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In Exercises 4752, if possible, find (a) (b) and (c) A2

College Algebra | 9th Edition | ISBN: 9781133963028 | Authors: Ron Larson ISBN: 9781133963028 204

Solution for problem 7.2.47 Chapter 7

College Algebra | 9th Edition

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College Algebra | 9th Edition | ISBN: 9781133963028 | Authors: Ron Larson

College Algebra | 9th Edition

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Problem 7.2.47

In Exercises 4752, if possible, find (a) (b) and (c) A2 AB, BA, . A 1422 B 2118 A

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Final Exam Study Guide Ch. 16: Respiratory Physiology  Respiration is made up of 3 functions that are separate, yet related. o Ventilation- breathing, mechanical process of moving air in and out of lungs o Gas exchange- occurs b/w alveolar air and blood in pulmonary capillaries o Oxygen utilization- occurs by tissues for energy liberating rxns of cell respiration  Ventilation o Moves by bulk flow  Internal respiration o In cells  External respiration o Atmosphere, heart and alveoli  Steps of ventilation o Ventilation (exchange of air between atmosphere and alveoli by bulk flow) o Exchange of oxygen and co2 between alveoli air and blood in lung capillaries by diffusion o Transport o2 and co2 through pulmonary and systemic circulation by bulk flow o Exchange of o2 and co2 between blood in tissue capillaries and cells in tissues by diffusion o Cellular utilization of o2, production of co2  Branching o Quick means of dispersing incoming air  Respiratory system o Conducting zone  Gets air into the pathway o Respiratory zone  Warms, humidifies, cleanses incoming air  Respiratory zone and site of exchange o Type I cells  Squamous, epithelium cells  Gas transfer occurs here o Type II cells  Surfactant—reduces STension, reduces the force to inflate lungs, higher compliance  Thoracic cavity o Visceral – covers lungs o Parietal – covers ribcage o Pleural cavity – space b/w the 2 pleura  Ventilation o What is it: movement of air from pressure difference between the ends of airways (atmospheric air and alveoli’s) o Pressure gradient: change in lung volumes o Airflow is directly proportional to pressure difference o Airflow is inversely proportional to frictional resistance to flow  Pressure relationship in thoracic cavity o Atmospheric pressure: 760 mmHG o Intrapulmonary – pressure within alveoli o Intrapleural – pressure within pleural cavity  Due to elastic tension of lungs with thoracic wall o Transpulmonary pressure – difference between intrapulmonary and intrapulmonary pressures  Acts as a vacuum  Intrapleural is always lower than intrapulmonary pressure because it needs to hold the lungs to the ribcage/in place  Boyles Law – pressure and volume of gases is represented by boyles law and it states: o For an ideal gas, if temp is constant, pressure of a gas varies inversely with its volume. o P1V1 = P2V2  Gases fill up the size of a container, in a large volume = less pressure. Smaller volume is greater pressure.  Increase in lung volume during inspiration decreases intrapulmonary pressure below atmospheric and air flows in. Decrease in lung volume raises intrapulmonary pressure above atm. Pressure, causing air to flow out.  Properties of lungs o Compliance – how stretchable the lung is  Defined as change in lung volume per change in trans pulmonary pressure (change V / change P)  Reduced by factors that produce resistance to distension o Elasticity – the structure and how it returns to its initial size after being distended  Normal lung has high elasticity o Surface tension  Thin fluid is left on alveolar surface  Tension exists because of water molecules that shrink alveoli resist further stretching.  Hard to change lung volume / makes breathing costly  The good thing about alveoli is that they have type II – surfactant producing cells!  Reduces cohesive forces between water molecules on the surface  Therefore, a decrease in ST = increase in compliance and lungs are easier to expand!  Law of Laplace – relationship b/w pressure, ST and radius of alveoli  P = (2 – T) / r  Mechanics of breathing o Pressure difference = air flow  Pressure difference air in alveolus and atmospheric ends o Breathing has 2 phases  Inspiration – alveolar is less than atmospheric pressure, air flows in  Expiration – alveolar pressure is greater than atmospheric, air flows out  Mechanical process o RULE OF BREATHING: Volume changes lead to pressure changes which lead to the flow of gases!  Pressure change is the driving force  But, it doesn’t occur unless there is a volume change  Mechanics of pulmonary Ventilation o Intrapleural is less than intrapulomary because the lungs are a vacuum o Rest: atmospheric air comes in (760 mmHg), intrapulmonary is 760 mmHg, intrapleural is 756 mmHg o Inspire: atmospheric air comes in because it is higher than intrapulmonary (757 mmHg), intrapleural is at 754 mmHg. o Expire: air flows out because it is higher than atmospheric air in the intrapulmonary (763 mmHg) and intrapleural is 757 mmHg  Gas exchange in the lungs o Why does gas exchange in the body occur  Bulk flow of gases and diffusion through tissues o Daltons Law of partial Pressures  In a mixture of gases the total pressure is the sum of partial pressure exerted independently by each gas in the mixture. o Air flow stops at….  Terminal bronchioles because the movement of gases from respiratory bronchioles to alveoli is by simple diffusion  Partial Pressure of Gases in Blood o Large SA and short diffusion distance along capillaries o Amount of dissolved blood reaches a value in accordance to Henry’s Law  Henry’s Law: if gases and liquid come in contact each gas will dissolve into the liquid in proportion to its partial pressure; thus the greater concentration of gas = the quicker it will move into the solution.  In conclusion Henry’s law focuses on concentration and solubility of the gas in proportion to the solution (also, consider the temperature— we warm everything that enters our body so temp. is not an issue)  Co2 > O2 > N2 o Why do we take in little Nitrogen  It is the least soluble of oxygen and carbon dioxide o Why aren’t alveolar air and atmospheric air the same  Residual volume (air is pulled in close to the alveolus, but not into them)  CO2 and O2 move in at the same rate because even though there is a pressure difference O2 doesn’t need a big pressure gradient to flow in and CO2 is soluble enough. o Why is it important to keep pulmonary circulation low  Low pulmonary bld pressure produces LESS filtration pressure and protects against pulmonary edema which occurs with pulmonary hypertension and leads to an increase in interstitial fluids that enter alveoli and impede ventilation and gas exchange.  Ventilation-Perfusion Coupling o Must be matched for gas exchange  Regulated by autoregulatory mechanisms that monitor alveoli  Regulation of Breathing o Inspiration and expiration is produced by contraction/relaxation of SkMs in response to somatic neuron activity. o Medulla and cerebral cortex control it o Rhythmicity center controls automatic breathing  I neurons – inspiratory, part of VRG, apneustic center  E neurons – expiratory, part of DRG, pontine respiratory centers (antagonistic against apneustic center)  I remember everything in the rhythmicity center by this: o D I V E (DRG and VRG have inspiratory neurons (“I” is sandwhiched between “D” and “V”) and VRG has Expiratory neurons  Pre-botzinger complex – sets inspiratory rate  Chemoreceptors – automatic control of breathing o Where: central and peripheral locations o What does it do: relays info on changes in pH of blood, PO2 and PCO2. In addition to changes in pH in brain If and CSF o In the brainstem, chemoR’s modify rate and depth of breathing  PCO2 and pH on Ventilation o O2 is not changed because PCO2 causes expiration and inspiration. o Blood brain barrier only lets CO2 move into CSF o Immediate increase in ventilation due to peripheral chemoR’s with a rise in arterial PCO2, whereas a sustained rise in arterial PCO2 activates central chemoR’s and takes longer to respond  Immediate peripheral chemoR’s, ex: blood pH  Sustainedcentral chemoR’s, ex: plasma CO2  Effects of Blood PO2 on Ventilation o Oxygen and carbon dioxide display a different curve  Co2 and breathing are linear  Oxygen – since CO2 is the principle gas to regulate ventilation oxygen displays a slower increase on the graph.  Hypoxic drive – related to PO2, static to an increase in the graph because oxygen chemoR’s are utilized instead on CO2.  You need to be below 70 mmHg to stimulate ventilation.  chemoR’s that respond to CO2 are enhanced when oxygen levels are low. CO2 is suppressed when oxygen levels are high.  Effects of pulmonary Rs on ventilation—what influences ventilation o Receptors act through the hypothalamus activate peripheral ChemoR’s and central chemoR’s  Peripheral—low O2, high CO2 and high H ions  Central, high CO2, slower to respond and high levels of H ions (R’s in muscles and joints)  Hering Breuer Reflex- prevents over inflation (stretch receptors in the lung)  Irritant R’s are stimulated by unmyelinated C fibers that respond to capsations when someone eats hot/spicy foods  higher brain centers like the cerebral cortex voluntarily control breathing  Hemoglobin and Oxygen transport o Oxygen carrying capacity is defined by Hb concentration  Anemia- below normal Hb  Polycythemia- above normal Hb o Whole blood has more oxygen carrying capacity than bubbling plasma o Why can hemoglobin bind to oxygen  It has iron o High elevations _______ oxygen carrying ability.  Increase o Loading reaction: oxygen binds to heme group o Acidic increases heme loading o Why is erythrocyte pH falling  Because CO2 has carbonic anydronase and when it is around water it turns into bicarbonate  Oxygen Hb Dissassociation Curve o At rest lungs are 98% saturated and at a 20 volume percent o Tissues: 75% saturated, 15 volume percent o Reserve of oxygen is in venous bld o Hb is almost saturated at 70 mmHg  Increase in PO2 causes a small increase in O2 binding.  When levels are below 70 mmHG like 55-60 then molecules want to quickly be saturated o What determines if Hb will unload/load oxygen  Picks up O2 in alveoli,  Unloads O2 in tissues o High PO2 means molecules are loading o Low PO2 means molecules are unloading  How does the environment effect affinity o A drop in pH – more unloading (Bohr Effect) o High temp – more unloading o Increase in PCO2 increases in loading o Increase DPG – more unloading  Oxygen transport o Oxygen travels in 2 ways  Blood plasma and it is taken up by erythrocytes making oxyhbglobin  Lungs – load oxygen  Tissue – unload oxygen  Carbon Dioxide Transport o CO2 moves in 3 ways  Dissolved in plasma, bound in Hb, transported as bicarb  Chloride shift: H makes blood acidic, bicarb is transported out of the cell and Cl ion is taken in.  Low CO2 in the lungs  As bicarb is taken in, it binds to H ion and forms carbonic acid and converts to water and CO2. It is released and comes in from plasma. In plasma it is bound to hb and released…CO2 is unloaded at the lungs.  At the tissues:  Binding O2 and CO2unloading O2 and CO2 (internal respiration)  CO2 is taken up by erythrocyte and converted into bicarb. Take Cl ions in o Bicarb binds to hb and some stays free o Binding to hb influences unloading of oxygen  What does the bohr effect do to the affinity between ocygen and hb o Supports oxygen unloading  Hb-NO partnership in Gas Exchange o NO is secreted by lungs or vascular endothelial cells  Vasodilation o Hb is a VC and scavenges NO (it takes away NO) o Whats the conflict  As O2 binds to Hb it changes shape and enables NO to bind to it by cysteine residues  Protects NO  As O2 is unloaded at tissues so is NO and this causes local vessel dilation and aids in O2 delivery  When CO2 binds, NO is picked up and carried to the lungs  Bottom line: Hb carries along is own VD and assists in CO2 exchange  Acid-Base Balance of Blood o Bld pH is kept within a range or .1 o Function of lungs- regulate bld CO2 levels o Kidney function- regulate bicarb ion o What is the major buffer in plasma  Bicarb ion o Acidosis  Respiratory- hypoventilation, increases bld CO2 levels  Metabolic- nonvolatile acids (lactic acid) or loss of bicarb o Alkalosis  Respiratory- hyperventilation  Metabolic- too much bicarb or inadequate nonvolatile acids o Absolute bld limits for life  pH: 7-7.8  below 7 depresses CNS, coma  above 7.8 – muscle tetni/death occurs due to respiratory arrest Chapter 17: Physiology of Kidneys  primary function of the kidneys o regulate ECF environment of the body  how is this accomplished through the formation of urine o Volume of bld plasma, concentration of waste products in blood, concentration of electrolytes (sodium, K, bicarb), pH of plasma  Kidneys considered most potent acid-base regulator (because it regulates bicarbonate ion)  The urinary system and the respiratory system regulate acid and base balance  Anatomy of the urinary system o Kidneys: urine formation o Ureter o Bladder: storage o Urethra: eliminates urine from body  Last 3 are referred to urinary tract because it is a conduit o Kidney  Renal cortex  Renal medulla (inner)  Slice of medulla – renal lobe  Kidneys are the workforce  Nephron: functional unit of kidney (found in cortex and medulla) made up of renal corpuscle and renal tubule  Collecting duct: conduit  urine taken to renal papilla and urine is released into minor and major calyx  Renal pelvis leads into the ureter  Nephron – functional unit of kidney, where urine is produced o It is made up of 2 parts – renal corpuscle and renal tubule  Renal corpuscle is made up of the glomerulus, which is a high capillary bed  It is a high capillary bed b/c it is fed and drained by an arteriole (afferent and efferent)  Arterioles are made for VD and VC  Bowmans capsule - a capsule-shaped membranous structure surrounding the glomerulus of each nephron in the kidneys of mammals that extracts wastes, excess salts, and water from the blood  Renal tubule  PCT  Loop of henle  DCT – connects to the collecting duct (where all the filtrate from nephrons collect) o 2 types of nephrons  Cortical – makes up 80% of nephrons, shortened  Juxtamedullar – loop of henle, long o Peritubular capillaries loop around renal tubule  In juxtamed. Nephrons the peritubular capillaries are referred to as vasa recta  Basic functions of Renal function (nephrons) o Glomeruluar filtrations (occurs in renal corpusule) o Tubular reabsorption (renal tubule) o Tubular secretion (renal tubule)  Glomerular filtration  Begins as the filtration of plasma arising from glomerular capillaries into bowman’s capsule. This is called filtrate. It uses a pressure gradient.  High pressure capillary bed  Process: nonselective o Construction: afferent and efferent arteriole, renal corpuscle Bowmans Capsule has 2 layers  Outer layer- parietal layer  Inner layer- podocytes forms the visceral layer  Foot processes come out of it to interdigitate with each other  Filtration memory – 3 filtration barriers  Fenestrated Capillaries – charged area, repels proteins. It keeps plasma proteins within the blood.  glomerular basement membrane – restricts fluid flow in lumen of BC, made up of proteoglycan  slit diaphragm (created in interdigitations in foot processes) – restricts things by size, keeps out plasma proteins and within blood o some proteins get through, but we reabsorb them later on. Very few get through.  Forces involved with filtration o Pressure gradient o Filtration due to opposing forces – hydrostatic pressure (BP) and protein conc in plasma (colloid osmotic pressure) o Forces favor filtration – hydrostatic pressure (BP within glomerulus), it is at 60 mmHg, capillary beds are usually at 40 mmHg or less (so this is a high capillary pressure bed!) o Opposing forces: Pressure in BC (hydrostatic pressure of filtrate), osmotic force in plasma proteins – pulls water from BC into plasma  3 players  Capillary hydrostatic pressure, colloid osmotic pressure and fluid pressure (hydrostatic pressure of BC on the tube)  Net glom. Filtration pressure = 16 mmHg ( what pushes fluid from plasma to glom capillaries into BC) o GFR – volume filtered from glomeruli into BC per unit of time  Blood volume is filtered about every 40 minutes  Blood plasma is reflective of IF components, whats coming from lymph is looked at on a regular basis for regulation  Regulation of GFR o Regulate through VC or VD in afferent (effecting hydrostatic pressure o Extrinsic mechanisms  Decrease in systemic BP  increase SN activity and VC of arterioles (leaving more fluid in blood and then BP is elevated)  Exercise (increases sympathetic nerve activity) o Intrinsic mechanism – happen regularly/adherently  BP fluctuates a lot throughout the day, GFR stays constant  Renal autoregulation – maintain constant GFR o Myogenic: stretch smm in a bld vessel constricts (since BP increases we VC) o Locally produced chemicals effect afferent tubules o Tubuloglomerular fdbk mechanism – results in JG apparatus  Cells called the macula densa – found in Renal Tubule and serves as a flow detector. (when it is already in the glomerulus and in the tubules)  Increase in filtrate flow, macula densa releases chm signal and makes arterioles VC.  Why should be regulate flow  To regulate blood composition. If it is too fast the good stuff goes to waste and if it is too slow you actually reabsorb waste you are trying to get rid of due to the nonselective process. You need balance to get flow rate at a certain rate.  Renal Reabsorption o Water and salt is filtered to bld by reabsorption o Reabsorption is returned of filtered molecules from the renal tubules bld o It can occur along the whole tubule but it is dominant in the PCT o Obligatory water loss – min volume needed to excrete metabolic wastes per day. This ensures you get rid of waste and reclaim nutrients you need. (400 ml urine/day) o Water transport is passive  Concentration gradient needed in RT and peritubular capillaries surrounding them  Filtrate = isosmotic to plasma  How do we move anything! We spend energy. We have active transport to let us run things passively. o Primary active transport: move Na in and K out o Begins in epithelial cells of PCT, joined by tight junctions, sealing off epithelium, creates regions of exchange o “All about the sodium, all about the sodium, no others” Meghan Trainer song  Sodium in the filtrate (tubular) and Proximal Tubule plasma are equal. Sodium is lower in PT capillary because of primary active transporter.  3 Na out and 2 K in  Na is high in IF space (making a pressure different in between cell wall)  It is + charged  Concentration gradient is set up for other ions to move (bicarb ions)  When Na is pulled water follows and water moves by osmosis  As water moves from filtrate, osmolality increases, then solutes can move passively. o Facilitated diffusion or cotransporter o Mechanisms for reabsorbing – water moving, cotransporters  Move Na across PT capillary, increase in local osmolality and water follows, its all about sodium. The osmosis is called obligatory water reabsorption (since it is following salt) now we can carry solutes behind the solvent, which is water!  Solvents moving are usually cotransporters  Transportation maximum on apical side of the cell  If conc. exceeds carries, solute will be excreted.  Fluid compartments are kept in balance if peritubular capillary can do its job.  Countercurrent multiplier system and countercurrent exchange o We usually have a hypoosmotic urine (we hold onto water) o Where does this occur  Loop of henle (in juxtamedullary nephrons) o Process: from the cortex  medulla kidneys we see a steep osmotic gradient from NaCl and urea (waste product of aa metabolism) o Apical surface (300 mOsm) and into the deep portion is close to 1400 mOsm o What does it do Creates an osmotic gradient o Countercurrent is due to descending (from the PCT) and ascending loop of henle  Ascending limb  Active transporters of Na, set up Cl to move passively, moving salt out into the environment, cannot move water (impermeable to water) which increases osmotic environment ie: the interstitial fluid  Descending limb  Permeable to water and water only  Pulling water out of the filtrate  Reflects concentration of IF o Creates a POSITIVE feedback mechanism multiplying concentration of IF of descending limb  Multiplies IF concentration due to active and passive transport system  Max concentration is determined by max activity of active transporters (depends on how much is inside the filtrate and if there is energy to run it) o Maintain hyperosmotic environment and we need to get rid of the water (it will dilute the concentration we established)  How With the vasa recta!  Counter current exchanger – the parts of the VR on the descending and ascending limb are in close proximity to each other  It maintains a hyperosmotic environment o It is permeable to salt, water and urea, but not plasma proteins  Descending VR o Salts and solutes diffuse IN (mimicking the environment)  Ascending VR o Pulling out NaCl (water moves in…why We still have plasma proteins that don’t move aka oncotic pressure in the blood that pulls water in!) *important characteristic  CCE maintains the gradient  CCM creates the gradient o Videos  Kidney function  Renal formation: occurs in RC (ions, water, solutes are filtered out of the blood)  PCT  loop  CCMultiplier system (NaCl diffusion, dips from cortex into the medulla of the kidney, elevates urine in the loop and elevates IF concentration) o Water is removed by VR in the descending limb o The more salt pumped out = higher concentration in the medulla o Final concen = in collecting ducts (where urine is diluted)  Walls are permeable to water in the collecting duct  Rate is determined by ADH in the blood. This causes the CD to be more permeable to water and more is excreted.  CCMultiplier system  Sequence of kidneys for a reference: Bowmans capsule is capped around the glomerulus and then flows to the PCT into the loop of henle and up into the DCT. Finally, it goes into the collecting duct and to the bladder.  ADH o Reabsorbing as much as water as possible creating highl concentrated urine o What 2 aspects drive CCM during ADH  Urea reabsorption in medullary collecting ducts  Urea = high concentration in the collecting duct and during ADH it flows into the IF increasing concentration  Secondly, active transport of NaCl on the loop of henle  Key points that drive the CCM: Urea and NaCl reabsorption (hyperosmotic IF promotes water reabsorption on descending loop of henle)  At the top of the DCT the fluid is hypo osmotic  This determines how much urine is diluted or concentrated  When the nephron is antidiuresis it lets out water = hypoosmotic urine!  Vasa Recta Counter Current Exchange (ADH) o VR is a specialized peritubular capillary for the Juxatamedullary nephrons that make a hyperosmotic fluid, especially in ADH  VR’s role: Minimizes solute that is carried away by the diffusion into the medullary fluid  Isosmotic to the bld plasma  gets hyperosmotic  Effects of urea o Trapped in medullary IF o Helps support high osmolarity o Osmotically active molecule o Recycling in and out of RT (keeps high osmolarity) o We have the ability to eliminate o Filtration = nonselective (if urea is there, it will be in the filtrate) o NaCl and urea make IF hypertonic (makes us remove water by osmosis) we remove water in the collecting duct  Everything is set up so we reclaim water  How  We use ADH  Role of ADH o Aquaporin’s are in the tubule cells and this is how water is transported out of the collecting duct (exocytotic vesicles have aquaporin’s in them and are placed in the tubule cells) o How do we pull water in the CT  By osmosis! Concentrated IF allows us to PASSIVELY pull water from filtrate = concentrated urine o Overhydrated – plasma osmolality goes down, so we decrease ADH and we cause formation of endocytoic vesicles. When ADH falls and is low in CT we take away ADH so water from the body will be elimated. o Eliminating water brings down high BP o Water reclaimed from tubular fluid is called facultative water reabsorption  Renal Plasma Clearance – Renal Secretion o removing excess ions and wastes is a major function of the kidneys o clearing the blood is accomplished through excretion in urine o renal clearance - ability of kidneys to remove molecules from bld plasma by excreting them in urine  urine is a result of filtration (Renal Corpusule), reabsorption, secretion (membrane transport mechanism- reabsorption in reverse) o for excretion to occur a molecule can be filtered and secreted (filtration rate + secretion rate) – reabsorption o renal plasma clearance: V * C / P [(urine volume per minute * concentration of urine) /(concentration of plasma)]  this tells us how the molecule is handled by the kidneys  clinically, this is important for disease states in the kidney or if the kidney is normal  Renal Control of Electrolytes o Match urinary excretion with dietary intake o 90% of Na and K are reabsorbed in Proximal Convoluted Tubule, although it can happen along the entire tubule o Secretion occurs along the proximal convoluted tubule  It is not subjected to hormonal regulation but in regards to body needs  It occurs at a constant rate  Regulated by aldosterone – regulates Na and K (K –direct, Na- complex regulation)  Na reabsorption: excrete around 30 grams a day in urine (2%) o Na concentration can diminish to 0 in the presence of aldosterone (reabsorb it all) o Na induces synthesis of all channels and pumps in collecting ducts to reclaim  Induces synthesis of collecting duct to reclaim Na or K  Regulatory mechanisms o K secretion  Occurs in DCT and collecting ducts in 2 ways  Aldosterone dep K secretion – K rich meal, increase rich levels of K and stimulates release of aldosterone which results in K secretion into filtrate  (intrinsic) Independent K secretion – eat a K rich meal and this causes insertion of K channels into PM of cortical collecting ducts due to Bld K concentration levels  Sensory mechanism – RT cells have cilium that bends to a degree determined by flow. This activates K channels, increasing K secretion. o This explains why diuretics cause hypokalemia – low bld K levels  Aldosterone Secretion – main regulators of sodium (not as sufficient as K) o Regulates Na – accomplished by a complex mechanism (involves in fall of blood volume that activates renin-angiotensin- aldosterone system)  Sympathetic nerve activity o Retain NA (concentrates urine and increases blood volume) and K secretion o Na – fall in bld volume along the activation of renin-angiotensin aldosterone system  Activation of juxtaglomerular cells that releases renin  ANP – regulates blood pressure o Increase in bld volume makes Na be secreted and water loss due to the inhibition of aldosterone however, ANP is released by the atria of the heart or BNP and influence GFR (increase in Na secretions and diuresis)  Whats great about naturietic peptides: ANP spares K – regulate Na without sacrificing K  Causes VD and decreases Bld pressure  Counter regulatory system for renin-angiotensin aldosterone system o Influences GFR and Na  Regulated Na and water secretion  Relationship between Na, K and H ion o Why does bld K concentration indirectly affect H concentrations (and vise versa)  Increase in H in the IF which causes K to move out (reest ions) if you move K you don’t move our H and vise versa.  in DCT & collecting ducts, observe that as Na moves, K &/or H+ are secreted to maintain charge balance  alkalosis – decrease in K, move K out and hold onto H ion  acidosis- increase in K (get rid of H ion)  hyperkalemia leads to acidosis…why  If we move K we cant move H ion. High blood K levels means you move K and you can move H ion, so H ion is increased in bld circulation and decreased in filtrate and become acidotic.  Acid base regulation: o Acidification of urine – H ions in urine (affects the pH) o The kidney can move bicarb indirectly which is why it is the most potent acid base regulator  Move bicarb by being found in acidic urine.  Bicarb ion found in acidic urine: sodium H antiport exchanger( takes in Na and pumps out H). carbonic anhydrase sits on renal tubule cells  carbonic acid water and carbon dioxidetaken up by cells and carbonic acid bicarbH ion is pumped put and we run through the process again  Alkalosis: less bicarb b/c less H is filtered and secreted  Acidosis: glutamine makes bicarb and in the process it makes NH3 which is used as a buffer.  Urinary buffers: urine can never get lower than 4.5 so we have to excrete more H ion, w/ out getting rid of bicarb. Phosphates and ammonium ion are alternatives so you don’t use bicarb. Chapter 18: The Digestive System  Function: organs of this system function to produce food and process it and eliminate it o Processes involved are ingestion, digestion, absorption and waste removal o Without this system the body would be unable to obtain needed materials for fuel and cell maintenance o Absorbed nutrients from the GI tract are used for structural elements  2 parts of the digestive system o GI tract—one continuous tube o Accessory organs – salivary glands, pancreas, liver and gall bladder  Digestive processes o Motility- move things by peristalsis in the wall of the GI tract. It involves mastication and deglutination (chewing and swallowing) o Digestion: break down of food into smaller elements to be absorbed  Physically (chewing) or chemically done (salivary amylase is saliva breaking down carbohydrates) o Secretion: exocrine—(secretions from the glands and pancreas, bile from the live rand gall bladder and saliva from the salivary glands.) Cells within the GI tract are Enteroendocrine cells and these produce Hs for regulation of digestive processes o Absorption: takes up broken down food and absorbs it through the epithelium that lines the GI tract  Liver is important in making bile and processing elements o The liver helps our body deal with fats, lymphatic’s, nutrients and toxins o Storage mechanism: rectum o Elimination: anus o When you have secretion it has the ability to get rid of wastes o What happens throughout the day: we take in solids and fluids, secreting/absorbing and excreting occurs. o o In a day we get rid of 100 ml of water and 50 g of salts are excreted  GI tract wall o Lined by an epithelium and supported by lamina propia o The ducts from the external exocrine glands have products expressed on the top of the epithelial layer (secretions) o Underneath this – submucosa: highly vascularized (enteric nervous system) o Muscularis: made up of 2 layers of SmM (circular and then the outer is parallel to the lumen)  Myenteric nerve plexus: modify contractile activity in the muscularis o The outer layer: serosa (binds, cover, protect) o Mucosa: in the small intestine the muscosa is different. Sometimes it has elevations and folds. In the small intestine there are villi. Within the villi there are capillary beds (for absorption) and lacteal (fat absorption)  Mucosa (inner tunic): on the top there are epithelial cells with tight junctions to seal off the layer and make it a physical barrier. There are immune cells in the lamina propia and this provides an immune barrier.  Enteric NS o Related to the autonomic o How it functions: example of peristalsis contract the lumen behind the bolus and contract. Motor neurons, sensory neurons… food bolus acts as a sensory element. Then a signal goes in front of the bolus, causing relaxation. Behind the bolus there is contraction. This is how the item moves.  This is how your esophagus works o Reflexes occur due to this NS o The digestive system is regulated extrinsically by ANS and ES and intrinsically regulated by the enteric nervous system and various paracrine factors  Digestive tract physiology o The process begins with ingestion and mastification. We mechanically and chemically digest things.  Carbohydrate digestion begins in the mouth.  From Mouth to Stomach o Deglutition- peristalsis wave down the esophagus  pharynx  stomach  Stomach: gastroesphogeal sphincter—bounded by pyloric sphincter  Sphincter: enlargement of muscularis  Compartments allow us to optimize the environment = more efficient in digestion o Unique aspects  Physical digestion – kneeding  Gastric juice is important for digestion  The stomach has a low pH. Our normal pH is around 7.4  How is the acidic environment created/how do we not digest out stomach o There are a lot of cell types  Gastric pitgastric glandMucus cells: make muscin (mucus barrier—protects from self digestion)  Parietal cells- produce HCl acid (“pH parietal cell HCL”) and vitamin B12  Chief cells produce pepsinogen – proenzyme, activated into pepsin which digests proteins  Enteroendocrine cells- within the epithelium there are endocrine cells that produce Hs. These Hs serve as Hs and paracrine factors— assist with digestive processes.  All the cells are impermeable to H ions (HCl)— how do we make acid o The presence of the Hydrogen K ATPase pump—found on the apical surface of the parietal cell. It is a primary active transport pump. It pumps out H and in exchange we pump in K. o At the basolateral surface—a secondary active transport is occurring because within the cell there is carbonic anhydrasecarbonic aciddisassociate H ions and these are pumped into the lumen. Bicarb is left over too. It is something we can use! Bicarb is shipped out and in exchange it pumps in Cl ions. The Cl ion moving out into the lumen is a passive process. o Energy is only used at the ion pump, everything else is used passively. o Bicarb causes alkaline tide because bld takes it up. Blood out of the stomach is high in bicarb. *very important. o Acid secretion: (you want acid secretion if you eat something high in fat) the parietal cells have vesicles that have ion pumps. The vesicle can insert it into the apical membrane, thus increasing the capacity to produce more acid.  Hs  Gastrin- positive effect (locally)  Somatostatin- negative (globally)  Histamine – unique cell type that is local and a paracrine factor makes this  Ach- coming from parasynthetic neurons. In the stomach it is stimulatory, NOT a break!!  Gastrin and histamine act synergistically and are the most potent regulators of HCl secretion!  Muscularis is modified to mix (innermost- oblique muscle) gives us the ability to kneed  Gastric rugae- folds of the mucosa  Allows the mucosa to stretch without tearing  Pepsin Activation: Why do we have a pH of 2  Pepsins optimal pH is around 2  Acidity of the stomach assists with pepsin activity  Pepsinogen goes from inactive to active state in the presence of HCl o Pepsin can then, auto activate o HCl causes unfolding of the pepsin molecule, allowing it to cleave itself.  Digestion and Absorption (carbohydrates and proteins) o Carbohydrate digestion begins in the mouth and protein digestion begins in the stomach o Hydrolysis rxns: Use water to split the bonds to take the disaccharide  monosaccharide o NZ’s break down elements in the lumen  Brush border NZs – on microvilli (small intestine)  Pancreatic lipase – comes from pancreatic juice: breaks down lipids (triglycerides)  Interesting: colipase—protein produced by the pancreas. It anchors lipase to attach to the emulsion droplet in the GI tract  Small Intestine – main site of digestion and absorption of nutrients o Modifications that assist us  Increase in SA – helps absorption of nutrients and move nutrients through the structure  Circular folds – elevations that increase SA and move chime along the tract  pH of the stomach – 2  pH of the small intestine is close to 7.4 o mechanism to buffer acidic chime – digestive elements and buffering agents  vilus are located on the circular folds o goblet cells – produce muscin  becomes mucus when in contact with water o intestinal cripts- digestive NZs in the pH comes from accessory organs but there are glands apart of the GI tract like this one.  Produce fluid to add to lumen fluid and provides buffers and lubricants  DO NOT produce digestive NZs  Intestinal contractions and motility o 2 types of contractile movements—peristalsis (weak in the SI) and segmentation- occurs simultaneously in different regions; serves to mix chime with luminal fluids o Slow waves- ICC (interstitial cells of Cajal)  Gap junctions between them for communication  Not a specific type of cell/tissue type  Graded depolarizations  Localized o Modified by the ANS works through the enteric NS modifies the contractions  ICC helps the elements move, but we can have modifications  Increases Ach, promoting contractility and motility in the region  Parasympathetic NS—“break” that enhances and SUPPORTS the digestive processes!  Digestion and Absorption of Fats o When fats are in an aqueous environment they form a fat globule o Emulsion droplets- formed due to bile salts (produced by liver)—interplay between hydrophobic and hydrophilic environments o Fats are not broken down! Bile salts make them into smaller fat droplets, called emulsion droplets.  Lipase digests more efficiently o Pancreatic lipase, bile salts and fats all work together to break fats down o Epithelial cells take these cells in  Taxi cab: my cell (takes fatty acids and glycerides to the intestinal epithelium to be released into the cells if they are not close) o Lacteal – chylomicron (triglycerides in a coat that get into a device to move through circulation) o Vitamins – NEVER broken down!!  Water soluble  Fat soluble – taken up by my cells  A, K, D and E  Liver, gallbladder and pancreas o impt accessory digestive organs, provide majority of digestive NZ’s for SI, as well as buffering substances to adjust acidic chyme coming from stomach o bile – liver o gallbladder – bile storage unit o hepatopancreatic sphincter- major duodenum papilli  Pancreas o Pancreatic juice is the product of acinar cells (produce zymogen granules—inactive NZs) and epithelial cells lining ducts o Zymogen, trypsinogen (inactive)activated by NZs in the brush border  Trypsin activates a lot of other NZs o Produces NZs impt for digeston of food molecules o Endocrine and exocrine organ o Produces bicarb  How do we make the bicarb ion  CO2 is taken in, bicarb is made and pushed out into the lumen of the duct, we counter it with Cl ion by recycling it. H ion is moved out into blood and we exchange it with N. o Pancreas: somewhere we can exchange charge! To keep a balance o H moving out is important because of the alkaline tide we produce and it balances it before it is sent out systemically. o Cl ion moves out through CFTR—cystic fibrosis transmembrane conducting factor (transporter)  Patients with cystic fibrosis have this but it is dysfunctional  Liver o Many functions: bld detox, CHO metabolism, lipid metabolism, protein synthesis & bile secretion o How does the liver work  Portal triad- 3 things; branch of the hepatic artery (bringing O2 rich blood), hepatic portal vein (O2 poor, nutrient rich blood, drains stomach, SI and LI), bile duct branch  Blood comes in through hep. Artery and hep. Portal vein. It meanders through the liver sinusoids. The capillaries are discontinuous—blood percolates. Then, it goes to the central vein and exits through it to drain from the liver.  Hepatocytes –produce bile, leads to the bile duct. It also processes blood borne nutrients, sort fat-soluble vitamins & detoxify  Kupffer cells- local macrophages (immune presence that looks for things that may have been absorbed)  The liver does a little of everything due to the hepatocytes!  Enterohepatic Circulation o some compounds absorbed by SI & enter hepatic circulation - - are recirculated between liver & SI o variety of exogenous compounds excreted by liver in bile, thus liver can “clear” bld of particular compounds, which are eliminated in feces  The liver AND the kidney can clear blood! o Bile salts recirculates between the liver and SI o Bilirubin – much like bacteria in the GI tract. It is broken down into urobilinogen. This compound is brown and this is why your poop is brown and pee is yellow/amber.  Lipid Transport and Utilization o Lipoproteins- lipid-protein complexes that solubilize the hydrophobic lipids as well as providing signals that regulate lipid entry/exit at target cells o Chylomicrons- deliver lipids of dietary origin  When chylomicrons come in contact with ApoE (signaling molecule to stop chylomicron to stop in a region)  Pulling things from chylomicrons brings things back to the liver o Lipid proteins are produced by the liver  All these shuttle things in the body…Lipoproteins  VLDL- very low density lipoproteins, deliver triglyceride to the body  LDL- bad cholesterol, travels through capillary walls and taken up by receptor mediated mechanism, building materials for the cell  HDL- picks up the high cholesterol that is released from the cell (low or high is cholesterol) “cholesterol sponges”  Large Intestine o Little to no digestive function o Job: absorb water and electrolytes. It takes chime and removes water from it, making the content into a semi solid  Absorbs water passively  Na/K ATPase pump – under influence of aldosterone (it can respond to aldosterone levels as well)  Secrete a little water – move Na or Cl out of intestinal cells  lumen  Intestinal microbiotia/microflora: Vitamin K is important for clotting factors, B vitamins and folic acid comes from interic bacteria  Spinal Cord Reflex: defecation (how elements are eliminated from our body)  The rectum fills up and the sensory R tell the spinal cord to relax sphincters (made up of Smooth Muscle) o “To void or not to void….” o Voluntary response  Neural and Endocrine Regulation of the Digestive System o Job: modify activity of the GI tract o GI tract: endocrine gland and target organ for various Hs o Gastric Functions  Cephalic Phase – sight, smell, thought of food  Relays info through the vagus nerve  If you smell something really yummy, like cookies, your stomach grumbles and you produce acids. The GI tract is prepping itself (what the cephalic phase does) o Secretes acid and pepsinogen! o Activates parietal and chief cells  Gastric Phase – sensory element (when food arrives) – acid secretrion and chemical nature (carbohydrates, proteins, fats) – gastrin is released and responds to proteins.  Gastrin initiates pepsinogen release from chief cells and acid secretion  Fats inhibit acid release  If your pH is 2.5 or below then gastrin is slowed down or not released.  G cell- enteroendocrine cell, produces gastrin, influences ECL cell (enteroendocrine cells) o Produce histamine – this causes the parietal cell to release HCl o Gastrin works as a H and histamine works as a paracrine factor within the gastric gland of the stomach o Positive fdback mechanism – aa stimulates HCl, G cells produce more gastrin and ECL releases more histamines o Negative fdback mechanism – HCl produced = pH falls (inhibits G cells) o The G cells look at aa and pH (keeps a balance—pH is kept at an optimal range and not too acidic)  Intestinal phase – as chime enters the small intestine (SI)  Sensory – stretching of duodenum and increase in osmolality o Signals and inhibits gastric motility and secretion (this is so contents wont overwhelm the intestine)  Hormonal –secretin (released below pH of 4.5) and CCK releases proteins and fats o What do both of these target with there functions  Increase in acid, translates into a decrease in pH and secretin is released. This targets the pancreas (ducts) and this increases bicarb  flowing into SI neutralizing acidity from the stomach  CCK is released when the SI sees fat (aa, free fatty acids) – causes an increase in granules that have NZs that

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Chapter 7, Problem 7.2.47 is Solved
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Textbook: College Algebra
Edition: 9
Author: Ron Larson
ISBN: 9781133963028

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In Exercises 4752, if possible, find (a) (b) and (c) A2