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KIN 272 Exam 3 Study Guide

by: Juliana Bernard

KIN 272 Exam 3 Study Guide 272

Marketplace > University of Massachusetts > Kinesiology > 272 > KIN 272 Exam 3 Study Guide
Juliana Bernard
GPA 4.0
Anatomy and Physiology II
Dr. Gordon

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About this Document

Detailed study guide on Exam 3 material. Includes: some blood vessel info, atherosclerosis, filtration/reabsorption of capillaries, and respiratory system material.
Anatomy and Physiology II
Dr. Gordon
Study Guide
50 ?




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This 4 page Study Guide was uploaded by Juliana Bernard on Tuesday March 24, 2015. The Study Guide belongs to 272 at University of Massachusetts taught by Dr. Gordon in Spring2015. Since its upload, it has received 128 views. For similar materials see Anatomy and Physiology II in Kinesiology at University of Massachusetts.

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Date Created: 03/24/15
Exam 3 Study Guide Circulatory SystemRespiratory System Unlike arteries veins cannot alter in diameter because they lack smooth muscle Tunica media of veins collagen and elastin no smooth muscle Total Peripheral Resistance total resistance in all vessels changes due to Change in diameter Larger diameter less resistance quicker flow Smaller diameter more resistance slower flow Blood viscosity The greater the viscosity the less easily molecules slide past one another and the more dif cult flow is Blood viscosity is fairly constant but having a higher than normal RBC count can increase blood viscosity and resistance while a lower RBC count can reduce viscosity and peripheral resistance Turbulent vs laminar ow In a tube of a given size the speed and position of fluid in the regions of the tube39s cross section remain constant this is called parabolic or laminar flow gt center travels quicker When blood encounters an abrupt change in vessel diameter or roughprotruding areas of tube wall the smooth laminar blood flow is replaced by turbulent flow gt irregular fluid motion high resistance ncreased HR increases turbulenceresistance Blood flow is inversely proportional to total peripheral resistance lf TPR increases the heart has to work harder to overcome the resistance Tissues dictate CO To return flow veins have One way valves once blood goes through it can39t go backwards doesn39t help with actual movement Rely on respiratory system pressure vacuum when we breathe we pull blood into the thoracic cavity Rely on contractions of the muscular system contracting skeletal muscles around veins pushes blood up We have flow down in the capillaries what happens in terms of diffusion We know RBCs are stacked like dinner plates in capillaries because they are so small but How do you get materials out of RBC plasma The RBC is so close to the thin wall of the capillary this close relationship and the fact that RBCs have thin membranes allows 02 to come out and C02 to come in On top of this we also want the nutrients glucose FFAs antibodies etc from inside the plasma The flow of blood at the beginning of the capillary entered from being arteriole is faster than it is at the end of the capillary it actually slows down Flow is associated with hydrostatic pressure At the beginning of the capillary water can be pushed out and with it nutrients that need to go into extracellular fluid can go with it This is known as the process of filtration Can you lter for the entire length of the capillary No because the speed of flow decreases towards the end of the capillary so the force alone will not allow you to continue pushing water out Filtering water out increases oncotic pressure so at the end of the capillary when water is no longer being pushed out water from the extracellular fluid is pulled back into the vessel due to this increased oncotic pressure As water goes in waste products from extracellular fluid go with it This is known as the process of filtration When reabsorption stops you are in a venule Hydrostatic pressure pushes water away Osmotic pressure attractspulls water in Filtration happens in the beginning because hydrostatic pressure forces it out Reabsorption happens in the end because osmotic pressure pulls it in Atherosclerosis Sedentary people with poor diets will have high LDL and low HDL LDLs like to migrate to coronary arteries and above the carotid arteries brain After a while WBCs will see LDLs as foreign invaders so they will attempt to clean them up Monocytes will consume LDL burrow itself in the tunica media and attempt diapedesis to get it out The monocytes will eventually get taken over by the fat and expands well beyond it39s size referred to a foam cell Build up of foam cells end up shrinking the size of the lumen increasing resistance in the vessel At this point if any tearing occurs fibrinogen will convert to fibrin to build a patch over the endothelial tear The patch is made of collagen elastin and smooth muscle The more foam cells grow however patches may end up ripping which could cause a clot in that location Myocardial infarction heart attack heart death due to blockage in the arteries Exercise increases HDLs which collect LDLs and return them to the liver good Over time good exercise and diet increase the thickness of the patch which pushes down on foam cell and increases the diameter of the lumen Clinical ways to increase artery diameter Angioplasty Coronary bypass place segments of the great saphenous around damaged vessel to form a new one Factors that effect blood flow 1 Autoregulation control factor that happens naturally and locally to balance back to homeostasis 2 Neural regulation brain fixes things when autoregulation is not enough to fix damage Autoregulation Local vasodilators things that result in vasodilation open precapillary sphincters increase C02 or H byproducts in tissues you induce vasodilation decrease 02 in tissues increase lactic acid in blood These A cause endothelium of arterioles to release nitric oxide gt a potent vasodilator local inflammatory chemicals histamines also increase vasodilation Local vasoconstrictor no actual chemicals Aggregation of platelets Neural Regulation Cardio centers are in the medulla of the brain Neurons for widespread vasoconstriction respond to norEPl Neurons for vasodilation norepi and epi release nitric oxide NO Reflex control change in size due to responses Baroreceptors pressure receptors senses amp regulates BP an autoregulated response most found in carotid sinuses and aortic sinuses when blood pressure rises these receptors stretch and send a rapid stream of impulses to the cardiovascular center ultimately decreasing blood pressure Chemoreceptors sense changes in chemicals H 02 C02 gt send signals to brain if need a response most found in carotid bodies and aortic bodies Respiratory System Major functions of the respiratory system 1 Gas exchange C02 and 02 between the air and the blood 2 Movement of air onto respiratory surfaces 3 Protection of the delicate respiratory surfaces 4 Provides a method of communication gt air over vocal chords 5 Provides us with one of the major senses olfactory Upper respiratory above the trachea includes Nose Nasal cavity Oral cavity also shared with digestive system Pharynx also shared with digestive system Lower respiratory includes Larynx located between thyroid cartilage cricoid cartilage and count 7 other cartilage rings down Trachea Lungs right lung contains 3 lobes eft lung contains 2 lobes and is slightly smaller than right lung Bronchi Right Left primary bronchi 3 2 secondary lobar bronchi 3 2 l tertiary segmental bronchi 89 78 terminal bronchioles respiratory bronchioles end in the air sacs known as alveoli Trachea has hard cartilage in the front connective tissue in the back follows this trend down to the bronchi Has connective tissue in back to stretch when too much food is swallowed lnitial bronchi segments are mostly cartilaginous rings like the trachea Cring cartilage As you move down the bronchial tree from primary bronchi gt respiratory bronchioles the tubes shift from being mostly cartilage to mostly smooth muscle Bronchiomotion bronchioconstrict pollen and bronchiodilate Alveoli air sacs at the bottom of each respiratory bronchiole made of simple squamous epithelium makes diffusion faster umped together to hold more oxygen diameter of thread Modes of protection Filtration nasal hairs filter out big particles cilia mucous production traps fine particles that get past nose hairs phagocytes are housed inside of epithelial cellsliningsmucous membranes WBC migration here too The simple squamous epithelial cells that make up alveoli are classified as either type 1 cells or type 2 cells Type 2 cells look slightly different a bit fuzzier are known as surfactant cells they produce surfactant Surfactant sticky substance that lines the inside of alveoli decreases surface tension without this alveoli would collapse and breathing would be extremely difficult Smokingchemicalsetc destroy type 2 cells so they have to inflate alveoli each time they breathe Respiration the exchange of gases 02 and C02 lnternal respiration in the tissues exchange between alveoli amp tissue gt mitochondria External respiration in the lungs exchange between alveoli amp capillaries Ventilation the actual act of breathing inhaleexhale there can39t be any respiration without ventilation 02 consumption how much 02 the mitochondria are using V02 Ventilation Boyle39s law gt P 1IV pressure and volume are inversely related As volume T pressure l Pleura thin double layer sac around the lungs one layer connects to the lungs the other connects to the outside of the thoracic cavitydiaphragm helps create the partial vacuum that exists in the intrapleural space To ventilate the lungs air moves from high pressure to low pressure you can39t alter pressure in the lungs so we rely on the diaphragm to change the volume which in turn changes the pressure When the diaphragm contracts it becomes flat and pulls on the pleura which also tugs on the vacuumlike system of the lungs this increases the volume in lungs therefore decreasing the pressure Now pressure in the thoracic cavity is lower than the pressure of the air where you are so air will go in inhale nhalation is only responsible for contracting the diaphragm to make sure pressure in the room is higher than pressure in the thoracic cavity When we exhale the diaphragm relaxes so lung volume goes back down and pressure increases pressure is now higher in the lungs than outside so air will travel outexhale lnhalation contracting the diaphragm volume T pressure l ACTIVE process Exhalation relaxing the diaphragm volume l pressure T PASSIVE process When we inhale The alveoli and tubes ventilate Only the alveoli respirate Compliance expandability Capillary beds are bound to alveoli sacs by elastic fiber network When we inhale we work to expand the alveoli when we exhale we don39t have to work because of compliance the elastic fibers bring it back to normal without force Elastic tissues cannot be repaired when damaged they are destroyed and compliance is lost This is why COPD patients and smokers struggle to exhale lnhalation muscles Exhalation muscles Diaphragm 75 of work nterna intercostals External intercostals External oblique Scalenes nterna oblique Sternocleidomastoid Transverses abdominis Pectoralis minor Rectus abdominis Lung capacity 56L Tidal volume TV amount of air that moves into and then out of lungs with each breath 500 mL rest lnspiratory reserve volume IRV the amount of air inspired forcibly beyond the tidal volume Expiratory reserve volume ERV the amount of air expelled from the lungs after a normal TV expiration Residual volume RV the amount of air that remains in lungs even after the most strenuous expiration 1 L Functional capacity FC TV lRV ERV quotwe can39t control these VE TV x RR how much you are ventilating per minute RR respiratory rate


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