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Pathophysiology Test 3 Notes

by: Hope Gulley

Pathophysiology Test 3 Notes BIOL 3123

Marketplace > Auburn University > Biology > BIOL 3123 > Pathophysiology Test 3 Notes
Hope Gulley
Dr. Davonya Person

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These are the notes for the third test in Pathophysiology under Dr. Davonya Person
Dr. Davonya Person
Class Notes
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This 28 page Class Notes was uploaded by Hope Gulley on Sunday August 16, 2015. The Class Notes belongs to BIOL 3123 at Auburn University taught by Dr. Davonya Person in Spring 2015. Since its upload, it has received 58 views. For similar materials see Pathophysiology in Biology at Auburn University.


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Date Created: 08/16/15
X Cardiovascular Svstem Blood Vessels and Blood Pressure A Vasculature 1 General a 5 vessel types Arteries branch Arterioles Capillaries gt gt gt gt gt 2 Arteries Venules Veins convert b The lumen of a blood vessel is the opening through which blood ows gt 3 layers of tissue surround the lumen a Functions gt Act as transit for blood from the heart to the tissues gt Exhibit elastic recoil 3 Arterioles Tunica intima 1 Inner most layer 2 In contact with blood Tunica media 1 Middle layer 2 Muscular 3 Vasodilates and vasoconstricts Tunica adventitia 1 Outermost layer 2 Anchoring layer During ventricular systole a greater volume of blood enters the arteries from the heart than leaves them to ow into downstream vessels Arteries have an abundance of the protein elastin in the tunica media allows them to expand to accommodate blood buildup During ventricular diastole arteries passively constrict forcing the excess blood being held into the downstream vessels This mechanism ensures continuous ow of blood through the vasculature even when the heart is not actively pumping 1 Blood vessels are never empty a Branch from arteries b Tunica media s smooth muscle is highly innervated by the sympathetic nervous system gt Svmpathetic stimulation vasoconstriction Alpha 1 receptors decrease in lumen diameter decrease in blood ow LACK OF svmpathetic stimulation vasodilation increase in lumen diameter increase in blood ow Cut off the sympathetic stimulation because there is not parasympathetic supply to most of the blood vessels because they are not sympathetic fibers gt These changes determine the amount of blood ow to capillaries beds that surround tissue cells c Local chemicaltemperature changes can also in uence lumen diameter gt Vasoconstrictors tissues get less blood High 02 Low C02 gt 1 Cold 1 Arteries are delivering 02 to tissue and picking up C02 but there is already high 02 and low C02 so there is no reason for blood to travel to that tissue so blood is shunt to a more metabolically active tissue so it can get more 02 and pick up the C02 Want to conserve heat Endothelin chemical produced by endothelial cells associated With Tunica Intima 1 Body s natural vasoconstrictor gt Vasodilators tissues get more blood Low 02 High C02 4 Capillaries 1 These tissues are metabolically active so they need 02 and they need their C02 picked up so more blood goes here Nitric oxide produced by endothelial cells Heat 1 2 Tissue is warm skin will take on a reddish hue Blood is brought to surface of body so you can cool off a Function in actual exchange processes between blood and tissue cells 5 Venules a Collect blood from capillaries b Converge to form veins 6 Veins a Have little elastin but lots of collagen this allows a high degree of distension without recoil gt Serve as blood reservoirs Under resting conditions when tissue demands are low the veins can contain up to 65 of the total blood volume When the stored blood is needed extrinsic factors drive the blood out of the veins and toward the heart 1 Sympathetic stimulation vasoconstriction decreases diameter decreases amount of blood that can be held and increases venous return 2 Skeletal muscle activity contracting muscles compress nearby veins forcing blood towards the heart and increasing venous return IX CARDIOVASCULAR SYSTEM THE HEART A Functional Anatomy 1 Pericardium a b c Fibrous multilayered covering around the heart holds heart in place and provides a barrier to infection brous pericardium outermost layer i prevents heart overdistension parietal pericardium middle layer i deep to the fibrous pericardium ii lines pericardial cavity walls iii attached at apex bottom of heart to the diaphragm visceral pericardium innermost layer i covers the surface of the heart ii when considering the 3 walls of the heart musculature synonymous to Epicardium outermost heart wall pericardial cavity i between parietal and visceral layers ii has 3050 ml of lubricating uid that minimizes friction during heart beats iii pericarditis in ammation of pericardium that leads to a decrease in uid production resulting in painful heart movements gt causes cells to stop making the uid which leads to friction 2 Myocardium a b muscular layer of the heart deep to Epicardium has sarcomeres made of actin and myosin contractile proteins 3 Endocardium a smooth inner surface of heart chambers 4 Atrioventricular AV valves a Separate atria from ventricles b Tricuspid right side 3 aps Bicuspid Mitral left side 2 aps 1 Open to allow blood ow from atria to ventricles but snap shut during ventricular systole contraction to prevent back ow of blood into the atria P i Mitral Valve Prolapse probably congenital valve is enlarged and does not close properly allows blood leakage into the left atrium TX usually none but if symptoms ie fatigue irregular heartbeat are severe may treat with a Betablocker i None bc usually the opening is small and pt has no symptoms at all and do not know until they go to the doctor and he listens to their heart VVVV 5 Aortic and Pulmonary Semilunar SL2 Valves a Aortic SL between left ventricle and aorta b Pulmonary SL between right ventricle and pulmonary trunk c Open to allow blood ow from ventricles into aortapulmonary trunk but snap shut during ventricular diastole relaxation to prevent back ow of blood into the ventricles i Ventricles move down during relaxation and are empty no blood bc it went to through the valves B Blood Flow 1 Pulmonarv Circulation a Deoxygenated blood from the tissues to the heart to the lungs b gigm side of heart tissues superiorinferior vena cavae right atrium tricuspid valve right ventricle pulmonary semilunar valve pulmonary trunk rightleft pulmonary arteries pulmonary capillaries i where gas and nutrient exchange takes place lungs VVVVVVVVV V 2 Systemic Circulation a oxygenated blood from the lungs to the heart to the tissues b side of the heart rightleft lungs rightleft pulmonary veins i vessels that dump blood into left atrium left atrium mitralbicuspid valve left ventricle aortic semilunar valve aorta systemic arteries systemic capillaries i surround body cells for gas and nutrient exchange gt body tissues VV VVVVVVV C Normal Electrocardiogram l 2 3 Showing electrical events depolarization and repolarization Assume there are Mechanical evens systole and diastole P Wave represents Atrial depolarization 3 Assume atrial systole happens after QRS Complex Ventricular Depolarization a Assume ventricular systole happens T Wave Ventricular Repolarization a Assume ventricular diastole happens PR Interval AV nodal delay point in time when atria have been stimulated and stimulation of ventricles is being held off ST Segment Plateau Phase contractile cells TP Interval heart is at rest ventricles are passively filling with blood and atria are getting ready to depolarize D Abnormal Electrical Events Arrhythmias 1 Abnormal Sinus Rhythm a Tachycardia gt Faster than normal heart rate resting HR6 i Normal avg HR is about 72 ii Faster gt100 gt Not necessarily pathological b Bradycardia gt Slower than normal heart rate i lt60 gt Can be seen in athletes with increased myocardial strength i Highly trained athletes ii Their heart musculature doesn t need to pump as many times to pump out their blood same blood amount as others gt Carotid Sinus Syndrome i Arteriosclerotic plaques in carotids ii Cause nearby baroreceptors to be extremely sensitive 1 Any mild pressure is perceived as an increase in BP a In response vagus nerve sends efferent signals to heart to decrease HR in order to decrease BP i Efferent signals ach sent to heart to bind to M2 receptors 2 Impulse Conduction Blocks a the AV node a 1st Degree incomplete gt Increase length of PR Interval i Atria have already contracted SA Node did that so now the ventricles need to contract but will take longer gt Amount of increase can be used to determine the severity of the cardiac condition b 2rld Degree incomplete gt Atria beat faster than ventricles gt Some ventricular beats are dropped i Reason if it takes too long SA node is pacemaker and AV node takes too long and ventricles are not stimulated before the SA node fires again then some of the beats will be missed ii Issue lies with how slowlyquickly the AV node fires 1 THE SA NODE IS WORKING FINE iii In relation to EKG may have more P waves than QRS complexes c 3rd Degree complete gt Atria beat regularly but the ventricles receive no impulses gt Purkinje fibers initiate APs at their own rate which can be up to 50 slower than when following normal sequence i Only getting 12 as much 02 delivered to body gt StokesAdams Syndrome i Pt s who have this don t have 3rd degree heart block but they have all the symptoms ii The block comes and goes don t have the symptoms all the time iii Basically When they get the block they have intermittent fainting iv So Sudden Fainting is the main characteristic V Once block removes itself they regain consciousness 3 Premature Contractions a Premature Atrial Contractions gt P Wave occurs early gt TP interval shortened b Premature Ventricular Contractions gt QRS wave occurs early PR interval shortened gt Decreases ventricular load i Could decrease a lot ii The affect on the interval determines how much of a decrease there is c Atrial fibrillation gt Decreases atrial contractile function due to uncoordinated stimulationcontraction i Areas of atria that are being stimulated and areas that aren t being stimulate gt Causes a decrease in ventricular functioning by 20 30 i Only 2030 because 7075 of blood fills ventricles passively gt Could be damaging if chronic d Ventricular Fibrillation gt Some areas of the ventricles are contracting While others are relaxing gt Results in ventricular chambers never being completely full nor empty gt Little to no blood at all is eventually being pumped out gt Unconsciousness can occur in less than one minute irreversible tissue death in less than 10 minutes i Immediately life threatening ii Use AED to reverse e Atrial Flutter gt SA node signals travel in circles around the openings of the superior and inferior vena cavae i Right side of heart gt Causes a rapid rate of atrial contraction and not all signals reach the AV node gt 23 P waves for every QRS i This is not normal ii Also seen in blocks gt Not immediately life threatening if ventricles contract With normal force C Functional Anatomy Microscopic 1 CONTRACTILE CELLS a Striated atrial and ventricle muscle b 99 of myocardial cell population c Cell membranes have intercalated discs types of cellular adhesions gt Areas of very low electrical resistance gt APs are quickly propagated from cell to cell Contractile AP happens second Conductile Cells AP happens first and stimulate the contractile cells to have an AP d AP in Contractile Cells gt Specifically What an AP looks like in a contractile cell gt 3 Phases Phase 1 Depolarization i Membrane permeability to Na increases Na channels open ii Increase Na in ux Phase 2 Plateau Phase i Sl Ca2 channels open Na gates close ii Ca2 in ux iii iv Membrane permeability to K decreases channels are delayed from opening preventing immediate K ef ux Prolongs inside positivity preventing Tetany smooth sustained contraction of the heart 393 Tetany will cause the ventricles to stay contracted and Will not be able to fill With blood so they wont be able to pump any blood out Heart Attack Phase 3 Repolarization 1 ii iii Ca2 channels close Membrane permeability to K increases K channels open K ef ux e Intrinsic Regulation of Contraction Contractile Cells gt Frank Starling Mechanism Amount of blood pumped per minute is dependent on venous return i Venous return is amount of blood returned to the right atrium from the vena cavae Blood volume in the atria blood volume in the ventricles The more the muscle of the ventricles is stretched by an increase in incoming blood the more forceful the next contraction Will be venous return increases contractility increase How do you increase the amount of blood ow to the right atrium 1 ii you are not increasing total blood volume but decreasing the amount of blood held onto by the veins 65 of blood is resting passively at the veins DO NOT INCREASE TOTAL BLOOD VOLUME BUT DECREASE AMOUNT OF BLOOD PASSIVELY HELD IN THE SYSTEMIC VEINS INCEASING BLOOD RETURN TO THE HEART f Extrinsic Regulation of Contraction Contractile Cells gt Svmpathetic Nervous Svstem Both atrial m ventricular contractile cells are highly innervated by sympathetic fibers fibers going to both the atria and ventricles When epinephrine and norepinephrine bind to Beta 1 gBlz receptors Ca2 in ux increases and contractility increases i Will cause heart to have a stronger contraction Stimulation of Alpha 1 receptors on VEINS causes vasoconstriction Which propels blood forward to the heart therefore venous return increases increasing contractile strength vasoconstriction of veins increases blood ow gt Parasvaathetic Nervous Svstem Innervation is ONLY to the atria via the vagus When Ach binds M2 receptors the membrane becomes less permeable to Ca2 Ca2 in ux and therefore atrial contractility decreases 2 CONDUCTILE CELLS a Clusters of cells that initiate and conduct the APs necessary for AF generation in contractile cells b 1 of myocardial cell population c Components i Sinoatrial SA node 0 90 Called the heart pacemaker because it depolarizes the fastest reaches threshold fastest and begins the sequence of excitation i Important especially for heart arrhythmias APs travel through intercalated discs to R m L atria causing APs in all atrial contractile cells and therefore contraction AP in SA node that AP travels to internodal pathway and to both atria i Internodal pathway 0 90 Electrically connects SA node to AV node ii Atrioventricular AV node 0 90 O 9 Functions to DELAY impulses coming from the SA node The delay gives atrial cells time to fully contract and empty all blood into ventricles before the ventricles are stimulated iii AV bundlebundle of His 393 Divides into L and R bundle branches going toward heart apex iv Purkinje bers 393 Generate action potentials which then stimulate APs in ventricular contractile cells 393 Due to their orientation the ventricles are stimulated to contract apex to base contract in an upward direction to pump the blood through the semilunar valves Therefore blood pumps upward through the semilunar valves amp toward the aorta and pulmonary trunk d AP in Conductile Cell 1 No true resting membrane potential in conductile cell a The membrane is always gradually DEPOLARIZING due to i Decreased membrane permeability to K less K ef ux due to inactivation of K channels keeping more K in the cell which will help depolarize the membrane ii Constant Na in ux iii Opening of Transient Ca2 channels Ca2 in ux 0 Called Transient but they are short lived open up and then close quickly 2 Sharp spike seen at threshold due to the opening of LONGER LASTING Ca2 channels Ca2 in ux 3 Repolarization due to an increase in membrane permeability to K K ef ux e Extrinsic Control of Excitation Conductile Cells gt Svmpathetic Nervous Svstem 1 SA node Epinephrine and Norepinephrine binding Beta 1 receptors i Increase in membrane permeability to Na increase in Na in ux ii Acceleration of inactivation of K channels decrease K ef ux therefore threshold is reached faster sequence of excitation is started faster increase in HR 0 AV node Epinephrine and Norepinephrine binding Beta 1 receptors i Increases Na and Ca2 permeability channel opening therefore decreases delay time ie conduction from AV node to bundle of His is faster increasing HR gt Parasvmpathetic Nervous Svstem Ach from the vagus stimulates M2 receptors on the SA node and the AV node Results in i Increase K ef ux and hyperpolarization more neg than at rest of conductile cells 393 SA node drift to threshold slows decrease HR 393 AV node increases delay time Which decreases HR HYPERTENSION Hypertension is defined as chronically elevated Blood Pressure normal BP 120180 mmHg Systolic pressure greater than 140 mmHg Diastolic pressure greater than 90 mmHg Lethal effects of hypertension C Types D Treatment 1 Excess workload on the heart leads to development of congestive heart disease heart disease accompanied by congestion excess uid of body tissues a The high pressure in vessels forces uid out of the capillaries and into the interstitial spaces 2 The high pressure can rupture a major blood vessel in the brain causing a cerebral infarct stroke An infarct is an area of dead or dying tissue resulting from inadequate blood ow to that area 3 High pressures can cause hemorrhaging in the kidneys Which can lead to renal failure a The afferent arteriole transports the entire volume of blood to the kidneys for filtering several times a day 1 Primary gt Hypertension With unknown origin idiopathic gt 90 of all cases gt Research suggests that there is a strong genetic correlation in the development of this type gt Susceptibility increases With obesity stress smoking dietary habits and race African American males are the most susceptible group 2 Secondary gt Cause can be diagnosed gt 10 of all cases gt Occurs secondary to some other pathologic condition gt EX Renal HvDertension An occlusion in the renal artery decreases filtration of blood through the renal tubules nephrons The decrease in renal blood ow is perceived by the body as a decrease in overall blood pressure This signals the release of renin and the formation of Angiotensin II This leads to an increase in BP but what if the patient already had a normal BP of 12080 0 Will cause pt to have hypertension 1 Nonpharmacological gt Weight loss gt Exercise helps strengthen heart muscle and increase blood ow gt Decrease exposure to stressors Which Will decrease sympathetic stimulation 2 Pharmacological gt Diuretic drugs O F urosemide decreases uid volume by increasing urine output I Call a loop diuretic I Will hold salt in the opposite direction Will cause NaCl to stay in kidney tubules and Will then be loss in urine gt Adrenergic inhibitors 0 Nadolol decreases sympathetic stimulation on heart I Beta 1 antagonist I decrease HR CO amp BP 0 Minigress vasodilator alpha 1 antagonist 0 Lack of sympathetic stimulation 0 Decrease in TPR BP gt Renin inhibitors blocking renin blocks formation of Angio II and all its effects 0 CaQtOQril gt Ca2 channel blockers O Nitedigine decreases heart rate CIRCULATORY SHOCK Circulatory Shock is a general term meaning that BP is so low that the body is unable to deliver blood ow to the tissues severe hypotension The heart musculature walls of the blood vessels and the cardiovascular system in general all begin to deteriorate Types and Causes 1 CardiOgenic shock inadequate cardiac output Myocardial infarction Severe heart valve dysfunctions blood ows back into atria during ventricular systole or back into ventricles during ventricular diastole 2 vaovolemic shock diminished blood volume Severe hemorrhage or loss of body uids due to mechanical trauma severe diarrhea burns or excessive urinary output if you lose body uids then that means you are losing blood volume Will get a decrease in BP 3 NeurOgenic shock Occurs without any loss of blood volume The vascular capacity increases so much that the normal volume of blood cannot fill the entire circulatory system Causes severe decrease in TPR Ie the dilation of the veins is such that the blood pools in them to an excessive extent massively decreasing venous return This occurs due to a loss of Vasomotor Tone general tone or TPR of vessels What is normal Can be caused by vasomotor tone Deep general anesthesia Spinal anesthesia Which blocks sympathetic out ow from the 4 5 CNS Brain damage Anaphylactic shock extreme hypersensitivity to an allergen Results from the formation of an antigenantibody complex antibodies of the immune system recognize and attach to an invading antigen allergen 1 Antibodies are What our bodies make to protect us Causes the release of histamine from basophils causes changes in vessels Vascular capacity increases because of venous dilation severe decrease in TPR Arterial pressure decreases because of arteriolar dilation not enough pressure to pump blood through vessesl Fluid is lost into tissue spaces because the permeability of capillaries is greatly increased AgAb complexes 831M Widely disseminated bacterial infection to many areas of the body With the infection being borne through the blood from one tissue to another and causing extensive damage Typical causes Peritonitis in ammation of peritoneal cavity spread from the uterus and fallopian tubes caused by an unsterile pregnancy termination Peritonitis resulting from rupture of the gut ex gunshot or knife wound Streptococcal or staphylococcal skin infection Bacilli from the colon traveling to the urinary tract and kidney then into general circulation C Treatment 1 2 3 Direct transfusion of blood increase Blood volume Infusion With Dextran A large polysaccharide related to glucose Restores loss of uid by increasing the plasma colloid osmotic pressure Treatment With sympathomimetics For Neurotlenic Shock restores vasomotor tone For Anaphylactic Shock opposes vasodilating effects of histamine causing vasoconstriction working on Alpha 1 receptors B Regulation of Blood Pressure 1 Introduction 61 BP measured as a function of Cardiac Output and Total Peripheral Resistance BP C0 X TPR 9 CO is the amount of blood pumped by the heart per minute gt Function of stroke volume SV and heart rate gt SV is the amount of blood pumped by the heart per m c TPR is the resistance to blood ow Within the vasculature gt Determined by blood viscositv and vessel diameter 0 Thicker blood Increase TPR I Vasoconstriction decreases diameter and increases TPR I Vasodilation increases diameter and decreases TPR d Any increase or decrease in SV CO TPR HR Will cause corresponding changes in BP gt Increase SV increase CO increase BP gt Decrease TPR decrease BP gt Increase HR Increase CO Increase BP gt Decrease viscosity of blood decrease TPR decrease BP 6 Short term changes regulated by the E f Long term changes regulated by hormones 2 CNS Mechanisms of BP Regulation 61 Cardiovascular Control Center gt Located in medulla oblongata gt Integrating center that receives afferent signals regarding state of BP and if necessary sends efferent signals for correction a Efferent signals go to heart to cause increase or decrease in HR or go to blood vessels and cause vasoconstriction or vasodilation gt Consists of 2 divisions 393 VASOMOTOR CENTER VMC If BP DECREASES sends efferent signals via the Sympathetic NS to cause an increase in BP back to normal I Epi amp Norepi on B1 receptors on the heart increase HR increase CO increase BP I Epi amp Norepi on Alpha 1 receptors on arteries Vasoconstriction increase TPR increase BP I Epi amp Norepi on Alpha 1 receptors on veins vasoconstriction increase venous return increase SV increase CO increase BP 393 VAGAL CENTER VC If BP INCREASES sends efferent signals via the Parasympathetic NS to cause a decrease in BP back to normal I Ach on M2 receptors on heart decrease HR decrease CO decrease BP I Most of our blood vessels do not have parasympathetic innervation except ones to external genitalia I What about TPR I Note When either center is activated the other center is inhibited SO lack of sympathetic stimulation via inhibition of Vasomotor center causes arterial vasodilation decrease TPR decrease BP Only direct organ affected by the vagal center is the HEART NOTE When either center is activated there is simultaneous inhibition of the other Therefore I Afferent signals are sent to the medulla control center via receptors in the periphery gt Baroreceptors pressure sensing receptors Stretch receptors located in the carotid arteries and the aorta Signals from the carotids travel afferently via the cranial nerve IX glossopharyngeal Signals from the aortic arch travel afferently via the cranial nerve X Vagus An INCREASE in BP results in the inhibition of the VMC and the activation of the VC A DECREASE in BP results in the inhibition of the VC and the activation of the VMC 3 Chemical Mechanism of BP Regulation 61 Slow acting and long lasting I Work by changing blood volume 6 Antidiuretic Hormone ADH gt gt gt Receptors in the right atrium are sensitive to atrial stretch due to venous return If blood volume entering is loW venous return is assumed to be low and this could mean there has been a decrease in BP Atrial receptors signal the release of stored A from the posterior pituitary into blood Which has actually been made in the hypothalamus a Hypothalamus makes ADH then sends to post Fit for storage Which releases it into the blood ADH causes an increase in water reabsorption at the kidneys a Increase blood volume increase venous return increase SV increase CO increase BP If blood volume is sensed to be mgh by the atrial cells ADH release is inhibited blood volume decreases and BP decreases a FYI usually a result of the first line of events When talking about chemical control Main initial stimulus is going to be a decrease in BP then you want an increase d ReninAngiotensin System gt gt gt gt gt Primary regulator of blood volume A DECREASE in BP signals the kidneys to release the hormone renin Once in the plasma renin acts as an enzyme to catalyze the formation of a protein called Angiotensin II a Directly causes vasoconstriction of peripheral arterioles increases TPR Increase BP by binding AT1 receptors Angiotensin 1 b Stimulates release of Aldosterone from the Adrenal M i Aldosterone increases NaCl reabsorption at the kidneys therefore increase water reabsorptions via osmotic movement ii Blood volume increases venous return increases increase SV increase CO increase BP ADH directly increases water reabsorption no middle man Aldosterone directly increases NaCl reabsorption but then H20 bc water follows salt XI Respiratorv Svstem A Introduction 1 Primary function a the exchange of O2 and C02 between the external environment and the cells of the body through ventilation breathing 2 Anatomic Pathway gt Nares nostrils gt Pharynx Nasopharynx behind nasal cavity Oropharynx behind oral cavity Laryngopharynx Larynx Trachea wind pipe Bronchi Bronchioles Alveolar ducts Alveolar sacs look like a sack of grapes Alveoli one little grape 3 Respiratory Membrane a Made of gt Epithelium of alveolar walls gt Endothelium of pulmonary capillaries b This is the surface across which gas exchange takes place c Alveolar epithelium is made of 2 cell types gt Tvpe I Pneumocvtes Majority of the cells gt Tvpe II Pneumocvtes Produce and secrete pulmonarv surfactant this substance coats the internal alveolar walls decreasing surface tension propensity of water molecules to want to join together and preventing alveolar collapse ie hinders adhesion of water molecules to each other i Pulmonary Surfactant coats over the water molecules and prevents them from sticking together 1 If you don t have it you could get alveolar collapse gas exchange will be hindered VVVVVVV B Gas Transport 1 02 a Circulating in the blood in 2 forms gt Physically dissolved in the plasma 15 gt Bound to Hemoglobin Hb within red blood cells Hb is the gas carrying protein in the RBCs 1 Hb molecule is made of 2 C02 a 4 protein subunits globin O 2 alpha subunits and 2 beta subunits that are circular 4 pigment subunits each containing an iron Fe group heme The O2 molecules specifically bind to the Fe portion of heme Because each Hb molecule has 4 Fe groups each one can carry a maximum of 4 O2 molecules gt Hb will load up on 02 at the pulmonary capillaries from the lungs and drop off 02 at the systemic capillaries to the tissues Circulating in the blood in 3 forms gt Physically dissolved 10 gt Bound to Hb 30 CO2 binds to the globin portion each Hb can carry up to 4 CO2 molecules gt As bicarbonate 60 gt Hb will load up on CO2 at the systemic capillaries from the tissues and drop off CO2 at the pulmonary capillaries to the lungs C Power Point Slides 1 Gas Exchange a b Partial Pressure PP the individual pressure exerted by one gas within a mixture of gases P02 PC02 When PP values differ for a gas on either side of a membrane a gradient is created A gas will always diffuse down its gradient from an area of higher PP to an area of lower PP Partial pressures before gas exchange gt In alveoli P02 100 mmHg gt Pulmonary capillaries P02 40 mmHg gt Systemic capillaries P02 100 mmHg gt Tissue cells P02 40 mmHg 2 Chloride Shift a b Looks at how CO2 is traveling in the body Start with CO2 in the tissue cells and move into the systemic capillaries RBC gt Moves down its PPG Once CO2 is in the RBC the enzyme needed to turn CO2 into bicarbonate is present There is more bicarbonate in the systemic capillaries than in the interstitial uid gt Bicarbonate will move down its concentration gradient into the interstitial uid C In order for this to happen bicarbonate Will use an antiport protein i Called a Band 3 Anion Exchanger 1 Transport protein 2 Specifically trades bicarbonate for C1 ion Use a Cl ion to replace the negative charge When bicarbonate leaves the RBC so Cl Will go into the RBC i Cl is helping maintain the neutrality between the RBC and interstitial uid 1 Will move down its electrical gradient Bicarbonate at the level of the pulmonary capillaries there is more in the plasma than in the RBC so it is going to move down its concentration gradient gt From the plasma into the RBC gt Once this happens Cl can be removed from the RBC Will move down its electrial gradient from the RBC to the plasma Bicarbonate Will then move to the alveoli by moving down its PPG D Regulation of Respiration by the CNS 1 Structures in the Medulla a DORSAL RESPIRATORY GROUP gt Located on the dorsal portion of the medulla gt Made of a group of neurons called the Nucleus Tractus Solitarius NTS gt These neurons are responsible for inspiration sends efferent signals to 0 Diaphragm via the phrenic nerve 0 Diaphragm contracts and moves inferiorly 0 External intercostals via intercostal nerves 0 External intercostals contract and ribs move superiorly and laterally up and outwards towards side 0 Both increase pulmonary holding capacity gt When signaling stops exhalation occurs passively due to relaxation of inspiratory muscles and elastic recoil of the lungs b VENTRAL RESPIRATORY GROUP gt Located in the ventrolateral portion of the medulla gt Made of 3 groups of neurons 0 Botsinger s Nucleus 0 Nucleus Ambigualis 0 Nucleus Retroambigualis gt Function to give a boost to exhalation when needed sends efferent signals to 0 Intercostals via intercostal nerves 0 Abdominal muscles via abdominal nerve causing contraction 0 This decrease pulmonary holding capacity gt Inactive during eupena normal quiet breathing breathing at rest 0 Only one set of muscles involved during eupena diaphragm and external intercostals only 0 Forceful breathing diaphragm and External intercostals internal intercostals abdominal muscles 2 Structure in the Pons a PNEUMOTAXIC CENTER gt Located dorsally in the superior portion of the pons gt Functions to limit inhalation by sending inhibitory signals to the DRG shutting off the NTS relaxing the external intercostals and diaphragm gt Allows smooth transition between inhalation and exhalation E Chemical Control of Respiration 1 Peripheral Chemoreceptors a Located in the aortic arch and bifurcation of the carotid arteries b Sensitive to arterial increases in H derived from CO2 and slightly sensitive to CO2 itself c Responsive to decreases in 02 but only if the decrease is life threatening gt 02 levels are normally controlled by Hb 0 If the P02 Partial Pressure of 02 is high Hb s affinity bond strength or attraction force for 02 is going to be high at lungs 0 If Hb is in an area with lots of 02 it will take advantage and pick up as many 02 molecules as possible 0 Where are high levels of 02 The lungs 0 If the P02 is low the Hb affinity for 02 is going to be low at tissues d When H concentration increases due to an increase in C02 receptors send efferent signals to the respiratory centers in CNS 0 Via Vagus nerve from receptors in aortic arch 0 Via glossopharyngeal nerve in the Carotids i Similar to baroreceptors 0 Respiratory centers dorsal and ventral in CNS increase efferent signaling to respiratory muscles 0 Not in eupena anymore Need additional boost to exhalation Thus external amp internal intercostals diaphragm and abdominal muscles e Ventilation increases to rid the body of the excess C02 2 Central Chemoreceptors a Located beneath the ventral surface of the medulla b Highly sensitive to increases in H derived from the C02 reaction that takes place in the CSF SENSITITY OF THE CENTRAL CHEMORECEPTORS IS THE DOMINANT CONTROLLING FACTORE IN RESPIRATION Respond more vigorously and faster than peripheral receptors because they are located in the medulla which is closerin the CNS gt The blood brain barrier made of capillaries with tight junctions at cellular adhesion designed to keep out everything that circulates in the blood ex hormones is impermeable to any H already formed in arterial blood 0 No matter how much H is in peripheral arteries it cannot cross the BBB 0 So C02 has to cross over BBB get into CSF and do the reaction into H and bicarbonate gt The reaction takes place after C02 diffuses from the blood and into the CSF c Stimulation of the receptors causes signals to be sent to the respiratory centers d Ventilation increases to rid the body of the excess C02 e Receptors are not sensitive to decreases in 02 no matter how severe Is the BBB permeable to H N0 only C02 that converts to H and bicarbonate F Respiratory Disorders a Adult Respiratory Distress Syndrome b Causes injury to the lung from trauma anaphylaxis viral pneumonia drug overdose inhalation of noxious gases near drowning c Pathophysiology injury involves both the alveolar epithelium and the pulmonary capillm endothelium the respiratory membrane the causative agent triggers a cascade of cellular and biochemical events that lead to severe in ammation primary mediator is histamine this in ammatory response increases capillary permeability causing proteins and uids to first leak into the interstitial space then into the alveoli PULMONARY EDEMA the edema along with vasoconstrictive substances cause decreased blood ow 02 nutrient delivery released in the immune response damage alveoli surfactant and impair the cells ability to produce more as a result alveoli collapse impeding gas exchange and decreasing lung compliance edema worsens in ammation leads to fibrosis laying down of fibrin strands yielding scar tissue and gas exchange is further hampered if not treated Within 48 hrs death from respiratory failure can occur 1 Cystic Fibrosis e Causes Inherited mutation of the gene that codes for a transmembrane protein channel that regulates Cl and Na transport This channel is specifically called the Cystic Fibrosis Transmembrane Conductance Regulator CFTR gt CFTR functions in C1 transport across cell membranes and Na transport is generally coupled to Cl transport gt Water will follow the NaCl Depending on the direction of movement glandular mucous secretions will become very viscous thick due to loss of water gt The increased thickness of the mucus is a breeding ground for bacteria which is the source of repeated respiratory infections the abnormally thick mucous is also the cause of transport problems in other systems Occurs once in every 2500 births in the Caucasian population The average life expectancy of a CF patient is 28 years f Pathophysiology epithelia affected followed by consequences gt Airway epithelia increase viscosity of alveolar mucus which hinders breathing gt Intestinal epithelia results in thick obstructing stool which hinders elimination gt Saltabsorbing epithelia in sweat ducts leads to sweat glands that secrete NaCl A crude test for CF in children involves tasting the sweat from their foreheads and assessing degree of saltiness A more modern test involves molecular analysis of sweat gland secretions for NaCl levels 1 NaCl is in a much higher concentration gt Volumesecretory epithelia in the pancreas results in ductal occlusion that prevents secretion of digestive enzymes The pancreas produces digestive enzymes g Treatments Salt supplements Pancreatic enzyme replacement Breathing exercises and chest percussion Inhaled Beta adrenergic agonists Current research is investigating gene therapy a method in which the defective gene can be replaced by a functional one Asthma type of Chronic Obstructive Pulmonary Disorder a group of lung diseases characterized by increased air ow resistance a Causes ExtrinsicAtopic asthma allergens gt pollen gt animal dander gt house dust gt mold IntrinsicNonatopic allergens gt emotional stress anxiety gt fatigue gt coughing or laughing b Pathophysiology bronchial linings overreact to various stimuli patient is hypersensitive upon inhalation of the allergen plasma antibodies specifically Immunoglobulin E stimulate the release of histamine and a chemical called slowreacting substance of anaphylaxis SRSA from mast cells and basophils gt histamine binds to receptors in the larger bronchi causing swelling of smooth muscle and resulting in constriction of underlying bronchioles and the release of excessive amounts of mucus gt SRSA binds to receptors in the smaller bronchi causing swelling of smooth muscle there This substance also causes fatty acids called prostaglandins to travel via the bloodstream to the lungs Where they enhance histamine s effects overall result is the closure of bronchial lumen and the inhibition of alveolar ventilation c Treatments Bronchodilators ex Ipratropium Corticosteroids antiin ammatory agents ex Funisolide subcutaneous epinephrine ex EpiPen antihistamines ex Cromolynsodium


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