Cilia 7. Mucus 8. Olfactory receptors are located on the cilia of the olfactory cells. G protein—coupled receptors on olfactory cells bind odorants. Binding activates signal transduction mechanisms, resulting in opening of ion channels and depolarization. These olfactory cells are afferent neurons, which send signals via their axons to the olfactory bulb. An olfactory receptor may bind a range of odorant molecules, and an odorant may be bound by more than one receptor type.
Olfactory Receptors See Figure 5. Identify each neuron and its function. Fibers from annulospiral endings; function in proprioception 4. Fibers from flower spray endings and from paciniform and Pacinian corpuscles; function in proprioception and detect pressure, respectively 5.
Fibers from free nerve endings; detect pain 6. Identify the spinal reflexes associated with the illustrated pathways. Explain the physiology of each reflex. Stretch reflex. An example is the knee jerk reflex. Simultaneously, activation of interneurons results in relaxation of opposing muscles.
Golgi tendon reflex. It is a bisynaptic reflex and constitutes a mechanism for preventing muscle damage due to excessive tension.
Simultaneously, antagonistic muscles contract. Flexor withdrawal reflex. This reflex occurs in response to pain or other noxious stimuli. Afferent signals are conducted through sensory nerves to the spine, where activation of multiple interneurons produces simultaneous flexion and relaxation of the appropriate muscles to withdraw the limb.
Identify each structure as you trace the descending pathway for voluntary motor control through the corticospinal pyramidal tract. Fibers originate in the motor cortex. Fibers descend via the posterior limb of the internal capsule. Fibers reach the basis pedunculi of the midbrain. Longitudinal bundles branch upon entering the basis pontis. Bundles rejoin to enter the pyramids of the medulla. At the lower medulla, the bulk of fibers cross the median plane to form the lateral corticospinal tract, whereas some fibers continue downward in the ipsilateral lateral corticospinal tract.
Other fibers descend via the ipsilateral anterior corticospinal tract. Synapse occurs at the spinal level, and secondary motor neurons innervate muscles at the motor endplates. Corticospinal Tract See Figure 6. Identify the three functional subdivisions of the cerebellum. The archicerebellum is composed of the lingula, flocculus, and nodule.
It is involved in regulation of posture and balance and control of eye and head movement. It receives afferent signals from the vestibular apparatus and sends efferent signals through the relevant descending pathways. The paleocerebellum spinocerebellum is composed of the uvula, pyramid, and vermis. It is involved in regulation of proximal limb movement. Afferent sensory signals regarding position and movement of limbs are used to fine-tune limb motion through relevant descending pathways.
The neocerebellum pontocerebellum is composed of the middle vermis and hemisphere. It has a coordinating role in the regulation of distal limb movement.
It receives input from the cerebral cortex via the pontine nuclei and aids in the planning and initiation of motor activity through its efferent fibers. These subdivisions cannot be directly equated to the subdivisions described above. Functional Subdivisions of Cerebellum See Figure 6.
General characteristics of the parasympathetic and sympathetic nervous systems Parasympathetic Sympathetic Characteristic nervous system nervous system Location of preganglionic? Neurotransmitter of preganglionic neurons?
Major neurotransmitter released by postgan-? Actions of the autonomic nervous system Parasympathetic Sympathetic nervous system nervous system Site of action Action Action Cardiac pacemaker? Cardiac muscle? Cardiac AV node?
Vascular smooth muscle? Gastrointestinal smooth muscle? Gastric parietal cells? Lung, bronchial smooth muscle? Sweat glands? Male reproductive system? Female reproductive system? Describe the three fractions of a centrifuged, anticoagulated blood sample, and state the types of formed elements found in each fraction. Compare plasma and serum in terms of preparation and composition.
The top fraction of a centrifuged, anticoagulated blood sample is plasma water containing plasma proteins and other solutes. There are no formed elements in this fraction. It is composed of platelets and white blood cells. The red blood cells constitute the bottom fraction. Hematocrit is the proportion of the packed cell volume mainly red blood cells at the bottom of the sample to the total sample volume.
Serum is plasma minus the coagulation proteins. Whereas plasma is prepared by centrifugation of anticoagulated blood, serum is prepared by centrifugation of blood collected in a tube that does not contain anticoagulant. Components of Blood See Figure 8. Identify the formed blood elements and describe the general functions of each.
Basophil: involved in anticoagulation; increases vascular permeability through histamine release 2. Neutrophil: phagocytoses bacteria; increases in number in acute bacterial infections 3. Lymphocyte: acts in humoral B cell and cellular T cell immunity 4. Monocyte: is motile; gives rise to tissue macrophages 5. Explain the role of thromboxane in this process, and relate this to the antithrombotic effects of aspirin.
Arachidonic acid, a polyunsaturated fatty acid, is a product of this action and is converted to thromboxane, a potent platelet activator and vasoconstrictor. The thromboxane then activates additional platelets and causes vasoconstriction.
When cyclooxygenase, the first enzyme involved in conversion of arachidonic acid to thromboxane, is blocked by aspirin, thromboxane synthesis is blocked, leading to the antithrombotic action of this drug.
Hemostasis See Figure 8. What are the approximate resting systolic and diastolic blood pressures mm Hg at the labeled points for a normal, healthy person? Pressures in the Circulation See Figure 9. What is cardiac output and its normal, resting value? Give the approximate percentage of cardiac output received by the organs at A through G. Cardiac output CO is the flow from one side of the heart flow from the right ventricle equals flow from the left ventricle.
The approximate percentages of CO delivered to various organs are: A. Distribution of Cardiac Output See Figure 9. Identify the chambers and valves of the heart and note whether the blood coursing through the chambers is oxygenated or deoxygenated. Left ventricle, oxygenated 2. Right ventricle, deoxygenated 3. Tricuspid valve 4. Right atrium, deoxygenated 5. Aortic valve 6. Mitral valve 7.
Left atrium, oxygenated 8. The right ventricle pumps blood into the pulmonary circulation. Oxygenated blood returns from the lungs to the left atrium, flowing into the left ventricle during diastole. The left ventricle pumps this oxygenated blood into the systemic circulation. The pulmonic valve is not visible in this illustration.
Chambers of the Heart See Figure 9. Identify the components of the cardiac conduction system and describe the sequence of conduction through these structures. Sinoatrial SA node 2. Internodal tracts 3. Atrioventricular AV node 4. Common AV bundle bundle of His 5. Right bundle branch 6. Left bundle branch 7. Depolarization of this node results in subsequent conduction of the wave of depolarization along internodal tracts to the AV node.
Conduction through the AV node is slow, allowing a pause between depolarization and contraction of the atria, and the subsequent depolarization and contraction of the ventricles. After the signal is conducted through the AV node, it is propagated rapidly along the bundle of His, to the bundle branches and Purkinje fibers, resulting in depolarization and contraction of the ventricular myocardium. Cardiac Conduction System See Figure Identify the three ionic currents and describe their contribution to the action potential illustrated in the top tracing.
The phase 0 upstroke of the action potential top panel is caused by opening of sodium channels when ventricular cells reach threshold. Inactivation of these channels contributes to the phase 1 rapid repolarization to the plateau phase 2.
Increased outward potassium current leads to the rapid repolarization of phase 3 top panel. Name each pressure in this tracing of arterial pressure and determine the value for each. Predict the effect of increased stroke volume on the arterial pressure curve. An increase in stroke volume will result in larger pulse pressure. Systolic pressure will be higher and diastolic pressure will be lower. The reduction in heart rate will be associated with higher pulse pressure, with higher systolic pressure and lower diastolic pressure.
Arterial Pressure Wave See Figure Identify the likely site of measurement of pressure waves shown based on the systolic and diastolic pressure and wave form, assuming that these tracings were obtained in a normal, resting subject. Give a simplified formula for the relationship among flow Q , pressure, and resistance. A doubling of the length of the tube, L 3. Q will double with a doubling of the pressure gradient.
Q will be halved by a doubling of the length of the tube. Q will be increased fold by a doubling of the radius of the tube. What is the relative velocity of fluid in the large tube V1 compared with the velocity of fluid in one of the small tubes V2 , assuming that each of the nine small tubes has a cross-sectional area equal to one ninth the area of the large tube?
Give the appropriate equation for determining the answer. In the cardiovascular system B , velocity is greatest in the aorta and large arteries, where total cross-sectional area is smallest; velocity is lowest in the capillaries, where the total cross-sectional area is greatest.
Give the formula that predicts whether flow in a tube will be laminar or turbulent. Explain how each of the variables in the formula affects the probability that flow will be laminar or turbulent. Assuming other variables are held constant, increased velocity, tube diameter, and density of fluid are associated with greater likelihood of turbulence; increased viscosity is associated with greater likelihood of laminar flow.
Laminar and Turbulent Flow See Figure What is the formula for wall tension in a vessel? Explain why an aneurysm of this type is prone to rupture based on this formula. Wall tension can be conceptualized as the force necessary to hold together a theoretical slit occurring in the wall of a vessel. In the case of an aneurysm, the increased vessel radius results in greater wall tension, and the vessel becomes susceptible to rupturing. Wall Tension See Clinical Correlate In this cardiac cycle diagram, identify the three waves of the atrial pressure curve dashed line.
Explain the cause of each of these waves. The a wave of the atrial pressure curve is caused by atrial contraction. The c wave occurs during isovolumetric contraction and is caused by bulging of the mitral valve back into the left atrium as the ventricle attempts to contract against a fixed volume.
The v wave occurs during the ejection phase of the cardiac cycle as left atrial pressure rises slowly while venous return from the pulmonary circulation fills the atrium. In this cardiac cycle diagram, identify the valve opening or closure occurring at the labeled points. Mitral valve closure 2. Aortic valve opening 3.
Aortic valve closure 4. In the cardiac cycle diagram below, identify the electrocardiographic wave or complex occurring near the labeled points. For each, describe the major electrical event s responsible for the wave or complex and the mechanical event following it. QRS complex: produced by ventricular depolarization and leads to ventricular contraction; seen in the diagram as a rise in ventricular pressure 2.
T wave: associated with ventricular depolarization; occurs during the latter half of ventricular systole and leads to ventricular relaxation 3. In this cardiac cycle diagram, identify the heart sounds that might be heard at the labeled points and the cardiac event associated with each sound. S4, associated with active ventricular filling atrial contraction ; it is not heard in healthy adults 2.
S1, associated with closure of the mitral and tricuspid valves 3. S2, associated with closure of the aortic and pulmonic valves 4. Identify the major neurotransmitters released at the labeled points. Acetylcholine ACh is released by preganglionic fibers of both the sympathetic and parasympathetic nervous systems. ACh is released by postganglionic fibers of the parasympathetic nervous system at the SA and AV nodes of the heart and in some vascular beds in the genital region and lower gastrointestinal tract.
Norepinephrine NE is released by postganglionic fibers of the sympathetic nervous system at the SA and AV nodes, ventricular myocardium, and blood vessels. Epinephrine two thirds and NE one third are released by the adrenal medullary chromaffin cells in response to sympathetic nervous system activation. Indicate the direction of change in the variables at the labeled points, and explain the sequence of events that occurs as a result of the baroreceptor reflex following a rise in mean arterial pressure MAP.
Increase in firing rate of baroreceptor afferent fibers. The rise in MAP produces stretch of the arterial baroreceptors, which initiate signals to the medullary cardiovascular center.
Increase in parasympathetic efferent output occurs in response to the increased firing of baroreceptor afferent fibers. Decrease in heart rate, and therefore cardiac output, as a result of increased parasympathetic stimulation of the heart. Decrease in sympathetic efferent output occurs in response to increased firing of baroreceptor afferent fibers.
Decrease in peripheral resistance and venous tone are produced by vasodilation in response to reduced sympathetic efferent activity. Decrease in contractility of the ventricle as a result of reduced sympathetic stimulation of the heart. Decrease in stroke volume, and therefore cardiac output, in response to reduced venous tone and myocardial contractility.
Decrease in MAP as a result of reduced peripheral resistance and cardiac output. The decrease in stroke volume is the result of both reduced contractility and reduced preload.
The latter is caused by the decrease in venous tone. Baroreceptor Reflex See Figure Identify the changes or events that would produce a displacement of the curve to 1 or 2 in B.
Cardiac function curve is shifted upward by sympathetic stimulation or administration of drugs that enhance myocardial contractility inotropic agents. Cardiac function curve is depressed by myocardial ischemia, infarction, and heart failure. Cardiac Function Curve See Figure Identify the change that would produce a displacement of the curve to 1 or 2.
Increased preload 2. When preload is increased, the curve is shifted upward, but Vm the maximal velocity, occurring at zero afterload is unchanged. Increased contractility, however, results in a shift in the curve with an increase in Vm. Force-Velocity Relationship See Figure Identify the manipulation that would change this relationship to the relationships represented in B.
Increased preload end-diastolic volume 2. Increased afterload arterial pressure 3. An increase in preload end-diastolic volume results in greater stroke volume through the Frank-Starling mechanism 1.
An increase in afterload results in opening of the aortic valve at a higher left ventricular pressure; stroke volume is reduced 2. Increase in contractility produces a greater stroke volume that is not dependent on a change in end-diastolic volume 3. Pressure-Volume Relationship See Figure Identify the manipulation or event that would result in vascular function curves 1 and 2. What effect would the altered vascular function have on cardiac output? Hemorrhage hypovolemia ; decreased cardiac output 2.
The new equilibrium between the cardiac and vascular function curves at point A reflects lower preload as reflected by lower right atrial pressure and cardiac output.
Hypervolemia causes an upward shift in the vascular function, and the new equilibrium at point B is at higher preload and cardiac output. Venoconstriction also causes an upward shift in the vascular function curve. Identify the manipulation or event that would result in cardiac function curves 1 and 2.
Sympathetic stimulation or administration of inotropic drugs 2. With heart failure, the cardiac function curve shifts downward, resulting in lower cardiac output and higher preload D. Name each tissue layer in the wall of this vessel and its predominant cell or tissue type. Tunica intima; this innermost layer consists of a single endothelial cell layer resting on a basement membrane 2.
Tunica media; consists mainly of smooth muscle 3. Connective tissue and cellular constituents of these layers vary between vessel types as well. Walls of large arterial vessels are rich in elastic tissue, with relatively thick adventitia compared with smaller arteries.
Smaller arteries have a relatively thicker tunica media. Capillaries contain no media or adventitia, and their vascular walls consist only of endothelial cells and basement membrane. The illustrated vessel is a small artery. Vascular Wall See Figure Identify the structures in the microcirculation. Arteriole 2. Precapillary sphincters 3. Metarteriole 4. Capillaries 5. Venules Microcirculation See Figure What is the Starling equation for net filtration pressure for diffusion of fluid out of a capillary?
Use the Starling equation to calculate the net filtration pressure for the arteriolar end of the capillary illustrated and describe the effect on interstitial fluid volume and lymphatic flow. The increase in interstitial hydrostatic pressure drives the excess fluid into the lymphatic vessels, removing the fluid from the interstitial space. Lymphatic Circulation I See Figure For the diagram below, describe the force s that produces flow of extracellular fluid into lymphatic vessels.
Contrast this to the forces that account for filtration or reabsorption of fluid across the capillary wall. Excess interstitial fluid is returned to the circulation through the lymphatic system. Fluid flows from the interstitium into lymphatic capillaries when driven by a falling hydrostatic pressure gradient from the interstitial space to the lymph.
The edges of lymphatic capillary endothelial cells overlap, acting as one-way valves. Lymph subsequently flows into larger lymphatic vessels in which there are also one-way valves. Flow is augmented by smooth muscle filaments of the collecting lymphatics, which contract when stretched. Lymph eventually flows into the central venous circulation through the thoracic duct and lymphatic duct. Points 3 and 4 represent pathways for endothelium- dependent constriction or relaxation of VSMC.
Associate the following A to D with one of these four pathways and briefly describe the pathway. Pulmonary hypertension; vascular injury B. Vasopressin ADH C. Acetylcholine; bradykinin D. ANP produces endothelium-independent vasodilation. Acetylcholine, bradykinin, and a number of other endothelium- dependent vasodilators stimulate nitric oxide NO and prostacyclin synthesis by endothelial cells.
Pulmonary hypertension and vascular injury are associated with release of endothelin, a peptide that induces contraction of VSMC.
Thus, pulmonary hypertension and vascular injury produce endothelium-dependent vasoconstriction. Identify and explain the mechanisms of local regulation of blood flow illustrated.
Reactive hyperemia. Occlusion of blood flow to a region results in buildup of metabolic products; when flow is restored, the accumulated vasodilator metabolites produce increased blood flow. Active hyperemia. Increased tissue metabolism results in greater local blood flow, caused by increased metabolic products with vasodilatory actions.
Myogenic regulation autoregulation. Arterial smooth muscle constricts in response to increased transmural pressure, resulting in autoregulation of local flow. Thus, when perfusion pressure is artificially increased, although flow immediately rises, in many vascular beds it subsequently returns toward normal.
Explain how vasopressin released in response to reduced blood volume helps restore homeostasis. Explain how atrial natriuretic peptide ANP , released by atrial myocytes during stretch, acts to reduce blood volume.
Explain the role of renin produced by the juxtaglomerular apparatus of the kidney in regulation of blood volume. Vasopressin ADH is released by the posterior pituitary in response to reduced blood volume or increased plasma osmolarity resulting from dehydration. ADH promotes water retention by the kidney.
ANP released by atrial myocytes during stretch has direct renal effects diuresis and natriuresis and inhibits aldosterone release by the adrenal cortex. Renin is an enzyme released by the kidneys in response to low renal blood flow as well as sympathetic nerve activity.
The action of renin on plasma angiotensinogen produces angiotensin I, which is cleaved to angiotensin II by endothelial cell angiotensin- converting enzyme. Angiotensin II has the direct effect of promoting sodium retention by the kidney and also stimulates aldosterone release by the adrenal cortex.
Identify the constituents of the renin-angiotensin-aldosterone system and explain their role in the response to decreased blood volume and pressure. Angiotensin II. Angiotensin-converting enzyme ACE is found on the surface of endothelial cells, particularly in the lungs, and converts angiotensin I to angiotensin II.
Through its various renal effects, angiotensin II reduces NaCl and water excretion. The liver produces angiotensinogen, the precursor for angiotensin I and II.
Angiotensin I. Angiotensin I is produced by the action of the enzyme renin on angiotensinogen. This enzyme is released by the kidney in response to reduced renal blood flow and sympathetic nerve activity; it cleaves angiotensinogen to form angiotensin I.
This steroid is produced by cells of the zona glomerulosa of the adrenal cortex in response to angiotensin II. At the kidney, its actions result in retention of NaCl and water. However, in states such as hemorrhagic shock, the vasoconstriction by angiotensin II may be important as one of the mechanisms that raise total peripheral resistance. Note that in contrast to other vascular beds, in the kidney, angiotensin II does have a physiologic role in regulating the tone of afferent and efferent arterioles.
Identify the labeled coronary arteries. In the bottom panel, explain the basis for the changes in left coronary artery flow at the points noted. Right coronary artery 2. Left coronary artery 3. Circumflex branch of the left coronary artery 4. Anterior descending anterior interventricular branch of the left coronary artery 5. This fall in left coronary flow occurs at the beginning of cardiac systole during isovolumetric contraction.
It is caused by extravascular tissue pressure, which compresses the coronary vasculature in the wall of the left ventricle as the heart contracts. For the remainder of systole, left coronary flow remains low and follows the pattern of the systolic aortic pressure curve. The great rise in left coronary flow during early diastole is caused by the fall in extravascular tissue pressure as the heart relaxes, along with vasodilator effects of metabolites particularly adenosine that build up during systole, when flow is low.
This is because extravascular tissue pressure in the right ventricular wall is much lower than in the left ventricular wall and therefore has only a modest effect on coronary flow. Coronary Blood Flow See Figure Identify the structures in the fetal circulation and explain the basis for closure after birth for each. Ductus arteriosus. In the fetus, blood flows from the pulmonary artery to the aorta through this structure.
With inflation of the lungs and reduced pulmonary artery pressure, and with increased systemic arterial pressure due to closing of the umbilical circulation, flow through the ductus is reversed. With higher oxygen tension in arterial blood, vasodilator prostaglandins formed in the ductus fall, resulting in vasoconstriction and closure of the ductus. Foramen ovale. In the fetus, right atrial pressure exceeds left atrial pressure, keeping the foramen open.
With inflation of the lungs after birth and, therefore, greater flow of blood to the left atrium from the pulmonary circulation, this pressure gradient is reversed, functionally closing the foramen as the tissue flap covers the opening. Ductus venosus. This structure shunts a fraction of the blood from the umbilical vein directly to the inferior vena cava, bypassing the liver.
It closes after the return of blood from the placental circulation falls, although the mechanism is not well understood. Umbilical vein. Closure of this vessel occurs after umbilical artery closure and is probably caused by catecholamines and other factors. Umbilical arteries. The paired umbilical arteries close in response to vasoconstrictor catecholamines, cold, and other factors associated with delivery of the baby and placenta.
Ligamentum arteriosum obliterated ductus arteriosus Fossa ovalis obliterated foramen ovale Ligamentum venosum obliterated ductus venosus Ligamentum teres round ligament of liver obliterated umbilical vein Medial umbilical ligaments occluded part of umbilical arteries Postnatal circulation Fetal Circulation See Figure Pulmonary artery versus aorta 2. Right ventricle versus left ventricle 3.
Pressures given above for the right and left atria are mean pressures. Pressures in the Pulmonary Circulation See Figure Describe the effects of pulmonary artery pressure on pulmonary vascular resistance, relating these effects to each panel. Not all capillaries in the pulmonary circulation are normally open; collapsed capillaries do not conduct blood.
An increase in pulmonary artery pressure results in recruitment of capillaries, in which collapsed vessels are opened when pulmonary artery pressure increases, resulting in a fall in pulmonary vascular resistance. Higher pressure also results in distention of pulmonary vessels, which also reduces resistance owing to increased radius of the vessels. In alveolar vessels, on the other hand, increase in lung volume raises resistance as they are compressed by the enlargement of alveoli.
Starting from the collapsed state, as a lung is inflated, pulmonary vascular resistance first falls as a result of distension of extra-alveolar vessels, and then rises as the lung is inflated further and alveolar vessels are compressed.
Describe the effect of alveolar hypoxia on pulmonary arterioles 3. Alveolar hypoxia constricts pulmonary arterioles, redirecting blood flow toward areas of the lung that are better ventilated. Name the labeled structures.
Which of these structures constitute the respiratory zone of the lungs? Acinus 2. Terminal bronchiole 3. Respiratory bronchioles 4. Alveolar sacs and alveoli 5. Structures distal to the terminal bronchiole constitute the respiratory zone of the lungs respiratory bronchioles, alveolar sacs and ducts, and alveoli. Intrapulmonary Airways See Figure Identify each cell type. Trachea and large bronchi Mucus Nerve 1 6 2 3 4 Nerve 5 B.
Ciliated cells 2. Goblet mucus cell 3. Basal cell 4. Brush cell 5. Kulchitsky cell 6. Serous cell 7. Ciliated cells are predominant in the bronchioles; club Clara cells increase distally through the airways, whereas goblet cells and serous cells decrease distally and are absent in the terminal bronchioles.
Ultrastructure of Airways See Figure Identify and describe the lung volumes 1— 4 and the capacities 5— 8 on this spirometry tracing. Inspiratory reserve volume IRV : the additional volume that could be inhaled after a normal, quiet inspiration 2. Tidal volume VT : the volume of air inhaled and exhaled during breathing. Expiratory reserve volume ERV : the additional volume that could be exhaled after a normal, quiet expiration 4.
Residual volume RV : the volume remaining in the lung after maximal exhalation 5. Inspiratory capacity IC : the maximum volume that can be inspired after expiration during normal, quiet breathing 6. Functional residual capacity FRC : the volume remaining in the lung after expiration during normal quiet breathing 7.
Vital capacity VC : the maximum volume that can be exhaled after a maximal inspiration 8. An additional technique such as nitrogen washout, helium dilution, or body plethysmography must be employed to measure FRC, after which RV and TLC can be calculated.
Lung Volumes See Figure Identify the muscles of breathing. Which muscles are involved in normal, quiet breathing? Sternocleidomastoid 2. Anterior, middle, and posterior scalenes from right to left 3. External intercostals 4. Internal intercostals interchondral portion 5. Diaphragm 6. Internal intercostals except interchondral portion 7. Abdominal muscles from top to bottom: rectus abdominis, external oblique, internal oblique, and transversus abdominis 8. The diaphragm is the main muscle used in normal, quiet breathing.
In quiet respiration, the diaphragm is the main muscle involved. The main muscles of expiration are the internal intercostals except the interchondral portion and the abdominal muscles. However, in normal, quiet breathing, no muscles are involved; expiration in this case is driven by passive recoil of the lungs. Respiratory Muscles See Figure Equate these percentages with partial pressures of the gases in dry air at sea level.
Give the partial pressure of O2 and CO2 in inspired air at sea level. Explain the basis for the difference in PO2 between the atmosphere and inspired air. Give the normal partial pressure of O2 and CO2 in mixed venous blood, alveolar air, and arterial blood.
Give the alveolar gas equation for determining partial pressure of oxygen in alveolar air. Given the various partial pressures in the diagram below, calculate the partial pressure of oxygen in the alveolar air PAO2. The alveolar gas equation can be used in a healthy person to predict PAO2 based on Paco2 measured during arterial blood gas determination, because PACO2 and Paco2 will be the same the partial pressures of oxygen and carbon dioxide completely equilibrate between blood and alveolar air as blood courses through the alveolar capillaries.
Alveolar Gas Equation See Figure Blood flow is present only when alveolar pressure is raised or arterial pressure is reduced. Zone 2: Arterial pressure exceeds alveolar pressure, and alveolar pressure exceeds venous pressure. Blood flow is determined by the difference between arterial and alveolar pressures. Zone 3: Arterial pressure exceeds venous pressure, and venous pressure exceeds alveolar pressure.
Flow through zone 3 depends on the A-V pressure gradient. The higher hydrostatic pressure in this region results in distention of vessels and, therefore, reduced resistance. Line 1 represents blood flow perfusion from the bottom to the top of the lung. Note the greater gradient for perfusion than for ventilation line 3. Note that the ratio is lowest at the bottom of the lung and greatest at the apex of the lung, and that ventilation and perfusion are best matched in the middle of the lung.
Line 3 represents ventilation from the bottom to the top of the lung. The gradient for ventilation is not nearly as steep as the gradient for perfusion. Ventilation—Perfusion Relationships See Figure Elastic recoil pressure of the chest wall 2. Elastic recoil pressure of the lung 3. Elastic recoil pressure of the lung and chest wall the algebraic sum of elastic recoil pressure of the chest wall and lung 4.
Total lung capacity 5. Functional residual capacity 6. This is the state after quiet expiration in breathing. Explain the concept of pulmonary compliance in the context of this diagram. A 90 80 B Lung vol. The slope of the pressure—volume relationship in this plot is compliance. In the graph, lung volume percent total lung capacity, or TLC is plotted against transpulmonary pressure; the latter is measured during periodic interruptions of a slow expiration from TLC.
The spirometry tracing during the procedure is illustrated at the left. Pulmonary Compliance See Figure Identify which tracing 1 or 2 is obtained in air-filled lungs and which is obtained in saline-filled lungs.
Tracing 1 is obtained in saline-filled lungs, and tracing 2 is obtained in air-filled lungs. In air-filled lungs, the surface tension associated with the liquid—air interface results in a higher pressure required to maintain a given lung volume. Hysteresis is the difference in the pressure—volume curve obtained during inspiration indicated in the diagram by upward arrows and the curve obtained during expiration downward arrows.
Lung volume associated with any pressure during inspiration is lower than volume at that pressure during expiration, mainly because surface forces must be overcome during inspiration. Surface Forces in the Lung See Figure Which of the two tubes has the higher resistance, assuming length is the same?
By what factor? Which of the two tubes has the higher resistance, assuming radius is the same? The smaller of the two tubes has the higher resistance, which is 16 times greater than in the larger tube.
Thus, resistance is inversely related to the fourth power of the radius, and therefore the smaller tube, with half the radius of the larger tube, has 16 times greater resistance. The longer of the two tubes has twice the resistance of the shorter tube. Resistance is directly related to the length of a tube. Airway Flow I See Figure Identify the type of airflow illustrated in each airway as well as the type of airway in which this type of flow is likely to occur.
Laminar flow; occurs mainly in small airways where diameter and velocity are low, with both factors favoring laminar flow 2. Turbulent flow; occurs mainly in trachea and larger airways, where velocity is high and diameter is large, with both factors favoring turbulent flow 3. Higher Re is associated with turbulence. Identify points 1 and 2 on these curves. Explain the convergence of the down slopes of the two curves in the segment labeled 3.
Peak expiratory flow rate PEFR at maximum effort during a forced vital capacity maneuver 2. PEFR at reduced effort 3. The downward slope expiratory phase of the flow—volume curve is effort independent. During this phase of the curve, flow is limited by dynamic compression of the airways. Thus, once maximum flow rate is reached, further increases in pleural pressure will only increase resistance proportionally, and the two lines overlap solid line represents a forced vital capacity maneuver; dotted line represents the flow—volume curve performed at reduced effort.
Identify the category of lung disease characterized by the expiratory flow—volume curve labeled 1. Describe how the following parameters are affected increased, decreased, or unchanged in this type of disease: 2. Total lung capacity TLC 3.
Functional residual capacity FRC 4. Residual volume RV 5. Forced vital capacity FVC 6. Forced expiratory volume in the first second of a vital capacity maneuver FEV1 7. Obstructive lung disease. TLC is increased in obstructive lung disease. FRC is increased. RV is increased. FVC is reduced slightly. FEV1 is reduced. Lung Disease I See Figure Restrictive lung disease. TLC is decreased in restrictive lung disease. FRC is decreased. RV is decreased. FVC is reduced. Identify line 1.
Give the formula for calculation of the maximum amount of oxygen that can be carried in blood in this form. Identify line 2. Give the formula relating the amount of oxygen carried in blood in this form to partial pressure of oxygen.
Oxyhemoglobin dissociation curve at pH 7. SO2 percentage saturation of hemoglobin with oxygen 2. O2 content of blood 3. Dissolved O2 in blood Oxyhemoglobin dissociation curve at pH 7. A fall in hemoglobin concentration will not affect saturation of hemoglobin with O2. A fall in hemoglobin concentration will proportionally reduce the concentration of oxyhemoglobin at a given PO2.
Dissolved oxygen bottom line on the graph will be unaffected by a change in hemoglobin concentration. The effect of changes in PCO2, pH, and temperature on the binding of oxygen by hemoglobin are illustrated by the dotted and dashed lines in graphs 1, 2, and 3, respectively. Describe the qualitative effects of an increase or decrease in PCO2, pH, and temperature on the oxyhemoglobin dissociation curve in the context of the graphs.
A rise in PCO2 shifts the oxyhemoglobin dissociation curve to the right dashed line , whereas a fall in PCO2 shifts the curve to the left dotted line. A rise in pH shifts the curve to the left dotted line , whereas a fall in pH shifts the curve to the right dashed line. A rise in temperature shifts the curve to the right dashed line , whereas a fall in temperature shifts the curve to the left dotted line. The rightward shift of the curve results in decreased affinity of hemoglobin for oxygen and therefore enhances delivery of oxygen to tissues.
Describe the effects of anemia on oxygen content of blood. Describe the effects of carbon monoxide poisoning on oxygen content of blood. Anemia 7. In anemia, the content of oxygen in blood is reduced at any PO2 in proportion to the reduction of hemoglobin concentration. Thus, on the graph, at any PO2, O2 concentration of the anemic blood line 3 is half that of normal blood line 1.
Carbon monoxide has much higher affinity for hemoglobin than oxygen. In carbon monoxide poisoning, CO displaces oxygen bound to hemoglobin, forming carboxyhemoglobin and therefore reducing the oxygen-carrying capacity of blood. What is the relative importance of these three forms of CO2 transport? CO2 binds to terminal amino groups of blood proteins. Thus, the left, upper line in the figure is the curve for venous blood the normal PVO2 marked , whereas the right, lower line represents the CO2 dissociation curve for arterial blood the point marked is the normal PaO2.
This shift is the Haldane effect. As a result of this effect, as hemoglobin is deoxygenated in systemic capillaries, its affinity for CO2 is increased, facilitating CO2 transport. In the lungs, as hemoglobin is oxygenated, its affinity for CO2 is reduced; as a result, transfer of CO2 from blood to alveolar air is facilitated. Write the Henderson-Hasselbalch equation as it applies to the bicarbonate buffer system. Write the equation in a form in which pH can be calculated based on PCO2 and plasma bicarbonate concentration.
Explain, in the context of this diagram, how the lungs act as a buffer for changes in blood pH. Explain, in the context of this diagram, how changes in respiratory function can be a cause of acidosis or alkalosis. CO2 formed during metabolism of lipids and carbohydrates is normally readily eliminated by the respiratory system. By adjusting respiration, the system can compensate for pH imbalances produced by metabolic disturbances. Thus, metabolic acidosis is compensated for in part by increased respiration, whereas reduced ventilation will occur in metabolic alkalosis.
Disturbances in respiration can result in acid—base imbalance because changes in CO2 elimination will directly affect carbonic acid levels. Hypoventilation will cause respiratory acidosis, whereas hyperventilation will cause respiratory alkalosis.
When a respiratory acid—base disturbance occurs, the compensation is primarily renal. Explain the role of central chemoreceptors in the regulation of respiration.
Discuss the relative importance of changes in arterial O2, CO2, and pH in this regulation. Explain the role of arterial chemoreceptors in the regulation of respiration. As illustrated, changes in arterial blood gas levels result in regulation of respiration. Brainstem respiratory centers adjust rate and depth of breathing, causing changes in PaO2 and PaCO2, and thus blood pH. Peripheral chemoreceptors in the carotid and aortic bodies respond to changes in arterial PaO2 as well as PaCO2 and pH.
Impulses from these chemoreceptors reach the medullary respiratory center via the glossopharyngeal and vagus nerves, resulting in regulation of ventilation and normalization of PaO2 and PaCO2. However, in states such as hemorrhagic shock, the vasoconstriction by angiotensin may be important as one of the mechanisms that raise total peripheral resistance. Note that in contrast to other vascular beds, in the kidney angiotensin II does have a physiological role in regulating the tone of afferent and efferent arterioles.
Control of Respiration See Figure What are the factors that account for the initial, rapid adjustment of ventilation with the onset of exercise and the termination of exercise? What are factors that play a role in the sustained elevation of respiration during exercise, and in the continued elevation in respiration during the recovery period? The rapid increase in respiration at the onset of exercise is through neural and reflexive mechanisms.
Although not all of the mechanisms are known, one mechanism is that activation of motor pathways results in collateral activation of the respiratory center.
Afferent signals from muscle and joint mechanoceptors result in further activation of respiration. The slow responses that play a role in sustained elevation of respiration during exercise and during the recovery period are feedback responses. Chemoreceptor activation by changes in PaO2, PaCO2, and blood pH is important; the rise in core body temperature during exercise also has a role in stimulating respiration.
Respiratory Response to Exercise See Figure Renal artery 2. Renal vein 3. Renal pelvis 4. Ureter 5. Minor calyces 6. Major calyces 7. Renal pelvis 8.
Cortex 9. Medulla Nephrons serve to filter the blood and process the ultrafiltrate. After the tubular fluid is processed, the remaining fluid urine flows through the medullary collecting ducts into the calyces; the calyces empty into the ureters that lead to the bladder, where urine is stored until excreted.
Anatomy of the Kidney See Figure In which area does the most sodium and water reabsorption occur? Juxtamedullary glomerulus 2. Proximal convoluted tubule 3. Thin descending limb of Henle 4. Thick ascending limb of Henle 5.
Distal tubule 6. Collecting duct 7. Cortical glomerulus 8. In humans, each kidney contains more than 1 million nephrons. Cortical, or superficial, nephrons have glomeruli near the surface of the kidney and short loops of Henle that are found in the cortex and outer zone of the medulla. The images take the form of anatomical or histological depictions or graphical representations of physiological processes. Though small, the images are excellent… overall, undergraduate students will likely find this review system helpful in their exam preparations.
As a naturally integrative fi eld of study, physiology cannot readily be learned by simple memorization or repetitive study of lecture notes or texts. Most students fi nd that the best understanding of this fi eld comes when multiple learning modalities are utilized. With this in mind, this set of over cards has been developed to be used in conjunction with textbooks, lectures, and problem sets to cover topics in each of the major areas of physiology: cell physiology, neurophysiology, cardiovascular physiology, respiratory physiology, renal physiology, gastrointestinal physiology, and endocrinology.
Medical students, allied health students, and undergraduate students taking an advanced course in human physiology will enhance their knowledge of physiology by working with these cards. Moreover Medicalstudyzone.
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