VPHY Exam 4 Study Guide PDF

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CHAPTER 161. Introduction to the respiratory system How does ventilation differ from gas exchange and what are the 3 different types of respiration? Ventilation- moving air into and out of the respiratory system Gas exchange- exchange of CO2 and O2 bw the atmosphere and lungs/ capillaries and tissue...

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CHAPTER 16 1. Introduction to the respiratory system How does ventilation differ from gas exchange and what are the 3 different types of respiration? Ventilation- moving air into and out of the respiratory system Gas exchange- exchange of CO2 and O2 bw the atmosphere and lungs/ capillaries and tissues 3 types of respiration 1. External- gas exchange bw air and lung capillaries 2. Internal- gas exchange bw systemic capillaries and tissues 3. Cellular respiration What is the sequence of the airways from trachea to alveoli? Nasal passages → pharynx → epiglottis → larynx → (inside lungs) trachea → bronchus → bronchiole → terminal bronchiole → (respiratory zone) respiratory bronchiole → alveolar sacs What are the corresponding trends in diameter, length, number, total cross-sectional area from trachea to alveoli? Diameter and length decrease, number and cross sectional area increase How do the conducting vs. respiratory zones differ in terms of anatomy and physiology? Conducting: air passage, warming, humidification, filtration, immune surveillance Respiratory: air passage, gas exchange***, immune surveillance What is the anatomy of the alveoli, especially in regards to movement of air and blood supply? CO2 enters the alveoli from vessels, O2 leaves What cell types comprise the alveoli and what are their functions? What are the layers of the diffusion barrier? Type 1 alveolar cells- the major lining cells of alveoli, 95-97% surface area Type 2 alveolar cells- production of surfactants Layers: 1. Fluid layer w surfactant 2. Type 1 alveolar cell membranes 3. Narrow interstitial space 4. Capillary endothelial cell membranes

What defines the pleural space? Fluid layer between lungs and thoracic cavity walls. What muscles are involved in inhalation and exhalation? Inhalation: Diaphragm, paraternal and external intercostals Exhalation: Abdomen involved in forced expiration, relaxation of inspiratory muscles in quiet exhalation What direction does each of the respiratory muscles move when contracting or relaxing, and how does each movement contribute to expansion or decrease of volume of the thoracic cavity? Contracting: diaphragm moves downward, intercostals raise the ribs and increase thoracic volume laterally Relaxing: diaphragm moves upward, intercostals lower the ribs How do active inspiration vs. passive expiration vs. active expiration differ? Active inspiration: contraction of diaphragm, intercostals contract; requires ATP Passive expiration: relaxation of inspiratory muscles Active expiration: forced, assisted by abdominal muscles 2. Physical aspects and mechanics of ventilation Be able to apply Boyle’s Law to understand how changes in thoracic cavity, pleural, and alveolar or lung volume and in pleural and alveolar pressure move air in and out of the lungs. P1V1 = P2V2 -Thoracic expansion and contraction lead to air movement -When alveolar and pleural pressure decrease, inspiration occurs allowing air to move into the lungs -When alveolar and pleural pressure increases, expiration occurs allowing air to move out of lungs -Thoracic cavity volume increases during inspiration/contraction allowing air to move into lungs -Thoracic cavity volume decreases during expiration/relaxation allowing air to move out of lungs -lungs expand and contract along with thoracic cavity so they follow the same patterns -Pleural space: lungs recoil inward and chest wall recoils outward at rest creating a negative pleural pressure of around -3 to -4 mmHg, need this so lung lobes don’t collapse and we can continue breathing -a new pressure gradient is created when air enters the pleural space (pneumothorax) causing the collapse of lung lobes

How do changes in pressure gradients in the airways move air in and out of the lungs? Net gas flow and diffusion from high pressure to low pressure How is negative intrapleural pressure created? Lungs recoil inward and the chest wall outward, these opposite forces create a negative intrapleural pressure How does air or fluid in the pleural space affect intrapleural pressure, and in turn the sequence of changes in volumes and pressures listed above? Physiologists love the diagram of lung volumes and alveolar and pleural pressures relative to atmospheric pressure during inspiration and expiration. Follow the changes of each and relative to each other during the respiratory cycle. Air or fluid → relative negative pressure lost → lung lobes collapse How do lung capacities differ from lung volumes? Understand what total lung capacity, vital capacity, tidal volume, and residual volume are and how they are related. Be able to identify them on a graph of lung volumes during the respiratory cycle. Lung capacities: sum of more than 1 volume

Total lung capacity: total amount of gas in lungs after a maximum inspiration Vital capacity: maximum amount of gas that can be expired after a maximum inspiration, equal to maximum inspiration+tidal volume Tidal volume: the volume of gas expired or inspired during an unforced respiratory cycle Residual volume: the volume of gas remaining in the lungs after a maximum expiration, should be very low

What creates the 3 different dead spaces in the lungs? How do anatomic vs. functional dead spaces participate in gas exchange? Physiologic dead space: anatomic dead space + alveolar dead space Anatomic dead space: air in the conducting airways of respiratory system that does NOT participate in the gas exchange as the air is a mix of inhaled fresh air and expired air Functional dead space: air in the respiratory zone that is ventilated but does NOT participate in gas exchange due to lack of blood flow to these alveoli How do increases or decreases in ventilation (V) or perfusion (Q) affect the V/Q ratio and efficiency of gas exchange across the respiratory membrane? How do V and Q change as you go from superior to inferior in the lungs? Efficient gas exchange occurs when the level of ventilation matches blood flow in the alveoli (V/Q ~ 0.8) Apices of the lungs → high V/Q (overventilated and underperfused) Bases of lungs → low V/Q (underventilated and overperfused) How do pulmonary arterioles differ from systemic arterioles in their response to increases or decreases in oxygen levels in the alveoli (PAO2)? What purpose does this serve in the lungs? Anatomy: Be able to follow the path of blood and RBCs through the pulmonary and systemic circuits including where the chambers of the right side vs. the left side of the heart are between the two circuits. Systemic arterioles: dilate if arterial O2 levels are low → more blood with oxygen is delivered Pulmonary arterioles: constrict if alveolar O2 levels are low, dilate if high, want to maximize V/Q ratio How do the circuits differ in blood flow rate vs. vascular resistance and what is the physiological purpose of each circuit and the relative blood flow rate and vascular resistance in each circuit? ?? The blood flow rate through pulmonary circulation = flow rate through the systemic circulation -pulmonary vascular resistance is lower, leading to lower BP -pulmonary circulation travels from right ventricle to left atrium -systemic circulation travels from left ventricle to right atrium -O2 is brought in from the atmosphere into the lungs via the pulmonary circuit where it enters the blood and travels to the heart and then the body tissues where the blood experiences cellular respiration via the systemic circuit leaving the blood with CO2. The blood then travels to the heart via the systemic circuit where it then travels to the lungs via the pulmonary circuit where the CO2 is removed from the blood and exhaled into the atmosphere. 3. Factors affecting ventilation

How do alveolar compliance and elastance differ? Increased compliance facilitates inspiration or expiration? Increased elastance facilitates inspiration or expiration? Realize that for each, the opposite relationship applies to the other part of the respiratory cycle. Compliance- stretchability (distensibility) - Increased compliance facilitates inspiration Elasticity- recoil ability - Increased elasticity facilitates expiration What creates surface tension in the alveoli? Increased surface tension facilitates inspiration or expiration? What are surfactants, where do they come from, and how are they beneficial to ventilation? Thin film of liquid creates surface tension Increased surface tension decreases compliance, facilitates expiration Surfactants- phospholipids and surfactant proteins - Produced by type 2 alveolar cells (pneumocytes) - Prevent collapse of smaller alveoli, decrease surface tension What happens if surfactant production is impaired? Alveolar collapse How do restrictive vs. obstructive pulmonary disorders differ? Which type impairs inspiration vs. expiration to a greater extent? Which diseases are examples of each? If the effects of a respiratory disorder that we did not cover are described, be able to classify the disorder as restrictive or obstructive. Restrictive: accumulation of fibrous connective tissue in alveolar wall - Decreases vital capacity, decreases compliance - Reduced lung volume - Ex: pulmonary fibrosis - Evident in inhalation Obstructive - FEV1 < 80% - Reduced airflow - Ex: asthma, cystic fibrosis - Evident in exhalation 4. O2 and CO2 transport What does Dalton’s Law, the law of partial pressures, tell us about the pressures that different gases exert in air? Ptotal = Pgas + Pgas + Pgas = 760 mm Hg

The pressure exerted by each component in a gaseous mixture is independent of other gases in the mixture How does Henry’s Law influence the concentration of a gas in liquid if the solubility or the concentration of a gas in the air is increased or decreased? Which will be equal at equilibrium of a gas between a liquid matrix and a gaseous matrix – the number of particles or the partial pressure of each gas? C = kP Concentration of gas in liquid = solubility * partial pressure in liquid At equilibrium, partial pressure is equal on the gas and liquid sides, but the number of molecules will vary depending on gas solubility Know the relative concentrations (not the actual values) of pO2 and pCO2 from the atmospheric air to the alveoli through the arterial circulation to the cytosol/mitochondria of the tissues in the body and then back through the venous circulation all the way back to the atmospheric air. If you understand the concept of pressure gradients as they apply to movement of gases then this is much easier to understand than it sounds. What are PA, Pa, and Pv? PA: partial pressure alveolar Pa: partial pressure arterial PV: partial pressure venous

Which is more soluble in the blood, O2 or CO2? CO2

What are the two forms in which O2 is transported in the blood, and what percent of total oxygen transport does each form represent? Dissolved O2: 98% What is the structure of each hemoglobin molecule (polypeptide chains and hemes) and how many O2 molecules does each Hb carry? How does oxygen tension (PO2) affect loading and unloading of O2 from Hb molecules? 4 polypeptide chains and 4 hemes Each Hb carries 4 O2 to Greater PO2 → greater loading of O2 Less PO2 → greater unloading of O2 How do oxyhemoglobin, deoxyhemoglobin, carbaminohemoglobin (part 5), methemoglobin, and carboxyhemoglobin differ? How does each state influence O2 transport in the blood? How do anemia vs. polycythemia influence O2 transport in the blood? Oxyhemoglobin: Hb-O2, O2 binds to Fe2+ of heme Deoxyhemoglobin: Hb and Fe2+only Carbaminohemoglobin: unloading O2 forms Hb-CO2, CO2 does not bind heme Methemoglobin: Fe2+ oxidized → Fe3+, cannot bind w O2 Carboxyhemoglobin: CO-Hb, carbon monoxide, transport of O2 to tissues is impaired Anemia: decreased RBCs → [Hb] below normal Polycythemia: increased RBCs → [Hb] above normalHow does the hemoglobin-oxygen dissociation curve reflect changes in affinity of Hb for O2 as PO2 conditions change? Which parts of the curve reflect what is happening in the alveoli, systemic tissue beds, and capillary beds in actively exercising muscles? How does myoglobin-oxygen dissociation curve fit in with these situations? As PO2 increases, affinity of Hb for O2 increases

How does a left shift vs. right shift of the hemoglobin-oxygen dissociation curve affect the affinity of Hb in the pulmonary capillary beds and in the systemic tissue beds? Which conditions cause left shifts vs. right shifts? Realize that a condition that causes a left shift when it changes in one direction can cause a relative right shift when it moves in the opposite direction. Left shift increases O2 affinity, right shift decreases O2 affinity ↓ pH (acidosis) → right shift, ↑ PCO2 (suggests hypoxemia) → right shift (Bohr effect), ↑ temperature → right shift, ↑ [2,3-DPG] in RBC → right shift

5. Acid-base balance What is the normal range for blood pH? 7.35-7.45 What defines acidosis vs. alkalosis? What is the difference between volatile vs. non-volatile acids and what do I mean when I refer to CO2 as being the equivalent of an acid? Acidosis: pH < 7.35 Alkalosis: pH > 7.45 Volatile acids can be converted to a gas Non-volatile acids cannot leave blood In the bicarbonate buffer system, CO2 can be converted to carbonic acid Know the bicarbonate buffer system, which steps carbonic anhydrase catalyzes, and which ways equilibrium will shift if H+, HCO3-, or CO2 is added to or removed from the system. We are just going to focus on the role of the lungs in this unit. Also know what is happening to blood pH with different changes.What if the extent of ventilation changes, and how does

ventilation change to compensate for acidosis or alkalosis from other causes. If you can follow the flow of hydrogen ion through the buffer system, then it will be easier to predict changes that occur with or result in acidosis or alkalosis, and the types of compensation that occur by the lungs (and kidneys). You will be asked to predict how a change in one of these 5 factors – H+, HCO3-, CO2, blood pH, and ventilation rate or depth – will alter the other factors, and what the compensatory response by the lungs (and kidneys) will be. The Henderson Hasselback equation as modified for this course will also allow you to understand changes in pH, blood bicarb, and blood CO2.

Henderson-Hasselbach equation: pH = 6.1 + log ( [HCO3-] / [CO2] ) Carbonic anhydrase catalyzes the first step. Understand how alterations in ventilation may result in respiratory acidosis or alkalosis. What happens with the other 4 factors? Be able to extrapolate how a physiologic event or disease may result in respiratory acidosis vs. alkalosis. Examples are given. Respiratory acidosis: caused by hypoventilation (increased PCO2 in blood, decreased blood pH) - CNS depression, neuromuscular disorders, chest wall restriction, pulmonary tissue disease, airway obstruction Respiratory alkalosis: caused by hyperventilation (decreased PCO2 in blood, increased blood pH) - CNS disease, acute asthma, hypoxemia What are the 3 forms in which CO2 is transported in the blood, and what percent of total carbon dioxide transport does each form represent? What is the role of carbonic anhydrase and the bicarbonate buffer system in the transport of CO2 in the blood? How is chloride ion also involved in this? 1. Dissolved CO2 (10%) 2. HCO3- (70%) 3. Carbaminohemoglobin (20%) Carbonic anhydrase is located in RBCs, CO2 readily crosses plasma membrane, HCO3- is exchanged for Cl- by antiporter when crossing plasma membrane Where does the chloride shift vs. reverse chloride shift occur – pulmonary capillary vs. systemic tissue capillary beds? In which tissue beds will a right shift vs. left shift of the

Hb-O2 dissociation curve occur, will pH be higher vs. lower, and will free chloride concentrations in the blood be higher vs. lower? Do you see how CO2 and O2 exchange in the lungs and systemic tissues complement each other? Chloride shift into RBCs at systemic capillaries Reverse chloride shift out of RBCs at pulmonary capillaries

6. Regulation of breathing Going back to homeostasis, what are the sensors (O2, CO2, or pH), integrators, and effectors organs that influence the rate and depth of breathing. Sensors: chemoreceptors for chemical changes, mechanoreceptors for mechanical changes Integrator: brain Effectors: respiratory muscles Where are central vs. peripheral chemoreceptors located, and which are the most important molecules each detects, O2, CO2, and/or pH? Central: located in medulla, more sensitive to blood CO2 Peripheral: located in carotid and aortic bodies, directly detects O2, indirectly detects CO2 through pH, most sensitive to blood pH How are the pulmonary stretch receptors involved in the Hering-Breuer inflation reflex? What roles do pulmonary irritant receptors and unmyelinated C fibers play? What category of receptors do all these belong to (hint: not chemoreceptors)? Mechanoreceptors:

Pulmonary stretch receptors: detect volume changes, function in the Hering-Breuer reflex to prevent over-inflation of the lungs Pulmonary irritant receptors: detect frequency of breathing, cause coughing in response to smoke, smog, and particulates Unmyelinated C fibers: sensory neurons in lungs, stimulated by noxious substances, produce initial apnea → rapid, shallow breathing How do the medullary dorsal respiratory group and ventral respiratory group, and pontine apneustic center and pneumotaxic center each affect inspiration and/or expiration? Rhythmicity center: - generate automatic basic rhythm of breathing - Basic rhythm is NOT normal (irregular, erratic, unstable) - Consists of interacting neurons that fire during either inspiration or expiration - Dorsal respiratory group- inspiration - Ventral respiratory group- expiration Pontine centers: - Basic rhythm generated by medullary rhythmicity center must be adjusted by the pons - Apneustic center: promotes long inspiration and sharp expiration - Pneumotaxic center: antagonizes the apneustic center’s effects - Inhibits inspiration

CHAPTER 17 1. Introduction – structure of the kidneys What are some broad functions of the kidneys? What stimulates secretion of the hormone erythropoietin from the kidneys and what does it cause? Primary function- regulate volume and components of ECF (plasma and interstitial fluid) through filtering of blood plasma into urine Other functions: regulate BP through volume of blood plasma, regulate electrolyte concentration, regulate fluid pH Hypoxia → increased erythropoietin → increased RBC production Be able to trace the path of urine formation from the glomerulus to the toilet bowl. This includes the nephron.

Nephrons → calyces → renal pelvis → ureters → bladder → urethra → exit What are the 3 muscles involved with the bladder and urethra, and what type of muscle is each one? When is each one constricted vs. relaxed during bladder filling and micturition? Detrusor: smooth muscle, bladder wall, relaxed during filling, contracted during micturition Internal urethral sphincter: smooth muscle, constriction during filling, relaxed during micturition External urethral sphincter: skeletal muscle, relaxed during micturition What are parts of the nervous system contribute to each phase – not the names of nerves but roles of brain, autonomic system, and somatic nervous system. Micturition (voiding): -

Somatic motor fibers control external urethral sphincter Pons signals inhibition of sympathetic and activation of parasympathetic neurons

Bladder filling: -

Pons is quiet Sympathetic relaxation Somatic motor fibers stimulate external urethral sphincter Afferent nerves along pelvic nerve detect stretch → stimulate sympathetic outflow and somatic firing

What is renal plasma/blood flow and how much of cardiac output do the kidneys get? What are its units of measurement? How much of renal plasma/blood flow to the glomeruli get? Renal plasma/ blood flow- volume of plasma (blood) delivered to kidneys over time (22% of cardiac output) Units: mL / min All of renal plasma flow passes through the glomeruli Be able to trace the path of renal blood flow starting on the arterial side with the afferent arteriole to the venous side. Afferent arteriole → glomerulus (1st capillary) → efferent arteriole → efferent arteriole ...