Pathophysiology Chapters 11, 12, 13, and 17
Pathophysiology Chapters 11, 12, 13, and 17 HLTHST 300
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This 20 page Class Notes was uploaded by email@example.com Notetaker on Monday September 19, 2016. The Class Notes belongs to HLTHST 300 at Boise State University taught by Jennifer Legget in Fall 2016. Since its upload, it has received 26 views. For similar materials see Pathophysiology in Biology at Boise State University.
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Pathophysiology: Chapter 11 - Disorders of White Blood Cells and Lymphoid Tissue Development of Blood Cells o Pluripotent Stem Cells In bone marrow Develop into Committed Progenitor Cells: develop into specialized cells Lymphoid Stem Cells and Myeloid Stem Cells o Multipotent Stem Cells Hematopoietic: complete maturation in bone marrow (B cells) Lymphopoietic: travel to lymph tissues to complete maturation (T cells) Types of White Blood Cells o Granulocytes Neutrophils Neutral staining granules 60 to 65% of WBCs Contain 3-5 lobar nuclei Maintain normal host defense against foreign agents First to arrive to area during inflammation Eosinophils Granules stain red 1 to 3% of WBCs Increase in number during allergic reactions Basophils Granules stain blue 0.3 to 0.5% of WBCs (least numerous) Contain heparin, histamine, and inflammatory mediators Related to mast cells o Agranulocytes Lymphocytes 30% of WBCs Reside in lymph organs 3 types o B Cells humoral mediated immunity Mature in the bone marrow o T Cells cell mediated immunity Mature in the thymus o Natural Killers innate immunity Destroy foreign cells Monocytes/Macrophages 3 to 8% of WBCs Largest cells Mature in bone marrow Phagocytize bacteria and tissue debris during inflammation Lymphoid Tissues o Lymph vessels, lymph nodes, thymus, spleen o B Cells, T Cells, and Natural Killers in nodes o Lymph vessels collect extra fluid from the tissues and bring it through the nodes to be filtered for pathogens Disorders of White Blood Cells o Normal numbers = 4,500 to 10,500 o Leukopenia Decrease in number of leukocytes in blood Most often affects neutrophils o Aplastic Anemia All myeloid stem cells are affected (monocytes, granulocytes, erythrocytes, megakaryocytes) Causes anemia, thrombocytopenia, agranulocytosis Agranulocytosis: virtual absence of neutrophils o Neutropenia Abnormally low number of neutrophils Less than 1500 Can be mild, moderate, or severe Risk for recurrent/severe bacterial infections – neutrophils are first defense Congenital Hereditary Kostmann Syndrome (autosomal recessive) Periodic/Cyclic Neutropenia (autosomal dominant) o Periods of low neutrophils, and periods of normality Acquired Caused by aplastic anemia, chemotherapy, radiation Fetly syndrome Splenomegaly o Infectious Mononucleosis Viral infection caused by Epstein Barr Virus Spread y contact with oral secretions Process Virus spreads to B cells Either kills B cell or incorporates itself into the cell’s DNA Infected B cells proliferate and produce heterophil antibodies o Presence of heterophils used to diagnose mono Once infected, you are asymptomatically infected for life Time from exposure to symptoms is 4 to 8 weeks Increase in number of WBCs Acute phase of 2 to 3 weeks Symptoms: malaise, anorexia, chills, fever, pharyngitis (sore throat), enlarged lymph nodes, hepatitis, splenomegaly, nausea, jaundice Treatment: bed rest, analgesics, and anti-inflammatories to treat symptoms Leukemia o Malignant neoplasms of cells coming from myeloid or lymphoid stem cells o Risk Factors Ionizing radiation Chemotherapy nd May occur as a 2 cancer after aggressive treatment for another cancer Family history o Causes chromosomal abnormalities that disrupt normal blood cell development o Complications Leukostasis: blast cell count is elevated Increases blood viscosity Can cause obstruction of small blood vessels Hyperuricemia: increased proliferation or breakdown of purine nucleotides after leukemic cell death from chemotherapy o Four Types Acute Lymphocytic Leukemia (ALL) Most common in children Neoplasms grow composed of immature B cells and T cells Symptoms: bleeding, fatigue, anemia, fever, weight loss, night sweats, bone pain Chronic Lymphocytic Leukemia (CLL) Most common in adults Rarely seen in people younger than 40 Clonal malignancy of B cells Can progress slowly without symptoms or be rapidly fatal Diagnosed by increase in number of lymphocytes Acute Myelocytic Leukemia (AML) Most common in adults Neoplasms grow affecting myeloid stem cells in bone marrow Symptoms: bleeding, fatigue, anemia, fever, weight loss, night sweats, bone pain Chronic Myelocytic Leukemia (CML) Excessive proliferation of myeloid stem cells in bone marrow Develops when a stem cell acquires a Philadelphia Chromosome 3 Phases o 1. Chronic Phase o 2. Short Accelerated Phase o 3. Terminal Blast Crisis Phase Lymphoma o Solid tumors composed of neoplastic lymphoid cells o Non-Hodgkin Lymphoma (NHL) One of the most common cancers Tumors originate from malignant transformation of B cell and T cells during their maturation processes Symptoms: fever, night sweats, weight loss, increased susceptibility to infections, impaired humoral immunity o Hodgkin Lymphoma Presence of Reed Sternberg cells Release factors that induce the accumulation of lymphocytes, macrophages, and granulocytes Symptoms: enlargement of a single lymph node (usually above diaphragm), fever, chills, night sweats, weight loss, impaired cellular immunity, fatigue, anemia Multiple Myeloma o Proliferation of malignant plasma cells in bone marrow and osteolytic bone lesions o Associated with chromosomal abnormalities o Unregulated production of M protein and Bence Jones proteins o Proliferation and activation of osteoclasts Cause bone reabsorption and destruction Impaired production of RBCs, WBCs, and platelets o More cases in men and African-Americans o Symptoms: fractures, hypercalcemia, high viscosity of blood, susceptibility to recurrent infections Pathophysiology: Chapter 13 – Disorders of Red Blood Cells Red Blood Cell o Most numerous blood cell o Structure Nonnucleated Biconcave shape more surface area for oxygen diffusion Thin membrane oxygen can diffuse rapidly on and out of the cell Flexible membrane can squeeze through tight vessels o Function Deliver oxygen to the tissues o Development Erythropoiesis: production of RBCs Production is governed by the body tissue’s oxygen needs Erythropoietin: hormone that signals the need for more RBCs Produced in red bone marrow Start as erythroblasts from pluripotent stem cells As the blast cells mature, they divide, accumulate hemoglobin, and lose their organelles to become mature RBCs Released into the blood as reticulocytes (almost RBCs) Life span of 120 days Destroyed in the spleen when they are old Hemoglobin o Found in red blood cells o Transports oxygen to tissues o Each molecule of hemoglobin can carry 4 molecules of oxygen o Rate of hemoglobin synthesis depends on availability of iron Lack of iron = low hemoglobin in RBCs Iron from dietary intake Bilirubin o When a RBC is destroyed in the spleen, iron and heme are recycled Iron goes to bone marrow to be used in other RBCs Heme is converted to bilirubin and excreted in bile o Accumulates in blood if liver cannot excrete it fast enough o Conjugated Bilirubin: water soluble o Unconjugated Bilirubin: water insoluble Accumulation results in jaundice Lab Tests o Red Blood Cell Count Counts the total number of RBCs in a blood sample o Percentage of Reticulocytes An index of the rate of RBC production When RBCs are produced at a faster rate, there will be more reticulocytes in the circulating blood o Hemoglobin Measures hemoglobin content of blood sample o Hematocrit Measures RBC mass in a blood sample Sample is centrifuged to separate the cells from the plasma Anemia o Sickle Cell Anemia Inherited disorder Caused by the presence of abnormal hemoglobin (HbS instead of HbA) Recessive gene Cause of Sickling HbS polymerizes when deoxygenated, creating a semisolid gel that makes the RBC rigid, distorts its shape, and damages the cell membrane The sickle cell can return to normal shape when oxygenated in the lungs After repeated times of deoxygenation, the sickling is irreversible Effects Chronic Hemolytic Anemia o Premature destruction of RBCs because of rigid membrane o Decrease in RBC numbers Blood Vessel Occlusion o Tissue ischemia Acute Chest Syndrome o Pneumonia from pulmonary infarction o Leading cause of death from sickle cell anemia Acute pain from tissue hypoxia Factors that increase sickling Cold, stress, physical exertion, infection, illness, hypoxia, dehydration, and acidosis o Thalassemia Inherited disorders caused by mutations that decrease the rate of synthesis of alpha or beta globin chains Heterozygous for the trait – thalassemia minor Homozygous for the trait – thalassemia major Severe growth retardation without blood transfusions Beta Thalassemia Deficient synthesis of beta globin chains Cooley Anemia or Mediterranean Anemia Alpha Thalassemia Deficient synthesis of alpha globin chains More common in Asians o Iron Deficiency Anemia Dietary deficiency or loss of iron from bleeding Deficiency in iron leads to decreased hemoglobin and impaired oxygen delivery More iron required for… Toddlers low iron levels at birth and a diet of mainly cow’s milk Adolescents growth spurts require more iron Menstruating women blood and reusable iron lost to menstruation Pregnant women expanding blood volume creates need for iron Symptoms: pallor, fatigue, dyspnea, tachycardia, epithelial atrophy, compulsive eating of ice or dirt o Megaloblastic Anemia Impaired DNA synthesis resulting in enlarged RBCs from impaired maturation Develops slowly Vitamin B12 Deficiency Essential for DNA synthesis and RBC maturation RBCs are oddly shaped, not fully developed with a short life span Found in all animal foods Severe cases cause demyelination of neurons o Paresthesia of hands and feet, loss of position sense, dementia Folic Acid Deficiency Required for DNA synthesis and RBC maturation RBCs are oddly shaped, not fully developed with a short life span Found in green-leafy vegetables, fruit, cereal, and meat o Lost in cooking though Dietary deficiencies, malnutrition, alcoholism Malabsorption from celiac disease Pregnancy increases the need for folic acid o Deficiencies in the fetus cause neural tube defects o Anemia of Chronic Disease Anemia as a complication of chronic infections, AIDS, osteomyelitis, cancer, autoimmune disorders, lupus, inflammatory bowel disease, and chronic kidney disease Polycythemia o An abnormally high total red blood cell count – hematocrit > 50% o Relative hematocrit rises because of a loss of plasma volume o Absolute hematocrit rises because of an increase in total RBC mass o Primary Polycythemia Vera Neoplastic disease of pluripotent stem cells in bone marrow Absolute increase in total RBC mass, elevated WBC and platelet counts Increased viscosity interferes with cardiac output, blood flow, blood pressure Blood clots from increased platelets Symptoms: hypertension, headache, dizziness, inability to concentrate, problems with hearing and vision, itching, pain in fingers/toes, night sweats Treatment to reduce viscosity o Secondary Caused by increase in erythropoietin in response to hypoxia Hypoxia from high altitude, heart and lung disease, smoking Erythropoietin causes increased formation of RBCs in bone marrow Could be caused by neoplasms secreting erythropoietin Treatment to relieve hypoxia Changes for Newborns o RBC count and hemoglobin are high at birth and fall until 2 months o Switch from fetal hemoglobin (HbF) to adult hemoglobin (HbA) within 6 months HbF has a higher affinity for oxygen Facilitates the transfer of oxygen across the placenta HbA has a lower affinity for oxygen Facilitates the unloading of oxygen into the tissues o Hyperbilirubinemia Increased levels of bilirubin – jaundice Very common, benign, self-limiting Caused by increased RBC breakdown, and the inability of the immature liver to conjugate bilirubin for excretion Increases risk of Kernicterus: accumulation of bilirubin in brain cells Causes brain damage Treated with phototherapy Exposure to blue light reduces bilirubin levels o Hemolytic Disease Erythroblastosis Fetalis When an Rh-negative mother has an Rh-positive baby after sensitization Rh antibodies from the mother are transferred to the baby through the placenta o Antibodies cause agglutination and hemolysis o Leads to severe anemia, hyperplasia, edema, enlargement of spleen and liver in the baby Changes in the Elderly o Anemia increases with age Associated with mortality, cardiovascular disease, cognitive disorders, reduced bone density o Hemoglobin levels decline after middle age o Capacity for RBC production declines Cells are not replaced as quickly after a bleed Pathophysiology: Chapter 12 – Disorders of Hemostasis Hemostasis o Maintains the integrity of the circulatory system after vessel injury o Not the same as homeostasis o Disorders are (1) inappropriate formation of clots and (2) failure of blood to clot o Purpose of coagulation – prevent excessive bleeding following injury o Components Platelets (thrombocytes) Come from megakaryocytes in bone marrow Normal level = 150,000 to 400,000 Thrombopoietin signals formation of platelets Coagulation Cascade Each coagulation factor performs a specific step o The activation of one factor is designed to activate the next Vitamin K controls the synthesis of factors VII, IX, X, and prothrombin in the liver Calcium is required for almost all steps Blood Vessels The endothelial cells usually maintain blood flow o Blocking platelet adhesion and activation o Inhibiting the coagulation process o Lysing blood clots In response to injury, they exhibit procoagulant properties o Release Von Willebrand factor Helps platelet adhesion and blood clotting Clotting Process o 1. Vessel Spasm Initiated by endothelial injury Smooth muscle in the vessel wall contracts and reduces blood flow Lasts less than a minute o 2. Formation of Platelet Plug Endothelial tissues release von Willebrand factor Binds to platelet receptors causing them to adhere to the exposed collagen fibers in the vessel wall Platelets release ADP and TXA Attract additional platelets platelet aggregation o 3. Clot Formation Starts the coagulation cascade Sequential activation of factors in the blood Results in conversion of fibrinogen to fibrin threads Create meshwork that cements platelets together to form the clot Intrinsic Pathway Initiated by the activation of factor XII Slower Extrinsic Pathway Initiated by tissue factor Faster In response to trauma o 4. Clot Retraction After the clot is completely formed Actin and myosin filaments in platelets contract like a muscle fiber Fibrin strands of the clot are pulled toward the platelets Squeezes serum out of the clot and shrinks it o 5. Clot Dissolution Initiated by activation of plasminogen Large amounts are trapped in the clot Plasminogen turns to plasmin which digests fibrin strands (fibrinolysis) Clot dissolves Increased Platelet Function o Causes Increased platelet count Disturbances in blood flow Damage to vascular endothelium Increased sensitivity of platelets to factors that cause adhesion and aggregation o Thrombocytosis: platelet count above 1,000,000 From iron-deficiency anemia, splenectomy, cancer, arthritis, Crohn’s disease o Effects Inappropriate blood clotting Endothelial damage Arteriosclerosis Increased Clotting Activity o Caused by an increase in procoagulation factors or a decrease in anticoagulation factors o Inherited Disorders (primary) Mutations in factor V and prothrombin Leiden Mutation: a specific mutation in factor V Associated with… Venous thrombosis Thromboembolisms in pregnancy Premature placental separation o Acquired Disorders (secondary) Caused by prolonged bed rest and immobility Hypercoagulability is associated with the use of oral contraceptives, smoking, and obesity Thrombocytopenia o Decrease in the number of platelets – less than 100,000 The greater the decrease, the greater the risk of bleeding o Manifestations Bleeding in the nose, mouth, GI tract, and uterus Bruises and pinpoint hemorrhages on the skin Petechiae: small red or purple spot on the skin caused by bleeding of small blood vessels o Causes Decreased platelet production Decreased platelet survival Splenic sequestration Dilution of the blood o Immune Thrombocytopenic Purpura Autoimmune disorder Platelet antibody formation and excess destruction of platelets Can be acute or chronic Purpura: rash of purple spots on the skin caused by bleeding of small blood vessels Associated with… AIDS Systemic lupus erythematosus Antiphospholipid syndrome Chronic lymphocytic leukemia Lymphoma Hepatitis C o Drug-Induced Drugs cause an antigen-antibody response that causes platelet destruction Fall in platelet count 7 days after taking the drug for the first time or 2-3 days after taking the drug for the recurrent time Commonly caused by Heparin o Thrombotic Microangiopathies Thrombotic Thrombocytopenic Purpura (TTP) Effects o Fever o Thrombocytopenia o Anemia o Neurologic abnormalities Treatment o Plasmapheresis: removing and replacing the patient’s plasma Hemolytic-Uremic Syndrome (HUS) Usually follows an E. Coli infection Effects o Anemia o Thrombocytopenia o Acute renal failure Coagulation Disorders o Von Willebrand Disease Hereditary Deficiency or defect in von Willebrand factor (vWF) Autosomal dominant Manifestations Bleeding from the nose, mouth, GI tract, excessive menstrual flow Severe cases – life threatening GI bleeds and joint hemorrhage o Hemophilia A X-linked recessive Primarily affects males Deficiency or defect in factor VIII Manifestations Bleeding from the hip, knee, elbow, and ankle joints o Inflammation, pain, and swelling in the joint o Causes joint fibrosis and contractures Treatment Must prevent trauma Avoid aspirin and NSAIDs Factor VIII replacement therapy Vascular Disorders o Nonthrombocytopenic Purpura o Mild bleeding o Structurally weak vessel walls or damaged vessels from inflammation Platelet count is normal Coagulation factors are normal o Manifestations Easy bruising Petechiae and purpura on the skin Disseminated Intravascular Coagulation o Widespread coagulation and bleeding o Not a primary disease – results from complications of other disorders o Process Begins with massive activation of coagulation cascade Leads to widespread fibrin deposition and clots RBCs squeeze through the clogged vessels Consumption of platelets and coagulation factors to stop the clotting Plasminogen is activated and leads to hemorrhage o Causes Infection and inflammation Trauma Bacterial sepsis Cancer Endothelial damage Viruses Infections Temperature extremes Anticoagulant Drugs o Heparin Binds to antithrombin III to inactivate thrombin and fibrin o Warfarin Prevents Vitamin K from controlling the synthesis of cofactors in the liver o Aspirin and NSAIDs Prevents platelet aggregation Nonsteroidal Anti-Inflammatory Drugs) Pathophysiology: Chapter 17 – Control of Cardiovascular Function Circulation o Distributes oxygen and nutrients needed for metabolic processes to the tissues o Carries waste products from cellular metabolism to the kidneys for elimination o Circulates fluids, electrolytes, and hormones that regulate body function o Pulmonary Circuit Central circulation Components = right heart, pulmonary arteries, arterioles, capillaries, and veins Pulmonary arteries are the only arteries that carry deoxygenated blood Pulmonary veins are the only veins that carry oxygenated blood Smaller system Low pressure system Blood moves through lungs slower – more time for gas exchange o Systemic Circuit Peripheral circulation Components = left heart, aorta, peripheral arteries and veins, and vena cava Larger system High pressure system Move blood all over the body, sometimes against gravity Volume and Pressure o Volume Distribution 4% in left heart 4% in right heart 16% in arteries and arterioles 4% in capillaries 64% in veins and venules o Blood must move from areas of higher pressure to areas of lower pressure Arterial pressure is MUCH higher than venous pressure Blood Flow o Hemodynamics: principles that govern the flow of blood Pressure Gradient difference in pressure between the two ends of a vessel Increased gradient = increased flow Vessel Radius size of the blood vessel’s lumen Increased radius = increased flow Vessel Length usually remains constant, increases with more tissue (fat) Increased length = decreased flow Cross Sectional Area surface area of the vessel Increased area = slower velocity of flow Viscosity determined by the number of components and RBCs in the blood Increased viscosity = decreased flow o Pressure and Resistance Flow = ΔP/R ΔP = Pressure difference between the two ends of a vessel R = Resistance the blood must overcome as it moves through the vessel Poiseuille’s Law Flow will increase as pressure gradient and vessel radius increase Flow will decrease as blood viscosity increases o Laplace’s Law P = T/r Pressure = tension/radius P = intraluminal pressure: pressure within the vessel T = wall tension: force of the vessel wall opposing outward pressure from blood inside the vessel r = vessel radius Intraluminal pressure expands the vessel until it is balanced by wall tension T = P x r Tension = pressure x radius Tension decreases in areas of smaller radii Tension increases in areas of larger radii Blood Vessels o Distensibility: the ability of a blood vessel to stretch and accommodate more blood Veins are the most distensible Can increase their volume with only a slight change in pressure o Compliance: the total amount of blood that can be stored in a given portion of circulation o Arteries have thicker, more +muscular walls than veins Allows for vasodilation and constriction when needed Anatomy of the Heart o Atria have thin walls, ventricles have thick muscular walls o Left ventricle wall is much thicker than the right ventricle Left ventricle pumps blood to the whole body, not just the lungs o Pericardium Fibrous outer covering around the heart Holds the heart in position in the thorax Barrier from infection 2 Layers 1. Tough outer fibrous layer – highly resistant to distention 2. Thin inner serous layer o Visceral layer (epicardium) o Parietal layer o Pericardial cavity in between – minimizes friction o Myocardium Muscular layer Cardiac Muscle Striated Sarcomeres composed of actin and myosin filaments Many, large mitochondria for energy Contractions are involuntary and last longer Fibers separated by intercalated discs o Allows the impulses to travel quickly and the heart to contract as a single unit Rely on extracellular calcium ions for contractions Troponin levels released from injured heart muscles are used to diagnose MI o Endocardium Thin membrane that lines the chambers of the heart and covers the valves Three layers o Fibrous Skeleton Separates the atria and ventricles Rigid support for attachments for the valves o Heart Valves Ensures blood only flows in one direction Atrioventricular Valves Supported by papillary muscles held down by chordae tendineae Bicuspid/Mitral between left atrium and ventricle Tricuspid between right atrium and ventricle Semilunar Valves Cuplike cusps catch the backward flow of blood when closed Pulmonic between right ventricle and pulmonary artery Aortic between left ventricle and aorta Electrical Activity of the Heart o Heart can generate its own action potentials o Conduction System 1. Sinoatrial (SA) Node Action potential is generated Fastest intrinsic rate = 60 to 100 bpm Pacemaker of the heart 2. Atrioventricular (AV) Node Conducts the action potential from the atria to the ventricles Intrinsic Rate = 45 to 50 bpm 3. AV Bundle (Bundle of HIS) Action potential is briefly delayed o Allows the atria to complete their contraction before the ventricles contract 4. Purkinje Fibers Conducts the action potential to all parts of the ventricles Intrinsic Rate = 15 to 40 bpm o Action Potentials Depends on sodium, potassium, and calcium 1. Resting Stage Positive on the outside, negative on the inside 2. Depolarization Polarity switches 3. Repolarization Polarity returns to normal state o Conduction Disorders Supraventricular Arrhythmias Originate in the SA node, atria, and AV node Ventricular Arrhythmias Originate in the Purkinje fibers More serious and life threatening Heart Block Action potential is blocked in the AV bundle In complete heart block, the atria and ventricles cannot communicate with each other – beat independently Ectopic Pacemaker Action potential comes from somewhere other than the SA node, when the SA node is working correctly Results in an extra, unnecessary beat Premature Ventricular Contraction (PVC) An action potential is generated from the ventricles, when the SA node is working correctly Results in an extra, unnecessary beat Fibrillation Disorganized current flow Heart doesn’t fully contract, just quivers Ventricular fibrillation can be immediately fatal o Electrocardiography A recording of the electrical activity of the heart P Wave atrial depolarization Line Between P Wave and Q Wave delay at the AV node QRS Complex ventricular depolarization T Wave ventricular repolarization Cardiac Cycle o Systole: Ventricles contract and pump blood o Diastole: Ventricles relax and fill with blood o First heart sound = begins systole, closing of AV valves o Second heart sound = ends systole, closing of semilunar valves Regulation of Cardiac Performance o Cardiac Output The amount of blood the heart pumps each minute Increases with exercise, decreases with rest/sleep CO = SV x HR Cardiac Output = Stroke Volume x Heart Rate Stroke Volume: amount of blood the heart ejects with each beat Heart Rate: number of time the heart beats each minute Cardiac Reserve: maximum percentage of increase in cardiac output that can be achieved above a normal level Preload: ventricular filling, volume work of the heart The amount of blood the heart must pump out of the ventricles Blood remaining in the ventricles after systole plus blood that filled the ventricles during diastole Afterload: pressure the heart must generate to pump blood out Pressure in the aorta creates afterload for the left heart Pressure in the pulmonary artery creates afterload for the right heart Cardiac Contractility: the ability of the heart to change its force of contraction without changing its resting length Heart Rate: frequency of contractions Determines the time spent in diastolic filling Faster heart rate o Less time for diastolic filling o Decrease in stroke volume o Decrease in cardiac output Blood Vessels o Three Layers Tunica Externa/Adventitia Collagen fibers Protection Tunica Media Smooth muscles Dilates and constricts the vessel Tunica Intima Single layer of endothelial cells Prevents platelet adherence and blood clotting o Capillaries Walls are only one cell thick – for gas exchange o Arterial System High pressure system Sympathetic nervous system signals for dilation or constriction Arterioles Take blood to the capillaries Lots of smooth muscle – control blood pressure Arteries Take blood from the heart to the body Lots of elastic fibers – for stretching o Venous System Low pressure system Thin walls, distensible, collapsible Can store lots of blood Valves counteract gravity Skeletal muscles in the legs contract to “milk” the blood up Venules Collect blood from the capillaries Veins Take blood back to the heart Lymphatic System o Takes extra fluid from the tissue spaces o Carries protein, fats, and fat soluble vitamins o Vessels carry the fluid to lymph nodes where it is filtered by WBCs for pathogens Microcirculation o Arterioles, capillaries, and venules Transport of nutrients to the tissues Removal of metabolites o Autoregulation Organs and tissues regulate blood flow depending on their metabolic needs Modifies the diameter of local capillaries Metabolic Mechanism Need for more blood signaled by o Decreased levels of nutrients and oxygen o Increased levels of metabolic wastes (potassium, lactic acid) Myogenic Mechanism Rely on stretch of the smooth muscle in the vessel walls Control of Blood Flow o List at least four tissue factors that contribute to local control of blood flow. o Describe the role of the endothelium in the synthesis and release of factors that control vessel dilatation. o Describe the role of the autonomic nervous system in the control of circulatory function. o Endothelial Control Release factors that affect the degree of relaxation or contraction Nitric Oxide vessel relaxation, inhibits platelet aggregation Continuously released o Humoral Control Relaxation and contraction factors in the blood Epinephrine & Norepinephrine vasoconstriction, sympathetic nervous system Angiotensin II vasoconstriction, increases arterial blood pressure Histamine vasodilation, capillary permeability, mast cells and basophils Serotonin vasoconstriction, controls bleeding, from platelets during clotting Bradykinin vasodilation, capillary permeability Prostaglandins some vasoconstrict, some vasodilate, from cell membrane o Neural Control Autonomic Nervous System (sympathetic and parasympathetic) Medulla oblongata Controls heart rate, contractility, and peripheral vascular resistance Vasomotor Center o Sympathetic control o Acceleration of heart rate o Blood vessel tone Cardioinhibitory Center o Parasympathetic control o Slowing of heart rate