Blood Exam Questions PDF

Blood 1.​ Blood transports oxygen collected from the lungs and nutrients from the small digestive tract. After delivering oxygen and nutrients to the different areas of the body, blood picks up carbon dioxide and delivers it back to the lungs to be exhaled out. Hormones from...

Blood 1.​ Blood transports oxygen collected from the lungs and nutrients from the small digestive tract. After delivering oxygen and nutrients to the different areas of the body, blood picks up carbon dioxide and delivers it back to the lungs to be exhaled out. Hormones from endocrine organs are transported by the blood. 2.​ Blood regulates the body by keeping the body cool by increasing blood flow to the skin. The components of the blood (proteins) maintain the pH balance in the body’s tissues. Blood also maintains an adequate fluid volume in the circulatory system. 3.​ The blood prevents the loss of blood from the body and prevents infections from attacking the body 4.​ The two major components of whole blood are plasma and packed red blood cells. Blood is considered a connective tissue because plasma is suspended in a fluid called matrix. Dissolved fibrous proteins (protein found in plasma) become visible as fibrin strands during blood clotting. 5.​ Blood's physical characteristic is a sticky and opaque fluid with a metallic taste. Approximately 8% of body weight is blood. Adult men can hold 5-6 L of blood and adult women can hold 4-5 L. 6.​ 55% of whole blood is plasma, less than 1% is buffy coat, and 45% of whole blood is 45%. 7.​ The buffy coat is the thin layer that sits between plasma and packed red blood cells after a blood sample has been placed in a centrifuge. Within the thin layer are leukocytes (WBCs) that act in various ways but they all protect the body from foreign invaders like bacteria or parasites. The buffy coat also contains platelets, fragmented cells that help the body to stop bleeding. 8.​ Hematocrit is the total volume of blood within a blood sample. It is also known as the blood fraction. Hematocrit is different in both men and women. In men, it is approximately 47% and in women it is approximately 42% 9.​ Plasma contains water, electrolytes, proteins, and other miscellaneous items like nutrients, hormones, and respiratory gases. Water absorbs electrolytes helps maintain osmotic pressure and maintain the pH balance within blood. The proteins within the plasma include albumin, Globulins, and fibrinogen. Albumin is the main contributor of maintaining osmotic pressure. There are three types of Globulins, Alpha and Beta, that transport proteins that bind to lipids, metal ions, and fat soluble vitamins, and Gamma, that contains antibodies that are released by plasma cells during an immune response. Fibrinogen forms fibrin threads used to clot blood. Serum is plasma but without the proteins. 10.​The formed elements refers to cells and cell fragments suspended in the plasma, including erythrocytes, leukocytes, and platelets. Erythrocytes have no nuclei or organelles, platelets are cell fragments and leukocytes are the only formed elements with completed cells. Most types of formed elements survive in the blood for only a few days. Most blood cells do not divide, instead, stem cells divide continuously in red bone marrow to replace them. 11.​The shape and the small size of the erythrocyte provides a large surface area relative to its volume. The concave disc shape is ideal for gas exchange between the cells. Oxygen  is delivered and carbon dioxide is picked up, because there is no point within the cytoplasm that is far from the surface. 12.​Hemoglobin is made up of two components, Heme, a red pigment that is bound to the protein globulin and contains iron. The protein globin contains 4 polypeptide chains, 2 alpha and beta chains. Hemoglobin is used to allow blood to have the ability to carry oxygen. 13.​The life cycle of an erythrocyte is approximately 120 days from when the erythrocyte is created to when it is destroyed. The process creating an erythrocyte takes about 15 days. The erythrocyte starts in the bone marrow where a stem cell turns into a proerythroblast, then turns into a basophilic erythroblast where ribosomes are synthesized. During the first two phases, the cells divide. Hemoglobin is synthesized and iron accumulates as the basophilic erythroblast transforms into a polychromatic erythroblast then into an orthochromatic erythroblast. When an orthochromatic erythroblast has accumulated almost all of its hemoglobin and it ejects its organelles. The nucleus degenerates and is pinched off, allowing the cell to collapse inward and eventually assume the biconcave shape, resulting in the reticulocyte. After the reticulocyte is created, it is then ejected from the bone marrow and into the bloodstream where within a day or two it matures into an erythrocyte. 14.​Erythropoiesis (the production of erythrocytes) is controlled by hormones and it requires an adequate amount of amino acids, iron and b12 vitamins, 15.​When erythrocytes are destroyed or damaged, they are sent to the spleen where they are picked apart for materials that can be recycled like the iron from the heme is sent back to the bone marrow for the production of new erythrocytes. The leftover heme is turned into bilirubin, a metabolic waste product is sent to the liver and is removed from the body through the intestines and any carbon dioxide found in the blood cells are exhaled out from the lungs. 16.​Anemia is where the blood's oxygen carrying capacity is compromised and is too low to support normal metabolism. The different types of anemia are cut up into three types: hemorrhagic anemia, not enough red blood cells are being produced, and when too many red blood cells are destroyed too quickly. Hemorrhagic anemia is caused when there is a rapid loss of blood in the body. There are four types of anemia that is caused when there are not enough red blood cells that are produced Typically this is caused by the lack of essential raw material such as iron. Iron deficiency anemia is the most common type of anemia and is generally the secondary result of hemorrhagic anemia. Luckily there is a quick fix to treat this type of anemia by supplementing with iron or with a blood transfusion. Pernicious anemia is an autoimmune disorder that mostly affects older adults. Their immune systems destroy the cells of their own stomach mucosa. Renal anemia is caused by the lack of EPO, a hormone that is produced in the kidneys and used in the production of RBCs, but when the kidneys are damaged or failing, EPO production is disrupted. Aplastic anemia stops the production of RBCs in the bone marrow by certain drugs, chemical exposure, ionizing radiation, or viruses. In the case where too many RBCs are being destroyed too quickly for the body to reproduce, the condition is called hemolytic anemia. RBC ruptures or lyses prematurely. This can be caused by genetic disorders like Thalassemia and sickle cell anemia, autoimmune  disorders like lupus, infections like malaria, or from a reaction from mismatched blood transfusion. Thalassemia is a genetic disorder common in people with Mediterranean ancestry. One of the globin chains in hemoglobin is absent or faulty causing the RBCs to be thin, delicate and deficient in hemoglobin. Sickle cell anemia is a genetic disorder common in people with African ancestry and caused by abnormal hemoglobin due to a change in just one of the 146 amino acids in a beta chain of the globin molecule. This change causes the beta chains to stick together under low oxygen conditions forming stiff rods so that hemoglobin S becomes spiky and sharp. This causes RBCs to be in the shape of a sickle when oxygen content of the blood is lower than normal as vigorous exercise and other activities increase metabolic rate. When these cells flow through the vessels they get stuck causing unbearable pain and organ failure. There is no cure but can be treated with pain medication, blood transfusion and other medication to prevent sickle cell crisis. 17.​Polycythemia is the abnormal excess of erythrocytes that increases blood volume and viscosity causing it to flow slower than normal and putting the patient at risk of clotting and stroke. Medication can be used to treat, so can a procedure called phlebotomy where a certain amount of blood is removed every so often to allow normal blood flow to occur. 18.​Leukocytes prevent and fight off infections within the body. Typical infections are bacterial, viral, parasitic, toxic, and tumor cells. White blood cells have the special ability to be able to slip out of the capillary blood vessels. 19.​Diapedesis is the action of white blood cells slipping out of the capillary blood vessels. Amoeboid motion shows how leukocytes move through the tissue spaces but forming cytoplasm that lets the leukocytes “walk” towards the affected areas. Positive chemotaxis is the chemical trail of molecules that are released by damaged cells or other leukocytes. It is used to pinpoint areas of tissue damage and infections so the leukocytes can destroy foreign substances and dead cells. 20.​Neutrophils are the most common type of leukocytes that fight bacteria in the body. Eosinophil kills parasitic worms. Basophil releases histamine and other mediators of inflammation during allergic reactions. Lymphocytes are the strongest types of leukocytes they are able to attack by direct cell attack or by antibodies. Typically goes after harder to “kill” invaders like tumor cells. Finally, monocytes fight against bacteria, viruses and fungi. When monocytes leave the blood vessels to attack invaders, they transform into macrophages 21.​Describe the formation of the different types of WBCs (explained above) 22.​Leukemia is the overproduction of abnormal leukocytes that contain cancerous cells that attack the lymph nodes and travel through the blood streams causing it to easily develop cancerous cells in other parts of the body. The other blood cell lines are crowded out resulting in severe anemia and bleeding problems. Leukopenia is an abnormally low white blood cell count. 23.​Mononucleosis is caused by the epstein-barr virus and is transmitted orally through saliva. It causes fatigue, sore throat, enlarged lymph nodes and spleen, and a low grade fever. 24.​Platelets are cell fragments found in the bloodstream. They play a crucial role in the clotting process that occurs when plasma when blood vessels are ruptured or their lining is injured by sticking to the damaged sites, platelets form a temporary plug that helps seal the break. Platelets are formed by secreted endothelial cells lining the blood vessels. 25.​Hemostasis is the process of clotting and restoring blood flow. The three mechanisms include vascular spasm, platelet plug formation, and coagulation. 26.​Vascular spasm is when chemicals released by damaged endothelial cells are activated by platelets. The reflexes are initiated by local pain receptors. 27.​Platelet plug formation is when temporary platelet plug is formed using proteins, ADP, serotonin and thromboxane A2. ADP is a potent aggregation agent that causes the platelets to stick to the affected area and release their contents. Both serotonin and thromboxane A2 are messengers that enhance vascular spasm and platelet aggregation. As more platelets aggregate they release more chemicals aggregating more platelets and so on in a positive feedback cycle. 28.​Coagulation happens in three phases. In phase 1, two pathways to the prothrombin activator can happen intrinsically and extrinsically. Intrinsic pathways as the clotting factors present in blood, triggered by negatively charged surfaces and are slower but create a stronger seal. Extrinsic pathway requires clotting factors outside the blood, triggered by tissue factor and happens faster because there are fewer steps required. Phase 2 is the prothrombin activator catalyzes the conversion of a plasma protein called prothrombin into the active enzyme thrombin. Phase 3 traps blood cells and effectively seals the hole until the blood vessel can be permanently repaired. Thrombin catalyzes the transformation of the soluble clotting factor fibrinogen into fibrin. 29.​Clot retraction happens 30-60 minutes after a wound has clotted. It is a platelet induced process that stabilizes the clot. 30.​Fibrinolysis removes any unneeded clots when healing has occurred. Without fibrinolysis, blood vessels would gradually become completely blocked. 31.​The removal of coagulation factors in contact with rapidly flowing blood and inhibition of activated blood factors. Prostacyclin (PGI2) and nitric oxide secreted by the endothelial cells help prevent undesirable clotting. 32.​Thromboembolic disorder is a type of hemostasis disorder, including thrombus; a clot forms in an unbroken blood vessel. If large enough the clot can block circulation leading to tissue death. Embolus; a thrombus that breaks away and travels through the bloodstream leading to conditions like pulmonary embolism or stroke. Other disorders of hemostasis are bleeding disorders including thrombocytopenia, hemophilia and liver disease. Thrombocytopenia is the deficiency of platelets causing spontaneous bleeding from small blood vessels. Hemophilia is a genetic disorder of certain coagulation factors, leading to prolonged bleeding. Liver disease can result in bleeding disorders since many coagulation proteins are produced in the liver. The last hemostasis disorder is Disseminated Intravascular Coagulation (DIC). It is a widespread clotting in unmanaged blood vessels and severe bleeding due to the consumption of clotting factors. 33.​Important factors must be taken into consideration during blood transfusion because blood from the donor and recipient may not match causing clotting. General transfusion  reactions include fever, chills, low blood pressure, rapid heartbeat, nausea, and vomiting. Severe reactions can lead to kidney shutdown and require immediate treatment to prevent kidney damage. 34.​ABO groups are determined by the presence or absence of two antigens on the surface of red blood cells. Rh blood groups system includes 52 antigens but the most significant is the D antigen that determines if a person's ABO blood type is positive or negative. 35.​Agglutination is the clumping of particles. It occurs when antibodies bind to antigens on the surface of RBCs causing them to clump together. Agglutinogens are antigens found on the surface of red blood cells that determine an individual's blood type. Agglutinins are the antibodies found in the plasma that react with specific agglutinogens. 36.​Blood typing is mixing a small sample of blood with anti a and b serums to observe agglutination (clumping). This process is broken up into three different steps. Step one is to divide the sample into three parts. Anti A serum is mixed with the first part of the divided blood sample, serum Anti B is mixed with the 2nd group and D serum is mixed with the last part. The 2nd step is to observe if any agglutination happens. The clumping determines the person's blood type. Step three is identifying the results from the blood. 37.​Blood testing is a crucial diagnostic tool used to give either an overall or more detailed look into a person's health by determining the amount of certain vitamins and metals, to see if there are active infections if a person has diabetes or at risk of heart disease. Even cans find inflammation markers that can determine if a person has an autoimmune disorder and allergy to certain things. Cardiovascular 1.​ Distinguish between the pulmonary and systemic circuits a.​ The right side of the heart receives poor-oxygenated blood from body tissues and then pumps this blood to the lungs to pick up oxygen and disposes carbon dioxide. The blood vessels that carry blood to and from the lungs form the pulmonary circuit i.​ The right atrium receives blood returning from the systemic circuit. ii.​ The right ventricle pumps blood into the pulmonary circuit b.​ The left side of the heart receives the oxygenated blood returning from the lungs and pumps this blood throughout the body to supply oxygen and nutrients to the body tissues. The blood vessels that carry blood to and from all body tissues form the systemic circuit. i.​ The left atrium receives blood returning from the pulmonary circuit ii.​ The left ventricle pumps blood into the systemic circuit 2.​ Describe the location of the heart within the body a.​ Slightly inferior to this position in a standing person. b.​ Obliquely within the mediastinum of the thorax, medial to the arm c.​ Enclosed within the mediastinum, the medial cavity of the thorax, the heart extends obliquely front he second rib to the fifth intercostal space. 3.​ Describe the structure and function of the coverings of the heart a.​ The heart is enclosed in a double walled sac called the pericardium. b.​ The loosely fitting superficial part of this sac is the fibrous pericardium.  i.​ Structure 1.​ Tough dense connective tissue layer ii.​ Functions 1.​ Protects the heart 2.​ Anchors it to surrounding structures 3.​ Prevents overfilling of the heart with blood c.​ Deep to the fibrous pericardium is the serous pericardium i.​ Thin, slippery, two layer serous membrane that forms a closed sac around the heart. ii.​ parietal layer 1.​ Structure: outer layer of the serous pericardium. Lines the internal surface of the fibrous pericardium. 2.​ Function: provides a smooth surface to reduce friction iii.​ The visceral layer, also called the epicardium, is an integral part of the heart wall. 1.​ Structure: inner layer of serous pericardium, also the outermost layer of the heart wall 2.​ Function: adheres to the surface of the heart providing lubrication and protection iv.​ Between the parietal and visceral layers is the site like pericardial cavity 1.​ Structure: contains a film of serous fluid. 2.​ Function: lubricates the serous membrane to glide smoothly past one another, allowing the mobile heart to work in a relatively friction-free environment. 4.​ Describe the structure of the heart wall a.​ Epicardium - outermost layer i.​ Structure: thin, serous membrane. Made up of simple squamous epithelial tissue and connective tissue. ii.​ Function: provides a smooth, lubricated surface to reduce friction as the heart beats and protects the heart b.​ Myocardium - middle layer i.​ Structure: composed mainly of cardiac muscle. Forms the bulk of the heart. Branching cardiac cells are tethered to one another by criss crossing connective tissue fibers and arranged in spiral or circular bundles. The connective tissue fibers form a dense network, the fibrous cardiac skeleton ii.​ Function: this is the layer that contracts. The interlacing bundles link all parts of the heart together. c.​ Endocardium - third layer i.​ Structure: glistening white sheet of endothelium resting on a thin connective tissue layer. Made up of simple squamous epithelium. Located on the inner myocardial surface, lines the heart chambers and covers the fibrous skeleton of the valves.  ii.​ Function: provides a smooth surface to minimize friction and turbulence within the heart, preventing blood clot formation. 5.​ Name the chambers of the heart a.​ The heart has four chambers i.​ Right atrium ii.​ Left atrium iii.​ Right ventricle iv.​ Left ventricle 6.​ Describe the anatomy of the atria a.​ The atria are two upper chambers of the heart and play a crucial role in relieving blood returning to the heart from the body and lungs. b.​ Right atrium i.​ Two basic parts: a smooth walled posterior part and an anterior portion in which bundles of muscle tissue form ridges in the walls. 1.​ The muscle bundles are called pectinate muscles c.​ Left atrium i.​ Mostly smooth and pectinate muscles are found only in the auricle. 1.​ The internal septum bears a shallow depression, the fossa ovalis, that marks the spot where an opening, the foramen ovale, existed in the fetal heart. 7.​ List the veins that carry blood into the right atrium and into the left atrium. a.​ Right atrium i.​ Blood enters the right atrium through three veins 1.​ Superior vena cava returns blood from body regions superior to the diaphragm 2.​ Inferior vena cava returns blood from the body areas below the diaphragm 3.​ Coronary sinus collects blood draining from the myocardium b.​ Left atrium i.​ Four pulmonary veins enter the left atrium. 1.​ These veins transport blood from the lungs back to the heart. Best seen in a posterior view. 8.​ Describe the anatomy of the ventricles. Include the arteries that receive blood from each a.​ The walls are much more massive than the atrial walls. b.​ Right ventricle i.​ Forms the hearts anterior surface ii.​ Internal walls are marked by irregular ridges of muscle called trabeculae carneae. Papillary muscles play a role in valve function and project into the ventricular cavity. iii.​ Pumps blood into the pulmonary trunk, which routes the blood to the lungs where gas exchange occurs. c.​ Left ventricle i.​ Dominates its posteroinferior surface  ii.​ Like the right ventricle, also has trabeculae carneae and papillary muscles. iii.​ Ejects blood into the aorta 9.​ Compare and give the reason for the relative sizes of the right and left ventricles a.​ Right ventricle i.​ Pumps deoxygenated blood to the lungs requiring lesser pressure and making the right ventricle thinner walled than the left b.​ Left ventricle i.​ Pumps oxygenated blood to the entire body requiring a greater pressure and making the left ventricle thicker walled than the right. 10.​Name and give the location, and describe the structure of each of the heart valves. Explain how each heart valve functions. a.​ Atrioventricular (AV) Valves i.​ Two total, one located at each atrial-ventricular junction to prevent backflow into the atria when the ventricles contract. 1.​ Right AV valve - Tricuspid valve a.​ Three flexible cusps 2.​ Left AV valve - bicuspid a.​ Two flexible cusps ii.​ Structure 1.​ AV valves a.​ Tricuspid - three flexible cusps attached to chordae tendineae 2.​ Chordae tendineae a.​ Tiny white collagen fibers anchored to the papillary muscles protruding from the ventricular walls. iii.​ Function 1.​ AV Valves a.​ When the heart is completely relaxed, the AV valve flaps hang limply into the ventricular chambers below. b.​ Blood flows into the atria and then through the open AV valves into the ventricles. c.​ When ventricles contract, compressing the blood in their chambers, the intraventricular pressure rises, forcing the blood superiorly against the valve flaps. d.​ The flap edges meet, closing the valve. 2.​ Chordae tendineae and papillary muscles a.​ Acts as tethers that anchor the valve flaps in their closed position. b.​ If these cusps were not anchored, they would be blown upward into the atria in the same way an umbrella is blown inside out by a gusty wind. c.​ The papillary muscles contract with the other ventricular musculature so that they take up the slack on the chordae  tendineae as the full force of ventricular contraction hurls the blood against the AV valve flaps. b.​ Semilunar (SL) Valves (semilunar = half moon) i.​ Aortic valve 1.​ At the junction of the left ventricle and the aorta ii.​ Pulmonary valve 1.​ located at the junction of the right ventricle and the pulmonary trunk. iii.​ Structure 1.​ Each SL valve has three pocket like cups shaped like a crescent moon iv.​ Function 1.​ When the SL valves open and close in response to differences in pressure 2.​ When ventricles contract and intraventricular pressure rises above the pressure of the aorta and pulmonary trunk, the AL valves are forced open and their cusps flatten against the arterial walls as the blood rushes past them. 3.​ When ventricles relax, and the blood flows backward towards the heart, it pushes on the cusps and closes the valves. 11.​Describe the coronary circulation. Name all coronary vessels listed in your text and state which areas of the heart they supply or drain. a.​ Coronary circulation i.​ The functional blood supply of the heart, providing oxygen and nutrients to the myocardium. Despite being filled with blood, the heart relies on its own network of vessels for nourishment due to the thickness of the myocardium b.​ Coronary arteries i.​ Left coronary artery (LCA) 1.​ Runs toward the left side of the heart and then divides into the major branches. a.​ Anterior interventricular artery follows the anterior interventricular sulcus and supplies blood to the interventricular septum and anterior walls of both ventricles. b.​ Circumflex artery supplies the left atrium and the posterior walls of the left ventricle ii.​ Right coronary artery (RCA) 1.​ Courses to the right side of the heart, where it also gives rise to two branches a.​ Right marginal artery serves the myocardium of the lateral right side of the heart b.​ Posterior interventricular artery runs to the heart apex and supplies the posterior ventricular walls. Near the apex of  the heart, this artery merges with the anterior interventricular artery c.​ Cardiac veins i.​ After passing through the capillary beds of the myocardium, the venous blood is collected by the cardiac veins, whose paths roughly follow those of the coronary arteries. These veins join to form an enlarged vessel called the coronary sinus, which empires the blood into the right atrium. ii.​ Great Cardiac Vein 1.​ Anterior interventricular sulcus 2.​ Empties into the coronary sinus iii.​ Middle Cardiac Vein 1.​ Posterior interventricular sulcus 2.​ Empties into the coronary sinus iv.​ Small cardiac vein 1.​ Running along the heart’s right inferior margin 2.​ Empties into the coronary sinus v.​ Functions 1.​ Arteries: deliver oxygen right blood to the myocardium when the heart is relaxed 2.​ Veins: collect oxygen-poor blood from the myocardium and return it to the right atrium 12.​Describe the microscopic anatomy of cardiac muscle. How is this related to its function? a.​ Structure i.​ Cardiac muscle is striated and contracts by the sliding filament mechanism. b.​ Cardiac cells i.​ are short, fat, branched and interconnected. Each cell typically contains one or two centrally located nuclei. Abundant mitochondria account for about 35% of the volume of cardiac cells. The remaining volume is occupied by myofibrils composed of fairly typical sarcomeres c.​ Intracellular spaces i.​ Filled with a loose connective tissue matrix (endomysium) containing numerous capillaries. This delicate matrix is connected to the fibrous cardiac skeleton d.​ Intercalated discs i.​ specialized junctions connected to cardiac muscle cells end-to-end, appearing as dark lines under a microscope. They contain Desmosomes and Gap Junctions e.​ Myofibrils i.​ Composed of fairly typical sarcomeres. 1.​ Sarcomeres have Z discs, A bands, and I bands that reflect the arrangement of the thick (myosin) and thin (actin) filaments composing them f.​ Function  i.​ Matrix (endomysium) 1.​ Acts both as a tendon and as an insertion, giving cardiac cells something to pull or exert their force against. ii.​ Desomes 1.​ Button together two adjacent cells, keeping them from separating during contraction iii.​ Gap junctions 1.​ Allow ions to pass from cell to cell, transmitting current across the entire heart. Makes the myocardium behave as a single coordinated unit or functional syncytium (syn = together, cyt = cell) iv.​ Cardiac cells 1.​ Highly resistant to fatigue because they produce large amounts of ATP. 13.​Explain the five differences between physiology of skeletal muscle and cardiac muscle. Why are these differences necessary for cardiac function? a.​ Gap Junctions and Functional Syncytium i.​ skeletal muscle: no gap junctions; each fiber is individually simulated ii.​ Cardiac muscle: has gap junctions, allowing the heart to contract as a unit iii.​ Necessary: the heart needs synchronized contractions to effectively pump blood. Without this, different regions of the heart would contract independently, leading to ineffective circulation. b.​ Tetanic contractions i.​ skeletal muscle: tetanus is possible due to a short refractory period ii.​ Cardiac muscle: tetanus is not possible because the refractory period is nearly as long as the contraction iii.​ Necessary: if tetanus occurred in the heart, it would be unable to relax and fill with blood, making it an ineffective pump. c.​ Source of calcium ions for contraction i.​ Skeletal muscle: calcium is released exclusively from the sarcoplasmic reticulum (SR) ii.​ Cardiac muscle: calcium comes from both the SR and extracellular fluid iii.​ Necessary: the heart relies on extracellular calcium to sustain contractions and regulate force generation. This ensures the heart can adapt to different physiological demands d.​ Pacemaker cells and autorhythmicity i.​ skeletal muscle: requires neural stimulation to contract ii.​ Cardiac muscle: has pacemaker cells that can spontaneously depolarize iii.​ Necessary: the heart must beat continuously without requiring direct neural input. Pacemaker cells ensure a consistent rhythm, even if neural connections are severed. e.​ Dependence and aerobic respiration i.​ Skeletal muscle: can generate ATP aerobically and anaerobically ii.​ Cardiac muscle: relies almost exclusively on aerobic respiration, with more mitochondria  iii.​ Necessary: the heart must function without fatigue, requiring a continuous oxygen supply. Unlike skeletal muscle, it cannot afford to accumulate lactic acid, which would impair contraction. 14.​What is a slow Ca2+ channel? How does it function in cardiac muscle contraction? a.​ Slow calcium ion channels are specialized calcium channels in the plasma membrane of cardiac cells. They are termed “slow” because their opening is delayed compared to fast sodium channels. b.​ Function i.​ Depolarization trigger 1.​ When the cardiac muscle cell membrane depolarizes, these slo Calcium ion channels open, allowing calcium ions to enter the cell from the extracellular fluid ii.​ Calcium influx 1.​ Accounts for about 10-20% of the calcium needed for muscle contraction. iii.​ Triggering further release 1.​ The entry of calcium ions through these channels triggers the release of additional calcium ions from the sarcoplasmic reticulum (SR) which provides the remaining 80-90% of the calcium required for contraction. iv.​ Prolonged depolarization 1.​ The calcium ion influx prolongs the depolarization phase, creating a plateau in the action potential, which ensures sustained contraction necessary for effective heartbeats. c.​ Importance i.​ Coordinated contraction 1.​ The prolonged depolarization ensures that the heart muscle contracts in a coordinated manner, essential for pumping blood effectively. ii.​ Calcium-induced calcium release 1.​ This mechanism ensures a robust and sustained contractions, critical for the hearts continuous activity 15.​What is the intrinsic conduction system? Name and give the location of its components a.​ Intrinsic conduction system i.​ Consists of non contractile cardiac cells specialized to initiate and distribute a wave of depolarization, throughout the heart, so that it depolarizes and contracts in an orderly, sequential manner. b.​ Sinoatrial (SA) node i.​ Located in the right atrial wall, inferior to the entrance of the superior vena cava. c.​ Atrioventricular (AV) node i.​ Located in the inferior portion of the interatrial septum immediately above the tricuspid calc. d.​ Atrioventricular (AV) bundle  i.​ Located in the superior part of the interventricular septum. e.​ Right and left bundle branches i.​ Runs along the interventricular septum toward the heart apex 16.​Describe how the intrinsic conduction system functions. Include the effects of dysfunction of the different parts a.​ Function of the intrinsic conduction system i.​ Consists of specialized cardiac muscle cells that generate and transmit electrical impulses, ensuring coordinated contractions. b.​ Sinoatrial (SA) Node (pacemaker) i.​ Function 1.​ Initiates each heartbeat by generating action potentials at about 75 impulses per minute. This sets the rhythm of the heart (sinus rhythm) ii.​ Dysfunction 1.​ If the SA node fails, the AV node can take over, but at a slower rate (40-60 bpm). This may lead to bradycardia or irregular rhythms, requiring a pacemaker in severe cases c.​ Atrioventricular (AV) Node i.​ Function 1.​ Delays impulses (by about 0.1 sec) to allow the atria to fully contract before the ventricles. Also serves a s backup pacemaker ii.​ Dysfunction 1.​ AV node damage can cause heart block, where impulses are partially or completely blocked from reaching the ventricles. This can result in slow or irregular ventricular contractions, sometimes requiring an artificial pacemaker d.​ Atrioventricular (AV) Bundle i.​ Function 1.​ Conduct impulses through the interventricular septum toward the apex of the heart ii.​ Dysfunction 1.​ Blockage in one of these branches causes the ventricles to contract asynchronously, reducing the efficiency of the heartbeat e.​ Purkinje Fibers i.​ Function 1.​ Distribute electrical impulse throughout the ventricles, ensuring coordinated contraction for effective blood ejection ii.​ Dysfunction 1.​ If purkinje fibers fail, ventricular contraction may be weak or uncoordinated, leading to conditions like ventricular arrhythmias or heart failure 17.​Explain the different arrhythmias that may occur. Include fibrillation, ectopic focus, extrasystole and heart block. What are the consequences of each? a.​ Fibrillation  i.​ A conduction of rapid and irregular or out of sync contraction b.​ Ectopic focus i.​ Takes over the pacing of the heart rate. The pace set by the AV node is 40-60 bpm, slower than sinus rhythm but still adequate to maintain circulation c.​ Extrasystole i.​ Premature contraction due to a hyperexcitable region of the heart. Usually harmless but resistant causes ended evaluation d.​ Heart block i.​ Damage to the AV node, AV bundle or bundle branches ii.​ Total heart blockage 1.​ no impulses reach the ventricles, causing them to beat too slowly iii.​ Partial heart blockage 1.​ Some impulses get through, leading to irregular heartbeats. Artificial pacemakers are often used to maintain proper rhythm. 18.​Explain how the basic rhythm of the heart is modified by extrinsic innervation a.​ The autonomic nervous system modifies the march like beat and introduces a subtle variability from one beat to the next b.​ The sympathetic nervous system increases both the rate and the force of the heartbeat c.​ Parasympathetic activation slows the heart 19.​Explain how action potentials are initiated by pacemaker cells. Explain two ways that this is different from action potentials of skeletal muscle or nerve cells. a.​ Pacemaker potential (slow depolarization) i.​ Do not have stable resting membrane potentials. Instead they depolarize due to slow Na+ influx and reduced K+ efflux ii.​ This gradual depolarization continues until the membrane potential reaches threshold b.​ Depolarization (threshold reached) i.​ When the membrane potential reaches threshold (~40 mV) voltage gated Na+ channels open, allowing Ca+2 influx, which generates the rapid depolarization phase of the action potential c.​ Repolarization i.​ After the peak, voltage-gated K+ channels open, allowing K+ to exit, which depolarizes the membrane ii.​ Once repolarization is complete, the cycle starts again due to the constant slow influx of Na+ d.​ Two difference between pacemaker and skeletal muscle/nerve action potentials i.​ Unstable vs. Stable Resting Potential 1.​ Pacemaker cells: have an unstable resting potential that gradually depolarizes on its own 2.​ skeletal muscle/Nerve cells: have a stable resting potential that requires external stimulation ii.​ Depolarization by calcium vs. sodium  1.​ Pacemaker cells: depolarize via Ca+2 influx 2.​ skeletal muscle/nerve cells: depolarize via Na+ influx 20.​Draw and label an electrocardiogram. Explain what each of the components represents a.​. 21.​Define diastole and systole a.​ Diastole i.​ The period of relaxation in the heart ii.​ During diastole, the heart chambers relax and fill with blood b.​ Systole i.​ The periods of contraction in the heart ii.​ During systole the heart chamber contracts to pump blood out. 22.​For cardiac cycle, explain how the pressure in the left atrium, left ventricle and aorta change as the atria and ventricles contract and relax. Describe the relative volume of the left ventricle. What makes the heart sounds and when are the different valves open and closed? a.​ Ventricular filling (mid-to-late diastole) i.​ Pressure 1.​ Low in atria and ventricles, higher in the aorta ii.​ Valves 1.​ AV valves open, SL valves closed iii.​ Volume 1.​ Left ventricle fills, reaching end diastolic volume (EDV) b.​ Atrial systole (final filling phase) i.​ Pressure 1.​ Slight increase in atrial pressure as it contracts ii.​ Valves 1.​ AV valves remain open, AL valves still closed c.​ Isovolumic contraction (early ventricular systole) i.​ Pressure 1.​ Ventricular pressure rises sharply, atrial pressure drops ​ ii.​ Valves 1.​ AV valves close (“Lub” S1) SL valves still closed iii.​ Volume 1.​ No change (both valves closed) d.​ Ventricular ejection (late ventricular systole) i.​ Pressure 1.​ Ventricular pressure peaks (~120 mmHg) aortic pressure rises ii.​ Valves 1.​ SL valves open, AV valves remain closed iii.​ Volume 1.​ Left ventricle ejects blood, volume decreases e.​ Isovolumic Relaxation (early diastole) i.​ Pressure  1.​ Ventricular pressure drops, aortic pressure briefly rises (dicrotic notch) ii.​ Valves 1.​ SL valves close (“Dub” S2) AV valves still closed iii.​ Volume 1.​ No change f.​ Ventricular filling begins again i.​ Pressure 1.​ Atrial pressure rises, eventually exceeding ventricular pressure ii.​ Valves ​ 1.​ AV valves open, SL valves closed iii.​ Volume 1.​ Left ventricle refills, restarting the cycle g.​ Heart Sounds and Valve timing i.​ S1 “Lub” AV valves close (start of systole) ii.​ S2 “Dub” SL valves close (start of diastole) 23.​Define cardiac output. What two factors produce it? What is cardiac reserve? a.​ Definition i.​ The amount of blood pumped out by each ventricle in 1 minute b.​ Factors i.​ Heart Rate (HR) ii.​ Stroke Volume (SV) iii.​ Cardiac reserve 1.​ The difference between resting and maximal cardiac output 24.​What is stroke volume? What three factors affect it? a.​ Stroke volume (SV) i.​ The volume correlates with the force of ventricular contraction. ii.​ SV represents the differences between end diastolic volume (EDV), the amount of blood that collects in a ventricle during diastole, and end systolic volume (ESV) the volume of blood remaining in a ventricle after it has contracted 1.​ SV = EDV - ESV b.​ Three factors i.​ Preload ii.​ Contractility iii.​ Afterload 25.​Explain preload and the Frank Starling law of the heart a.​ Preload i.​ the degree to which cardiac muscle cells are stretched just before they contract. Aids to automatically control stroke volume b.​ Frank Starling law i.​ The principle that increased blood volume return to the heart results in a corresponding increase of the cardiac muscle fibers before contraction 26.​Explain contractility and the factors that affect it  a.​ Contractility i.​ The contractile strength achieved at a given muscle length b.​ Factors i.​ Rises when more Ca+2 enters the cytoplasm from the extracellular fluid and the AR ii.​ Enhanced contractility means more blood is ejected from the heart and so ESV is lower iii.​ Effect of norepinephrine or epinephrine binding is to initiate a cyclic AMP second messenger system that increases Ca+2 entry, which in turn promotes more cross bridge binding and enhances ventricular contractility. 27.​Explain afterload and its effects on stroke volume a.​ Afterload i.​ The pressure that the ventricles must overcome to eject blood. ii.​ Essentially the back pressure that arterial blood exerts on the aortic and pulmonary valves. b.​ Effects on SV i.​ In healthy individuals, afterload is not a major determinant of SV because it is relatively constant ii.​ People with hypertension, afterload is important because it reduces the ability of the ventricles to eject blood. iii.​ More blood remains in the heart after systole increasing ESV and reducing stroke volume 28.​What factors affect heart rate? Which will increase heart rate and why? Which will decrease heart rate and why? a.​ Factors that increase heart rate i.​ Autonomic Nervous System 1.​ Emotional or physical stressors activate the SNS causing the SA node fires more rapidly and the heart responds by beating faster ii.​ Chemical Regulation of Heart Rate 1.​ Hormones a.​ Epinephrine during SNS activation enhances heart rate and contractility b.​ Thyroxine increases metabolic rate and production of body heat. When released in large quantities, it causes sustained increase in heart rate 2.​ Ions a.​ Normal heart rate functions depend on having normal levels of intracellular and extracellular ions. 3.​ Other a.​ Exercise raises HR by acting through the SNS b.​ Heat increases HR by enhancing the metabolic rate of cardiac cells b.​ Factors that decrease heart rate  i.​ PNS activation 1.​ Fatal tone a.​ Under resting condition the PNS dominates, releasing acetylcholine, which hyperpolarizes the heart cells, reducing HR 2.​ Ions a.​ High levels of potassium ions can lead to heart block and cardiac arrest, while low levels cause weak and arrhythmic heartbeats 3.​ Cold a.​ Directly decreases HR by lowering the metabolic rate of cardiac cells 29.​Define tachycardia and bradycardia a.​ Tachycardia abnormal fast resting heart rate of more than 100 bpm i.​ May result from elevated body temp, stress, certain drugs, or heart disease b.​ Bradycardia i.​ Resting heart rate slower than 60 bpm 1.​ May result from low body temperature, certain drugs, or PNS activation. 30.​Explain the factors that can contribute to homeostatic imbalance of cardiac output. Include the consequences of each a.​ Coronary atherosclerosis i.​ Essentially fatty buildup that clogs the coronary arteries, impairs blood, and O2 delivery to cardiac cells. Heart becomes increasingly hyposix and begins to contract ineffectively b.​ Persistent high blood pressure i.​ When aortic diastolic blood pressure rises to 90 mmHm or more, the myocardium must exert more force to open the aortic valve and pump out the same amount of blood. If afterload is chronically elevated, ESV rises and the myocardium hypertrophies. Eventually the myocardium becomes progressively weaker c.​ Multiple myocardial infarctions i.​ A succession of MIs (heart attacks) depresses pumping efficiency because noncontractile fibrous (scar) tissue replaces the head heart cells d.​ Dilated cardiomyopathy (DCM) i.​ Ventricles twitch and become flabby and myocardium deteriorates often for unknown reasons. Drug toxicity or chronic inflammation may be involved. 31.​Explain the difference between fetal circulation and normal circulation after birth. a.​ Fetal circulation i.​ Fetus receives O2 and nutrients front he placenta bot the lungs ii.​ Two key shunts bypass the lungs since they are not yet functiona; 1.​ Foramen ovale  a.​ A hole between the right and left atria, allowing O2 blood from the palcenta to bypass the right ventricle and lungs 2.​ Ducuts arteriosus a.​ Vessel connecting the pulmonary trunk to the aorta diverting blood away fromt he lungs iii.​ Blood is oxygenated in the placenta and returns via the umbilical vein then mixes with deoxygenated blood before being distributed to the body b.​ Postnatal circulation i.​ At birth the lungs expand and pulmonary resistance drops ii.​ The foramen ovale closes becoming the foaas ovalis ensuring blood flows normally through the lungs iii.​ The ducuts arteriosus constricts becoming the ligamentum arteriosum directling all blood from the right ventricle to the lungs for pxygenation. iv.​ The placenta is no longer used and the babys own cirulatory system supplies oxygen c.​ Key changes i.​ Foramen ovale bypasses lungs by shunting blood between atria and after birth it closes to form fossa ovalis ii.​ Ducuts arteriosus connects pulmonary trunk to aorta and after birth they close forming ligamenteum arteriosum iii.​ Umbilical vein and arteries supply oxygen/nutrients from placenta and after birth they close and become fibrous remnants