDGF)

Developmental pathway Stem cell Developmental pathway Hemocyto- blast Promegakaryocyte Megakaryoblast Megakaryocyte Platelets Figure 17.12

Hemostasis- stoppage of bleeding Platelets: 250,000-500,000 cells/mm3 Tissue Damage Clotting Factors Platelet Plug

Hemostasis: Vessel injury 2. Vascular spasm 3. Platelet plug formation 4. Coagulation

Hemostasis (+ feedback) Clotting Factors thromboplastin Prothrombin Thrombin Fibrinogen Fibrin Traps RBC & platelets Platelets release thromboplastin

Blood Clot RBC Does this look like spider webs? Platelet Fibrin thread

Disorders of Hemostasis Thromboembolytic disorders: undesirable clot formation Bleeding disorders: abnormalities that prevent normal clot formation

Thromboembolytic Conditions Thrombus: clot that develops and persists in an unbroken blood vessel May block circulation, leading to tissue death Embolus: a thrombus freely floating in the blood stream Pulmonary emboli impair the ability of the body to obtain oxygen Cerebral emboli can cause strokes

Thromboembolic Conditions Prevented by Aspirin Antiprostaglandin that inhibits thromboxane A2 Heparin Anticoagulant used clinically for pre- and postoperative cardiac care Warfarin Used for those prone to atrial fibrillation

Bleeding Disorders Thrombocytosis- too many platelets due to inflammation, infection or cancer Thrombocytopenia- too few platelets causes spontaneous bleeding due to suppression or destruction of bone marrow (e.g., malignancy, radiation) Platelet count <50,000/mm3 is diagnostic Treated with transfusion of concentrated platelets  

Impaired liver function Bleeding Disorders Impaired liver function Inability to synthesize procoagulants Causes include vitamin K deficiency, hepatitis, and cirrhosis Liver disease can also prevent the liver from producing bile, impairing fat and vitamin K absorption

Bleeding Disorders Hemophilias include several similar hereditary bleeding disorders Symptoms include prolonged bleeding, especially into joint cavities Treated with plasma transfusions and injection of missing factors

Hemophiliac- a sex-linked recessive trait, primarily carried by males (x chromosome)

Blood Types Type A Type B Type AB Type O

Blood Typing Blood type is based on the presence of 2 major antigens in RBC membranes-- A and B Blood type Antigen Antibody A A anti-B B B anti-A A & B AB no anti body Neither A or B O anti-A and anti-B Antigen- protein on the surface of a RBC membrane Antibody- proteins made by lymphocytes in plasma which are made in response to the presence of antigens. They attack foreign antigens, which result in clumping (agglutination)

Type A b b b b b b b

Type B a a a a a a a

Type O a b a a a b b a a b

Type AB

Rh Factor and Pregnancy                                                                                                               RH+ indicates protein RH+ indicates protein RH- indicates no protein

Rh Factor and Pregnancy Rh+ mother w/Rh- baby– no problem Rh- mother w/Rh+ baby– problem Rh- mother w/Rh- father– no problem Rh- mother w/Rh- baby-- no problem RhoGAM used @ 28 weeks

Type AB- universal recipients Type O- universal donor Rh factor:   Rh factor: Rh+ 85% dominant in pop Rh- 15% recessive Blood Type Clumping Antibody A antigen A anti-A serum antibody anti-b B antigen B anti-B serum antibody anti-a AB antigen A & B anti A & B serum - O neither A or B no clumping w/ either anti A or B anti-a, anti-b

agglutinates with both sera) Blood being tested Serum Anti-A Anti-B Type AB (contains agglutinogens A and B; agglutinates with both sera) RBCs Type A (contains agglutinogen A; agglutinates with anti-A) Type B (contains agglutinogen B; agglutinates with anti-B) Type O (contains no agglutinogens; does not agglutinate with either serum) Figure 17.16

Blood Type & Rh How Many Have It Frequency O Rh Positive 1 person in 3 37.4% Rh Negative 1 person in 15 6.6% A 35.7% 1 person in 16 6.3% B 1 person in 12 8.5% 1 person in 67 1.5% AB 1 person in 29 3.4% 1 person in 167 .6%

ABO Blood Types Phenotype Genotype O i i A I A I A or I A i B I B I B or I B i AB I A I B

Punnett square Type A and Type B cross IB i IA IAIB IAi IA IAIB IAi