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msu pre med

msu pre med

Description

School: Michigan State University
Department: Physiology
Course: Introductory Physiology
Professor: Patrick dillion
Term: Fall 2015
Tags: PSL, 250, PSL250, Physiology, P.Dillon, Dillon, premed, medical, and med
Cost: 50
Name: PSL 250 Test 3 study guide
Description: This contains all the content that will be on exam 3
Uploaded: 11/07/2016
29 Pages 193 Views 1 Unlocks
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What are premature atrial contractions?




What is the atrioventricular node?




​What is the only vein in the body that has a high oxygen content?



PSL 250 - Test Review - 3 PSL 250 - Lecture 21 - Cardiac Structures and activation Cardiac Cell Structures Structure? ● Cylindrical shaped cells with intercalated disks that join cells end-to-end. ● Thin filament activation by Ca2+ binding to Troponin Type? ● About 95 percent of cells in your heart are muscle cells. ● OthDon't forget about the age old question of bacteriology exam
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ers are autorhythmic, which start your heartbeat Intercalated Disks Structure? ● Intercalated disks are loaded with two particular substructures - have desmosomes that connect the two different cells. Purpose? ● Gap junctions for electrical activation spread. Cardiac Activation Purpose? ● All the cells are acting as a unit - your heart contracts to effectively pump blood around your body. Requirements? ● When the blood is leaves your heart, it needs to have sufficient momentum - when you go all the way down to your feet and all the get all the way back up again. Similar to? ● The activation of cardiac cells is identical to activation in skeletal muscle - ○ Have calcium - with cardiac cells having two sources of the calcium from both the sarcoplasmic reticulum and inside your heart. ○ And you have calcium channels on the cell membrane when the calcium enters into your heart. Baby hearts ™ When? ● You need to have your heart working starting at about five weeks post-conception by five weeks post-conception. ● The growing embryo is so large that it cannot survive on diffusion alone. ● You've got to have a blood supply circulatory system that's carrying blood around the developing embryo, essentially so that the different parts of the body can get the oxygen they need and then get rid of the carbon dioxide they have to get rid of five weeks post-conception day.Circulatory Flow Circuit Systemic flow circuit? ● Left valves to aorta to body to vena cava to right arteries Systemic flow purpose? ● Carries oxygenated blood away from the lungs, carrying it throughout the body and then returning the deoxygenated blood back to the heart. Pulmonary flow circuit? ● Right valves to pulmonary artery to lungs to pulmonary vein to left arteries. Pulmonary flow purpose? ● PFC is the circuit through the lungs, where blood becomes oxygenated. Heart circulation Structure? ● Double pump. cAMP and blood flow? ● When the blood is used in cAMP, it is then returned back by venous circulation to the right side of your heart where you begin the pulmonary circuit. ​What is the only vein in the body that has a high oxygen content? ● The answer is your pulmonary vein = test question. Cardiac Activation Structures Structure? ● Activation pathway has autorhythmic cells Atria ● Site of normal heartbeat initiation Sinoatrial node Location? ● Right atrium Purpose? 1. Spontaneous depolarization (pacemaker potential) that triggers the AP once the MP reaches threshold between -40 and -30 mV). 2. ​The depolarization phase of the AP. 3. ​Repolarization. Once the cell is completely repolarized at about -60 mV, the cycle is spontaneously repeated. What is the atrioventricular node? ● Conducts electrical impulses from sinoatrial node from the atria to the ventricles. What are premature atrial contractions? ● Premature beats occurring from an ectopic focus within the atria. ● Spontaneous depolarization of ectopic focus causes premature atrial contractions. Ectopic focus? ● Excitable group of cells.Blood Venous blood? ● Venous blood is the low oxygen blood. ● Even in the pulmonary artery, it's low oxygen blood. Blood motion? ● The blood has to be pushed upwards in order to get out of your heart. ● The amount of work that your heart has to do is going to be proportional to how much pressure - how much distance you ask the pump for blood. Atrial Muscle How is it activated? ● Right Atrium activated by Sinoatrial node - spreads toward the left atrium using the interatrial pathway ● Contraction spreads through gap junctions ● Not autorhythmic - contraction spreads downward Heart Structure Left ventricle structure? ● The heart wall around your left ventricle is a lot thicker than the wall that's around your right ventricle. ● Left has to pump all the way to your feet and then back up - about four feet. Right ventricle structure? ● The right side of your heart can have a thinner wall - the muscle doesn't have to be strong because the distance it has to pump the blood to your lungs (right next door) is not very great. Heart attack Cause? ● When someone has a heart attack, you have it because some part of your heart muscle does not have sufficient oxygen to make the ATP it needs to do its work, and it can result in the death of those particular cells. Cardiac cells post attack? ● You do not regrow new cardiac muscle cells. - ○ Those dead cells are replaced with scar tissue. Explain additive attacks? ● Heart attacks are additive. If somebody has one heart attack, you can generally pick that up on the electrocardiogram. ● Additional heart attacks cause additional changes which can be picked up by cardiograms. Attack location + cause? ● Most heart attacks occur on the left side, because the left side has to generate more force to pump the blood.● Since the left side is generating more force, it uses more energy and is closer to reaching the edge of not having enough ATP to pump blood. ● Majority of heart attacks are due to not having sufficient oxygen getting to their blood and through their blood vessels Rare cause ● There are seldom heart attacks that occur for energetic reasons. ● On the right side of your heart if you had an embolism that blocked the blood vessel going to to the right side of your heart, you could still have a heart attack there. Atrioventricular node What is it? ● Electrical connection from atria to ventricles What does it do? ● Delays SAP spread, allows ventricular filling to be completed ● Atrioventricular node takes signal from the Sinoatrial node, slows it down and regulates it and sends the impulses from the atria to the ventricles (bundle of His) Purpose of block? ● Atrioventricular block produces separate atrial and ventricular activation. Ventricles How? ● AP enters septum, first spreading to the apex, then up to ventricular muscle. ● Ventricle muscle contraction spreads upward. Purpose? ● Pumps blood away from the heart via powerful contractions. Bundle of His Location? ● Off of AV node, down the septum. Purpose? ● A band of cardiac muscle fibers connecting the atria with the ventricles of the heart. Alternate name? ● Also called the atrioventricular bundle. Purkinje Fibers Location? ● Branch off of septum to ventricular muscle Activated by? ● Activated by bundle of His through gap junctions. Purpose? ● Conduct nerve signals faster than other muscle cells in the heart. ● Send nerve impulses to heart cells in the ventricles, causing them to contract and send blood throughout the body.Ventricular muscle Activated by? ● Apex cells activated first by Purkinje fibers, the muscle cell-to-cell through gap functions ● Contraction spread upward, forcing blood into aorta and pulmonary artery Activity type? ● No pacemaker activity. Pacemaker cells Characteristics? ● Autorhythmic, no stable baseline potential What parts have pacemaker cells? ● Sinoatrial nodes and Atrioventricular nodes, some cells of the B of H and Purkinje Fibers Depolarization How? ● Closing of K+ channels, opening of Ca2+ channels ● Little Na+ influence Neural influences How do sympathetic neurons increase heart rate? ● Sympathetic neurons -- NE opens Ca2+ channels How do parasympathetic neurons decrease heart rate? ● Parasympathetic neurons (vagus n.)- ACh decrease K+ closing rate, ACh decrease Ca2+ channel opening Electrocardiogram What is it? ● Sum of changes in cardiac APs. Measures electrical output by the heart. Relation to cardiac AP What does the electrocardiogram do? ● Detect changes in the sum of APs ● Changes in membrane potential detected by different distances to leads Ventricular Fibrillation What is it? ● Life threatening- no coordinated emptying- no blood delivery How to fix it? ● Need electrical shock to re-coordinate APs P wave Size? ● 0.05 to 0.25 mV Time?● 80 to 100 ms OR 0.08 - 0.1 seconds. What is it? ● The wave of atrial depolarization that spreads from the SA node through the atria, ● Start of atrial contraction QRS complex Time? ● 0.06 to 0.1 seconds - if longer then conduction is impaired within the ventricles. Why can there be a conduction issue? ● A bundle branch blocks or a ventricular foci (abnormal pacemaker site) becomes the pacemaker driving the ventricle. What is it? ● Ventricular depolarization. ● End of atrial contraction, start of atrial filling. ● Start of ventricular contraction. What does it hide? ● Masks atrial repolarization T wave What is it? ● Ventricular repolarization ● End of ventricular contraction, start of ventricular filling. Why is it slower than the P wave? ● Repolarization wave does not utilize the high-velocity bundle branch and purkinje system, and therefore primarily relies on cell-to-cell conduction. Lecture 22 - Cardiac Pumping Cardiac cycle What is it? ● Sequence of contraction and relaxation ● 4 valves ● 2A-V What does it do? ● Aortic/pulmonary, keep blood flow one-way Diastole What is it? ● The relaxation and dilation of the heart chambers, during which they fill with blood. ● End diastolic volume ~130mL Atrial Systole What is it?● Contraction of the atria, which fills the ventricles with blood. Ventricular Systole What is it? ● The contraction of the ventricles, forcing blood into the aortic and pulmonary artery. ● Contraction spreads upward. How should the pressure be? ● Pressure must be greater than aorta to open aortic valve. Aortic Pressure What is it? ● Load left ventricle works against. ● High BP puts greater load on heart Ejected Blood Volume Blood ejected characteristics? ● ~>0-90 mL of blood ejected/ beat ● ~ 65% of end diastolic volume ● Lower HR means higher ejected volume Heart Rate dependence Maximum heart rate? ● The maximum heart rate is (200 age) ○ Rates about 180 decrease filling time Can you go above it? ● Must be motivated to exceed 180 ○ This can decrease cardiac output ○ Potentially life threatening Arterial Pulse How? ● Arterial walls expand to hold blood What is it? ● Pulse - feeling the shockwave of the heart’s contractions through the arteries. ● Little drop in BP throughout arteries Heart Sounds Cause of sounds? ● Closing of valves-- turbulent blood flow creates sounds ● Low pressure AV (mitral and tricuspid) first, then high pressure aortic and pulmonary valves ● Different sounds intensities MurmursWhat is it? ● Non-laminar (non-smooth) flow creates an unnatural sound when valves should be closed. Valve Stenosis What is it? ● Any narrowing of the heart valves. ● Stiff Valve- small opening ● Turbulent flow as blood squirts through Valve insufficiency What is it? ● Valve leaves don't properly mesh ● Children with improper valve closure sometime outgrow this murmur as growth alters valve alignment Cardiac output ● Amount of blood pumped per minute. Stroke volume x Heart Rate = CO. Typical CO? ● ~70 ml at 70 beats/min = ~5 liters per minute. Amount of blood typical? ● Body has about 5 liters of blood. Circulation rate? ● Circulation time - 1 minute. Starling’s law What is it ● Stroke volume control. How? ● Increase in venous return stretches cardiac muscle leading to an increase in force causing an increase in CO. What increases/ decreases? ● More actin-myosin interaction: Less thick z line contact then thin-thin overlap, more Ca++ release. ● Stronger contraction, more SV and more CO. ● When you get more venous return, you get more CO.Neural influences ● Both SV and HR changes. Parasympathetic Characteristics? ● Dominant at rest. ● Cut vagus nerve to heart = HR increases from 70 to 100 immediately. Impact of exercise? ● Exercise increases parasympathetic output, decreasing the resting heart rate. ● May go to 30s and 40s. Sympathetic Caused by? ● Increased Ca++ channel opening. What causes increased HR? ● Faster depolarization causes increased HR. ● More Ca++ causes more force, causes increased SV. PSL 250 - Lecture 23 - Arteries - Arterioles Blood vessels How many layers + names? ● Have three layers - endothelium, vascular smooth muscle, connective tissue. Exception? ● Capillaries only have endothelium. Blood vessel types Types? ● Arteries, arterioles, capillaries, veins.Lymph vessels do what? ● Lymph vessels carry excess filtered fluid. Physical Factors Constant factor? ● Vessel length Flow factor? ● Flow = pressure/resistance. Vessel radius Why is it important? ● Most important variable factor - increase in radius sharply decreases resistance. Resistance ~ 1/(radius)^4 Small constriction effect? ● Small constriction causes large increase in resistance, decrease in flow. Small dilation effect? ● Small dilation causes large decrease in resistance, increase in flow. How to compensate for blockages? ● Short blockages can compensate with increased velocity until greater than 80% closed. Viscosity What is viscosity? ● Thickness of blood Controlled by what + above what concentration is it bad? ● Controlled by hematocrit(%RBCs in blood, 45 males, 42 females) - need large change to influence blood flow. ● Above about 48%, RBC interaction with arteriole walls greatly increases resistance. Arterial Conductance When does high pressure blood enter the aorta? ● High pressure blood enters aorta at ~93 mmHg. How wide are arteries + how they transport blood to tissues? ● Large arteries expand to hold blood, little change in BP, 2-4 mm wide. ● Momentum of moving blood carries blood forward to tissues. Arterial pressure What is systolic and diastolic pressure? ● Systolic P is 120 mmHg , Diastolic P is 80 mmHg. What is pulse pressure? ● Pulse pressure is Sys-Dias: 120 - 80 = 40 mmHg. What is the mean pressure? ● Mean arterial pressure = Dia + ⅓ PP = 80 + 13 = 93 mmHgCoronary circulation Dependent upon? ● Heart rate dependent. What does it do? ● Decreases diastole at high heart rate leading to a decrease in filling time and a decrease in coronary flow. What can cause potential heart failure? ● Coronary flow only occurs during diastole HR > 180 decreases cardiac output and can cause potential heart failure. Atherosclerosis What is it? ● Plaque forming within the inside of the blood vessels. Why is it problematic ™ ● Causes a disruption in the blood flow - more problems with blood clots, up your carotid or down artery. Stages? ● Multiple stages: ● 1: Low density lipoprotein is depositing fatty streak. ● 2: WBCs and fibroblasts overgrow fatty streak. ● 3: Calcium infiltration hardens overgrowth, leading to the hardening of the arteries. ● Overall - ○ Fatty streaks are overgrown by fibroblasts, infused with calcium leads to calcification. Healthy arteries vs unhealthy characteristics? ● Healthy artery - spongy soft. ● Unhealthy - stiff, uncooked spaghetti. Alcohol EffectPositive impact of alcohol? ● Modest alcohol consumption can solubilize fatty streak. ● Can reverse atherosclerosis stage 1. ● Biophysical effect, not receptor effect. ● No effect on other stages. Arteriolar Flow Structure of arterioles? ● Arterioles branch off arteries ~ 30 microns wide, 93 mmHg at artery end. Purpose? ● Carries blood to capillaries: 37 mmHg at capillary end. ● Arteriole radius can go in either direction. Tone What is it? ● Partial activation of smooth muscle without no stimulus. ● Can relax (vasodilate) or contract (vasoconstrict) Perfusion What controls arteriole smooth muscle? ● Sympathetic neurons, metabolites, paracrines control arteriole smooth muscle. ● NE, adenosine, NO. NO impact on BP? ● NO - results in 5 microns blood pressure dilution. Lowering BP and health? ● If someone has high blood pressure, just lowering it results in a healthier individual without addressing any one possible cause specifically. PSL 250 - Lecture 24 - Capillaries - Lymph - Veins Capillary blood flow ● Very slow - many capillaries spread flow out and decrease speed. ● Capillary pressure 37 mmHg at arteriolar end down to 17 mmHg at venous end. Capillary fluid exchange ● Balance of BP forcing fluid out and osmotic pressure from plasma proteins drawing fluid in. ● Fluid moves through capillary pores. Filtration ● Dominates at high pressure end (arteriolar) ● BP is greater than osmotic pressure causing fluid to be forced out.Reabsorption ● At venous end lower BP, BP is greater than osmotic pressure, fluid reenters. ● Net: fluid sweeps volume around capillary . ● Slightly more fluid filtered than reabsorbed. Lymph flow ● Return of excess filtered fluid to circulation. Return of filtered fluid ● Fluid enters closed ended lymph vessels, which merge with others. ● Lymph nodes are sites of large lymph vessel merger ● Large lymph vessels have valves ● Lymph enters vena cava BP = 0 at thoracic duct in chest Edema ● Swelling ● Excess filtration due to broken capillaries ● Low blood protein either caused by starvation or alcoholism. ● Bacteria presence and destruction draw fluid osmotically. ● Parasites - filariasis - block lymph flow - fatal. ● Elephantiasis - fluid is taken into the lymph system. Venous flow ● Capacitance vessels ● Hold largest blood volume Venous Pressure ● 17 mmHg at capillary end to 0 at vena cava. ● During inspiration, vessel in thorax may have negative pressure. ● BP needs help getting blood up to heart. Venous valves Purpose? ● Prevent backflow Location interval? ● Every 1-2 inches in large veins. Skeletal pump How blood goes to heart? ● Muscle contraction squeezes veins - forces blood to heart Varicose veins Caused by?● Ruptured valves - column of blood , slow return. ● Clots may form. How blood bypasses varicose veins? ● Blood bypasses varicosities through different veins. Lecture 25 - Red blood cells - Platelets Plasma ● Liquid portion of blood ● Water, electrolytes, metabolites, hormones, proteins. Plasma proteins ● Albumin: highest amount - draws fluid into capillary - binds hydrophobic hormones. ● Globulins: many subgroups - gamma globulins are antibodies. ● Fibrinogen: final protein for blood clot formation. Erythrocytes - RBC’s ● Carry oxygen and CO2 ● No organelles, only hemoglobin - Hb ● In the course of being manufactured, lose nucleus and all of their organelles. Production ● In bone marrow from stem cells. ● ~ 20 ml of RBC per day ( ~50 ml of blood per day) ● Low blood oxygen causes release of EPO from kidneys. Shape ● Biconcave disks ~ 8 microns across. ● Spectrin net under the membrane helps maintain the blood cell’s shape. ● Fluidity of membrane allow squeeze through capillary. ● Membrane to membrane squeeze increases the transport of gas. Destruction ● RBC membrane lose cholesterol over time. ● Rupture in spleen capillaries at 120 days. ● If you lose your spleen, liver ruptures RBCs. Adult hemoglobin ● 2 alpha and 2 beta chains ● Each subunit has a protein (globin) with a heme group in the center ● Each heme has an iron atom at its center. ● Oxygen binds to the iron atom. ● Cooperativity increases binding at lugs and release at tissues.Fetal Hemoglobin ● 2 alpha and 2 gamma chains. ● Higher affinity for oxygen than adult hemoglobin. ● Draws oxygen from maternal blood ● Replaced by 2-3 months post natal Anemias ● Lack of oxygen (altitude) ● Reduce RBCs (bleeding), no anemia with menses (50 ml/ 5 days) ○ Can have reduced delivery of oxygen if you have poor circulation. ○ Diabetics lose feet as a result of veins collapsing in feet from poor circulation. ● Reduced delivery (circulatory) ● Reduced use (cyanide) Sickle cells ● Single Hb mutation. ● Low oxygen leads to Hb forming stacks, changing the cell’s shape. ● Sickled cells hang up on branch points. ● Survival value: protection from malaria - parasites lay eggs in RBCs. ● Growing malarial parasites rupture weakened RBCs before they reach maturity. Iron deficiency ● Not caused by using aluminum skillets lmao. ● Lack of iron results amount of Hb. ● Not from using non iron cookware, wrong form of iron in cookware - dietary deficiency. Platelets ● Pinched off parts of megakaryocytes in bone marrow. Production of Platelets ● Megakaryocytes in bone marrow. ● Platelets pinch off and enter circulation. ● Spleen, kidneys, and liver make thrombopoietin ThrP ● ThrP stimulates platelet formation. ● ThrP binds to platelets in blood, when platelets low causing an increase of free ThrP. Activation ● Activated y collagen and other proteins in connective tissue of blood vessels. ● Platelets adhere, increase ADP release, more P’s come and stick. ● Make platelet plug. Hemostasis● Stoppage of bleeding. Vasoconstriction ● Decreased blood pressure at the site of cut, tone constricts small vessels. Platelet plug ● Exposure of collagen leads to platelet sticking leads to an ADP positive type feedback. ● Prostacyclin from healthy blood vessels blocks platelet adherence. Coagulation ● Blood clotting: 2 systems. ● Both lead to fibrinogen (soluble) leading to fibrin (self adhering) ● Forms meshing that traps RBCs. Intrinsic System ● Inside plasma - collagen activated. ● Cascade needs Ca++ and all factors in pathway. Extrinsic System ● Thromboplastin from damaged tissue starts the cascade. ● Merges with Intrinsic system halfway. Clot removal ● Plasminogen trapped in clot - cascade caused by collagen - Plasmin ● Plasmin is an enzyme that slowly dissolves a clot over the course of 2 weeks. Lecture 26 - White blood cells - Innate immunity Cell types - Leukocytes ● 5 types - all have different defense functions. ● Multi-lobed nuclei granulocytes: ○ neutrophils , eosinophils, basophils. ● Stained by neutral, acidic or basic dyes. ● Single-lobed nuclei agranulocytes: ○ Monocytes, lymphocytes. Phagocytes ● Phagocytosis of bacteria and dead cells. ● Order of attack: resident macrophages , neutrophils, new monocyte - macrophage migration. Neutrophils ● Rapid response - move from the blood to damaged tissue.Diapedesis ● Squeeze through capillary pores. Monocytes - Macrophages ● Monocytes move into tissue and become macrophages ● Resident macrophages wait for bacteria to come. ● During infection, vast movement of monocytes into infected area. ● Massive macrophage attack of bacteria. Eosinophils ● Produce acids that kill parasites. ● High in GI tract, lungs, skin, reproductive tract. ● Produce allergic responses. Basophils ● Release histamine. ● Histamine results in inflammation. ● Increases blood flow (arteriolar dilation) ● Increases pore size (allows diapedesis) Defense Mechanism ● Innate (nonspecific immunity) ○ Defense mechanism not influenced by prior exposure ● Acquired ( specific immunity) ○ B and T lymphocytes attack specific antigens. Inflammation ● Nonspecific response. ● Occurs with any infection or injury. Chemotaxis ● Chemical signals from damaged areas draw phagocytes. Complement System ● Series of 9 plasma factors - C1-C9 ● Major bacteria killer. Activation ● By antibodies or by the protein properdin. ● This is opsonin tagging of surface carbohydrates on bacteria. ● Leads to pore formation in bacterial membranes. Pore formation● C5-C9 can form pores in membrane ● Very local, inactive activation. ● Pore allows osmotic lysis. ● Na+ enters, H20 follows, cell swells and bursts. ● Ill feeling cause: bacterial toxins, activation of pain receptors from partially digested proteins of dead bacteria / dead cells. Histamine ● Increases blood flow: brings phagocytes, oxygen, amino acids. ● Increase capillary permeability. ○ Opens pores for liquid and diapedesis. Interferon ● Cytokine - released from virus infected cells. ● Activate antiviral defenses in cells near virus infected cells. ● Blocks proteins synthesis, many side effects. Natural killer cells ● Non T cell lymphocytes. ● No prior exposure needed for activation. Activation ● Lipids and carbs on bacteria, tumors, transplants and by antibodies on cell surface. ● Forms pores by injecting perforin - kills by lysis. Lecture 27 - Adaptive Immunity: B lymphocytes Antigens ● Substances that activate B and T lymphocytes. ● Most foreign, some self antigens in autoimmune diseases. ● Can be serious like viral infection or benign like poison ivy. Antigen presentation ● Protein antigens ● TAken in and partially digested by macrophages. ● Part of antigen linked to MHC protein and put into cell membrane ● T or B cells then find MHC protein complex causing the activation of T cells which attack cells which have that protein or those who have B cells producing antibodies B lymphocytes ● Bind antigens - full activation requires T helper cell contact. ● Antigen binding triggers cell proliferation into plasma (B cell clone) cells and memory cells.Plasma cells ● Antibody factories - make antibodies to antigen that bound High ER for Ab production loses other organelles ● Limited lifetime - 1 week Primary response ● Activation of T or B cells is slow short and weak Secondary response ● Activation of memory cells is fast, strong and long. ● Massive response upon secondary exposure. Immunoglobulins - Antibodies ● IgG, IgA, IgD, IgM, IgE, are y shaped proteins ● Variable region - Arm tips of the y shaped protein ● Can bind to antigens/ Ab, must be same type of antigen. ● Constant region - Tail region ● Activates some aspect of immune system when antigen bound. Antibody functions ● Major functions: activate complement system to kill bacteria ● Labels cells for ingestion by lymphocytes. ●● Minor physiological function: neutralization by binding ● Used for lab testing. Blood types ● Based on surface carbs ● Genes code for enzymes that add carbs. ● Transfusion reaction if there is a mismatch. ABO system ● A factor, B factor, AB has both factors ● O has neither A or B antigens. Rh factor ● 2 gene system: gene for factor, activator gene. ● No activator: weak + reaction, formerly missed. ● Rhogam given to Rh- mothers of Rh+ children. Lecture 28 - T lymphocytes - Self T lymphocytes ● Attack cells with both a foreign antigen and self-antigen (MHC) ○ Cancer, virus infected cells and transplants are attacked. 1. Virus invades host cells.2. Viral antigen (piece of viral protein coat) is displayed on the surface of the host cell alongside the cell’s self-antigen. Cytotoxic T cells ● Bind to cell and inject perforin - form the pore. ● Osmotic lysis then occurs. Helper T cells ● Release cytokines that activate all B and T lymphocytes. AIDS ● HIV attack on helper T cells, causing a decreased immune response. ● Opportunistic diseases can now attack. ● Avoid multiple concurrent infections. ● HIV needs broken skin to enter - hard to get. Helper T cell Cytokines ● Paracrines that regulate immune response ● Increased proliferation, growth and function. ● When cytokine structure known, renamed an interleukin. Major Histocompatibility Complex ● Previous known as HLA antigens. ● MHC Class 1 - self antigens - on surface of all cells ○ Identify cells as self. ○ 3-6 out of 100 possible antigens on every cells. ○ Others in foreign cells attacked. MHC Class 2 - Ingest and present antigens - activate T cells Transplants ● Non matching MHC-1 cells are attacked by antibodies. ● Partial match has both self and foreign antigen, triggering T lymphocyte attack. ● TRy to match MHC Class 1 proteins. ● T cells may attack - suppress T cells - more infections ● Leukemia - replace marrow - fungus risk. Tumors ● Benign tumors stay localized, no infiltration of surrounding tissues ● Malignant tumors have transformed cells - cancers. ○ Can infiltrate nearby tissues. ○ Can metastasize to other parts of the body.Allergies ● Immune reaction to a harmless substance. ● Allergens can produce responses. ‘ Immediate Hypersensitivity ● Immune response in 20 minutes. ● B cell is mediated - antibody production. Stimuli ● Non bacterial - pollen, bee stings, penicillin, mold, dust, IgE antibodies ○ Many in skin, eyes ,lungs , GI tract. ● System designed to attack parasitic worms. ● Chemical Triggers - ● Histamine vasodilation and capillary permeability increase ● SRS-A strong bronchial contraction, potentially lethal. Symptoms ● Localized reactions ● Upper respiratory - hay fever, congestion, edema, sneezing, runny nose. ● Bronchioles- asthma: inflammation, constriction, increased mucus, difficulty breathing. Anaphylactic Shock ● Allergens spread by blood. ● Severe hypotension due to increased capillary permeability. ● Bronchoconstriction ● Treat with epinephrine. Delayed hypersensitivity ● Immune response in 24 hours ● T cell mediated. ● Poison Ivy, some toxins stimulate. ● T cells migrate to area of contact and produce a rash. Skin ● Mechanical barrier with defense mechanisms. ● Different layers. Epidermis ● Layers of epithelial cells. ● Dead cells outermost, with dividing cells beneath. ● No blood supply, supplied by diffusion from the dermis. ● Desmosomes and keratin fibers hold cells together, with keratinized layer remaining after death.● Pathogen tight, air-tight, fairly water- tight, prevents evaporation. ● Burns destroy epidermis, causing hypotension and shock. Dermis ● Connective tissue beneath the epidermis. ● Blood vessels, nerve endings and many cell types. ○ Rings slip off fingers easily during the cold because of blood flow - reducing circulation to prevent cool off vs when it is hot, fingers get puffier from increased circulation as an attempt to cool. ● Blood regulates heat loss. ● Sweat glands - sweat has variable Na+ content. ● Sebaceous glands - oil waterproofs skin. ● Hair follicles - increase touch sensitivity. ● Melanin absorbs uv light - UV sensitive Langerhans cells present antigens, UV resistant Granstein cells slow immune responses. ● Increased exposure to UV light increases skin cancer. Hypodermis ● Adipose tissue - insulates body from heat loss. Lecture 29 - Lung structure - breathing External respiration ● Exchange of gases (o2 and CO2) between body and environment ● Internal respiration - use of O2 by mitochondria Non Respiratory Lung Functions ● Can’t see water vapor - its ice crystals ○ Potential test question, apparently. ● Water and heat loss, increases venous return, acid base balance, speech, pathogen defense, circulatory modification (ACE), sense of smell. ● Negative pressure draws blood back into right atrium - venous return. ● ACE inhibitors - entry drug for blood pressure regulation. Mild hypertension. ● trachea bronchi bronchioles alveoli ● more than 20 gen bronchioles, alveoli are air sacks sites of gas exchange Type 1 Cells ● Epithelial cells - 1 micron thick. ● Separate air from interstitial fluid. ● Malfunction here, causes death in the case of pneumonia. ● More water - reduce rate of oxygen diffusion. ● Don’t die from bacteria / virus - die from the edema in the lungs.Type 2 Cells ● In alveoli. ● Produce surfactant - leading to a decrease in resistance to the alveolar opening. Lung Mechanics ● Air flows from high pressure to low pressure. Atmospheric, Intra-alveolar, intrapleural pressures ● A: 760 at sea level, 600 at Denver (1 mile above sea level) ● I-A: variable, exhale 1-2 > atm, inhale 1-2 < atm ● IP: between lungs and thoracic wall. ○ Always 4 mmHg < atm ○ Lower pressure keeps lungs always inflated. Boyle’s Law ● PxV = constant. ● Decrease in volume is a result of an increase in pressure. ● An increase in volume is a result of a decrease in pressure. Tidal Volume ● Normal breathing volume ● Inspiratory reserve volume - extra amount you can inspire. ● Expiratory reserve volume - extra amount you can expire. Inspiration ● Regular - phrenic nerve from medulla sends AP to the diaphragm. ● Diaphragm contraction increases thorax volume, leading to a decrease in pressure. ● Decreased pressure causes inspiration. Extra Inspiration ● External intercostal muscles contract- expand thorax. ● Internal intercostal muscles between the ribs contract. ● Abdominal muscles contract also. ● Squeeze thorax Expiration ● Normally passive ● As diaphragm relaxes, volume decreases and pressure increases - causing expiration. Compliance ● Ease of lung expansion ● Normally easy● Increase fibrosis (asbestosis ) of lungs to decrease compliance. Alveolar Surface Tension ● Adherence of H2O molecules creates surface tension on inside of alveoli. ● Surface tension must be overcome to open alveoli. Surfactant ● Several phospholipids, mix with water and decrease surface tension. ● Also prevents edema in lungs. ● First made at the 36th week of gestation. ● Glucocorticoids increases surfactant production in premature infants. ● Presence of surfactant helps reduce edema in the lungs as humans age - keeps gas exchange happening easily. Anatomical dead space ● Normal tidal volume is 500 ml. ● 150 ml of mouth, pharynx, trachea, bronchi, bronchioles is dead space. ● 350 ml is normal alveolar inflation. ● Long slow breathing minimizes dead space effect. ● Short,, rapid breathing still must fill 150 ml dead space. Lecture 30 - Gas exchange Partial pressures ● Gas equivalent to concentration ● Sea level: 760 mmHg = 600 N2 + 160 O2 ● CO2 = 0.3 mmHg ● Gases are independent of one another. ● Air in lungs is water saturated. Alveolar air ● PO2 = 100 mmHg, PCO2 = 40. ● Venous blood: PO2 = 40, PCO2 = 46. ● The air pressure will always match the surrounding tissues concentration. ● Surrounding tissue 100 - match 100 with capillary. Diffusion through alveolar wall ● Gases follow partial pressure gradients ● Capillary gases match tissue it goes through. ● O2: O2 enters pulmonary capillaries until PO2 is 100 ● CO2: CO2 leaves pulmonary capillaries until PCO2 is 40Pulmonary circulation ● Lower BP than aorta. ● ~15 - 20 mmHg MAP of pulmonary artery. Ventilation/ Perfusion ratio ● Very little people have diseases with this. ● Ventilation and perfusion normally well matched, 0.8 ● Areas that have open alveoli get more blood flow. ● As need for gas exchange increases both blood flow and ventilation increases in new lung areas. Tissue gas exchange ● Reverse of lungs. ● O2: 100 mmHg arterial blood loses O2 to 40 mmHg tissue until capillary is 40 mmHG. ● CO2: 40 mmHg arterial blood receives CO2 from 46 mmHg tissues until capillary is 46 mm Hg. Oxygen transport ● 1.5% carried by dissolved O2 ● 98.5% carried by binding to hemoglobin. Oxygen Hemoglobin Binding ● Sigmoidal curve - cooperativity between 4 hB subunits. ● 26 27 28 6-12 ● 12-4 29 Plateau region + Steep region ● P: at lungs - all hB is O2 bound - no effects of extra O2 ● S: at tissues - fall in PO2 - unloads O2 ● At lower PO2- even more O2 delivery. ● Work hard, get oxygen Bohr Effect ● Shifts oxygen hemoglobin curve to the right. ● CO2, acid shifts hb-O2 curve to right = more O2 unloading at given PO2 Carbon Monoxide ● 2 effects - binds Hb 200x stronger than O2 - less O2 available. ● Never dissociates - must lyse RBC to lose CO ● Shifts Hb-O2 curve to left, less O2 delivery ● Simulated anemia.Hypoxia ● Low blood O2 ● Low O2 air = high altitude or O2 deprivation. ● High altitude ethnic groups - higher Hb even at sea level. ● Sea level ethnic groups - low O2 training increases Hb, lose when return to sea level. Hyperoxia ● Breathe high O2 air - no additional Hb binding (already full) ● Increase in dissolved O2 may decrease breathing rate = benefit is only psychological. ● 26,27,28,2,3,4 6 am ● 5 - 12-4 ● 29 12-4 Carbon dioxide transport ● 10% dissolved, 30% bound to plasma protein and Hb. ● 60% converted to bicarbonate by carbonic anhydrase (CA) ● CA catalyzes - H20 + CO2 = H2CO3 = HCO3- + H+ Carbonic Anhydrase ● In RBC’s ● Converts CO2 to bicarbonate at your tissues, as CO2 is added. ● At lungs, reversal - bicarbonate is converted to CO2 and then breathed out. Hypocapnia ● Low CO2 ● Hyperventilation decreases CO2 in blood = feeling faint. ● Breathing into a bag = increase of CO2, which then goes back to normal. Hypercapnia ● High CO2 = increased breathing rate. ● Increased CO2 in blood is the strongest stimulus for increased respiration. Lecture 31 - Regulation of respiration - lung diseases  Medullary Control Centers ● Dorsal respiratory group - DRG - rhythmic discharge - phrenic nerve - diaphragm. ● Initiates normal breathing. ● Ventral respiratory group - VRG - causes an increase in inspiration + expiration. Pontine Control Centers ● Modify medullary centers ● Pneumotaxic Center - switches off inspiration● Apneustic center- prolongs inspiration, normally inhibited. ● If PC damaged, Hering Breuer reflex from the lungs stops inspiration. Chemical control of inspiration ● Most powerful controller of rate. ● Increase of blood CO2 leads to increase in brain CO2 leads to increase of H+ and HCO3- ● H+ in brain increases DRG rate Peripheral Changes ● In carotid bodies and aortic bodies ● Increases H+ or increase of CO2 or decrease in O2 will increase rate of respiration. ● Little effect in normal range. ● PO2 lower than 60 mmHg increases rate, no help in CO poisoning. Sleep apnea ● Decreased DRG activity / airway obstruction. ● In REM, pharyngeal muscles relax and tongue blocks trachea ● Decreased restful sleep SIDS - Sudden infant death syndrome. ● Exact cause unknown ● May be due to congenital DRG problem or cardiac arrythmia ● Baby sleeping on the back = decreased risk of SIDs. ● Mother smoking during pregnancy = increased risk of SIDs ● Child abuse may have skewed SIDs stats. Pneumothorax ● Rupturing of thorax - air enters intrapleural space. ○ Common in car accidents - rib punctures lung. ● Pressure equalizes, lung collapses on ruptured side. ● Decreased flow in the good side. ● Danger of kinking off great veins if opening remains ● Reclosed = normal breathing on good side, the lung reinflates. Asthma ● Episodic or chronic wheezing, tightness in chest ● Increased morbidity and mortality. Airway obstruction ● Increased mucus production in response, blocks airway. ● Reduces air flow.Inflammation ● Response to allergies - increase in IgE ● Increase in mast cells release of histamine and other cytokines ● Edema decreases air flow. Bronchoconstriction ● Some cytokines are bronchoconstrictors ● Also cool air and exercise ● Constriction decreases air flow SRS-A ● Slow reactive substance of anaphylaxis, leukotrienes. ● Powerful bronchoconstrictors during allergic attacks ● Potentially fatal attack Epinephrine ● Beta 2 receptors bind Epi, relax bronchioles, increase air flow. ● Rescue from serious allergic attacks. ● Steroids decrease inflammation - however, have significant side effects. Emphysema ● Cigarette smoke and coal tar are the most common causes. Decreased a-Antitrypsin ● Lungs have digestive enzymes for defense ● Alpha-Antitrypsin protects lung tissue from digestion. ● Inhibit Alpha-AT production, and enzymes digest alveoli. ● Decreased amount of alveoli and increases the size of the remaining alveoli. Surface Area ● Progressive decrease in surface area. ● May need pure O2 to fill Hb. ● Irreversible - right heart enlarges and fails. Cystic fibrosis ● Recessive gene - decrease Cl- channel activity ● Loss of airway Na+ and water - mucus sticky and digestive enzymes increase ● Increased infection, lung destruction - fatal.

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