Chapter 17 blood - Lecture notes ch 17 PDF

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Chapter 17 blood Blood Composition • Blood is the only fluid tissue in body • Type of connective tissue composed of two things 1. Plasma (fluid component = nonliving extracellular matrix) 2. Formed elements (living cells suspended in the plasma) − Erythrocytes (red blood cells, or RBCs) − Leukocytes (white blood cells, or WBCs) − Platelets

Blood Composition Spun tube of blood yields three layers: • Plasma on top (~55%) • Buffy coat (< 1%) - WBCs and platelets in thin, whitish layer between RBCs and plasma layers • Erythrocytes on bottom (~45% of whole blood) • Hematocrit: percent of blood volume that is RBCs • Normal values: • Males: 47% ± 5% Females: 42% ± 5%

Physical Characteristics and Volume • Sticky, opaque fluid − 5x viscosity of water • Color: scarlet to dark red depending on O2 content • pH 7.35–7.45 • 38C - slightly warmer than core body temp • ~8% of body weight • Average volume: 5–6 L for males, and 4–5 L for females

Functions of Blood 1. Transport of • O2 and nutrients to body cells • Metabolic wastes to the lungs and kidneys for elimination • Hormones from endocrine organs to target organs 2. Regulation of • Body temperature by absorbing and distributing heat • Normal pH using buffers • Adequate fluid volume in the circulatory system Functions of Blood 3. Protection against • Blood loss − Plasma clotting proteins and platelets initiate clot formation • Infection − Antibodies in plasma − Complement proteins WBCs defend against foreign invaders

Blood Plasma Composition • Blood plasma is straw-colored sticky fluid − About 90% water • Over 100 dissolved solutes - Proteins are most abundant solutes by weight − 3 classes of proteins (most are produced by the liver) 1. Albumin (60% of total) – responsible for capillary colloid osmotic pressure 2. Globulins (36% of total) • Antibodies are a type of globulin, but are not produced by liver Fibrinogen (4% of total) – clotting protein

Other Blood Plasma Solutes

• Organic − Nitrogenous waste products of metabolism • uric acid, urea, creatinine − Nutrients − glucose, carbohydrates, amino acids − Hormones • Inorganic − Electrolytes − Na+, K+, Ca2+, Cl–, HCO3– • Most abundant solutes by number − Respiratory gases − O2 and CO2

Formed Elements – Overview • Only WBCs are complete cells • RBCs have no nuclei or organelles • Platelets are cell fragments (no nuclei) • Most formed elements survive in the bloodstream for only a few days • Most blood cells originate in bone marrow and do not divide after entering blood Erythrocytes • 90% of cells in blood – about 1/3 of total cells in the body • Biconcave discs, anucleate, essentially no organelles • Filled with hemoglobin (Hb) for gas transport • Contain the cytoskeletal protein, spectrin, and other proteins • Provide flexibility to change shape as necessary • Are the major factor contributing to blood viscosity

Erythrocytes • Structural characteristics contribute to gas transport

− Biconcave shape—huge surface area relative to volume allows rapid diffusion of respiratory gases into and out of cell − >97% hemoglobin (not counting water) − No mitochondriaATP production is anaerobic; no O2 is used to make ATP • A superb example of complementarity of structure and function! Erythrocyte Function • RBCs are dedicated to respiratory gas transport • Hemoglobin (Hb) binds reversibly with oxygen • Hemoglobin structure − Tetramer of globin protein: two alpha and two beta chains − Heme pigment bonded to each globin chain − One iron atom in each heme can bind one O2 molecule − Each Hb molecule can therefore transport four O2

Hemoglobin (Hb)

• O2 loading in the lungs − Produces oxyhemoglobin (ruby red) • O2 unloading in the tissues − Produces deoxyhemoglobin or reduced hemoglobin (dark red) • CO2 loading in the tissues − Produces carbaminohemoglobin (carries 20% of CO2 in the blood)

Hematopoiesis • Hematopoiesis (hemopoiesis): blood cell formation − Occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur − Hematopoietic stem cell (hemocytoblast) gives 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 to leave marrow

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  erythropoietin • Direct stimulus for erythropoiesis • Released by the kidneys in response to hypoxia (low oxygen levels in blood) • Target tissue is red bone marrow • Adequate supplies of iron, amino acids, and B vitamins

Fate and Destruction of Erythrocytes

• Life span: 100–120 days • Old RBCs become fragile, and Hb begins to degenerate • Macrophages in spleen and liver engulf dying RBCs

Fate and Destruction of Erythrocytes (cont.) Inside macrophages, heme and globin are separated • Globin is broken down into amino acids • Iron from heme is salvaged for reuse - stored in spleen bound to specific iron binding proteins (hemosiderin and ferritin) • The rest of the heme molecule is degraded to the orange-yellow pigment, bilirubin. • Bilirubin binds to albumin in blood and is transported to liver • Liver secretes bilirubin (in bile) into small intestine • Degraded pigment leaves the body in feces as stercobilin (gives feces its brown color)

Erythrocyte Disorders • Anemia: blood has abnormally low O2-carrying capacity − Like fever, anemia is a symptom rather than a disease itself − Blood O2 levels cannot support normal metabolism − Accompanied by fatigue, paleness, shortness of breath, and chills − Three primary causes: 1. decreased hemoglobin 2. decreased hematocrit 3. abnormal hemoglobin

Causes of Anemia . Decreased hemoglobin • Iron deficiency anemia - most common form of anemia − Caused by inadequate dietary iron intake or reduced intestinal absorption of iron − Without functional heme groups, developing RBCs are unable to synthesize hemoglobin

Causes of Anemia . Decreased hematocrit – results from reduced number of erythrocytes in blood • Hemorrhagic anemia – caused by blood loss − Acute injury or bleeding stomach ulcer can lead to a significant loss of circulating erythrocytes • Pernicious anemia – most common type of B12-deficiency anemia − Caused by autoimmune disease that destroys certain cells that line the stomach (synthesize intrinsic factor) − Intrinsic factor needed for absorption of B12 by intestines

− Lack of B12 interferes with DNA synthesis of rapidly dividing cells, including hematopoietic cells in bone marrow

Causes of Anemia Decreased hematocrit (continued) • Hemolytic anemia: RBCs rupture prematurely − Multiple causes: • transfusion reactions from mismatched blood • bacterial infections

Causes of Anemia

. Abnormal hemoglobin – most common example of abnormal hemoglobin is sickle-cell disease (SCD) • Caused by mutation in hemoglobin gene • Mutant hemoglobin protein forms abnormal clumps when O2 levels are low, resulting in change in shape of erythrocyte • In United States, occurs most often in black people of African descent

Erythrocyte Disorders • Polycythemia: excess of RBCs that increase blood viscosity • Results from: • Polycythemia vera—bone marrow cancer • Secondary polycythemia—when less O2 is available (high altitude) or when erythropoietin production increases Blood doping Leukocytes • Make up 30 types of glycoprotein antigens that are − Perceived as foreign if transfused blood is mismatched − Unique to each individual − Called agglutinogens because they promote agglutination (clumping of RBCs) • Presence or absence of each antigen is used to classify blood cells into different groups • The most vigorous transfusion reactions are caused by ABO and Rh blood group antigens

ABO Blood Groups • Based on the presence or absence of two antigens on surface of RBCs − Presence of A antigen = type A blood − Presence of B antigen = type B blood − The presence of both antigens A and B is called type AB blood

− The lack of these antigens is called type O ABO Blood Groups • Anti-A or anti-B antibodies form spontaneously in the blood at about 2 months of age − No previous exposure to antigen − Because these antibodies promote agglutination, they are called agglutinins • Blood type AB can receive A, B, AB, and O blood − Universal recipient • Blood type A can receive A and O blood • Blood type B can receive B and O blood • Blood type O can receive O blood Universal donor Rh Blood Groups • Named because of the presence or absence of one of eight Rh antigens originally discovered in Rhesus monkeys • D antigen is most important clinically • 85% of Americans are Rh+(Rh positive) • Problems can occur in mixing Rh+ blood into a body with Rh – (Rh negative) blood

Rh Dangers During Pregnancy • Danger occurs only when the mother is Rh – and the father is Rh+, and child inherits Rh+ factor from father

Rh Dangers During Pregnancy Mismatch of an Rh – mother carrying an Rh+ baby can cause problems for the unborn child • First pregnancy usually proceeds without problems • Mother’s immune system is sensitized after the first pregnancy (mother is exposed to baby’s blood during birth when placenta detaches from uterus) • In a second pregnancy, mother’s immune system produces antibodies that attack Rh + blood of fetus (hemolytic disease of newborn)

• RhoGAM injection during first pregnancy can prevent buildup of anti-Rh+ antibodies in mother’s blood  agglutination of Rh factor by injected antibody blocks mother’s immune response

Blood Typing • Blood samples are mixed with anti-A and anti-B serum • Blood type is determined by observing whether the blood sample clumps or not − Clumping = agglutination • Typing for ABO and Rh factors is done in the same manner • Cross matching—tests for agglutination of donor RBCs by mixing whole blood with the recipient’s serum, and vice versa Developmental Aspects of Blood • Sites of blood cell formation − The fetal liver and spleen are early sites of blood cell formation − Bone marrow takes over hematopoiesis by the seventh month • Fetal hemoglobin differs from hemoglobin produced after birth • Physiologic jaundice occurs in infants whose liver cannot rid the body of fetal hemoglobin breakdown products fast enough...