Blood and Circulatory System- Week 8 PDF

Summary

This document provides information on the cardiovascular system, including the functions of the circulatory system and blood vessels, blood cell types, and blood clotting. It also discusses blood types, the Rh group, and various clinical cases related to blood disorders. The information seems to be suitable for secondary-level biology.

Full Transcript

Blood and the Circulatory System CARDIOVASCULAR SYSTEM The, also known as the circulatory system, is the body's network of blood vessels and the heart that delivers oxygen, nutrients, and other substances to the body's cells and organs Function of Circulatory Syst...

Blood and the Circulatory System CARDIOVASCULAR SYSTEM The, also known as the circulatory system, is the body's network of blood vessels and the heart that delivers oxygen, nutrients, and other substances to the body's cells and organs Function of Circulatory System Transport: Delivers oxygen, nutrients, hormones, and waste products. Regulation: Helps maintain body temperature, blood pressure, and fluid balance Protection: Fights infection and clotting. Blood vessels and circuits 1.Pulmonary circuit To and from gas exchange surfaces in the lungs 2. Systemic circuit To and from rest of body What is blood Transport dissolved gases, nutrients, hormones, and metabolic wastes Oxygen—lungs to peripheral tissues Carbon dioxide—tissues to lungs Nutrients—from digestive tract or storage in adipose or liver Hormones—gland to target Wastes—to kidneys (excretion) Stabilize body temperature Absorbs heat generated in one area; distributes to other tissues High body temperature—blood directed closer to skin Low body temperature—blood directed to brain, internal organs Normal count of blood cells RBCs are biconcave discs—thinner centers, thicker edges Functional aspects of red blood cells Large surface area–to– volume ratioPacked with hemoglobin (= protein that carries oxygen) Form stacks (rouleaux)— facilitate transport in small vessels Flexible—RBCs can move through narrowest capillaries with diameters smaller than RBC Red blood cell characteristics Lose most organelles during development Mature RBCs lack nuclei (anucleate) and ribosomes Cannot divide/repair Life span < 120 days Primary function—transport respiratory gases 95 percent of RBC intracellular proteins are hemoglobin molecules Hemoglobin Complex quaternary structure Each Hb molecule has: Two alpha (α) chains Two beta (β) chains Each chain has a single heme molecule Each heme contains an iron ion that interacts with oxygen molecule to form oxyhemoglobin(HbO2) An RBC has ~280 million Hb molecules Each Hbmolecule has four heme units Hemoglobin OXYGENATED VS DEOXYGENATED BLOOD Red blood cells are continually produced ~1 percent of circulating RBCs are replaced each day (short lifespan) ~3 million new RBCs enter circulation each second End of RBC life Plasma membrane ruptures (hemolysis) or RBC is engulfed by macrophages in spleen, liver, or bone marrow Erythropoiesis= red blood cell formation The body has two types of hemopoietic tissue Red bone marrow—found in the ends of long bones and in flat irregular bones such as the sternum, cranial bones, vertebrae, and pelvis—produces all types of blood cells. Lymphatic tissue—found in the spleen, lymph nodes, and thymus gland—supplement blood cell production by producing lymphocytes, a specific type of WBC Events occurring in macrophages Macrophages monitor condition of circulating RBCs Engulf old RBCs before rupture (hemolyze) Remove Hb molecules/cell fragments Heme units stripped of iron Iron is stored in phagocyte or enters blood and binds to transferrin (plasma protein) Heme→biliverdin→bilirubin→bloodstream→liver Globular proteins disassembled and amino acids recycled Hemoglobin that is not phagocytized breaks down into its protein chains and is excreted in urine White blood cells (WBCs) leukocytes are the fewest of the formed elements. they are the body’s line of defense against invasion by infectious pathogens. Have nuclei and other organelles, unlike RBCs, but no hemoglobin WBCs are capable of movement, allowing them to migrate to sites of infection or injury. Types of white blood cell Types: There are five main types of WBCs, each with specific functions: Neutrophils: Phagocytic cells that engulf and destroy bacteria. Eosinophils: Involved in allergic reactions and parasitic infections. Basophils: Release histamine and other inflammatory substances. Monocytes: Mature into macrophages, which are phagocytic cells. Lymphocytes: Involved in specific immune responses, including antibody production and cell-mediated immunity. Platelets play a key role in stopping bleeding Formation of a Blood Clot Vascular phase of hemostasis Lasts ~ 30 minutes after injury Dominated by endothelial response and vascular spasm(smooth muscle contracts) Exposed endothelium in contact with blood; releases chemicals/local hormones Platelet phase of hemostasis Begins with attachment of platelets to sticky endothelial surfaces, basement membrane, exposed collagen fibers, and other platelets Coagulation phase of hemostasis Starts 30 seconds or more after damage Coagulation(blood clotting) involves complex sequence of steps leading to conversion of circulating fibrinogen to insoluble fibrin Blood cells and platelets are trapped in fibrin network (blood clot) Two pathways lead to common pathway—extrinsic and intrinsic Extrinsic pathway Begins with release of tissue factor(factor III) from damaged endothelial cells or peripheral tissues Tissue factor combines with Ca2+and another clotting factor to activate factor X (first step in common pathway) Intrinsic pathway Begins with activation of proenzymes exposed to collagen fibers at injury site Pathway proceeds with assistance of PF-3(factor released by aggregating platelets) Sequence of enzyme activations leads to factor X Common pathway Activated factor X activates prothrombin activator, a complex that converts the prothrombin(a proenzyme) to the enzyme thrombin Thrombin converts fibrinogen to fibrin Completes clotting process ▪Clot retractionRBCs and platelets stick to the fibrin threads Platelets contract to form tighter clot and pull edges together Continues for 30–60 minutes Fibrinolysis Process of clot dissolving Begins with activation of: Plasminogen by thrombin (from common pathway) Tissue plasminogen activator, or t-PA, from damaged tissues Produces plasmin—erodes the clot Blood types Antigens =substances that can elicit immune response Agglutination= clumping together of RBCs Occurs when surface antigens (agglutinogens) are exposed to corresponding antibodies (agglutinins) from another blood type Blood Type Rh group Difference between ABO and Rh blood types Six Rh antigens , each is called Rh factor C,D,E, c,d,e Type D antigen is most prevalent and more antigenic Person having antigen - - Rh positive Person not having D antigen – Rh negative Clinical Module: Hemolytic disease of the newborn is an RBC- related disorder caused by a cross-reaction between fetal and maternal blood types Background Blood type is determined by combining genes from both parents Child can have blood type different from either parent During pregnancy, mother’s antibodies may cross the placenta and attack/destroy fetal RBCs. Condition is hemolytic diseases of the newborn (HDN) Many forms—some very dangerous, others undetectable Most common involves Rh–mother who has carried Rh+fetus ▪First pregnancy—rarely poses a problem because fetal cells are mostly isolated from maternal blood—mom’s immune system is not stimulated to produce anti-Rh antibodies Birth: bleeding at placenta/uterus mixes fetal and maternal blood Mother exposed to Rh antigens; stimulates her immune system to produce anti-Rh antibodies (= sensitization) 20 percent of Rh–mothers who carried Rh+ children are sensitized within 6 months of delivery, but first child usually not affected (antibodies develop after delivery) Subsequent pregnancy with Rh+fetus: Maternal anti-Rh antibodies can cross placenta; destroy fetal RBCs, causing severe anemia Fetal demand for RBCs increases; erythroblasts enter bloodstream before maturity—leads to alternative name, erythroblastosisfetalis High fatality rate without treatment Newborn with severe HDN is anemic/jaundiced (from high bilirubin concentrations) Maternal antibodies remain active 1–2 months after delivery May require replacement of infant’s entire blood volume ▪HDN can be prevented by giving mother anti-Rh antibodies (RhoGAM) at weeks 26–28 of pregnancy and during/after delivery ▪The antibodies destroy fetal RBCs that crossed placenta before RBCs stimulate maternal immune response (= no sensitization) Obtaining blood for diagnosis Venipuncture Withdrawal of whole blood from superficial vein, such as median cubital vein Commonly used because: 1.Easy to locate superficial veins 2.Vein walls are thinner than walls of comparable arteries 3.Venous blood pressure is relatively low, so vein seals quickly Clinical case: Pernicious anemia Vitamin B12 - deficiency prevents normal stem cell divisions Fewer RBCs produced; often misshaped, large (macrocytic) Can be from lack of intrinsic factor—secreted in stomach; needed for vitamin B12absorption Ca2+ and vitamin K deficiencies Calcium is required for all clotting pathways Vitamin K is required by liver to synthesize clotting factors Clinical cases - Sickle cell disease (SDC) Sickle cell disease (SDC)—group of inherited RBC disordersGenetic mutation affects amino acid sequence of the beta globin subunit in hemoglobin RBCs take on sickle shape when they release oxygen RBCs more fragile, easily damaged Can get stuck in smaller vessels, block flow Clinical cases - Hemophilia Inherited bleeding disorder Affects 1 person in 10,000; ~80–90 percent are males Caused by missing or reduced production of a clotting factor Severity of disorder varies In severe cases, extensive bleeding occurs with minor contact Bleeding also occurs at joints and around muscles Clinical cases - Thalassemia diverse group of inherited disorders Unable to adequately produce normal Hb protein subunits Severity depends on which/how many subunits are abnormal Clinical cases - Sepsis Widespread infection of body tissue Septicemia Sepsis of the blood (“blood poisoning”) Pathogens present, multiplying in blood, and spreading Clinical cases - Malaria Malaria—parasitic disease caused by several species of Plasmodium Kills 1.5–3 million people per year (up to half are under age 5) Transmitted by mosquito Initially infects liver; later infects RBCs every 2–3 days, all Infected RBCs rupture, release more parasites Causes cycles of fever/chills; dead RBCs block vessels to vital organs Clinical cases - Leukemias Leukemias—cancers of blood-forming tissues Cancerous cells spread from origin in red bone marrow First symptoms appear with presence of immature and abnormal WBCs in circulation Fatal if untreated Two types Myeloid leukemia Lymphoid leukemia Both have elevated WBCs HEART The human heart beats about 100,000 times in one day and about 35 million times in a year. During an average lifetime, the human heart will beat more than 2.5 billion time Location of the heart The middle mediastinum contains the heart and large vessels entering or leaving the mediastinum Structures of the Heart Surrounding the heart is a double-walled sac called the pericardium. Anchored by ligaments and tissue to surrounding structures, the pericardium has two layers Relationship between heart and pericardium ▪Push fist into partly inflated balloon ▪Fist = heart ▪Wrist = base of heart, with great vessels ▪Inside of balloon = pericardial cavity ▪Pericarditis= inflammation of the pericardium ▪Cardiac tamponade= excess accumulation of pericardial fluid Walls of the heart Heart Chambers The heart is divided into four chambers or cavities two atria two ventricles These chambers are divided into right and left sides by walls called the interatrial septum and the interventricular septum. Right atrium receives blood from systemic circuit ▪Right ventricle pumps blood into pulmonary circuit ▪Left atrium receives blood from pulmonary circuit ▪Left ventricle pumps blood into systemic circuit Structures in the Atria Right atrium-receives deoxygenated blood from superior and inferior venae cavae and coronary sinus Fossa ovalis—remnant of fetal foramen ovale that allowed fetal blood to pass between atria; closes at birth Left atrium receives oxygenated blood from pulmonary veins Pectinate muscles—muscular ridges located inside both atria along the anterior atrial wall and in the auricles Structures in the ventricle Right ventricle—receives blood from right atrium through tricuspid valve (has three cusps or flaps), also called the right atrioventricular (AV) valve With contraction, blood exits through the pulmonary valve(pulmonary semilunar valve) into the pulmonary trunk Left ventricle—much thicker wall than right ventricle Receives blood from left atrium through mitral valve, also called bicuspid valve(two cusps) or left atrioventricular valve With contraction, blood exits through the aortic valve (aortic semilunar valve) into the ascending aorta Trabeculae carneae—muscular ridges inside both ventricles Comparison between chambers Atria have similar workloads; walls about same thickness Ventricles have very different loads Right ventricle—thinner wall; sends blood to adjacent lungs (pulmonary circuit) Contraction squeezes against left ventricle, forces blood out pulmonary trunk efficiently; minimal effort, low pressure Left ventricle—very thick wall, rounded chamber –4–6 times the pressure of right; sends blood through entire systemic circuit –Contraction decreases diameter and apex-to-base distance –Reduces right ventricular volume, aiding its emptying Right and left atria are separated by the interatrial septum Right and left ventricles are separated by interventricular septum(much thicker) Atrioventricular (AV) valves— between each atrium and ventricle Allow only one-way blood flow from atrium into ventricle ▪Semilunar valves—at exit from each ventricle; allow only one-way blood flow from ventricle out into aorta or pulmonary trunk Heart Valves Four valves act as restraining gates to control the direction of blood flow. They are situated at the entrances and exits to the ventricles Properly functioning valves allow blood to flow only in a forward direction by blocking it from returning to the previous chamber. Heart Valves 1. Tricuspid valve: an atrioventricular valve (AV), meaning that it controls the opening between the right atrium and the right ventricle. 2. Pulmonary valve: a semilunar valve, -Located between the right ventricle and the pulmonary artery, this valve prevents blood that has been ejected into the pulmonary artery from returning to the right ventricle as it relaxes. 3. Mitral valve: also called the bicuspid valve, indicating that it has two cusps. Blood flows through this atrioventricular valve to the left ventricle and cannot go back up into the left atrium. 4. Aortic valve: a semilunar valve located between the left ventricle and the aorta. Blood leaves the left ventricle through this valve and cannot return to the left ventricle. AV valve structure (tricuspid and mitral valve) Each has three (tricuspid) or two (mitral/bicuspid) cusps Cusps attach to tendon-like connective tissue bands = chordae tendineae Chordae tendineae anchored to thickened cone-shaped papillary muscles Moderator band—thickened muscle ridge providing rapid conduction path; tenses papillary muscles just before ventricular contraction; prevents slamming or inversion of AV valve Pulmonary and aortic (semilunar) valves Each has three half-moon shaped cusps Prevent backflow of blood from aorta and pulmonary trunk back into ventricles No muscular brace needed— cusps support each other when closed When ventricles are relaxed, they fill AV valves—open Chordae tendineae are loose Semilunar valves— closed Blood pressure from pulmonary and systemic circuits keeps them closed When ventricles contract, they empty AV valves—closed Pressure from contracting ventricles pushes cusps together Papillary muscles tighten chordae tendineaeso cusps can’t invert into atria; prevents backflow (regurgitation) Semilunar valves—open Ventricular pressure overcomes pressure in pulmonary trunk and aorta that held them shut Visible on anterior surface ▪All four chambers ▪Auricle of each atrium (expandable pouch) ▪Coronary sulcus—groove separating atria and ventricles ▪Anterior interventricular sulcus—groove marking boundary between the two ventricles ▪Ligamentum arteriosum—fibrous remnant of fetal connection between aorta and pulmonary trunk Visible on posterior surface: All four chambers Pulmonary veins (4)returning blood to left atrium Superior and inferior venae cavae returning blood to right atrium Coronary sinus—returns blood from myocardium to right atrium Posterior interventricular sulcus—groove marking boundary between the two ventricles Coronary circulation Continuously supplies cardiac muscle (myocardium) with oxygen/nutrients Left and right coronary arteries arise from ascending aorta; fill when ventricles are relaxed (diastole) ▪Myocardial blood flow may increase to 9 times the resting level during maximal exertion Right coronary artery ▪Supplies right atrium, parts of both ventricles, and parts of cardiac (electrical) conducting system ▪Follows coronary sulcus (groove between atria and ventricles) Left coronary artery ▪Supplies left ventricle, left atrium, interventricular septum Coronary circulation—veins (anterior) Great cardiac vein—in anterior interventricular sulcus Drains area supplied by anterior interventricular artery Empties into coronary sinus posteriorly Anterior cardiac veins Drain anterior surface of right ventricle Empty directly into the right atrium Coronary circulation—veins (posterior) Coronary sinus—expanded vein that empties into right atrium Posterior vein of left ventricle— drains area supplied by circumflex artery Middle cardiac vein—drains area supplied by posterior interventricular artery; empties into coronary sinus Small cardiac vein—drains posterior of right atrium/ventricle; empties into coronary sinus Blood flow through the coronary circuit is maintained by changing blood pressure and elastic rebound ▪Left ventricular contraction forces blood into aorta, elevating blood pressure there, stretching aortic walls Left ventricular relaxation—pressure decreases, aortic walls recoil (elastic rebound), pushing blood in both directions Forward into systemic circuit Backward into coronary arteries Cardiac skeleton (fibrous skeleton) Flexible connective tissue frame Interconnected bands of dense connective tissue Encircle heart valves, stabilize their positions Also surrounds base of aorta and pulmonary trunk Electrically isolates atrial from ventricular myocardium Cardiac cycle Cardiac cycle = period between start of one heartbeat and the next; heart rate = number of beats per minute Two atria contract first to fill ventricles; two ventricles then contract to pump blood into pulmonary and systemic circuits Two phases: Contraction (systole)—blood leaves the chamber Relaxation (diastole)—chamber refills Sequence of contractions 1.Atria contract together first (atrial systole) Push blood into the ventricles Ventricles are relaxed (diastole) and filling 2.Ventricles contract together next (ventricular systole) Push blood into the pulmonary and systemic circuits Atria are relaxed (diastole) and filling Typical cardiac cycle lasts 800 msec Phases of cardiac cycle, diagrammed for heart rate of 75 bpm.Cardiac cycle begins—all four chambers are relaxed (diastole; ventricles are passively refilling) Atrial systole(100 msec)—atria contract; finish filling ventricles Atrial diastole(270 msec)—continues until start of next cardiac cycle (through ventricular systole) Ventricular systole—first phase. Contracting ventricles push AV valves closed but not enough pressure to open semilunar valves (= isovolumetric contraction—no volume change) Ventricular systole—secondphase. Increasing pressure opens semilunar valves; blood leaves ventricle (= ventricular ejection) Ventriculardiastole—early.Ventricles relax and their pressure drops; blood in aorta and pulmonary trunk backflows, closes semilunar valves Isovolumetric relaxation. All valves closed; no volume change; blood passively filling atria Ventriculardiastole—late. All chambers relaxed; AV valves open; ventricles fill passively to ~70% Heart sounds ▪S1( “lubb”)—when AV valves close; marks start of ventricular contraction ▪S2(“dupp”)—when semilunar valves close ▪S3and S4—very faint; rarely heard in adults S3—blood flowing into ventricles S4—atrial contraction Cardiac output (CO) = amount of blood pumped from the left ventricle each minute ▪ Heart rate (HR)= # contractions/minute (beats per minute) ▪Stroke volume= volume of blood pumped out of ventricle per contraction Conducting system Auto rhythmicity= cardiac muscle’s ability to contract at its own pace independent of neural or hormonal stimulation Conducting system = network of specialized cardiac muscle cells (pacemaker and conducting cells) that initiate/distribute a stimulus to contract Electrocardiogram (ECG or EKG) Recording of heart’s electrical activities from body surface To assess performance of nodal, conducting, and contractile components If part of heart is damaged by heart attack, may see abnormal ECG pattern Appearance varies with placement and number of electrodes (leads) electrocardiogram (EKG or ECG) P wave= atrial depolarization ▪Atria begin contracting ~25 msec after P wave starts QRS complex= ventricular depolarization ▪Larger wave due to larger ventricle muscle mass ▪Ventricles begin contracting shortly after R wave peak ▪Atrial repolarization also occurs now but is masked by QRS T wave= ventricular repolarization P–R interval ▪Period from start of atrial depolarization to start of ventricular depolarization ▪>200 msec may mean damage to conducting pathways or AV node Q–T interval ▪Time for ventricles to undergo a single cycle ▪May be lengthened by electrolyte disturbances, medications, conduction problems, coronary ischemia, myocardial damage Resting heart rate Varies with age, general health, physical conditioning Normal range is 60–100 bpm ▪Bradycardia Heart rate slower than normal (100 bpm) Cardiac centers of the medulla oblongata ▪Cardioinhibitory center Controls parasympathetic neurons; slows heart rate Parasympathetic supply to heart via vagusnerve (X);synapse in cardiac plexus Postganglionic fibers to SA/AV nodes, atrial musculature ▪Cardioacceleratory center Controls sympathetic neurons; increases heart rate Sympathetic innervation to heart via postganglionic fibers in cardiac nerves; innervate nodes, conducting system, atrial and ventricular myocardium Factors affecting stroke volume End-diastolic volume (EDV) Venous return = amount of venous blood returned to the right atrium Varies directly with blood volume, muscular activity, and rate of blood flow Filling time = length of ventricular diastole; the longer it is, the more filling occurs (higher EDV) Factors affecting stroke volume Preload= amount of myocardial stretch –Greater EDV causes greater preload; more stretching causes stronger contractions and more blood being ejected (Frank-Starling law of the heart) Factors affecting stroke volume Contractility= amount of force produced during contraction at a given preload –Increased by sympathetic stimulation, some hormones (epinephrine, norepinephrine, thyroid hormone, glucagon) –Reduced by “beta blockers” and calcium channel blockers Factors affecting stroke volume Afterload= ventricular tension required to open semilunar valves and empty –As afterload increases, stroke volume decreases –Afterload increases whenever blood flow is restricted, such as with vasoconstriction Factors affecting cardiac output ▪Cardiac output varies widely to meet metabolic demands ▪Cardiac output can be changed by affecting either heart rate or stroke volume Heart failure= condition in which the heart cannot meet the demands of peripheral tissues Blood vessels Blood vessels conduct blood between the heart and peripheral tissues Arteries(carry blood away from the heart) Veins(carry blood to the heart) Capillaries(exchange substances between blood and tissues) Three layers of arteries and veins Three layers of arteries and veins Layer Arteries Veins Innermost layer, composed of endothelium and Similar to arteries, but often Tunica intima subendothelial connective thinner tissue Middle layer, primarily Thinner than in arteries, with Tunica media composed of smooth muscle less elastic tissue cells and elastic fibers Outermost layer, composed of Thicker than in arteries, often Tunica connective tissue and vasa containing more collagen adventitia vasorum (vessels that supply fibers blood to the vessel wall) Type of Arteries Elastic arteries Large vessels close to the heart that stretch and recoil when heart beats Include pulmonary trunk, aorta, and branches Muscular arteries Medium-sized arteries Distribute blood to skeletal muscles and internal organs Arterioles Poorly defined tunica externa Tunica media is only 1–2 smooth muscle cells thick Capillaries Only blood vessels to allow exchange between blood and interstitial fluid Very thin walls allow easy diffusion Capillaries Continuous capillary Fenestrated capillary Endothelium is a complete lining Contains “windows,” or pores, Located throughout body in all penetrating endothelial lining tissues except epithelia and Permits rapid exchange of water cartilage and larger solutes Permits diffusion of water, small solutes, and lipid-soluble materials Prevents loss of blood cells and plasma proteins Some selective vesicular transport Capillaries Sinusoids(sinusoidal capillaries) Resemble fenestrated capillaries that are flattened and irregularly shaped Commonly have gaps between endothelial cells Basement membrane is thin or absent Permit more water and solute (plasma proteins) exchange Occur in liver, bone marrow, spleen, and many endocrine organs Capillaries Capillary bed Interconnected network of capillaries Contains several connections between arterioles and venules Veins Large veins Contain all three vessel wall layers Thin tunica media surrounded by thick tunica externa Include superior and inferior venae cavaeand tributaries Vein Range from 2 to 9 mm in internal diameter Thin tunica media with smooth muscle cells and collagen fibers Thickest layer is tunica externa with longitudinal collagen and elastic fibers Venules Those smaller than 50 μmlack a tunica media and resemble expanded capillaries Collect blood from capillaries Pressure and blood flow in veins Blood pressure in peripheral venules is

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