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Exam 3 Study Guide (Chapters 13 and 14)

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Exam 3 Study Guide (Chapters 13 and 14) BI 315

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These are reading notes from the textbook on required readings for Chapters 13 and 14, which will appear on exam 3 on 5/3
Systems Physiology
Dr. Widmaier
Study Guide
Biology, Physiology
50 ?




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"I was sick all last week and these notes were exactly what I needed to get caught up. Cheers!"
Madisyn Cole

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This 19 page Study Guide was uploaded by JordanK on Saturday April 30, 2016. The Study Guide belongs to BI 315 at Boston University taught by Dr. Widmaier in Spring 2016. Since its upload, it has received 187 views. For similar materials see Systems Physiology in Biology at Boston University.

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Date Created: 04/30/16
CHAPTER 13 Not required: Case Study, Figures 2, 16-20, 23- 24, 32, 42; The neuroanatomical details of Section 13.7 titled “Neural Generation of Rhythmic Breathing” p474 “Other ventilatory responses” Sections 13-8 and 13-9: only the short part on emphysema is required but nothing else from these two sections 13.1 – Organization of the Respiratory System  Right and left lungs consist of tiny air-containing sacs: alveoli o Sites of gas exchange with blood o Airways flow air between alveoli and external environment  Upper airways: mouth/nose  pharynx (common to both food and air)  larynx (air only)  Conducting zone: (larynx)  trachea  2 bronchi (one for each lung)  bronchioles  terminal bronchioles  No alveoli or gas exchange  Respiratory zone: (terminal bronchioles)  respiratory bronchioles  alveolar sacs full of alveoli  Site of gas exchange  Low resistance of blood flow  low BP to prevent fluid accumulation in lung interstitium o Inspiration and exhalation  respiratory cycle  Right ventricle of heart pumps blood to capillaries surrounding each alveolus (at rest: 4 L of air and 5 L of blood flow through this site per minute; increases during exercise) o Mucous elevator traps airborne particles in mucus covered nasal hairs; mucus slowly moved by cilia towards pharynx to be swallowed  Keeps lungs clear from matter and bacteria  Ciliary activity negatively affected by smoking ( “smoker’s cough”) o Cystic fibrosis: mucous layer becomes thick and dehydrated and obstructs airways/leads to lung infections; autosomal recessive mutation in epithelial chloride channel (CF transmembrane conductance regulator protein)  Treat with therapy to improve mucus clearance and aggressive antibiotics to prevent pneumonia or lung transplant  Most lethal genetic disease among Caucasians, life expectancy 35 years o Bronchioles will constrict when irritated to prevent matter from entering sites of gas exchange  Macrophages in airways and alveoli provide 2 line of defense  Smoking and air pollutants can damage these defenses o Alveolar walls contain capillaries and small interstitial space (blood separated from air by about 0.2 µm to allow rapid exchange of O 2nd CO vi2 diffusion)  Type I alveolar cells: flat epithelial cells; make up one cell-thick layer on air-facing surfaces of walls separating two adjacent alveoli  Type II alveolar cells: interspersed between type I cells; thicker and secrete detergent-like substance (surfactant) to prevent collapse of alveoli  Some alveolar walls contain pores to permit air flow between alveoli  important when some alveoli are occluded by disease  Relation of lungs to thoracic (chest) wall o Lungs are situated in the thorax (synonymous with chest)  Closed compartment bounded at neck by muscles and connective tissue; wall formed by spine, ribs, breastbone, and intercostal muscles  Thorax is separated from abdomen by the diaphragm (dome-shaped sheet of skeletal muscle)  Contains large amount of connective tissue for elasticity o Each lung is surrounded by its own pleural sac (consists of thin sheet called the pleura)  Visceral pleura coats lungs and is firmly attached by connective tissue  Parietal pleura attaches to/lines interior thoracic wall and diaphragm  Intrapleural fluid separates two pleura, allows sliding of pleura during breathing; intrapleural pressure (P ) caipes lungs/thoracic wall to move in and out together during breathing 13.2 – Ventilation and Lung Mechanics  Ventilation: exchange of air between the atmosphere and alveoli; occurs from high to low pressure in bulk flow (F = ΔP(ressure)/R(esistance); ΔP = P – P ) alv atm o Pressures are relative to atmospheric pressure (760 mmHg at sea level; decreases with increasing altitude)  Palv 0 mmHg between breaths = same at atmospheric pressure; therefore F = 0 and no airflow occurs o When P alv P atm, air moves into the lungs (moves out when >); caused by changes in dimensions of chest wall/lungs (change in volume first, change in pressure as response second)  Boyle’s Law: P V 1 P1V (P2an2 V are inversely proportional) o Lungs are not attached to muscles to expand/contract them; change volume based on other factors:  Transpulmonary pressure: ΔP between inside (P ) and oualvde (P = ip intrapleural fluid) of lung; Ptp  Ptp P alv– P ip  Always positive because lungs always have air in them (at rest when P =alv P musipbe negative to keep lungs open)  How stretchable the lungs are: determines how much lungs will expand for given P tp o P itptransmural pressure of lungs that governs static properties of lungs  Transmural pressure acting on chest wall: P cw= P ipP atm  Chest wall muscles and diaphragm contract  chest wall expands  thoracic cavity volume expands  P decreases  P becomes positive ip tp  lungs expand  P alvbecomes negative compared to P atm inhalation  Airflow ceases when P alv P atm  Elastic recoil of lungs drives passive expiration when respiratory muscles relax o Figure 3.10 shows all pressures in relation to each other  Elastic recoil: tendency of an elastic structure to oppose stretching or distortion o Natural tendency of lungs is to completely collapse  Positive P tpir in lungs always opposes this o Natural tendency of chest wall is to expand o At rest, opposing transmural pressures balance each other out  Elastic recoil creates subatmospheric pressure that keeps them from moving apart due to intrapleural fluid between them o Important concept in pneumothorax (when atmospheric pressure enters intrapleural space through wound due to chest wall being pierced but lung is undamaged)  P ipcreases to a value equal to P atm, which eliminates P tpd causes lung to collapse o Lung volume is stable when transpulmonary pressure is balanced by the elastic recoil of the lungs (at end of inspiration and expiration when there is no airflow)  Inspiration is initiated by the neurally induced contraction of the diaphragm (most important inspiratory muscle) and the external intercostal muscles located between the ribs o Motor neurons in phrenic nerves innervating diaphragm cause contraction towards the abdomen, allowing enlargement of the thorax o Motor neurons in intercostal nerves cause contraction upward and outward to further increase thorax volume  Expiration begins when motor neurons in diaphragm and inspiratory intercostal muscles stop firing and muscles begin to relax (lungs and diaphragm passively recoil due to decreased P tp o Alveoli become temporarily compressed (P > P alv atm  air flows out of alveoli into atmosphere (figure 13.15) o During certain conditions (exercise), different set of intercostal muscles and abdominal muscles actively decrease thoracic dimensions  Lung compliance (C ): Lagnitude of the change in lung volume (ΔV ) produLed by a given change in transpulmonary pressure o C =LΔV /ΔP L tp o Greater lung compliance = easier to expand lungs at any given change in P tp o Low lung compliance (stiff) = requires more vigorous contractions of diaphragm and inspiratory intercostal muscles (more energy) due to need for bigger ΔP fotp inspiration  Causes shallow breathing at higher frequency to inspire adequate volume of air to minimize work needed to breathe o Determinants of lung compliance  Stretchability: thickening of lung tissues decreases lung compliance  Surface tension (attractive forces between water molecules) at air-water interfaces within alveoli  Water lining of alveoli constantly tend to shrink and resist further stretching; energy required to overcome surface tension & expand lungs  Surfactant (mixture of lipids and proteins) secreted by type II alveolar cells reduces cohesive forces between water molecules to ease expansion  deep breaths cause stretching of these cells which releases more surfactant (Table 13.3)  Law of Laplace: P = 2T(surface tension)/r(adius)  as radius of alveoli decrease, pressure increases o Respiratory distress syndrome of the newborn: leading cause of death in premature infants due to inadequate function of surfactant-synthesizing cells (lack of surfactant)  Breathing requires strenuous effort by newborn due to low lung compliance  exhaustion leads to inability to breathe  lung collapse and death  Mechanical ventilator and administration of surfactant through trachea have markedly reduced mortality rates  Airway resistance is determined by tube length, tube radius (most important; resistance = 1/r ), and interactions between moving molecules (gas) o Usually so small that very small ΔP produce large volumes of airflow (ex: ΔP of 1 mmHg can move about 500 mL of air) o P ptpvents smaller airways from collapsing  exerts a distending force on airways like in alveoli (airway radius increases when Ptpncreases  lower airway resistance  easy lung expansion during inspiration) o Lateral traction: elastic connective-tissue fibers that link outside of the airways to alveolar tissue also keep airways open (pull airways open when they are pulled on during lung expansion  decrease airway resistance) o Limit to how much airflow rate can increase during forced expiration exists due to increased air resistance when airways compress to push air out o Neuroendocrine and paracrine factors influence airway resistance  Epinephrine = relaxes smooth muscle in airway via beta-adrenergic receptors  Leukotrienes = contract muscles (released during inflammation of lungs)  Asthma: characterized by intermittent episodes in which smooth muscle in airways strongly contracts and airway resistance increases  hard to breathe o Caused by chronic inflammation due to allergy, viral infections, sensitivity to environmental factors  lungs are hyperresponsive o Treatment: reduce chronic inflammation via anti-inflammatory drugs (leukotriene inhibitors, inhaled glucocorticoids) and overcome excessive airway contraction via bronchodilator drugs (blocks actions of bronchorestrictors; ex: mimics epinephrine)  Chronic obstructive pulmonary disease (COPD): emphysema, chronic bronchitis, or combination of the two o Caused by damage and collapse of smaller airways o Chronic bronchitis: excessive mucus production in bronchi (causes obstruction) and chronic inflammation in small airways; caused by agents such as smoking  May be acute in response to viral infections, resolves in 2-3 weeks  Lung volumes and capacities o Tidal volume (TV): volume of air entering lungs during a single inspiration, equal to volume leaving on subsequent expiration (~500 mL) o Inspiratory reserve volume (IRV): maximum amount of air in deepest inspiration (~3000 mL; 6x greater than TV) o Functional residual capacity (FRC): air remaining in lungs after tidal expiration (~2400 mL) o Expiratory reserve volume (ERV): maximum amount of air in forced expiration (~1200 mL) o Residual volume (RV): amount of air that will always be in lungs (lungs are never completely without air, ~1200 mL) o Vital capacity (VC): IRV + ERV + TV; important in assessing pulmonary function ( pulmonary function test)  FEV :1fraction of total forced vital capacity expired in 1 sec (healthy = 80%)  Obstructive lung disease: FEV le1s than 80% (ex: asthma)  Restrictive lung disease: normal airway resistance, reduced VC o Minute ventilation (V ): Eidal volume (V, mLtbreath) x respiratory rate (f, breaths/min)  Healthy = ~ 500 mL air with each breath and 12 breaths/min = 6000 mL/min  Dead space prevents all of this air from being available for blood exchange  Anatomical dead space (V ):Dspace within airways; no gas exchange can occur o ~150 mL is left in airways when 500 mL is breathed out; next inspiration of 500 mL causes previous 150 mL + 350 mL of new air to enter alveoli (leaving new 150 mL of air in airways) o Alveolar ventilation (V ): Aresh air entering alveoli per minute = (V –tV ) D f  Important in evaluating effectiveness of gas exchange  Rapid, shallow breathing can cause lightheadedness/unconsciousness = if small volumes of air being inhaled are less than VD, no fresh air is reaching alveoli (no alveolar ventilation)  Deeper breaths are more effective in increasing V than increasing A breathing rate ( important for exercise)  Alveolar dead space: volume of air in alveoli not used for gas exchange (some alveoli have little or no blood supply), small in healthy people o V + Dlveolar dead space = physiological dead space (wasted ventilation) 13.3 – Exchange of Gases in Alveoli and Tissues  In steady state, amount of O that leaves tissue capillaries and is consumed by the body 2 cells is equal to the volume of 2 added to the blood in the lungs per unit of time o Rate of CO bei2g produced by body also equals rate of CO leavi2g lungs  Respiratory quotient (RQ): ratio of CO pr2duced to O cons2med; depends on which nutrients are used for energy (each pathway produces different amount of CO )2 o Carbs: RQ = 1; fats: RQ = 0.7; proteins: RQ = 0.8  overall average RQ of 0.8 for normal mixed diet (8 CO m2lecules produced per 10 O mole2ules consumed)  Partial pressures of gases are directly proportional to concentration; net diffusion of a gas is always from high to low pressure o Dalton’s Law: pressure of each gas in a mixture is independent of the others o Atmospheric pressure: sum of all partial pressures of gases in atmosphere; varies by weather conditions and altitude (760 mmHg at sea level)  Pgas= fraction of that gas x atm(ex: O 2s 21% of air  0.21 x 760 = 160 mmHg P O2 at sea level)  Diffusion of gases in liquids o Henry’s Law: the amount of gas dissolved in a liquid will be directly proportional to the partial pressure of the gas with which the liquid is in equilibrium with  higher P gasn air = more gas dissolving in liquid  When diffusion equilibrium is reached (P gasis same in air and liquid), no more net diffusion of gas  Seen when soda can is opened (more gas in liquid than in air  gas leaves liquid when can is opened) o Gas diffusion must always be thought of in terms of partial pressures, not concentrations (concentration depends on partial pressure & solubility; 2 gases can have same equilibrium partial pressures but different concentrations due to solubility) o *** alveolar P O2 and PCO2 determine systemic arterial P O2and P CO2***  Alveolar gas pressures o Typical P O2 = 105 mmHg, P CO2 = 40 mmHg (versus typical pressures in air being breathed: O 2 160 mmHg, CO = 0.32mmHg)  Alveolar P O2 is less than atmospheric PO2(due to oxygen leaving alveoli to enter capillaries) while alveolar CO2 is much greater than atmospheric PCO2 (due to CO 2ntering alveoli from capillaries)  Alveolar P O2 is determined by atmospheric P O2irect correlation), rate of alveolar ventilation (direct), and rate of total-body oxygen consumption (inverse correlation: more oxygen consumption = less oxygen in alveoli)  Any increase in concentration gradient of oxygen leads to increase in oxygen diffusion rates  Same principles for CO e2cept atmospheric P CO2 can be ignored (= 0)  When considering multiple factors changing at once, determine ratio of factors to see which has bigger effect (Table 13.5) o Relationship between alveolar ventilation and metabolism (figure 13.22)  Hypoventilation: increase in ratio of CO p2oduction to alveolar ventilation, causes increased alveolar PCO2(cannot expire it fast enough)  Hyperventilation: decrease in ratio of CO p2oduction to alveolar ventilation, causes decreased alveolar PCO2 (too much ventilation compared to CO pr2duced)  *** not synonymous with “increased ventilation” (such as during exercise)  Gas exchange between alveoli and blood o Blood coming from tissues to pulmonary capillaries has P CO2 = ~ 46 mmHg (relatively high) and PO2 = 40 mmHg (relatively low)  Differences in partial pressures between blood and alveoli cause net diffusion of gases (oxygen into blood, CO i2to alveoli for expiration)  In a healthy person, gas diffusion is fast enough and blood movement is slow enough that equilibrium is reached before blood reaches end of capillaries o Diffusion disease symptoms: shortness of breath, poor oxygenated blood (no effect on CO 2limination because it diffuses more rapidly)  Pulmonary edema: some alveoli are filled with fluid, which increases diffusion barrier for gases  gases diffuse more slowly  Diffuse interstitial fibrosis: fibrosis arises from infection/autoimmune disease/hypersensitivity to inspired substances/toxic airborne chemicals/etc., which causes alveolar walls to thicken with connective tissue  slower diffusion  Matching of ventilation and blood flow in alveoli o For alveoli to be most efficient, the correct proportion of alveolar airflow (ventilation) and capillary blood flow (perfusion) should be available to each alveolus  Ventilation-perfusion inequality: when that doesn’t happen (mismatching) o When mismatching occurs, major effect = decrease P O2 of systemic arterial blood (about 5 mmHg less in blood than in alveoli)  Upright posture increases filling of blood vessels at bottom of the lung due to gravity, contributing to this mismatch (Table 13.6) o Disease states (changes in lung compliance, airway resistance, and vascular resistance) can cause bigger ventilation-perfusion inequalities  There may be ventilated alveoli with no blood supply (dead space/wasted ventilation)  There may be blood flowing through areas of lung receiving no ventilation (shunt) due to collapsed alveoli o P CO2 not affected as drastically; disease states lead to increase in arterCO2 P o Homeostatic responses to minimize mismatch/maximize gas exchange efficiency (Figure 13.24):  Decrease in ventilation in group of alveoli (ex: due to mucus)  decrease in alveolar PO2 vasoconstriction to divert blood flow away from poorly ventilated area  Local decrease in blood flow (ex: due to clot)  decrease in systemic P CO2 coming to region of lungs  bronchoconstriction to divert airflow towards areas of lung with better perfusion  Can never fully eliminate mismatch  Gas exchange between tissues and blood o Capillary walls/interstitial fluid/cell membranes are all highly permeable to O2 and CO 2  Metabolic reactions require constant consumption of O a2d production of CO (lowest P in mitochondria = most metabolic activity) 2 O2  Net diffusion of O2into cell/mitochondria and net diffusion of CO 2ut 13.4 – Transport of Oxygen in Blood  Table 13.7 – oxygen content of systemic arterial blood  oxygen is present in 2 forms (dissolved in plasma/erythrocyte cytosol and reversibly combined with hemoglobin)  Hemoglobin: protein made up of four subun2+s bound together o Each subunit: heme (contains Fe atom that binds to molecular oxygen) + polypeptide (all 4 polypeptides together: globin) o Each Fe atom can bind 1 oxygen; 4 oxygens per hemoglobin molecule  O 2 Hb ↔ HbO where2Hb = deoxyhemoglobin and HbO = 2 oxyhemoglobin o Percent hemoglobin saturation = O bound 2o Hb/maximal capacity of Hb to bind O 2oxygen-carrying capacity) x 100  Anemia: significant decrease in hemoglobin present in blood  causes significant decrease in oxygen content in blood  Low hematocrit (due to chronic blood loss/dietary deficiencies) reduces hemoglobin content in blood (due to low erythrocyte production)  Effect of PO2on hemoglobin saturation o Oxygen-hemoglobin dissociation curve: as blood P O2 increases, HbO s2ould increase (Figure 13.26)  Sigmoid shape  each addition of O mol2cule to hemoglobin makes it easier for the next O2to bind  Steep slope between 10 and 60 mmHg P ; atO20 mmHg, 90% of total hemoglobin is combined with O 2  Between 60 and 100 mmHg (normal arterial P ), oO2y 10% more combine with O 2provides safety factor so that moderate limitations of lung function still allow significant binding to hemoglobin  20-60 mmHg part of curve is ideal for unloading O to2tissues  Presence of hemoglobin determines how much O will diffuse 2 (when O 2inds to hemoglobin, it is no longer considered in the pressure gradient between two places)  Mitochondria are constantly consuming oxygen, so gradient into cell is always favored for unloading of O2 o At rest, most hemoglobin is 75% saturated after passing through tissues (25% dissociation)  Increased activity (exercise)  more oxygen consumed  increase blood- cell PO2gradient  more dissociation of O fr2m RBCs at a faster rate  decrease in RBC P O2 causes additional dissociation (25+ % dissociation)  Effect of carbon monoxide on O bin2ing to hemoglobin o Has a binding affinity for oxygen-binding sites 210x greater than O  r2duces amount of O b2nding to hemoglobin o Alters oxygen-hemoglobin dissociation curve to left  decreases unloading of O 2 from hemoglobin into tissues o Causes sickness and death  Effects of CO 2nd other factors in the blood and different isoforms on hemoglobin saturation o Degree of hemoglobin saturation depends on blood P CO2 , H concentration, temperature, and concentration of 2,3-diphosphoglycerate (DPG, substance produced by RBCs during glycolysis)  Increase in [H ], [DPG], and temperature = curve shifts right  hemoglobin has less affinity for O  O dissociates more 2 2  Effects of increased P CO2, [H+], and temperature are continuously exerted  each factor is greater in tissue capillary blood than arterial blood o The more metabolically active a tissue is, the greater its increased P , [H ], and CO2 [DPG] will be  allows more O to b2 released from hemoglobin which is needed o DPG reversibly binds with hemoglobin in RBCs to allosterically cause it to have a lower affinity for oxygen  Increased [DPG] is caused by variety of conditions resulting from decreased O supply to tissues (ex: decreased P in blood at high altitude) 2 O2 o Fetal hemoglobin: contains subunits coded for by different genes that those expressed postnatally  higher affinity for oxygen than adult hemoglobin  Allows for increased oxygen uptake through placental diffusion barrier 13.5 – Transport of CO in 2lood +  CO i2 a toxic waste product because it generates H ( changes in pH affect enzyme function in body which is bad)  Average person generates 200 mL CO /min, 2hich diffuses from tissues into blood as arterial blood flows through capillaries (total-blood carbon dioxide: sum of following:) o Blood carries more dissolved CO than 2 (more s2luble)  only ~ 10% of CO 2 that diffuses into blood remains in plasma as is or diffuses into cytosol of RBCs o 25-30% form carbaminohemoglobin by reacting reversibly with amino groups in hemoglobin (CO + H2 ↔ HbCO ) 2 - + o Other 60-65% undergoes: CO + H O ↔2H CO2↔ HCO + H2 3 3  First step is rate limiting and must be catalyzed by carbonic anhydrase  HCO m3ves through a “chloride shift” transporter out of RBC into plasma  At lungs, P CO2 is lower in alveoli than in blood, so CO 2iffuses out of blood and is expired - + o HCO and3H recombine to form H CO , which2brea3s back down into CO and 2 H 2; HbCO dis2ociates + 13.6 – Transport of H Between Tissues and Lungs  Deoxyhemoglobin has a greater affinity for H than oxyhemoglobin, and binds most of it to act as a buffer + o HbO + H2↔ HbH + O 2 o Venous blood: pH = 7.36; more acidic than arterial blood: pH = 7.40 + -  In normal situations, all H that is formed from tissue capillaries recombines with HCO 3 to form H 2O to3break down into CO when n2eded +  Respiratory acidosis: increased arterial [H ] due to carbon dioxide retention (increased PCO2 ), due to hypoventilation or a lung disease (Table 13.8)  Respiratory alkalosis: opposite of respiratory acidosis, due to hyperventilation 13.7 – Control of Respiration  Important chemoreceptors for automatic control of ventilation at rest o Peripheral chemoreceptors: located high in the neck; included carotid bodies and aortic bodies; close to baroreceptors and arterial blood  Receptors on bodies recognize decrease in arterial PO2 and an increase in arterial [H ]  Communicate with medullary inspiratory neurons + o Central chemoreceptors: located in medulla; stimulated by increase in [H ] of brains extracellular fluid and communicate with medullary inspiratory neurons  Control by PO2 o Low arterial P O2 causes increase in rate at which peripheral chemoreceptors discharge  more action potentials to medullary inspiratory neurons  increase in ventilation to provide more O2 o Total oxygen transport by blood is not decreased very much until P O2decreases below 60 mmHg (oxygen-hemoglobin dissociation curve)  Control by PCO2 o Figure 13.36  increased atmosphere P CO2 = increased arterial CO2 = increased ventilation  Very sensitive to promote elimination of CO 2rom body/prevent change in body pH due to [H ] – Figure 13.37  Central chemoreceptors in brain that recognize increase in brain PCO2 are more important in reflex response  Stabilized PCO2around 40 mmHg o At very high levels, CO ca2 completely prevent ventilation and may be lethal  act directly on medulla to inhibit respiratory neurons with anesthesia-like effect  Other side effects: severe headaches, restlessness, loss of consciousness  Control by [H ] not produced from CO 2 o Metabolic acidosis: H increase not due to change in P CO2  Ex: addition of lactic acid in blood after exercise  causes hyperventilation o Metabolic alkalosis: H decrease not due to change in P CO2  Decrease in [H ] due to vomiting + o Peripheral chemoreceptors more important than central ones (H does not reach brain)  PCO2 must change in response to metabolic acidosis/alkalosis, even if it is normal (due to change in ventilation)  Control of ventilation during exercise o Alveolar ventilation can increase as much as 20-fold during exercise o Unclear if P CO2, PO2 [H ], or other factors stimulate increased ventilation  PCO2?  only P CO2 of venous blood would increase, not systemic arterial blood (arterial CO2 only dependent on alveolar P CO2); alveolar ventilation increases exactly with or faster than increased CO2production  P ?  similar to CO , only venous blood partial pressure would O2 2 decrease; arterial O2shouldn’t change because oxygen consumption is matched with alveolar ventilation  [H ]?  if PCO2 does not change in arterial blood, there should be no change in [H ] during exercise except for due to lactic acid buildup (stimulates some hyperventilation)  Other factors?  includes reflex input from mechanoreceptors in joints/muscles, increased body temp, inputs from motor neurons in exercising muscles, increased plasma [epinephrine] or [K ]; figure 13.43 Emphysema: characterized by loss of elastic tissue and the destruction of the alveolar walls leading to an increase in compliance; chronic obstructive pulmonary disease  Can lead to atrophy and collapse of lower airways  self-destruction of lungs by proteolytic enzymes secreted by leukocytes o Notably caused by smoking  When alveolar walls break down, adjacent alveoli fuse together to form fewer and larger alveoli  loss of pulmonary capillaries and total surface area available for diffusion  impairs gas exchange  Associated with large airway resistance  makes it harder to breathe, can cause hypoventilation o Decreased elastic coil CHAPTER 14; Sections A & B only NOT REQUIRED: Tables 14-2, 14-3 and 14-4; Section 14.5; the second half of Section 14.7 beginning with “Urine Concentration: The Countercurrent Multiplier System,” including figures 17-21; Sections 14.11, 14.12, 14.13, 14.14, 14.15 14.1 – Renal Functions  Renal: pertaining to the kidneys o Kidneys process plasma in blood by removing substances from it (rarely adding substances to it)  Kidneys have a central function in regulating water concentration, inorganic ion composition, acid-base balance, and fluid volume of internal environment o Excrete just enough water and inorganic ions to keep amounts within narrow range + -  Ex) if salt (NaCl) intake increases, kidneys will excrete more Na and Cl in urine  Kidneys excrete metabolic waste products in urine as they are produced o Prevents toxic waste from accumulating in the body o Includes urea (from protein catabolism), uric acid (from nucleic acids), creatinine (from muscle creatine), end products from hemoglobin breakdown etc.  Kidneys excrete foreign chemicals (drugs, pesticides, food additives, etc.) into urine  Kidneys perform gluconeogenesis  synthesis of glucose from amino acids and other precursors during prolonged fasting  Kidneys also act as endocrine glands o Release erythropoietin,1,25-dihydroxyvitamin D, and renin (enzyme important for control of BP and sodium balance) 14.2 – Structure of the Kidneys and Urinary System  2 kidneys, lie in back of abdominal wall but are not in abdominal cavity o Retroperitoneal  just behind peritoneum (lining of abdominal cavity)  Urine flow: kidneys  ureters  bladder  urethra  excreted  Indented surface of kidneys: hilum; contains blood vessels and nerves, connected to ureter (renal pelvis inside kidney that branches into calyces – Figure 14.2) o Renal artery (into kidney) and renal vein (out of kidney) o Urine drains from calyces  renal pelvis  ureter  Kidneys are divided into renal cortex (outer part) and renal medulla (inner part) o Papilla: connection between tip of medulla and a calyx o Renal cortex contains all renal corpuscles o Renal medulla contains all medullary collecting ducts  Each kidney contains appx. 1 million nephrons o Each nephron consists of initial filtering component (renal corpuscle) and a tubule that extends from renal corpuscle (very narrow; single layer of epithelial cells)  Renal corpuscle forms a filtrate from blood that is free of cells, larger polypeptides, and proteins  filtrate enters tubule to be processed  Renal corpuscle anatomy o Contains many capillaries to greatly increase surface area for waste product filtration from plasma  Glomerulus (glomerular capillaries): compact tuft of interconnected capillary loops; protrudes into a fluid-filled capsule (Bowman’s capsule)  afferent arteriole: supplies blood to each glomerulus o 20% of plasma from blood in glomerulus enters Bowman’s capsule for filtration through tubule  Rest of blood/plasma leaves via the efferent arteriole  Bowman’s capsule fluid space: Bowman’s space o Blood in glomerulus is separated from fluid in Bowman’s space by a filtration barrier: single-celled capillary endothelium  noncellular proteinaceous layer of basement membrane  single layer of podocytes (epithelial cells lining Bowman’s capsule) o Mesangial cells: modified smooth muscle cells that surround glomerular capillary loops (not part of filtration pathway)  Proximal tubule: segment of tubule that drains Bowman’s capsule (proximal convoluted and proximal straight tubules – Figure 14.3b)  Loop of Henle: sharp, hairpin-like loop after proximal tubule o Consists of descending limb (from proximal tubule) and ascending limb (leads to distal tubule)  Distal convoluted tubule: after loop of Henle, fluid flows from here to collecting-duct system (cortical and medullary collecting ducts)  Each nephron is completely separate from others until cortical collecting ducts merge to allow all urine to drain into central cavity of kidney (renal pelvis)  Each tubule in cortex is surrounded by peritubular capillaries (second set of arterioles and capillaries after glomeruli  unusual)  Two types of nephrons o Juxtamedullary: renal corpuscle lies in the part of the cortex closest to cortical- medullary junction (loops of Henle plunge deep into medulla; responsible for generating osmotic gradient in medullar to reabsorb water)  Vasa recta: capillaries associated with juxtamedullary nephrons o Cortical: most nephrons; renal corpuscles are located in outer cortex (Henle’s loops do not penetrate deep into medulla or do not even have a Henle’s loop)  Involved in reabsorption and secretion  Juxtaglomerular apparatus: macula dense and JG cells; involved in ion regulation and water blance o Macula densa: patch of cells in wall of ascending limb of Henle’s loop as it passes between afferent and efferent arterioles of the nephron o Wall of afferent arteriole contains secretory cells (juxtaglomerular (JG) cells) 14.3 – Basic Renal Processes  Glomerular filtration: filtration of plasma from glomerulus capillaries in Bowman’s space; filtrate = glomerular filtrate (cell and protein-free; only solutes with low MWs appear  ultrafiltrate) o Certain low MW substances that are bound to plasma proteins will not be filtered 2+ (ex: plasma Ca and fatty acids) o Filtration is determined by opposing Starling’s forces (hydrostatic and osmotic forces)  Glomerular capillary hydrostatic pressure favors filtratioGC(P )  Hydrostatic pressure from fluid in Bowman’s space and osmotic force from proteins in glomerular capillary plasma oppose filtration (less water concentration in plasma than fluid of Bowman’s space due to proteins) (PBSnd π )GC  Net glomerular filtration pressure: PGC - PBS π GC = 60 – 15 – 29 = 16 mmHg (usually positive value because P is so large; favors filtration GC and movement of plasma from Bowman’s capsule to tubules) o Glomerular filtration rate (GFR): volume of fluid filtered through glomeruli into Bowman’s space per unit of time  Determined by net filtration pressure, permeability of corpuscular membrane, and surface area available (all directly related to GFR)  Average GFR for 70 kg person = 180 L/day (compared to net filtration of 4 L across all other capillaries in body)  kidneys filter entire plasma volume 60x a day  Subject to physiological control via neural/hormonal input from afferent/efferent arterioles (ex: constriction of afferent arterioles = decreased PGC constriction of efferent arterioles = increaseGCP simultaneous change of both arterioles in same way = no net effect) o Filtered load: total amount of any non-protein or non-protein-bound substance filtered into Bowman’s capsule; GFR x plasma concentration  Use to compare substances and determine whether substance undergoes net tubular reabsorption or net secretion (compare to conc. In urine)  Tubular reabsorption: movement of substances from tubular lumen to peritubular capillary plasma o Reabsorption rates of most organic nutrients (ex: glucose) are always very high and not physiologically regulated  Complete reabsorption of filtered loads; none in urine o Reabsorptive rates for water and many ions is usually very high, but under physiological control (ex: decreased water intake = more water reabsorption) o Can occur via diffusion (ex: reabsorption of urea by proximal tubule to facilitate water reabsorption later) down concentration gradient o Can occur by mediated transport from apical membrane (luminal membrane) through cytosol and through basolateral membrane ( transcellular epithelial transport)  Substances don’t have to be actively transported across both; can passively diffuse on one side and them be actively transported (ex: Na ) +  Reabsorption of many substances is coupled to Na movement (ex: glucose, amino acids, etc.)  Transport maximum (T ): limit to amount of material that can be transported per unit of time (binding sites become saturated) o Diabetes mellitus: significant hyperglycemia leads to plasma glucose concentration that exceeds threshold (200 mg/100 mL; normal is only 150 mg/100 mL), leads to glucosuria – Figure 14.11  Diabetic nephropathy: high filtered loads of glucose lead to significant disruption of normal renal function  Tubular secretion: solute movement from peritubular capillary plasma or kidney cells interiors to tubular lumen o Can occur by diffusion or mediated transport like reabsorption can  Usually coupled to Na reabsorption o Tubules secrete H and K (most important), and also organic ions (choline, creatinine) and foreign chemicals (penicillin)  Amount excreted = amount filtered + amount secreted – amount reabsorbed o Figure 14.7: not all substances can do all of this (ex: glucose is usually always reabsorbed, most toxins are completely excreted) o Rates of secretion/reabsorption are dependent on physiological control (homeostasis)  Ex: if normally hydrated person drinks a lot of water, they will excrete all of this water because they don’t need it  Kidneys can metabolize certain substances (make them “disappear”) or produces substances to add to blood or tubular fluid (ex: NH4, H , HCO ) 3- o Can synthesize glucose and add to blood during prolonged fasting  Regulation of membrane channels and transporters o Under physiological control via regulating activity/concentrations of membrane channel and transporter proteins  Use of hormones, paracrine/autocrine factors o Ex) genetic mutations leading to abnormality of Na -glucose cotransporter lead to appearance of glucose in urine (familiar renal glucosuria)  Division of labor occurs in tubules o Proximal tubule: primary role is to reabsorb most of filtered water and non-waste plasma solutes and secrete solutes (except for K )+  Ensures masses of solutes and volume of water after Henle’s loop are relatively small o Henle’s loop: reabsorbs large quantities of major ions, some water o Distal tubules: fine-tuning for most low MW substances and determining final amounts excreted in the urine by adjusting Reabsorptive rates/secretion  Most homeostatic controls act upon these segments 14.4 – The Concept of Renal Clearance  Clearance: volume of plasma from which a givens substance is completely removed by kidneys per unit time o Clearance of X = mass of X excreted per unit time/plasma concentration of X  Mass of X per unit time = urine concentration of X * urine volume per unit time  C =x(U V)/x x o Ex) clearance of glucose  U glzero under normal conditions (no glucose is excreted in urine)  C gl(0*V)/P = 0gl clearance of glucose is 0 because all glucose filtered from blood plasma into glomeruli is reabsorbed back into the blood o Ex) inulin: polysaccharide that is not subject to physiological control as its filtered (“ignored” by renal tubular cells; freely filtered)  Filtered load (GFR x plasma concentration) entering nephrons = amount excreted (nothing secreted or reabsorbed)  GFR x P = U xin  Gin = U inP (Gin is equal to clearance of inulin) o Creatinine clearance (C ): ucrd clinically to determine kidney disease by assume creatinine behaves like inulin (C wCrl slightly overestimate GFR because some creatinine is excreted in urine; but close enough)  When clearance > GFR, substance undergoes tubular secretion o Renal plasma flow: measured by clearance of given substance from all plasma that enters kidneys per unit time  Ex) organic anion paraaminohippurate (PAH)  When clearance < GFR, substance undergoes tubular reabsorption o Useful in finding new drugs  rate of clearance of drug determines how fast kidneys absorb it (useful in determining safety and effectiveness)  If drug clearance is > than GFR, higher doses may be needed to reach optimal concentration in blood 14.5 – SKIP 14.6 – Totally-Body Balance of Sodium and Water  2 sources of body water gain: water produced from oxidation of organic nutrients and water ingested from liquids and foods  4 sites of body water loss: skin, respiratory airways, GI tract, urinary tract (and menstrual flow in women) o Insensible water loss: continuous water evaporation from skin and respiratory airways  Sweating causes additional water loss via evaporation from skin o GI tract water loss is usually minimal except with diarrhea and vomiting  Under normal conditions, water and NaCl loss should equal gain  no net change o Can vary considerably (ex: urinary water excretion can vary between 0.4 L/day to 25 L/day) 14.7 – Basic Renal Processes for Sodium and Water (first half only)  Bulk of Na and water reabsorption occur in proximal tubule (2/3); fine-tuning after Loop of Henle  Primary active Na reabsorption + + o Achieved by Na /K -ATPase pump in basolateral membrane of cells  keeps intracellular concentration of Na low so Na moves downhill out of tubular lumen into tubular epithelial cells (across apical membrane) o In proximal tubule, diffusion through apical membrane down gradient is coupled + + to transport of organic molecules (gl+cose) or countertransported with H (H moves out of cell into lumen and Na moves into cell)  Proximal tubule contains brush border with microvilli to increase surface area/reabsorption o In cortical collect duct, apical entry step occurs by diffusion through Na channels +  Coupling water reabsorption to Na reabsorption o Water passively follows ion reabsorption via osmosis:  Na is transported from lumen  interstitial fluid (across epithelial cells) (other solutes that reabsorb based on Na transport also influence osmosis)  Removal of solutes from tubular lumen decreases local osmolarity of tubular fluid  favors osmosis into area  Difference in water concentration between lumen and interstitial fluid causes net diffusion of water +  Water, Na , and anything else has moved together by bulk flow into peritubular capillaries (reabsorbed) o Water movement can only occur if tubular epithelium is permeable to water  Water permeability varies from segment to segment and is dependent on amount of aquaporins in membrane (higher in proximal tubule) o Permeability in cortical and medullary collecting ducts is subject to regulation  Vasopressin (antidiuretic hormone – ADH): peptide hormone produced by posterior pituitary gland  stimulates insertion of more aquaporins (via fusion of vesicles with aquaporins to plasma membrane) to increase reabsorption of water when necessary  Water permeability is low without vasopressin  Increased urine excretion due to low vasopressin: water diuresis o Diabetes insipidus: caused by failure of posterior pituitary gland to release vasopressin (central DI) or by inability of kidneys to respond to vasopressin (nephrogenic DI)  Permeability of water is low even when dehydrated o Osmotic diuresis: increased urine flow due to primary increase in solute excretion (ex: failure of Na to be reabsorbed or in diabetes mellitus when glucose is present in urine) 14.8 – Renal Sodium Regulation  In healthy individuals, urinary Na excretion increases when excess of sodium is in body and decreases with deficit + + + o Na excreted = Na filtered – Na ab+orbed  Kidneys can adjust Na excretion by changing either process on the right side  No important receptors exist capable of detecting total amount of Na in body o Responses are mainly initiated by various cardiovascular baroreceptors (ex: carotid sinus) and sensors in kidneys that monitor Na filtered load  Baroreceptors regulate total-body Na because total-body Na is associated with + extracellular volume (Na and associated anions are appx. 90% of extracellular solute that determine distribution of water between compartments) o Extracellular volume = plasma volume and interstitial volume  Plasma volume = important determinant of BP in veins/cardiac + +hambers/arteries  thus BP is associated with Na in body o Low Na in body  low plasma volume  decrease in cardiovascular pressure  baroreceptors stimulate renal arterioles/tubules to decrease GFR and increase Na absorption  decrease Na excretion +  Opposite for high body Na  Control of GFR o Figure 14.22 – increased Na and water loss = decrease in GFR  Due to decreased net glomerular filtration pressure (initiated by decreased arterial pressure in kidneys and reflex responses  baroreceptors cause vasoconstriction release) o Increase in GFR is usually elicited by neural and endocrine inputs due to increased plasma volume/increased Na in body  contributes to increased renal + Na loss so extracellular volume can return to normal  Aldosterone: steroid hormone produced by adrenal cortex; stimulates Na reabsorption via distal convoluted tubule and cortical collecting ducts when Na ingestion is low o Acts slowly  induces change in gene expression and protein synthesis  Induces synthesis of ion channels and pumps in cortical collecting duct to promote Na transport  Angiotensin II: component of renin-angiotensin system (Figure 14.23), acts directly on adrenal cortex to stimulate secretion of aldosterone; causes constriction of arterioles o Renin: enzyme secreted by juxtaglomerular cells of juxtaglomerular apparatuses in kidneys; splits angiotensin I from angiotensinogen (produced by liver) o Angiotensin I (inactive) undergoes further cleavage to form angiotensin II (active); mediated by angiotensin-converting enzyme (ACE)  found in high concentrations on apical surface of capillary endothelial cells o High concentration during NaCl depletion and low when NaCl intake is high  Plasma renin concentration acts as rate-limiting factor in angiotensin II formation  NaCl depletion  increased renin secretion  increased plasma renin concentration  increased plasma angiotensin I concentration  increased angiotensin II concentration  increased aldosterone release  increased plasma aldosterone concentration  Figure 14.24 – mechanisms that cause increase in renin secretion o Increased renal sympathetic nerve activity  Direct innervation of juxtaglomerular cells; increased activity = increased secretion  Nerves are reflexively activated via baroreceptors when Na concentration decreases (= decrease in BP) o Intrarenal baroreceptors detect decreased arterial pressure  When BP in kidneys decreases (due to plasma volume decrease), cells are less stretched and secrete more renin o Decreased GFR  decreased flow to macula densa  Located near ends of ascending loo+ of Henle  Macula densa sense amount of Na in tubular fluid flowing past it  decreased amount causes release of paracrine factors that difuse from macula dense to nearby JG cells ( release renin) o Redundancy of mechanisms = importance of renin secretion (all mechanisms can be working at same time)  Drugs that manipulate angiotensin II (all effective in treating hypertension  associated with failure of kidneys to adequately excrete Na and water) o Lisinopril: ACE inhibitor o Losartan: prevents angiotensin II from binding to receptors on target tissues (ex: smooth muscle and adrenal cortex) o Eplerenone: blocks binding of aldosterone to receptors on kidneys  Atrial natriuretic peptide (ANP): synthesized by cardiac atria cells; acts on several tubular segments to inhibit Na absorption (increased amount when increased amount of + Na exists) + o Can act on renal blood vessels to increase GFR  more Na secretion o Natriuresis: increased osmotic diuresis caused by increase in Na secretion o Inhibits aldosterone secretion to allow more Na secretion  Interaction of blood pressure and renal function o Arter+al blood pressure constitutes a signal for important reflexes that influence Na reabsorption (renin-angiotensin system and aldosterone) o Increase in arterial pressure inhibits Na reabsorption  pressure natiuresis 14.9 – Renal Water Regulation  GFR c+anges initiated by baroreceptor afferent input has same effects on water excretion as Na excretion  Rate of water reabsorption is most important factor for determining how much water is excreted o Determined by vasopressin; total body water regulated by reflexes that alter secretion of vasopressin  Osmoreceptor control of vasopressin secretion – changing total-body water with no corresponding changes in Na excretion o Water has little effect on extracellular volume because it is in all body compartments  cardiovascular pressures/baroreceptors are only slightly affected by pure water gains/losses o However, water has big effect on osmolarity of body fluids  osmoreceptors are responsive to this  Ex) drink 2 L of water  decrease body fluid osmolarity  inhibition of vasopressin secretion via hypothalamic osmoreceptors  excretion of water in urine (decreased permeability of water in collecting ducts)  Opposite effects for dehydration (Figure 14.26)  Baroreceptor control of vasopressin secretion – input to vasopressinergic neurons in hypothalamus o Decreased extracellular fluid volume (ex: diarrhea or hemorrhage)  increase water permeability of collecting ducts  more water reabsorbed  Initiated by baroreceptors: decreased firing when pressure decreases (due to decrease blood volume)  fewer impulses to hypothalamus = increased vasopressin secretion (Figure 14.27)  Opposite effects for increased plasma volume o Has a relatively high threshold to initiate  need big reduction in BP to trigger it (not as prominent of reflex as osmoreceptors)  Vasopressin causes widespread arteriolar constriction  helps restore arterial BP towards normal  Other stimuli to vasopressin secretion o Hypothalamic cells can receive input from other brain areas  vasopressin secretion can be altered by pain, fear, variety of drugs  Ex) ethanol inhibits vasopressin release  excess urine production when drinking o Nausea can cause vasopressin release  vasoconstrictor effects on blood vessels in small intestines help shift blood flow away from GI tract to decrease absorption of ingested toxic substances 14.10 – A Summary Example: the Response to Sweating  Figure 14.28  Sweat is hypoosmotic compared to body fluids (less solutes in sweat)  sweating causes decrease in extracellular volume and increase in body fluid osmolarity o Renal retention of water and Na minimize deviations from normal caused by loss + of water and Na in sweat Rest of Chapter 14 not required


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