Bio 2301 Human Physiology Final Exam 2025

Where do blood cells develop? - - - Red bone marrow - About 2 million new RBCs are produced every second RBC development steps - -- Hemosytoblast (occurs in red bone marrow) - Reticulocyte (young RBC - red bone marrow) - Erythrocyte (REC - occurs in blood stream) Hematopoiesis - -Blood cell formation Erythropoiesis - -Red blood cell formation Function and types of white blood cells - -- Function in phagocytosis, immunity, protection - Types: neutrophils, eosinophils, basophils, monocytes, and lymphocytes Function of platelets - -Play a role in blood clotting Function of RBCs - -- Oxygen transport What is the significance of a bioconcave disk shape of RBCs? - -Allows for a high surface to volume ratio so oxygen and carbon dioxide can diffuse rapidly to and from the interior of the RBC Function of erythropoietin - -- A hormone made by the kidney that stimulates RBC production - Released whenever pO2 is low (lung disease, heart disease, anemia, or high altitudes) RBC average life in the circulation - -- Lifespan of RBC: 120 days - During their lifespan they carry oxygen - As they approach the end of their lifespan, they become stiff and rigid and become stuck in small blood vessels - must be removed from blood Removal of RBCs from the blood - -- Done in the small capillaries of liver and spleen - When RBCs get stuck in those capillaries, they are destroyed by phagocytic cells Breakdown of RBCs - - BIO 2301 BIO 2301 BIO 2301 What happens when bilirubin accumulates? - -- The person will turn yellow because bilirubin is a yellow-orange pigment - Can happen when RBCs are being broken down too fast or if the bile can't get into the small intestine or with liver failure Antigen - -- on RBC membranes - Like "cell name tags" - Recognized by cells of the immune system so the immune system knows which RBC are "self" and which are "non-self" Antibody - -- Consists of antigens A & B and antibodies against A & B - A & B antigens are codominant - The antibodies are preformed, meaning that you have them even if you have never been exposed to foreign blood - Whatever antigens you have is what blood type you are - You have antibodies against whatever antigens you don't have Four blood types in the ABO system - -- Type AB: has A & B antigents on RBC and no antibodies - Type A: has antigens on RBC and antibodies against B in plasma - Type B: has antigens on RBC and antibodies against A in plasma - Type O: has no antigens on RBC and antibodies against A & B Rh System - -- Involves a different antigen on the RBC membranes, the Rh antigen - If someone has the antigen, they are Rh positive and they will not make the antibodies against Rh - If someone does not have the antigen, they are Rh negative and they will make antibodies against Rh Erythroblastosis fetalis - -- A problem when you have an Rh negative mother pregnant with Rh positive baby - During pregnancy, there is no mixing of mother's and baby's blood, however at the time of placental separation, some of the baby's blood can enter the mother's bloodstream - The mother recognizes the RH antigens as foreign and fights against those RBCs by making antibodies against RH - The next time a woman gets pregnant with an Rh positive baby, her antibodies will enter that baby's bloodstream and destroy the baby's RBCs - if that baby lives to be born, it will be very anemic and need a complete blood transfusion at birth How do you prevent erythroblastosis fetalis? - -RHoGAM injections given to Rh negative mothers during pregnancy? What is hemostasis? - -The stoppage of bleeding and consists of three processes: vasospasm, platelet plug formation, and blood clotting BIO 2301 BIO 2301 Vasospasm - -- Mechanism: the damaged blood vessel spasms down - caused by a reflex of the blood vessel and serotonin that is released by the damaged blood vessel - Significance: decreases blood loss from that vessel - you get more vasospasm with increased damage to the vessel Platelet plug formation steps of development - -Damage to blood vessel - collagen from deeper layers of the blood vessel is exposed - platelets adhere to those sticky collagen fibers - platelets release ADP and Thromboxane A2 and the damaged endothelial cells release von Willebrand's factor - more platelets come to the area - formation of a platelet plug that plugs up the hole Limiting plug growth - -- Nearby undamaged endothelial cells inhibit platelet adherence by release Prostacyclin (PGl2) and nitric oxide (NO) - This makes sure the plug does expand onto the undamaged entothelium What are the two pathways along which a clot is formed? - -Intrinsic pathway and extrinsic pathways What do both factors involve? - -Calcium and clotting factors/proteins Where are clotting factors made? - -They are made by the liver and circulate in the plasma in inactive form What coenzyme helps the liver make clotting factors? - -Vitamin K What happens when a person has liver failure? - -They are not able to make those clotting factors and they will bleed excessively What can act to prevent that liver from making clotting factors? What is an antidote? - -- Rat poison (warfarin) and Coumadin (a blood thinner) prevent the liver - Antidote for warfarin toxicity is vitamin K What anticoagulants function to prevent clotting and how? - -- EDTA and citrate function to prevent clottign by chelating calcium - they bind up the calcium in the blood so it is not present to cause clotting The intrinsic pathway of clotting - -- Forms a clot in 3-6 minutes - Is initiated only when there is damage to the lining of the blood vessel wall - Uses the clotting proteins XII, XI, IX, VIII, X, Thrombin, and Fibrin The extrinsic pathway of clotting - -- Forms a clot in 15 seconds - Is initiated when there is damage to the blood vessel and tissue around it - Uses clotting factors VII, X, Thrombin, Firbin, and Tissue Thromboplastin What is fibrin - -The clot itself BIO 2301 BIO 2301 What is thrombin? - -The enzyme right before the clot - if you have thrombin, you can form a clot Clot development involves... - -the polymerization of the fibrin to form a meshwork which traps blood cells within the clot Clot retraction occurs and causes... - -the cut edges of the vessel to be brought closer together, giving you a smaller hole to repair What do platelets release and what does it stimulate - -- Release PDGF (platelet derived growth factor) - Stimulates the healing of the blood vessel wall What happens once healing has occurred? - -- TPA (Tissue Plasminogen Activator) is released from the healed endothelial cells and activates plasminogen - Faxtor IIa and Thrombin also activate plasminogen - Plasminogen becomes plasmin when it is active and the plasmin will digest the clot Plaminogen is ___________ into the clot when the clot is made and the clot has a _________ way of getting rid of itself - -- incorpoated - built in Why don't you want the clot around after you do not need it anymore? - -- A piece of the clot can break off and start traveling in the blood stream, becoming an embolus - These emboli can get stuck in small blood vessels, causing strokes, heart attacks, and pulmonary emboli What happens with over-aggressive clot formation? - -- Can cause strokes, heart attacks and pulmonary emboli What else causes unwanted clot formation? - -- Rough tissue inside the blood vessels - The rough lining of the blood vessel with stimulate platelet plug formation and then clots will form - Example: Atherosclerosis which causes cholesterol deposits in the arteries - Blood pooling: the pooling of blood will activate clotting factors How does aspirin prevent clot formation? - -Inhibits thromboxane A2 therefore inhibiting the formation of the platelet plug What substances does the body have that limit clot growth? - -- Antithrombin III: present in the plasma, binds thrombin and inactivates it so thrombin cannot form clots elsewhere - Herapin-Like Molecules on endothelial cells: increase the activity of antithrombin III Boyle's Law - -- States that pressure of a gas varies inversely with volume - If volume goes up, pressure goes down BIO 2301 BIO 2301 - It volume goes down, pressure goes up Relevant pressures - -- Atmospheric: 760mmHg at sea level - Intrapulmonic: pressure in the alveoli and it changes with the phases of breathing but it always eventually equalizes with atmospheric pressure - Intrapleural: pressure within the pleural cavity, it changes with the phases of breaking but is always less than intrapulmonic pressure Muscles of inspiration - -- Resting inspiration: diaphragm and external intercostals - Deep inspiration: neck and back muscles Volume and pressure changes during inspiration - -Volume goes up, pressure goes down and air goes in Muscles of expiration - -- Resting expiration: no muscles needed - the external intercostals and diaphragm relax, causing decrease volume - elastic recoil of the lungs increases pressure in lungs - air goes out - Forced expiration: abdominal muscles - these increase pressure in the abdomen which increases pressure in the chest and forces air out Compliance - -The ability to expand the lungs for inspiration Consequences of decreased compliance - -Decreased ability to inhale Restricted airway diseases - -- Cause decreased vital capacity and restrict the ability to expand the lungs, causing decreased compliance - Examples: fibrosis (scar tissue in lungs), silicosis (talc or other substances in the lungs) Other causes of decreased compliance - -Anything that decreases the flexibility of the thoracic cage like a chest wrap that is too tight or something heavy on someone's cgest What is the significance of surface tension in compliance? - -- The tension at the air water interface within the alveoli - If the surface tension is not lowered, the work to breath would be too great - too hard to expand the alveoli - and you would not be able to breath in What chemical is produced by the cells of the alveoil and what does it do? - -- Surfactant is the chemical produced - It decreases surface tension and therefore decreases the energy needed to expand