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Ch 19 cont'd, Ch 20

by: Gail Chernomorets

Ch 19 cont'd, Ch 20 BIOL 224

Gail Chernomorets

GPA 3.2

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Week 4 notes 9/20 & 9/22
Human Anatomy and Physiology II
Sean Neiswenter
Class Notes
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This 13 page Class Notes was uploaded by Gail Chernomorets on Thursday September 22, 2016. The Class Notes belongs to BIOL 224 at University of Nevada - Las Vegas taught by Sean Neiswenter in Fall 2016. Since its upload, it has received 21 views. For similar materials see Human Anatomy and Physiology II in Biology at University of Nevada - Las Vegas.


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Date Created: 09/22/16
09/20 & 09/22 Chapter 19 cont’d Blood Types  Genetically determined  Single gene  By presence or absence of RBC surface antigens A, B, and Rh (D)  States the antigens present on the RBCs  Type O: nonfunctional alleles Surface Antigens  Cell surface proteins that identify cells to the immune system  Normal cells are ignored and foreign cells attacked  Over 50 antigens found on RBCs - 2 are used for typing Four Basic Blood Types 1. A (surface antigen A) 2. B (surface antigen B) 3. AB (surface antigen A&B) 4. O (neither A nor B)  In some cases you need to have been exposed to that type in the past to have antigens Blood Plasma  Contains antibodies that “attack” and agglutinate (clump) foreign antigens - starting point for clot  Recipient blood type is what is focused on  Wrong type given could lead to hemolysis - end result ugly Blood Plasma Antibodies  Type A cells - Anti-B antibodies in plasma  Type B cells - anti-A antibodies in plasma  Type O - both anti-A and anti-B antibodies in plasma  Type AB cells - no anti-A or –B antibodies The Rh Factor  Aka D antigen  Either Rh positive or negative  (+) are functional allele  (-) are nonfunctional allele  Only sensitized Rh blood has anti-Rh antibodies - are not already there, have to be exposed Testing for Transfusion Compatibility  Evaluate antigens on donor cell (RBCs) and antibodies in recipient plasma  Agglutination - blood clots - caused when wrong blood enters system and attacks itself Erythroblastosis fetalis  Hemolytic disease of newborn  Mother (Rh-) and father Rh (+)  Pertains to Rh factor only  Baby (Rh+) - not a problem in 1 pregnancy  Mother becomes sensitized - produces anti-Rh antibodies - during pregnancy not a problem since in separate vessel, blood is separated  Each additional Rh+ baby - antibodies cross placenta - attack baby’s RBCs - mom attacking baby - erythroblastosis fetalis occurs  Mom can pass immune system to offspring White Blood Cells  Leukocytes  Involved in immune system  Do not have hemoglobin  Have nuclei and organelles  Functions - defend against pathogens - remove toxins and wastes - attack abnormal cells - some can attack own cells  damaged cells (clean up) WBC Circulation and Movement  Most located in connective tissue proper and lymphatic system organs  Small numbers in blood - 5,000 to 10,000 per microliter Types of WBC  Neutrophils  Lymphocytes (involved in adaptability)  Monocytes  Eosinophils  Basophils Characteristics of Circulating WBCs  Can migrate out of bloodstream  Have amoeboid movement - by attaching to pseudopods  Attracted to chemical stimuli - positive chemotaxis  Some are phagocytic - monocytes - eosinophils - neutrophils WBC Production  All blood cells originate from hemocytoblasts - stem cells that turn into something else - can become 2 different types of stem cells  Progenitor cells - myeloid stem cells - lymphoid stem cells ** Myeloid stem cells produce RBCs and all WBCs except lymphocytes and platelets  Lymphoid stem cells produce lymphocytes Regulation of WBC Production  **Colony-stimulating factors - hormones that regulate blood cell populations Platelets  Cell fragments involved in human clotting  Circulate 9-12 days  Removed by spleen  1/3 reserved for emergencies in the spleen & other vascular organs  used when you have serious bleeding Platelet Functions  Release important clotting chemicals - slows down breeding - clotting factors signal other proteins  coagulation  Platelet production occurs in bone marrow  Megakaryocytes - giant cells in bone marrow  cytoplasmic shedding yields platelets Hemostasis  Cessation of bleeding  3 phases (not mutually exclusive; overlap) 1. Vascular phase  Vascular spasm for up to 30 min  Contraction of smooth muscle 2. Platelet phase  Begins 15 seconds after injury  Platelet adhesions - stick to damaged ends of endothelial cells  Platelet aggregation - stick together  Form platelet plug 3. Coagulation phase  Begins 30 seconds or more after the injury  Blood clotting - coagulation - many clotting factors - chain reactions of enzymes and proenzymes - 3 pathways ** All end with fibrinogen converting to fibrin Three General Coagulation Pathways  Complex 1. Extrinsic pathway  Begins outside of bloodstream in damaged cells of the vessel wall 2. Intrinsic pathway  Begins within bloodstream as platelets release specific molecules (signal) 3. Common pathway  Where the intrinsic and extrinsic pathways converge  Ultimately leads to the production of fibrin from fibrinogen ** end up in same place no matter where you start, end with production of fibrin - meeting point **Common Pathway may be on exam  Extrinsic or intrinsic pathway activates Factor X  Factor X forms the enzyme prothrombinase  Prothrombin converted to thrombin  Fibrinogen converted to fibrin  Fibrin = insoluble fibers - clot Clot Retraction **end result of clot formation  Pulls torn edges of vessel closer together - reduce residual bleeding and stabilizing injury site  Reduces size of damaged area - making it easier for fibrocytes, smooth muscle cells, endothelial cells to complete repairs (easier) Fibrinolysis  Slow process of dissolving clot with enzymes -digest fibrin Ex. plasmin - works against formation of fibrin  Ca 2+ and vitamin K (pick up in environment) are important at several stages of clotting 2+  All 3 pathways require Ca - anything that lowers blood calcium will impair clotting  Vitamin K is fat soluble - 50% from diet  found in green leafy vegetables – kale, spinach, etc. - 50% made by bacteria in your gut  microflora - required for prothrombin synthesis Blood Clot in Bloodstream  Can be bad  Anticoagulants in plasma - Ex. antithrombin III Heparin  Released by WBC Ex. basophils and granulocytes  Accelerates antithrombin III - increases anti-coagulation  Used clinically Thrombomodulin  Released by endothelial cells  Protein C in plasma - Stimulates plasmin Aspirin  Anti-inflammatory/blood thinner  Inhibits prostaglandins  Prevents platelet aggregation and clot formation - work against Vampire Spit  Vampire bats - blood drinking bats  Draculin - anticoagulant in vampire saliva - noncompetitive inhibitor of Factor X - common pathway  Desmoteplase - converts plasminogen to plasmin  dropped from Phase 4 trials Chapter 20 The Heart The Cardiovascular System Consists of:  a pump  a conducting system (blood vessels)  a fluid medium (blood) The Pulmonary Circuit  Closed loop (#1)  O 2CO 2  Carries blood to and from gas exchange surfaces of lungs The Systemic Circuit  Closed loop (#2)  High O i2 blood  CO O 2 2  Blood to the body  Blood alternates with pulmonary Three Types of Blood Vessels 1. Arteries  Carry blood away from heart  Long vessel that branches out smaller and smaller 2. Veins  Carry blood to the heart 3. Capillaries  Only site of exchange  Networks connecting arteries and veins  Exchange vessels Heart Chambers  Right Atrium - collects blood from systemic circuit - returning to heart from body  Right Ventricle - pumps blood to pulmonary circuit  Left Atrium - collects blood from pulmonary circuit - returning to heart from lungs  Left Ventricle - pumps blood to systemic circuit  Pump - high blood pressure  lungs  exchange gases and change in pressure  lower blood pressure  heart The Heart  Great veins and arteries at the base  Pointed tip is apex  Surrounded by pericardial sac  In mediastinum  Base Apex Analogy of Heart  Fist in a balloon - heart is fist - pericardial sac is balloon Superficial Anatomy of the Heart  Empty atria are wrinkly - fold down on each other - auricle  atrial appendage  right atrium  Sulcus - between ventricles - groove  Coronary sulcus - superficial - divides atria and ventricles  Anterior Interventricular sulcus  Posterior Interventricular sulcus  Contains coronary vessels and fat - energy source - doesn’t preserve well Structure of the Heart  Cardiac muscle - aerobic The Heart Wall has Three Layers  Epicardium - outer layer - surrounding the heart - attached to sac - is the same as the visceral pericardium  Myocardium - middle layer - majority of the heart - muscular wall  cardiac muscle  Endocardium - inner layer - SSET  Simple squamous epithelial tissue - continuous with endothelium Cardiac Muscle Tissue  Single nucleus per cell  Intercalated discs interconnect cardiac muscle cells - secured by desmosomes  transfer force of contraction - linked by gap junctions  propagate action potentials - continuous membrane between cell (cytoplasm) - structural connection  Ex. Velcro Characteristics of Cardiac Muscle Cells  Compared to skeletal muscle  Small size  Single, central nucleus  Branching interconnections between cells  Intercalated discs Internal Anatomy and Organization  Internal septum - partition between atrium and ventricles  Interventricular septum  Atrioventricular septum - between - function  ensure one-way flow of blood from atrium to ventricle  one direction only The Right Atrium  Before birth Foramen ovale  At birth - closes  Forms fossa ovalis  Pectinate muscles - prominent muscular ridges on the anterior atrial wall and inner surfaces of the right auricle  Superior vena cava - receives blood from head, neck, upper limbs, and chest  Inferior vena cava - receives blood from trunk, viscera, and lower limbs  Coronary sinus - receives blood from cardiac veins The Right Ventricle  Only flow one direction  The right atrioventricular (AV) valve - aka tricuspid  Chordae tendinae from papillary muscles - prevent backflow during ventricular contraction - only found in atrioventricular valves  Trabeculae carneae - muscle ridges - similar to appearance of spongy bone The Pulmonary Circuit  The right ventricle pumps blood through pulmonary semilunar valve into pulmonary trunk  The pulmonary trunk divides into left and right pulmonary arteries  To L and R lung The Left Atrium  Left and right pulmonary veins - collects in left atrium  Left atrioventricular (AV) valve - aka bicuspid or mitral valve  Same volume thicker muscle as R 4-6x force Systemic Circulation  Aortic semilunar valve  Into ascending aorta  Turns (aortic arch)  Then descending aorta The Heart Valves Atrioventricular (AV) valves - backflow: serious force - blood pressure closes valves - papillary muscles tense chordae tendinae  Semilunar valves - 3 flaps - backflow: passive movement - have no muscular support - the valve supports itself (like a tripod) when closed and opens under pressure Connective Tissues and the Cardiac Skeleton Connective Tissue Fibers  Function - physically support cardiac muscle fibers - distribute forces of contraction - prevent overexpansion of heart - provide elasticity that helps return heart to original size and shape after contraction The Cardiac Skeleton  Bands of tough elastic tissue that encircle the valves as well as the base of the pulmonary trunk and aorta - stabilize valve positions - electrically insulate ventricular cells from atrial cells - provides electrical insulation - allows for proper timing The Blood Supply to the Heart  Has its own blood supply Coronary circulation - supplies blood to muscle tissue of the heart  The left and right coronary arteries originate at the base of the aorta - when contraction occurs, the aortic semilunar valve blocks coronary circulation and when it relaxes, the blood flow is restored Continued Anatomy  Arterial anastomoses - interconnections between arteries - small branches help stabilize blood supply - common in vascular system, not seen much in heart - provides alternate ways for blood flow to get to certain tissues - if block occurs can lead to severe tissue damage because no alternate route to provide blood supply  Coronary artery disease (CAD) - areas of partial or complete blockage of coronary circulation Myocardial infarction (MI) - heart attack - coronary circulation blocked and ischemic tissue dying - severity depends on where blockage occurs - heart muscle dies really quickly due to it being very aerobic - blood slows and clots occur; reaction is to calcify and allows for less elasticity Cardiac Physiology  A single cardiac contraction (heartbeat) - heart contracts in series – atria then ventricles  Two types of cardiac muscle cells - conducting system controls and coordinates heartbeat  specialized type of myocardium  create and send action potentials - contractile cells produce contractions that propel blood The Conducting System  A system of specialized cardiac muscle - initiates and distributes AP - aka pacemaker Autorhythmicity - cardiac muscle tissue contracts automatically - creates its own rhythm  SA and AV nodes exhibit prepotential - can spontaneously create an action potential - pacemaker potential  they spontaneously depolarize - conducting cells  SA node is the pacemaker - the one in control  Conducting cells go down and give up - rhythmic pattern depends on sodium entering cell Sinoatrial (SA) Node - right atrium - contains pacemaker cells - SA node generates 80-100 action potentials per minute - Parasympathetic stimulation slows HR - Generates more action potential than anything else  Atriventricular (AV) Node - receives AP from SA node - impulse slows ~100msec - atrial contraction during delay - during a heart attack, tissue dies here, next fastest source takes over  not as fast, HR drops significantly  AV Bundle - interventricular septum - splits into left and right bundle branches - deep Purkinje fibers propagate AP - throughout ventricular myocardium At this point: - atrial contraction completed - ventricular contraction begins  wave from apex to base - entire process requires 225 msec The Cardiac Cycle  One heartbeat  All 4 chambers contracting correctly  Begins with an action potential at the SA node - transmitted through conducting system - produces action potentials in contractile cells  Electrocardiogram (ECG or EKG) - electrical events in the cardiac cycle can be recorded on an ECG The Electrocardiogram (ECG or EKG)  A recording of electrical events in the heart - EKG patterns are different than the action potentials that occur along individual cell membranes  Obtained by electrodes at specific body locations  Abnormal patterns diagnose damage - measuring Features of an ECG ** Be able to identify waves and what occurs  P Wave - indicates atrial depolarization - signal for contraction - atrial contraction begins about 25 msec later  QRS complex - indicates ventricular depolarization - ventricular contraction begins just after the R peak - atrial repolarization occurs at this time but it masked by electrical events in the ventricles  complex pattern  AP wave from base to apex  T Wave - indicates ventricular repolarization Tension Production and Contraction Types  Rate of neural stimulation effects tension in skeletal muscle  Wave summation - increasing tension or summation of twitches  Incomplete tetanus - rapid stimulation causes muscle fibers to reach near maximum levels of tension  Complete tetanus - stimulation frequency is high = continuous contraction and maximum tension  Control tension by alternating contraction  Cardiac muscle can’t reach complete tetanus The Action Potential in Cardiac Muscle Cells  Resting potential = -90 mV  Threshold = -75 mV  Stimulus is the excitation near intercalated discs **Steps in Cardiac Muscle Action Potential Possible Essay Question 1. Rapid depolarization  Voltage gated fast sodium channels open a few msec  Duration: 3-5 msec  Ends with: closure of voltage-gated fast sodium channels 2. Plateau  Membrane potential remains near 0  Na+ channels close/Na+ pumped out  Voltage-gated slow calcium channels open 2+  Ca leaks in for ~175 msec 3. Repolarization  Slow calcium channels close and slow potassium channels open  Duration: 75 msec ** Reason why cardiac muscle cant reach complete tetanus is because action potential is too long  Refractory period - absolute refractory period - 200 msec - unable to respond Relative refractory period - 50 msec - can respond Compare/Contrast System  Skeletal Muscle - speed of refractory periods are like a twitch (msec) Cardiac Muscle - speed of refractory periods are long, slow contractions


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