Anatomy and Physiology II- week of notes
Anatomy and Physiology II- week of notes Biol 2230-001
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This 12 page Class Notes was uploaded by Madeline Notetaker on Thursday February 4, 2016. The Class Notes belongs to Biol 2230-001 at Clemson University taught by Dr. John Cummings in Spring 2016. Since its upload, it has received 21 views. For similar materials see Human Anatomy & Physiology II in Biological Sciences at Clemson University.
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Date Created: 02/04/16
Blood Blood is only liquid tissue in body Is connective tissue- has cells embedded in matrix Is contained within blood vessels Have about 5 liters in body (5000 mL) Temp of blood is about 100 degrees F is a mechanism for regulating body temperature 8% of body weight is blood pH needs to be between 7.35-7.45 Functions Delivers oxygen And nutrients, and sugar Transports metabolic wastes Ex: carbon dioxide, nitrogenous wastes Transports hormones Chemical messengers to affect every cell with receptors Maintains body temperature Maintains body pH Narrow range (slightly basic), if outside range you get health issues Blood has buffers Maintains fluid volume of body Fluid exchange between blood and tissues Prevents blood loss With clotting factors to seal Prevents infection Part of immune system; has antibodies Components Formed Elements (within the liquid portion) Erythrocytes Red blood cells Function to carry respiratory gases 45% of total blood volume Not really living cells (lost nucleus, organelles) All are produced in bone marrow No longer divide when outside bone marrow Leukocytes White blood cells True cells with nuclei, can reproduce Function as part of immune cells Less than 1% blood volume Platelets Fragments of other cells that have pinched off Can have vesicles that contain proteins Involved in blood clotting Less than 1% blood volume Plasma 55% blood volume Liquid portion Plasma is mostly water (90%) Has lots of proteins Albumin Clotting proteins Enzymes Hormones Nitrogenous wastes Electrolytes (charged ions) Respiratory gases Erythrocytes (RBCs) Approx. 5 million per mL of blood Men have higher amount than women on average Small Biconcave Anucleate NO nucleus or organelles! Contain hemoglobin Carries oxygen Contain antioxidant enzymes Eliminate free radicals that become toxic Hemoglobin Globin protein bound to heme pigment Heme pigment: makes our blood red 2 alphas, 2 betas each with heme in middle Each hemoglobin binds to 4 molecules of oxygen Approx. 250 million hemoglobin molecules in a single RBC Each RBC can carry a billion oxygen molecules Globin Complex with 4 subunits: 4 polypetide chains 2 alphas 2 betas Each globin attaches to one heme Heme Contains oxygen binding iron Iron loves to bind to oxygen Hemoglobin Oxi- vs. Deoxyhemoglobin Oxygen dissociation curve S-shaped, NOT linear As Deoxyhemoglobin starts to pick up oxygen, it changes affinity of hemoglobin to oxygen Oxygen binds to hemoglobin called oxyhemoglobin Hemoglobin without oxygen is called Deoxyhemoglobin Carbaminohemoglobin Globin part binds to carbon dioxide Thus, hemoglobin can transport CO2 But only 20% of carbon dioxide is transported as Carbaminohemoglobin Most transported in plasma as bicarbonate Erythropoiesis= production of RBCs Produce about an ounce a day, which contain about 100 billion cells Type of cells depend on type needed (ex: exercising, sick, have cold) All hematopoiesis occurs in bone marrow Takes about 3-5 days to complete 1. Hemocytoblast (pluripotent cell=can give rise to many things) produces myeloid stem cell (also pluripotent) 2. Myeloid stem cell becomes proerythroblast (can only become RBC) 3. Proerythroblast becomes early erythroblast 4. Early erythroblast becomes late erythroblast 5. Late erythroblast becomes normoblast 6. Normoblast loses organelles and nucleus and accumulates hemoglobin to become reticulocyte 7. Reticulocytes leave bone marrow and mature in bloodstream to become erythrocytes Regulation of Erythropoiesis Erythropoietin protein produced in kidneys that regulates RBC production Kidneys asses level of oxygen in the blood; if low, make more RBC Testosterone Stimulate kidneys to release erythropoiesis This is why men have more RBC than women because they have more testosterone Iron Need iron to make heme Get iron in diet and stored in cells as ferritin and hemosiderin Transported in blood as transferrin We recycle iron B vitamins Specifically B12 and folic acid Dietary nutrients Need enough to make cells in general Proteins, lipids, carbohydrates Erythrocyte Longevity Last somewhere between 100-120 days Old erythrocytes destroyed by macrophages (phagocytes) Heme is split from globin Iron bound to proteins and stored (as ferritin and hemosiderin) Bilirubin is produced Picked up by liver, and secreted as bile into intestine Bile stored in gallbladder Pigment degraded and expelled in feces Globin broken down to amino acids Erythrocyte Disorders Anemias Any time our blood has a low oxygen carrying ability Can be insufficient number of RBC Can be irregularly shaped RBC Ex: sickle cell anemia Polycythemia Too many RBCs Circulation is compromised, cant move as well Diapedesis =The ability for our blood cell to leave blood vessel Passes out of circulation RBC cant, some WBC can do this Leukocytes White blood cells Complete cells with nuclei and organelles Display positive chemotaxis Can be attracted to an area due to release of chemical 4800-10800 per mL of blood 2 categories: 1. Granulocytes= with granules Neutrophils- most common, lobed nucleus, phagocytic cells that function during inflammatory response Eosinophils- 2 lobed nucleus, 2-4% WBC, contain enzymes in granules that will digest parasitic worms Basophils- rarest, have histamine in granules that dilates blood vessels and attracts more blood to are 2. Agranulocytes= without granules Lymphocytes-most of cell made up of nucleus, major immune cells, B & T lymphocytes, 25% WBC volume Monocytes- 3-8%, largest WBC, big U-shaped nucleus, phagocytic cells, can leave circulation and then called macrophage Leukopoiesis= formation of WBC Hemocytoblasts give rise to myeloid stem cells and lymphoid stem cells Granulocyte Leukopoiesis 1. Myeloid stem cells become myeloblasts(committed cell, can only become granulocyte) 2. Myeloblasts accumulate lysosomes (granules) to become promyelocytes 3. Promyelocytes differentiate into myelocytes 4. Cell division stops and nuclei arch to form band cells 5. Nuclei constrict and segment to become mature granulocytes Agranulocyte Leukopoiesis 1. Myeloid stem cells become monoblasts (committed cell) 2. Monoblasts become promonocytes 3. Promonocytes leave bone marrow and become monocytes in lymph tissues Agranulocyte Leukopoiesis of lymphocytes 1.Lymphoid stem cells become lymphoblasts (committed cell) 2. Lymphoblasts become prolymphocytes 3. Prolymphocytes leave bone marrow and become lymphocytes in lymph tissue Regulation of Leukopoiesis 2 chemical messenger controllers: Interleukins Colony-stimulating factors The accumulation of either one stimulates leukopoiesis in bone marrow Leukocyte Disorders Leukemia Cancer of the WBCs Abnormal division Infectious mononucleosis Response to infection of virus (Epstein Barr virus) Causes increase in production of Agranulocytes Leukopenia Deficiency in number of WBCs Blood- day 2 Platelets Anucleated cytoplasmic fragments of megakaryocytes Chucks of cytoplasm that pinches off Granules contain clotting chemicals *because the role of platelets is to cause clots (VERY COMPLEX) Thrombopoiesis= formation of platelets (aka thrombocytes) Hemocytoblasts give rise to myeloid stem cells Myeloid stems cells become megakaryoblasts Megakaryoblasts undergo repeated mitosis but no cytokinesis to form megakaryocytes Cytoplasmic extensions of megakaryocyes break off to be platelets Regulation of Thrombopoiesis Thrombopoietin Regulatory chemical Something has to communicate to bone marrow Hemostasis= process of preventing loss of blood 3 major steps: Vascular spasm Constriction of damaged blood vessel Slow down passage of blood because smaller diameter Platelet plug formation Platelets will collect at site of damage Chemical signal causes them to stay there Coagulation “gels up” Stimulates repair of blood vessel Platelet Plug Formation Damage to blood vessel exposes underlying collagen fibers (connective tissue) to blood *healthy blood vessels don’t accumulate platelets Also releases von Willebrand factor (plasma protein) and thromboxane A (prostaglandin) 2 Accumulate von Willebrand factor from blood and thromboxane A re2eased from damaged blood vessels Causes platelets to collect and adhere at site of damage Platelets will not stick unless Willebrand factor and and thromboxane A are 2 present They stick to collagen fibers Once attached, thrombin activates platelets to breakdown and release chemical contents (clotting factors) Limitations to Platelet Plug What limits platelets? Intact (undamaged) endothelial cells secrete PGI (prostacyclin) and heparin 2 PGI 2revents platelets from sticking Heparin is also secreted by healthy cells and also prevents platelet attachment Vitamin E quinone Intrinsic Pathway to Coagulation (simplified version) Series of reactions in which clotting factors converted from inactive to active forms Ultimately aggregated platelets release PF 3 PF activates other intermediates leading to activation of factor X 3 Activated factor X combines with calcium, PF 3nd factor V to form prothrombin activator Which activates prothrombin Prothrombin activator catalyzes conversion of prothrombin to thrombin Thrombin catalyzes polymerization of fibrinogen into fibrin Thrombin also activates factor XIII which links fibrin strands together Makes mesh Extrinsic Pathway to Coagulation (shortcut; skips intermediate steps) Injured cells release tissue factor Tissue factor interacts with P3 (from platelets) to allow shortcut to factor X activation Clot Retraction We don’t need clot anymore but it needs to be broken down slowly: Platelets contain contractile proteins Cause platelets to contract and squeeze out serum to compact clot Clot hardens and becomes more dense This draws ruptured edges of vessel closer together Facilities repair PDGF stimulates vessel repair As platelets start to break down, release Platelet Derived Growth Factor Neighboring cells start dividing Fibrinolysis= breakdown of fibrin Have to break down the fibrin that’s holding everything together! Then debris can be phagocytized Clot produces plasminogen (inactive) New endothelial cells produce tissue plasminogen activator (or TPA) Plasminogen is activated to plasmin Plasmin digests fibrin So clot gets digests Clot Limiting Factors Clotting factors carried away from site by circulating blood Antithrombin III inactivates thrombin Slows down clotting process Protein C inhibits intrinsic pathway events Interrupts some intermediate steps in activating factor X Heparin enhances activity of antithrombin III and inhibits intrinsic pathway events Keep clot from getting too big Hemostasis Disorders Thromboembolytic disorders: excessive blood clot Thrombus Forms in otherwise healthy blood vessels Stationary; blocks flow of blood Embolism A moving blood clot Ultimately finds area it cant pass through, and Bleeding disorders: don’t get enough blood clotting Thrombocytopenia Insufficient amount of platelets in body Perhaps due to infection Hemophilia Genetic disorder in which they cant produce any one of the 13 clotting factors Human Blood Typing Determined by presence of agglutinogens Markers on the surface of red blood cells Use 3 marker system: Specifically ABO and Rh (D) A: blood type A B: type B Both: AB Neither: O Rh (D): + Markers directs production of agglutinins If you have A agglutinogen, produce anti-B agglutinin Will attack B agglutinogen markers *O Negative is universal blood donor- can give blood to anyone *AB positive is universal recipient (don’t produce any agglutinin) Hemolytic disease of the newborn or eythroblastosis fetalis If women is RH negative, and baby is RH positive, first baby is fine, but second baby is not Accumulation of anti RH as soon as its born its blood coagulates Give shot of RhoGAM which prevents production of RH agglutinin The Heart Heart Orientation Mediastinum Cavity that heart is in Base of heart is actually on top Apex is actually on bottom Coverings Heart is covered by pericardium with 2 layers: Fibrous pericardium Made of dense connective tissue- protects it Attaches to wall and anchors it Serous pericardium (2 layers) Parietal layer: belongs to cavity Visceral layer: outermost layer of heart (aka epicardium) Pericardial cavity: between these two layers, filled with pericardial fluid The fluid protects the heart, prevents friction, dissipate heat Heart Layers Epicardium Same as visceral layer of serous pericardium Myocardium Muscle layer that does beating Endocardium On inside of heart Squamous epithelial Chambers and Markings Atria (2) In base of heart Ventricles (2) In apex of heart *all chambers are separated from each other Interatrial septum Separates 2 atria Before birth, not completely separated because does not need to go to lungs Interventricular septum Separates two ventricles Coronary sulcus Interventricular groove Atria Auricles extension of atria to increase surface area Pectinate muscles Bands of pectinate muscles on upper surface of atria Fossa ovais Where used to be an opening between left and right atrium until born and takes first breath Ventricles Trabeculae carneae Muscle bundles in wall of ventricles Papillary muscles Muscles that extend off wall of ventricle Connected to flaps/valves Chamber-related Blood Vessels Vena cava Brings blood from body to right atrium Superior From head Inferior Coronary sinus All of blood empties here and meets with vena cava Pulmonary veins Empty into left atriam Right Left Pulmonary artery Goes to lungs Carries oxygen poor blood Aorta Pumps to entire body Circulation 2 circuits: Pulmonary circuit To and from lungs Systemic circuit To and from body
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