Ebook Lippincott illustrated reviews flash cards Physiology Part 2

(BQ) Part 2 book Lippincott illustrated reviews flash cards Physiology presentation of content: Respiratory system, respiratory system, gastrointestinal system, gastrointestinal system, living and dying.

5.1 Question Lung Airways Contrast the properties of airways that make up the bronchial tree’s conducting zone with those of the respiratory zone Why are smokers prone to coughing episodes and bronchitis? Conducting zone Which airways create the greatest resistance to airflow in a normal lung, and why? Trachea Bronchi Bronchiole Respiratory zone 17 18 Respiratory bronchiole 19 20 Alveolar 21 duct 22 Alveolar 23 sac Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 197 Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM 5.1 Answer Lung Airways Conducting zone versus respiratory zone airways: Respiratory zone • Houses the blood–gas interface Trachea Conducting zone Conducting zone • Do not participate in gas exchange • Mechanically supported with cartilage (larger airways) • Lined with a ciliated epithelium Bronchi Bronchiole The sites of highest resistance to airflow are the pharynx and larger airways (generations through ϳ7) Resistance is proportional to cross-sectional area Although larger airways are wider than smaller airways, the latter are far more numerous so their collective cross-sectional area is proportionally greater [Note: Airflow resistance is calculated with the Poiseuille law (see 4.18).] 17 Respiratory zone Tobacco smoke immobilizes respiratory cilia, which normally propel mucus with entrapped particulates, including bacteria, upward and out of the lungs (the mucociliary escalator) When allowed to accumulate, these inhaled irritants cause epithelial inflammation and infection, thereby predisposing smokers to coughing and bronchitis 18 Respiratory bronchiole 19 20 Alveolar 21 duct 22 Alveolar 23 sac Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 198 Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM 5.2 Question Blood–Gas Interface What are the functions of the structures located at the blood–gas interface, as indicated by boxed numerals? How does the pulmonary circulation differ from the bronchial circulation? What effect does aspirating freshwater have on pulmonary function, as seen in a case of nonfatal drowning? Alveolus (airspace) Alveolus (airspace) Alveolus (airspace) Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 199 Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM 5.2 Answer Blood–Gas Interface Blood–gas interface structures and their functions: Pulmonary capillary: brings the circulation into close proximity to air Type I pneumocyte: creates a thin barrier between air and the pulmonary interstitium Type II pneumocyte: synthesizes surfactant and repairs alveolar damage Lamellar inclusion body: contains surfactant Alveolus (airspace) Pulmonary versus bronchial circulations: Pulmonary • Low-pressure circuit • Presents the entire contents of the circulation to the blood–gas interface Bronchial • Circuit of the high-pressure systemic circulation • Provides the airways with nutrients [Note: The bronchial circulation drains O2-poor venous blood into the pulmonary veins, creating a physiologic shunt.] Alveolus (airspace) Alveolus (airspace) Aspirating freshwater decreases pulmonary compliance, which increases the work of breathing Fluid in the airways additionally prevents gas exchange, resulting in hypoxia The compliance effects are due to water entering the pulmonary vasculature under the influence of colloid oncotic pressure (␲c) Capillary hydrostatic pressure is very low in the pulmonary circulation, so ␲c dominates [Note: Drowning victims not absorb sufficient water to affect serum electrolyte levels and ventricular function, as originally hypothesized.] Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 200 Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM Surfactant 5.3 Question What is surfactant’s composition and origin? In what ways does surfactant assist lung function? Surfactant molecules What is the cause and what are the symptoms of infant respiratory distress syndrome (IRDS)? Alveolus (airspace) Water molecules Alveolar lining fluid Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 201 Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM 5.3 Answer Surfactant Surfactant is a mixture of phospholipids and a small number of essential proteins (ϳ5% by weight) that is produced and secreted by type II pneumocytes Surfactant phospholipids are amphipathic, causing them to localize to the air–water interface when secreted into the alveolar lumen Surfactant reduces alveolar lining fluid surface tension, which has several benefits, including: • Helps stabilize alveolar size Surface tension favors alveolar collapse, but collapse concentrates the surfactant molecules which negates the effects of surface tension Alveolar inflation has the opposite effect • Increases lung compliance Decreasing surface tension decreases the work of breathing • Helps keep lungs dry Surface tension promotes fluid movement from the vasculature into alveoli Surfactant reduces this tendency Surfactant Water molecules Surfactant molecules interpose themselves between water molecules and reduce surface tension Alveolus (airspace) IRDS is caused by surfactant deficiency in preterm infants Immature lungs secrete inadequate amounts of surfactant, so work of breathing is high Such infants show signs of respiratory distress and hypoxia, including tachypnea, use of accessory respiratory muscles, and cyanosis Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 202 Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM 5.4 Question Pleura Identify the structures and compartments indicated by the boxed numerals Compartments [3] and [4] are filled with fluid What are its principal functions? What happens if air is introduced into either compartment [3] or [4]? Right lung Left lung Diaphragm Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 203 Mediastinum Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM 5.4 Answer Pleura Four structures: Parietal pleura Visceral pleura Left pleural space Right pleural space [Note: The right and left lungs are completely enclosed within their own pleura.] Pleural spaces are filled with ϳ10 mL of pleural fluid, whose functions include: • Lubrication: The fluid allows the pleurae to slide over each other during breathing movements • Cohesion: Fluid is spread in a thin film that creates cohesion between the two pleurae, allowing forces generated by chest wall movement to be transferred to the underlying lungs If air is allowed to enter the pleural space (pneumothorax), the lung collapses, causing dyspnea and chest pain Pneumothorax occurs when the pleurae are breached following chest wall trauma, for example, or spontaneously as a result of underlying lung disease The lung’s elastic recoil holds the pleural space at a negative pressure relative to the atmosphere, which is why air flows in when the pleurae are compromised Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 204 Right lung Left lung Diaphragm Mediastinum Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM 5.5 Question Pressure–Volume Loop Explain the features of the red plot Why does the loop begin and end at a positive value? How might restrictive pulmonary disease (e.g., pulmonary fibrosis) affect a pressure–volume loop compared with a healthy lung? 100 Lung volume (% TLC) What the red [1] and blue [2] plots in the graph represent? 75 50 20 0 10 20 Transpulmonary pressure (cm H2O) Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 205 Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM Pressure–Volume Loop Plots represent: Lung-volume changes during inspiration (ascending limb, right) and expiration (descending limb, left) Volume changes in a saline-filled lung The difference between the two reflects the effects of alveolar lining fluid surface tension on lung compliance Features of the pressure–volume loop: Inspiration: Smaller airways are collapsed and sealed by surface tension at low lung volumes After sufficient pressure has been applied to reopen them, lung inflation proceeds linearly Hysteresis: Inflation recruits surfactant to the alveolar lining, decreasing the force favoring lung deflation Offset: Airway collapse seals and traps air within alveoli, so lung volume does not fall to zero upon expiration Pulmonary fibrosis and other restrictive diseases impair lung expansion, so higher transpulmonary pressures are required to achieve inflation, which manifests as a rightward shift in the loop Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 206 100 Lung volume (% TLC) 5.5 Answer 75 50 20 0 10 20 Transpulmonary pressure (cm H2O) Copyright © 2015 Wolters Kluwer 5/2/14 8:02 PM 9.15 Answer Ischemic Cascade Enzymes that protect against reactive O2 species: Superoxide dismutase Catalase Glutathione peroxidase Key events in an ischemic cascade include: • O2 deprivation forces cells to switch from aerobic to anaerobic metabolism Lactic acid accumulation causes acidosis • Falling ATP levels cause ion pumps to slow, allowing ion gradients to dissipate • Rising intracellular Ca2؉ activates Ca2ϩ-dependent degradative enzymes • Mitochondria accumulate reactive oxygen species, damaging their membranes Release of electron chain constituents initiates apoptosis • Cell breakdown and lysis (necrosis) initiates inflammatory reactions, causing further tissue damage Cooling body temperature to ϳ32°C for 12–24 hr following cardiac arrest (i.e., therapeutic hypothermia) reduces mitochondrial breakdown and limits inflammatory mediator release These mediators cause reperfusion injury and neurologic damage when circulation is restored after an ischemic event Reactive O2 species Cellular defense enzyme O2 e– (Oxygen) O2• – e– H2O2 e– (Hydrogen peroxide) OH• e– (Superoxide) (Hydroxyl radical) H2O (Water) Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit09.indd 392 Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM 9.16 Question Shock What are the three broad shock categories, and how are they characterized? Arterial system Loss of arterial pressure precipitates shock What compensatory systems help maintain arterial pressure (e.g., after hemorrhage, as shown)? What is sepsis? Venous system Blood loss from vasculature impairs left ventricular filling and reduces output Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit09.indd 393 Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM 9.16 Answer Shock Three broad shock categories: • Hypovolemic: Blood volume falls (e.g., through hemorrhage or ECF volume contraction), which compromises cardiac preload and output • Cardiogenic: Cardiac output (CO) falls due to pump failure (e.g., arrhythmia, cardiomyopathy) • Distributive: Loss of vascular tone (e.g., due to inflammatory responses) compromises mean arterial pressure (MAP) and prevents adequate tissue perfusion Hemorrhage Central venous pressure Transcapillary refill Preload Stroke volume Shock compensation mechanisms: • Baroreflex: ↓ MAP initiates a sympathetic response ᭺ ↑ Heart rate and ↑ cardiac inotropy helps support CO ᭺ ↑ Venous pressure increases preload and CO ᭺ ↑ Systemic vascular resistance helps sustain MAP • Transcapillary refill: ↓ Venous pressure causes capillary hydrostatic pressure to fall also, allowing for fluid recruitment from the interstitium • ↓ Renal fluid loss: Glomerular filtration rate falls due to a drop in MAP, renal artery pressure, and in response to SNS activation Sepsis is a systemic inflammatory response to local infection that causes widespread tissue damage and may result in septic shock Shock develops through inappropriate NO and prostacyclin (PGI2) release, causing systemic vasodilation and hypotension Cardiac output Arterial pressure Sympathetic activity Systemic vascular resistance Heart rate Cardiac inotropy Venous tone Baroreceptor reflex Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit09.indd 394 Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM Heart Failure 9.17 Question The process shown results in heart failure if left unchecked by timely medical intervention Identify three or more disadvantages to the process shown What is Cheyne–Stokes breathing, and how does it relate to heart failure? Cardiac output What process is shown? l rma No Failing heart Central venous pressure Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit09.indd 395 Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM Heart Failure [Note: The deleterious effects of volume loading can be reversed by diuresis (see 4.29).] G IN LO AD E UM Compensation disadvantages: • Length-dependent sarcomeric activation has limits, meaning that loading eventually becomes futile (as shown) • Volume loading increases wall stress (law of Laplace) and cardiac workload • Heart enlargement distorts electrical conduction pathways to cause dysrhythmias • Heart enlargement may also unseat the heart valves and allow regurgitation • Rising venous pressure ultimately causes systemic and pulmonary edema The ESPVR plateaus, so supporting cardiac output by volume loading has limited benefits VO L The figure shows ongoing heart failure compensation A failing heart initiates long-term fluid retention pathways (the renin–angiotensin– aldosterone system) to increase ECF volume Blood volume increases also, which supports cardiac output through increased ventricular preload Cardiac output 9.17 Answer l rma No Excessive preloading stresses the heart and causes edema Failing heart Pulmonary Central venous pressure congestion End-systolic pressure–volume relationship (ESPVR) Cheyne–Stokes breathing (CSB) is common in patients with heart failure and is associated with high rates of cardiac mortality compared with failure patients with no breathing disorder CSB is characterized by periods of apnea followed by breaths with a crescendo–decrescendo airflow pattern Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit09.indd 396 Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM 9.18 Question Respiratory Failure Is fluid in the lungs (e.g., blood, pus, or other exudates) more likely to cause hypoxemic respiratory failure or hypercapnic respiratory failure? How does severe hypercapnia (e.g., PCO2 Ͼ90 mm Hg) present clinically? Lung volume (% of total) What is the significance of the rightward shift in the pressure–volume loop in the patient with acute respiratory distress syndrome (ARDS) shown, and what causes the shift? Normal Inflation ARDS patient Deflation Transpulmonary pressure Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit09.indd 397 Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM 9.18 Answer Respiratory Failure The presence of fluid in the airspaces creates a V˙A /Q˙ mismatch and hypoxemia, although hypoxemia is typically accompanied by some degree of hypercapnia [Note: Hypercapnic respiratory failure usually occurs when ventilation is impaired.] Hypercapnia has anesthetic-like effects on the CNS (“CO2 narcosis”), causing confusion and lethargy Hypercapnia also depresses the respiratory center and suppresses ventilatory drive, thereby exacerbating the hypercapnia Normal Lung volume (% of total) The lungs of patients with ARDS are characteristically noncompliant, requiring high transpulmonary pressure to expand Stiffening occurs due to lung infiltrates that inactivate surfactant and inhibit surfactant synthesis by pneumocytes, causing atelectasis The infiltrates also interfere with gas exchange and reduce functional residual capacity Surfactant loss and atelectasis increase the pressure required to inflate the lungs Inflation ARDS patient Deflation Transpulmonary pressure Exudates reduce functional residual capacity Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit09.indd 398 Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM A-1 Key Equations Diffusion (Fick law) J ϭ P ϫ A (C1 Ϫ C2) Equilibrium potential (Nernst) Ex ϭ Hemodynamic Ohm law PϭQϫR Vascular resistance SVR ϭ Mean arterial pressure MAP ϭ DBP ϩ Resistance (Poiseuille) Rϭ Turbulence (Reynolds) NR ϭ Wall stress (Laplace) ␴ϭPϫ r 2h Cϭ Cardiac output CO ϭ HR ϫ SV Ejection fraction EF ϭ Starling law of the capillary Q ϭ Kf [(Pc Ϫ Pif) Ϫ (␲c Ϫ ␲if)] Alveolar ventilation VA ϭ (TV Ϫ VD) ϫ breaths/min 8L␩ ␲r4 Alveolar gas equation PAO2 ϭ PiO2 Ϫ vϫdϫ␳ ␩ Forced vital capacity FVC ϭ TV ϩ IRV ϩ ERV RT ln [X]o [X]i zF MAP Ϫ CVP CO Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Key_Equations.indd ⌬V ⌬P Compliance (SBP Ϫ DBP) Renal clearance Cϭ SV EDV PACO2 R UϫV P Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM A-2 Key Equations [U]Creatinine ϫ V [P]Creatinine Glomerular filtration rate GFR ϭ Henderson-Hasselbalch pH ϭ pK ϩ log Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Key_Equations.indd [HCO3Ϫ] [CO2] Serum anion gap Anion gap ϭ [Naϩ] Ϫ ([ClϪ] ϩ [HCO3Ϫ]) Plasma osmolality Osmolality ϭ 2[Naϩ] ϩ [BUN] [glucose] ϩ 2.8 18 Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM A-3 Abbreviations ABBREVIATION EXPANSION ABBREVIATION EXPANSION 2,3-DPG 5-HT3 AA ABG AC ACE ACh AChE AChR ACTH ADH ADP AF AIN AKI Ang-I Ang-II ANP ANS AoP AoV AP AQP 2,3-diphosphoglycerate 5-hydroxytryptamine afferent arteriole arterial blood gas adenylyl cyclase angiotensin-converting enzyme acetylcholine acetylcholinesterase acetylcholine receptor adrenocorticotropic hormone antidiuretic hormone adenosine diphosphate atrial fibrillation acute interstitial nephritis acute kidney injury angiotensin I angiotensin II atrial natriuretic peptide autonomic nervous system aortic pressure aortic valve action potential aquaporin AR ARDS AS ASD ATP AV BBB BPPV CA cAMP CaSR CCK CCr CD CF CFTR adrenergic receptor acute respiratory distress syndrome aldosterone synthase atrial septal defect adenosine triphosphate atrioventricular blood–brain barrier benign paroxysmal positional vertigo carbonic anhydrase cyclic 3Ј,5Ј-adenosine monophosphate calcium-sensing receptor cholecystokinin creatinine clearance collecting duct cystic fibrosis cystic fibrosis transmembrane conductance regulator cyclic 3Ј,5Ј-guanosine monophosphate Ca2ϩ-induced Ca2ϩ release creatine kinase Charcot-Marie-Tooth disease cranial nerve central nervous system Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Abbreviations.indd cGMP CICR CK CMTX1 CN CNS Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM A-4 Abbreviations ABBREVIATION EXPANSION ABBREVIATION EXPANSION CO COPD COX CP CRH CSB CSF CVO CVP DA DAG DBP DHEA DHP DI DIT DL DTL EA ECF ECG ECL EDV cardiac output chronic obstructive pulmonary disease cyclooxygenase corticopapillary corticotropin-releasing hormone Cheyne–Stokes breathing cerebrospinal fluid circumventricular organ central venous pressure ductus arteriosus diacylglycerol diastolic blood pressure dehydroepiandrosterone dihydropyridine diabetes insipidus diiodotyrosine lung diffusing capacity descending thin limb efferent arteriole extracellular fluid electrocardiogram enterochromaffin-like end diastolic volume EF EGF EK ENa ENaC ER ERP ERV EX FD FEV1 FHH FHHNC ejection fraction epidermal growth factor potassium equilibrium potential sodium equilibrium potential epithelial Naϩ channel endoplasmic reticulum effective refractory period expiratory reserve volume equilibrium potential functional dyspepsia forced expiratory volume in second familial hypocalciuric hypercalcemia familial hypomagnesemia with hypercalciuria and nephrocalcinosis familial hemiplegic migraine, type functional residual capacity follicle-stimulating hormone ␥-aminobutyric acid ␥-aminobutyric acid receptor stimulatory G protein alpha subunit guanylyl cyclase gastroesophageal reflux disease glomerular filtration rate Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Abbreviations.indd FHM3 FRC FSH GABA GABAAR G␣s GC GERD GFR Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM A-5 Abbreviations ABBREVIATION EXPANSION ABBREVIATION EXPANSION GH GI Gi GLUT GnRH Golf GPCR GPI GTO GTP Hb HbA HbF hCG HCM HCN growth hormone gastrointestinal inhibitory G protein glucose transporter Gonadotropin-releasing hormone olfactory G protein G protein–coupled receptor glycophosphatidylinositol Golgi tendon organ guanosine triphosphate hemoglobin adult hemoglobin fetal hemoglobin human chorionic gonadotropin hypertrophic cardiomyopathy hyperpolarization-activated, cyclic nucleotide– dependent, nonspecific ion channel hematocrit hypokalemic periodic paralysis heart rate hypertension inflammatory bowel disease inspiratory capacity ICa ICF If IGF-1 IK Im INa IOP IP3 IRDS IRV Ito IV JGA LAP LASIK LES LH LQTS LV LVP mAChR MAP Ca2ϩ current intracellular fluid funny current insulin-like growth factor Kϩ current membrane current Naϩ current intraocular pressure inositol trisphosphate infant respiratory distress syndrome inspiratory reserve volume transient outward Kϩ current intravenous, -ly juxtaglomerular apparatus left atrial pressure laser-assisted in situ keratomileusis lower esophageal sphincter luteinizing hormone long QT syndrome left ventricle left ventricular pressure muscarinic acetylcholine receptor mean arterial pressure Hct HPP HR HTN IBD IC Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Abbreviations.indd Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM A-6 Abbreviations ABBREVIATION EXPANSION ABBREVIATION EXPANSION MG MH MI MIT MLC20 MLCK MS MV nAChR NE NIS NKCC NMJ NO NSAID OI OTE OVLT PA PaCO2 PAH PaO2 PBS myasthenia gravis malignant hyperthermia myocardial infarction monoiodotyrosine 20-kDa myosin regulatory light chain myosin light-chain kinase multiple sclerosis mitral valve nicotinic acetylcholine receptor norepinephrine Naϩ-IϪ symporter Naϩ-Kϩ-2ClϪ cotransporter neuromuscular junction nitric oxide nonsteroidal anti-inflammatory drug osteogenesis imperfecta otoacoustic emission organum vasculosum of the lamina terminalis alveolar pressure arterial PCO2 para-aminohippurate arterial PO2 hydrostatic pressure within Bowman space ␲BS ␲c Pc PCO PCO2 Pcr PDE PepT1 PepT2 PFTs PG PGE2 PGI2 PH PIG-A PIP2 PKA PKC PKG PLC PO2 POS PP ultrafiltrate oncotic pressure plasma colloid oncotic pressure capillary hydrostatic pressure partial pressure of carbon monoxide partial pressure of CO2 creatine phosphate phosphodiesterase peptide transporter peptide transporter pulmonary function tests prostaglandin prostaglandin E2 prostaglandin I2 pulmonary hypertension phosphatidylinositol glycan A phosphatidylinositol 4,5-bisphosphate protein kinase A protein kinase C protein kinase G phospholipase C partial pressure of O2 polycystic ovary syndrome pulse pressure Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Abbreviations.indd Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM A-7 Abbreviations ABBREVIATION EXPANSION ABBREVIATION EXPANSION Ppc PPHN pulmonary capillary hydrostatic pressure persistent pulmonary hypertension of the newborn pyrophosphate intrapleural pressure proximal tubule parathyroid hormone pulmonary vascular resistance renin–angiotensin–aldosterone system right atrial pressure red blood cell renal blood flow rho-kinase renal outer medullary potassium channel refractory period renal plasma flow residual volume right ventricular pressure sinoatrial short-acting beta-agonists systolic blood pressure sarco/endoplasmic reticulum Ca2ϩ-ATPase subfornical organ SGLT SHBG SIADH sodium-dependent glucose transporter sex hormone–binding globulin syndrome of inappropriate antidiuretic hormone release sympathetic nervous system sarcoplasmic reticulum stroke volume systemic vascular resistance triiodothyronine thyroxine thick ascending limb total body water tubuloglomerular feedback total lung capacity maximal transporter capacity thyroid peroxidase thyroid hormone receptor thyroid-releasing hormone transient receptor potential cation channel, subfamily M, member transient receptor potential cation channel, subfamily V, member thyroid-stimulating hormone PPi Ppl PT PTH PVR RAAS RAP RBC RBF ROCK ROMK RP RPF RV RVP SA SABs SBP SERCA SFO Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Abbreviations.indd SNS SR SV SVR T3 T4 TAL TBW TGF TLC Tm TPO TR TRH TRPM6 TRPV5 TSH Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM A-8 Abbreviations Proudly sourced and uploaded by [StormRG] Kickass Torrents | The Pirate Bay | ExtraTorrent ABBREVIATION EXPANSION ABBREVIATION EXPANSION TV UES UT UV V˙A/Q˙ VC tidal volume upper esophageal sphincter urea transporter ultraviolet ventilation/perfusion ratio vital capacity Vm VOR VR Vth WPW ZES membrane potential vestibuloocular reflex venous return threshold potential Wolff-Parkinson-White Zollinger-Ellison syndrome Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Abbreviations.indd Copyright © 2015 Wolters Kluwer 5/2/14 8:05 PM ... bronchiole 19 20 Alveolar 21 duct 22 Alveolar 23 sac Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 198 Copyright © 20 15 Wolters Kluwer 5 /2/ 14 8: 02 PM 5 .2 Question Blood–Gas... mortality Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 22 2 100 % Saturation with O2 5.13 Answer 50 0 40 80 120 PO2 (mm Hg) Copyright © 20 15 Wolters Kluwer 5 /2/ 14 8: 02 PM... membranes.] CO2 120 RIGHT LEFT HEART CO2 O2 SYSTEMIC CIRCULATION Lippincott Illustrated Reviews Flash Cards: Physiology Preston_Unit05.indd 21 4 Copyright © 20 15 Wolters Kluwer 5 /2/ 14 8: 02 PM 5.10