Study Guide Exam 3 Fall2024 PDF

When: 1:00-2:30 pm, Wednesday, October 23, 90 minutes Questions: 60 (multiple choice, true/false, and short answer/essay), 100 points total Topics: Respiratory, Renal, and Acid/Base Physiology (Class Sessions 23-36) Equations: The equations and information on the l...

When: 1:00-2:30 pm, Wednesday, October 23, 90 minutes Questions: 60 (multiple choice, true/false, and short answer/essay), 100 points total Topics: Respiratory, Renal, and Acid/Base Physiology (Class Sessions 23-36) Equations: The equations and information on the last page of this study guide will be provided during the exam. Complex calculations will not be expected but be familiar with relationships. Learning Objectives Lung Structure 1. Remember the structures and order of the conducting and respiratory airways. https://www.youtube.com/watch?v=v_j-LD2YEqg - Conducting Zone: o Nose o Nasopharynx o Larynx o Trachea o Bronchi o Bronchioles o Terminal bronchioles - Respiratory Zone: o Respiratory bronchioles o Alveolar ducts o Alveolar sacs 2. Understand the functions of the conducting and respiratory zones. - Conducting Zone Function: o Bring air to respiratory zone o Humidify o Filter - Respiratory Zone Function: o Where gas exchange occurs (alveoli are sites of gas exchange) o The process where oxygen moves from the air in the lungs into the bloodstream and carbon dioxide moves from the blood into the lungs 3. Understand the patterns of cilia, smooth muscle, and cartilage as you move down the airway - Cilia: o Present in the upper airways (trachea to bronchioles) o Absent in the lower respiratory zone (alveolar ducts and sacs). - Smooth Muscle: o Present in the conducting zone o Sparse in the respiratory bronchioles. o Absent in alveolar ducts and sacs. - Cartilage: o Present in the trachea and bronchi o Absent in the bronchioles and lower respiratory structures. - This distribution allows for structural support and airway flexibility, while the presence of cilia in the upper airways aids in trapping and moving particles out of the lungs. 4. Understand the function of the cells located in the alveolus (type I pneumocytes, type II pneumocytes, alveolar macrophages). https://www.youtube.com/watch?v=B_XzUDClgac - Pneumocytes: alveolar cells - Alveolar walls are made up of type 1 and 2 pneumocytes - Type 1 pneumocytes: o Comprise 70% of surface area of alveolus o Gas exchange occurs here - Type 2 pneumocytes: o Produce surfactant and assist cell regeneration o Surfactant lines alveoli and prevents lungs from collapsing when inhaling § Puts a barrier on alveoli to separate air and water o Regenerates type 1 and 2 pneumocytes and produce surfactant - Alveolar Macrophages: o Clear debris (primarily) and pathogens o Clean up alveoli (dust particles, foreign bodies) 5. Understand the difference between bronchial and pulmonary circulation. - Bronchial circulation: supplies oxygenated blood to the lung tissue and removes waste o Does not participate in alveolar gas exchange - Pulmonary circulation: carries deoxygenated blood from the right ventricle of the heart to the lungs for oxygenation and returns oxygenated blood to the left atrium of the heart for systemic circulation o Its primary role is gas exchange in the alveoli. 6. Understand the different lung volumes and capacities (know this cold). !!!! https://www.youtube.com/watch?v=BP- uPD92DMk - Inspiratory reserve volume: extra volume you can breathe in o 3000 mL o 50% of lung capacity - Tidal volume: volume of a normal breath o 500mL o 10% of lung capacity - Expiratory reserve: extra volume you can breathe out o 1200 mL o 20% of lung capacity - Residual volume: extra volume you cannot breathe out o 1200 mL o 20% of lung capacity - Inspiratory capacity: Inspiratory reserve volume + tidal volume (3500 mL) o Air that enters when you breathe in - Vital capacity: Inspiratory reserve volume + tidal volume + Expiratory reserve volume (4700 mL) o Deep breathe in up to IRV and forceful breath out up to the ERV - Functional residual capacity: Expiratory reserve volume + residual volume (2400 mL) o Air that in lungs at state of rest - Total lung capacity: all (5900 mL) 7. Understand the concepts of the anatomic, functional, and physiologic dead space. - Dead space is the volume of air in the lungs that fills with air but does not participate in gas exchange - Functional dead space: volume of air in alveoli that does not participate in gas exchange - Anatomic dead space: volume of air in the conducting airways that does not participate in gas exchange  - Physiologic dead space: total dead space. Includes anatomic + functional dead space 8. Apply understanding of dead space ventilation to calculate alveolar minute ventilation. - VD = dead space ventilation - VT = tidal volume - PaCO2 = alveolar CO2 partial pressure - PECO2 = expired CO2 partial pressure - Alveolar minute ventilation measures the air reaching the alveoli for gas exchange, unlike total ventilation, which includes air stuck in the airways. 9. Apply understanding of dead space ventilation to predict changes in alveolar and end-tidal carbon dioxide measurements. 10. Understand the relationship between alveolar minute ventilation and alveolar CO2. 11. Understand the alveolar ventilation equation, and how it relates alveolar CO2, rate of CO2 production, and alveolar ventilation rates. 12. Understand the alveolar gas equation, and how it relates alveolar O2 to the partial pressure of inspired O2 and the partial pressure of alveolar CO2. 13. Remember the terms forced vital capacity, FEV1, and the relationship between them in different pathologic conditions. Lung Mechanics 1. Know the major muscles used in inspiration, passive expiration, and inspiration/expiration during exercise. - Inspiration: o Diaphragm § Downward movement with contraction § Increase in thoracic volume thus a decrease in pressure § PV = PV o External intercostal muscles § Pull outward § Allows for further increase in tidal volume - Expiration o Diaphragm § Relaxes to return to its resting position, reducing the superior/inferior dimension of the thoracic cavity. o External intercostal muscles § Relax to depress the ribs and sternum, reducing the anterior/posterior dimension of the thoracic cavity. o Internal intercostals: pull chest inward, expelling air more quickly o Abdominal muscles: push diaphragm up, compress abdomen § Examples: exercise, asthma, COPD 2. Understand the definitions of and apply the concepts of compliance and elastance. Watch vid over graph https://www.youtube.com/watch?v=KYmrI_vYCus - Compliance: lungs ability to stretch o Lungs and chest wall o C = ∆V/∆P o High compliance = distensible (lots of give) lungs can expand and contract easily o Low compliance = stiff (small changes in volume affect pressure) lungs are stiff and resistant to changes in pressure - Elastance: tendency of lungs to return to original shape after stretched or compressed o Compliance is inversely related to elastance o Transmural Pressure: pressure across a structure  o Ex transpulmonary pressure: pressure between intra-alveolar pressure and pressure intrapleural pressure 3. Understand the concept of hysteresis as it relates to lung compliance. https://www.youtube.com/watch?v=NSn4-BFacAQ - Hysteresis: reason why the graphs do not line up during inspiration/expiration. o The difference in pressure between inhalation and exhalation o The pressure required for inspiration is greater than the pressure required for expiration o The space between the curves represents the energy lost during the process. 4. Understand the roles of surfactant. https://www.youtube.com/watch?v=7ZMweT5o3Io - Surfactant reduces surface tension in the lungs. - During inhalation: o Water molecules are close together, making the lungs less stretchy (low compliance). o As the lungs fill with air, surfactant spreads out, decreasing tension and increasing compliance (lungs become easier to expand). o At high volumes, compliance decreases again because surfactant spreads too thin. o During inhalation, the surface area increases, which creates space for new surfactant molecules to be recruited. Surfactant proteins help spread surfactant lipids during inhalation. - During exhalation: o The lung’s surface area is initially large compared to the amount of surfactant, leading to higher tension and lower compliance. o As the lungs contract (lungs get smaller during exhalation), surfactant density increases, reducing surface tension and maintaining higher compliance. o During exhalation, the pressure in the thoracic cavity decreases, which can cause the alveoli to collapse. Surfactant prevents this by lowering surface tension, keeping the alveoli inflated, and ready to accept oxygenated air during inhalation. - More surfactant = easier lung expansion (higher compliance). 5. Describe the composition, origin, and properties of surfactant. - Surfactant: a mixture of phospholipids that line the alveoli and reduce surface tension o Surfactant reduces surface tension by spreading out between water molecules in the lungs. This makes it easier for the lungs to expand during breathing. Without surfactant, the water molecules would stick together more, making the lungs harder to inflate. - They are secreted by the type II pneumocytes - Most important component is: dipalmitoyl phosphatidylcholine (DPPC) - Amphipathic: polar and nonpolar ends o Benefit #1: keeps alveoli open at small alveolar pressure o Benefit #2: increases compliance (higher volumes at lower pressures) o Benefit #3: keeps alveolar size uniform Benefit of uniform alveolar size: V/Q matching 6. Understand the forces acting on the airway at functional residual capacity (FRC). Specifically know the forces acting on the lungs, chest wall, and intrapleural space. - Lungs naturally want to collapse inward (elastic recoil). - Chest wall wants to expand outward. o At a balanced point, these forces cancel each other out, and airway pressure is zero. This is called "equilibrium pressure." - When lung volume is less than FRC (Functional Residual Capacity): o The chest wall tries to expand more. o The lungs' inward pull is weaker. o The overall airway pressure becomes negative, so air flows in (from positive to negative pressure). - When lung volume is more than FRC:  o The lungs try to collapse harder. o The chest wall stops expanding (pressure from the chest wall becomes zero). o The overall airway pressure is now positive, so when you relax, air flows out (from positive to negative pressure). - Conditions: o In emphysema, the lungs are more stretchy (increased compliance), so FRC is higher. o In fibrosis, the lungs are less stretchy (decreased compliance), so FRC is lower. 7. Understand the relationship between air flow, pressure, and resistance. - Air flow is dependent on pressure gradients and resistance - Pressure is thus the driving force for air flow o Inspiration: pressure gradient from outside (zero) to inside (negative) o Expiration: pressure gradient from inside (positive) to outside (zero) o At rest: equilibrium, no pressure change, no air movement o This force competes with airway resistance - Airway resistance is dependent on length, viscosity, and radius of the airway o Length increases resistance (e.g. breathing through a long tube) o Viscosity: increases resistance (e.g. humid air) o Radius: inversely related to resistance o Please note: if radius halves, resistance increases by 16! Exponential relationship! o Medium Sized Bronchi: highest resistance o Despite small bronchioles having the lowest diameter, they are arranged in parallel. o Regardless, biggest changes in resistance areas still effected by modifying airway diameter 8. Understand and the relationship between resistance, length, and cross-sectional radius. - Thinner width/ longer length/ more viscous = more resistance - Wider width/ shorter length/ less viscous = less resistance 9. Understand the role that the autonomic nervous system plays in regulating airway resistance and flow. - Sympathetic: bronchodilation and smooth muscle relaxation; signals in epinephrine - Parasympathetic: bronchoconstriction and smooth muscle contraction; signals in acetylcholine 10. Name specific signaling molecules (e.g. norepinephrine, albuterol, ipratropium) and the role they play in regulating resistance and flow. - Bronchodilation: norepinephrine, albuterol, ipratropium o Sympathetic - Bronchoconstriction: Histamine and acetylcholine o Parasympathetic Gas Exchange / Control of Breathing 11. Understand the relationship between pressure and volume at fixed temperature (Boyle’s law). - P1V1 = P2V2 - Pressure and volume are inversely related 12. Understand Dalton’s Law of Partial Pressures. - Px = PB x F o Px= partial pressure of gas (mmHg) o PB = barometric pressure (mmHg) o F = fractional concentration of gas o PH2O = water vapor pressure at 37ºC (47 mmHg) - If accounting for water pressure, subtract the vapor pressure from the barometric pressure 13. Be able to apply Dalton’s Law of Partial Pressures to calculate a partial pressure, including adjustment for water vapor. 14. Understand the relationship between the concentration of dissolved gases, solubility, and pressure. - If pressure increases, concentration will increase, and solubility will increase - If pressure decreases, concentration will decrease, and solubility will decrease 15. Understand how Fick’s Law dictates relationship between volume of gas transferred per unit time (VX) to diffusion coefficient (D), surface area (A), partial pressure difference (∆𝑃), and thickness of the membrane (∆𝑋). - If the diffusion coefficient (D), surface area (A), or partial pressure difference (ΔP) increases: o The volume of gas transferred per unit time (Vx) will increase. This means more gas can move through the membrane faster. - If the thickness of the membrane (ΔX) increases: o The volume of gas transferred per unit time (Vx) will decrease. This means less gas will diffuse through the membrane because it’s harder for gas to move through a thicker barrier. - Increased D, A, or ΔP = Increased Vx (more gas transfer). - Increased ΔX = Decreased Vx (less gas transfer). !" - VX=D×A×!# 16. Be able to apply Fick’s law to determine how a change in one of the above variables: D, A, ∆𝑃, or ∆𝑋, might affect gas transferred per unit time (VX). 17. Be able to name conditions that can increase or decrease Diffusion Capacity of Carbon Monoxide (DLCO). - Increase DLCO o Exercise - Decrease DLCO o Emphysema/ COPD o Pulmonary edema o Pulmonary fibrosis (increase thickness) 18. Be able to define shunting. https://www.youtube.com/watch?v=q1_0kx7DVwA - Shunting occurs when blood flows through the lungs without going through the alveoli (the tiny air sacs where gas exchange happens). o Blood flow without aeration: lack of O2 § Blood is flowing through the body, but not receiving the necessary oxygen it need to supply the tissues effectively - This means deoxygenated blood moves from the right ventricle of the heart to the left side of the heart without picking up oxygen. - As a result, the blood returns to the heart still deoxygenated. - Shunting is different from dead space, which refers to alveoli that are filled with air but not getting enough blood flow (not perfused). In shunting, the alveoli are supplied with blood (perfusion) but are not ventilated (not getting air). 19. Be able to describe the effect shunting may have on the gradient between alveolar oxygen content and arterial blood oxygen content. - Shunting increases the A-A gradient (alveolar – arterial gradient) - Shunting, which refers to blood bypassing the alveoli and not being oxygenated, significantly increases the gradient between alveolar oxygen content and arterial blood oxygen content, meaning the difference between the oxygen level in the alveoli and the oxygen level in the arterial blood becomes larger, resulting in hypoxemia (low blood oxygen levels) that cannot be corrected by simply increasing the inspired oxygen concentration; this is because the shunted blood is not exposed to oxygen in the alveoli, causing a larger discrepancy between the two values. - Shunting is when blood skips the lungs and doesn’t get oxygen. This means the blood has low oxygen levels even though the air in the lungs is normal. As a result, there’s less difference between the oxygen in the lungs and the oxygen in the blood, leading to low oxygen in the body. 20. Be able to define perfusion and diffusion limited gas exchange. - Perfusion limited gas exchange: o Gas exchange happens easily when blood flow is normal and the levels of gases (partial pressure) stay consistent. o During normal respiration - Diffusion limited gas exchange: o Gas exchange is hindered because the levels of gases aren’t balanced, usually due to low blood flow. o Equilibrium doesn’t happen by the end o Makes it difficult for oxygen to reach equilibrium by end of capillary - Perfusion-limited: good gas exchange with normal flow - Diffusion-limited: gas exchange is poor because of problems with blood flow. 21. Name conditions that might cause diffusion limited gas exchange. - Emphysema/ COPD - Fibrosis - Strenuous exercise 22. Describe the roles of central chemoreceptors, peripheral chemoreceptors, lung stretch receptors, and muscle and joint receptors. https://www.youtube.com/watch?app=desktop&v=zjSBtRjgFjE - Central Chemoreceptors o Function: They detect levels of hydrogen ions (H+) and indirectly measure carbon dioxide (PCO2) levels. o How It Works: If breathing slows down (decreased ventilation), carbon dioxide levels rise. § This increase in carbon dioxide raises H+ levels, which then signals the body to breathe more. - Peripheral Chemoreceptors o Function: They monitor changes in carbon dioxide (CO2), hydrogen ions (H+), and oxygen (O2) levels in the blood. o How It Works: When they sense changes, they trigger an increase in breathing to help restore balance. - Lung Stretch Receptors o Function: They detect when the lungs stretch. o How It Works: They help prevent over-inflation of the lungs by signaling when to stop inhaling. - Muscle and Joint Receptors o Function: They respond to movement in muscles and joints. o How It Works: They stimulate breathing when the body is active to meet increased oxygen demands. - In summary, these receptors work together to monitor gas levels and body movements, ensuring that breathing adjusts appropriately to maintain proper oxygen and carbon dioxide balance. 23. Understand how changes in PCO2 might indirectly affect central chemoreceptors.  - PCO2 and ventilation indirectly affect central afferent signals and control of breathing by way of pH (adding H+ ions) o When carbon dioxide levels increase, it leads to more hydrogen ions (H+), which lowers the pH (makes the blood more acidic). o This change in pH sends signals to the brain, helping it adjust our breathing rate to maintain balance. 24. Describe how the body responds to changes in CO2, O2, and PO2 in the periphery. - O2 and CO2 are sensed in the periphery o Increase O2 cases a decrease in respiratory rate o Increase CO2 causes an increase in respiratory rate o Increased CO2 will cause H+ to increase § H+ are sensed centrally and periphery 25. Understand how physiologic changes might indirectly trigger activation of these receptors. - Hypoxia: decreased oxygen in tissues stimulates peripheral chemoreceptors - Acidosis: decrease in blood pH stimulates peripheral and central chemoreceptors 26. Recognize abnormal patterns of breathing including: Cheyne stokes breathing, Kussmaul breathing, and ataxic/cluster breathing. - Ataxic/cluster breathing: irregular respirations followed by periods of apnea groups of ataxic breathing episodes - Kussmaul breathing: deep and fast breaths Normal respiration o Typically to decrease CO2 and compensate for metabolic acidosis Respiratory amplitude - Cheyne-stokes breathing: Periodic hyperventilation followed by hypoventilation and apnea normopnoea Time (s) 27. Recognize conditions that might induce abnormal patterns of Biot's respiration Respiratory aka ataxic respiration amplitude — Periodic breathing: breathing. hyperpnoea (or normopnoea) and apnoea — Poor prognosis — Neuron damage - Ataxic/ cluster breathing: hyperpnoea apnoea hyperpnoea o Brain damage Time (s) - Kussmaul breathing: o Metabolic acidosis Kussmaul breathing Respiratory amplitude — Metabolic acidosis (Diabetes mellitus) o Hyperpnea — Hyperpnoea K = Ketones (Diabetic ketoacidosis) U = Uremia o Ketoacidosis S = Sepsis S = Salicylates M = Methanol o Uremia A = Aldehydes (U) Time (s) L = Lactic acid/Lactic acidosis o Sepsis - Cheyne- stokes breathing: Cheyne–Stokes respiration o Present in someone who is stick from another cause Respiratory — Periodic breathing: amplitude Gradual hyperpnoea/hypopnoea and Apnoea o Sleep — Sleep/Hypoxemia/Drugs — Hypoperfusion of the brain (respiratory center) o Hypoxemia gra dua l hype rpno ea apnoea gra dua l hype rpno ea gra dua l hypo pno ea o Drugs gra dua l hypo pno ea Time (s) o Hypoperfusion of the brian Kidney Structure / Body Fluids & Clearance 28. Describe the external structure of the kidney, including its location, support structures, and covering. - Structure: o Bean shaped organs o Outer layer: renal cortex o Inner layer: renal medulla - Location: o Upper abdomen below the ribcage on each side of the spine  - Support structures: o Adipose tissue o Renal fascia o Renal Sinus - Covering: o Tough fibrous tissue: renal capsule 29. Describe the major functions of the kidney. - Filtering waste - Regulating fluid balance - Regulating electrolyte balance - Regulating blood pressure 30. Name structures found in the cortex and medulla. - Proximal convoluted tubule (C) - Distal convoluted tubule (C) - Vasa Recta (M) - Nephron loop (M) - Collecting duct (M & C) 31. Be familiar with the components of the nephron including glomerulus, proximal convoluted tubule, descending loop of Henle, ascending loop of Henle, distal convoluted tubule, and collecting duct. - Glomerulus: filter blood - Proximal convoluted tubule: tubular reabsorption and water conversion - Descending loop of Henle: Na+ and Cl- ions out of tubule - Distal convoluted tubule: tubular secretion and regulation of electrolytes - Collecting duct: carrier urine from the nephrons to the uterus and bladder Renal Blood Flow / Glomerular Filtration 32. Describe the basic kidney functions of glomerular filtration, tubular reabsorption, tubular secretion, and micturition. - Glomerular filtration: filter waste products and excess substances from the blood (water, ions, etc.) - Tubular reabsorption: reabsorb valuable substances like water, glucose, and amino acids back into the blood stream - Tubular secretion: actively transport substances like hydrogen ions and certain drugs from the blood into the urine - Micturition: expel urine from the body 33. Identify the major blood vessels associated with the kidney and trace the path of blood through the kidney. - Renal artery à afferent arterioles à glomerulus à efferent arteriole à peritubular capillaries à vasa recta à renal vein à inferior vena cava 34. Be familiar with the renal vasculature including afferent arteriole, efferent arteriole, glomerulus, peritubular capillaries and vasa recta. o Large blood vessels that carry blood from your heart to your kidneys - Afferent arteriole: carries blood to the glomerulus - Glomerulus: network of capillaries where filtration occurs - Efferent arteriole: carries blood away from the glomerulus - Peritubular capillaries: surround the tubules of the nephron and reabsorb substances - Vasa recta: long, straight capillaries involved in urine concentration  35. Know the different factors controlling renal blood flow and GFR - Autoregulation: o Myogenic: Arterioles constrict/relax based on blood pressure. o Tubuloglomerular Feedback: Macula densa adjusts afferent arteriole tone based on sodium levels. - Neural: o Sympathetic Activity: Causes vasoconstriction, reducing RBF and GFR. - Hormonal: o RAAS: Angiotensin II constricts efferent arterioles to maintain GFR. o ANP: Vasodilates afferent arterioles, increasing RBF and GFR. - Local Factors: o Prostaglandins/Nitric Oxide: Vasodilators, increase RBF and GFR. o Endothelin: Vasoconstrictor, reduces RBF and GFR. 36. Mechanisms responsible for autoregulation of renal blood flow - Myogenic Mechanism: o When blood pressure increases, arteriolar smooth muscles in the afferent arterioles stretch, causing them to contract and reduce blood flow. o When blood pressure decreases, the arterioles relax, allowing more blood flow. - Tubuloglomerular Feedback (TGF): o The macula densa cells in the distal tubule detect changes in sodium chloride concentration. o If there’s increased sodium (indicating high filtration), the macula densa triggers vasoconstriction of afferent arterioles to reduce glomerular filtration rate (GFR). o If sodium is low, it promotes vasodilation to increase GFR. 37. Describe the effects of vasoconstrictors and vasodilators on RBF and GFR. - Vasoconstrictors decrease renal blood flow and GFR. - Vasodilators increase renal blood flow and GFR 38. Be familiar with myogenic and tubuloglomerulus feedback mechanisms. - Myogenic Mechanism: o Function: Regulates blood flow based on pressure changes in the afferent arterioles. o Process: § Increased blood pressure → Arteriole walls stretch → Smooth muscles contract → Afferent arteriole constricts → Reduces blood flow, maintaining GFR. § Decreased blood pressure → Afferent arterioles relax → Increases blood flow to maintain GFR. - Tubuloglomerular Feedback (TGF): o Function: Regulates GFR based on sodium chloride concentration in the distal tubule. o Process: § High sodium (high GFR) → Macula densa signals afferent arteriole constriction → Reduces GFR. § Low sodium (low GFR) → Macula densa signals afferent arteriole dilation → Increases GFR. - Both mechanisms help stabilize GFR despite changes in blood pressure or filtration rates. Renal Tubular Reabsorption and Secretion 39. List specific transport mechanisms occurring in different parts of the nephron, including active transport, osmosis, facilitated diffusion, and passive electrochemical gradients. - Proximal convoluted tubule: o Active transport: Na+/K+ ATPase, SGLT, K+/H+ ATPase o Facilitated diffusion: glucose, amino acids, urea o Osmosis - Loop of henle: o Osmosis: descending limb o Active transport: ascending limb - Distal convoluted tubule: o Active transport: Na+/K+ ATPase, Na+/Cl- cotransporter, H+/K+ ATPase - Collecting duct: o Osmosis 40. List the different membrane proteins of the nephron, including channels, transporters, ATPase pumps. - Channels: aquaporins, ion channels - Transporters: SGLTs, Na+/K+ ATPase pump, proton ATPase pump, OATs, OCTs - ATPase pumps: Na+/K+ ATPase pump, H+/K+ ATPase pump 41. Compare and contrast passive and active tubular reabsorption. - Passive reabsorption: substances move down their concentration gradient from high to low concentration without using energy - Active reabsorption: substances move up their concentration gradient from low to high concentration with the use of energy 42. Describe where in the nephron and the mechanisms involved, that the following ions or molecules are reabsorbed or secreted: sodium, potassium, hydrogen, glucose, amino acids, bicarbonate. - Sodium o Reabsorption: PCT o Secretion: DCT - Passport o Reabsorption: PCT o Secretion: DCT, collecting ducts - Hydrogen o Reabsorption: PCT, DCT o Secretion: PCT (minimal) - Glucose o Reabsorption: PCT - Amino Acids o Reabsorption: PCT - Bicarbonate o Reabsorption: PCT, DCT o Secretion: DCT, collecting ducts 43. Identify and describe the characteristic of loop of Henle, distal convoluted tubule and collecting ducts for reabsorption and secretion. - Loop of Henle focus on water reabsorption and creating an osmotic gradient o Relies on passive transport - The DCT and collecting ducts are involved in regulating electrolyte balance and pH o Influenced by hormones: aldosterone and ADH 44. Describe situations that would result in glucose being found in the urine. - Diabetes - Use of diuretics 45. Identify the site and describe the influence of aldosterone on Na+ and K+ regulation. - Aldosterone acts on DCT and collecting ducts  - Increases Na+ reabsorption and K+ secretion - Helps maintain fluid volume and electrolyte balance 46. Be familiar with the site of actions of common diuretics. - Carbonic anhydrase inhibitors: proximal convoluted tubule - Osmotic diuretics: everywhere - Loop diuretics: loop of Henle - Thiazide diuretics: distal convoluted tubule - Potassium sparing diuretics: btw distal convoluted tubule and collecting ducts 47. Explain which channels targeted by different classes of diuretics. - Osmotic diuretics: induce diuretics because it is not reabsorbed in the renal tubule, thereby increasing the osmolarity - Loop diuretics: block Na+/K+/2Cl- cotransporter - Thiazide diuretics: Block Na+/Cl- cotransporter - Potassium sparing diuretics: block aldosterone receptors - Vaptans: aquaretic (loss of water without the loss of electrolytes) that are vasopressin antagonist - Aliskerin: renin inhibitor - Empagliflozin: Na+ glucose cotransporter 2 inhibitors that treats type ii diabetes 48. Describe how sodium-glucose cotransporters work on nephron level - SGLT’s in the proximal convoluted tubule use the energy of the Na+ electrochemical gradient to reabsorb glucose from the tubular lumen back into the blood stream 49. Identify drugs of the renin-angiotensin-aldosterone system, how they modify blood pressure, and where in the pathway they work. - ACE inhibitors: block conversion of Ang 1 to Ang 2 o Drugs that end in -pril: Lisinopril, ramapril, enalapril - Angiotensin 2 receptor blockers (ARB): block action of ang 2 o Drugs that end in -sartan: losartan, valsartan, irbesartan - Renin inhibitors: directly inhibit the release of renin in the kidnets o Aliskerin - Aldosterone antagonist (potassium sparing diuretics): block aldosterone receptors o Spironolactone Acid Base Physiology 50. Identify and be able to describe the 3 main mechanisms for Acid Base Balance. - Buffers: o Controls the amount of H+ ions in the ECF and adds or removes H+ ions based on pH o Buffers do NOT reverse pH change, only limit it. o Buffer systems do not work independently in body fluids but work together. o This is the first line of defense o Only takes seconds to work o Least powerful regulator - Respiratory Regulation: o Controls the rate of CO2 removal from the plasma through adjustments in pulmonary ventilation to regulate pH. o Second line of defense against acid-base disturbances in the body o It works within minutes. o Acidosis results in hyperventilation. o Alkalosis results in hypoventilation. - Renal Regulation: o When there is excess acid or base the kidneys excrete acidic (H+0 ) or alkaline (HCO3-) urine to regulate pH  o Third line of defense against acid-base disturbances in the body. o Most powerful defense mechanism. o This process takes days to work. o Regulates by excreting either an acidic or alkaline urine. Case Study: Secondary Hypertension / Renal Artery Stenosis 51. Define the meaning of hypercholesterolemia, atherosclerosis and angiographic studies. - Hypercholesterolemia- high levels of cholesterol in the blood - Atherosclerosis- plaque buildup in the walls of arteries, narrowing, or blocking them. - Angiographic studies- procedure that uses X-rays to view blood vessels and blood flow in the body 52. Correlate between smoking as a risk factor and cardiovascular disorders. - Smoking is a risk factor for cardiovascular disease and can cause a heart attacks, stroke, heart failure, or heart disease. 53. Be familiar with renin- angiotensin-aldosterone system (RAAS). 54. Recognize the difference between primary and secondary hypertension. - Primary hypertension is high blood pressure with no underlying cause - Secondary hypertension is high blood pressure caused by an underlying medical condition. 55. Discuss factors controlling renal blood flow and glomerular filtration rate. - Renal blood flow- arterial pressure, venous pressure, ureteric hydrostatic pressure, plasma oncotic pressure - Glomerular filtration rate- blood volume and blood pressure 56. Be familiar with autoregulation including myogenic mechanism and tubuloglomerulus feedback. - Myogenic Mechanism- how arteries and arterioles react to an increase or decrease of blood pressure to keep the blood flow constant within the blood vessel; when BP increases, smooth muscle constricts Tubuloglomerular Feedback- high GFR increases the amount of NaCl → macula densa cells secrete ATP → mesangial cells metabolize ATP into adenosine → adenosine stimulates granular (JG) - cells → afferent arteriole constricts → reduces GFR 57. Know the mechanisms of actions of different treatment as Beta blockers, diuretics and angiotensin converting enzyme (ACE) inhibitors. - Beta blockers- block beta-1 receptors which blocks the effects of EP and NEP resulting in decreased contractility, heart rate, and blood pressure. - Diuretics- increase urine flow by reducing the amount of sodium and water reabsorbed by the kidneys. - ACE inhibitor- inhibit the conversion of angiotensin I to angiotensin II, angiotensin II narrows blood vessels so inhibiting ACE prevents vasoconstriction. FiO2 fraction of inspired oxygen