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Midamor

By E. Ramirez. Hebrew College.

ABP is found at high con- olytic enzyme that assists in the release of the mature sperm centrations in the human testes and epididymis proven midamor 45mg arteria networks corporation. Sertoli cells also synthesize large amounts a carrier of testosterone in Sertoli cells purchase midamor 45mg fast delivery arteria esfenopalatina, as a storage protein of transferrin, an iron-transport protein important for for androgens in the seminiferous tubules, and as a carrier sperm development. During the fetal period, Sertoli cells and gonocytes form Other products of the Sertoli cell are inhibin, follistatin, the seminiferous tubules as Sertoli cells undergo numerous and activin. The pituitary gonadotrophs and testic- cease proliferating, and throughout life, the number of ular Sertoli cells form a classical negative-feedback loop in sperm produced is directly related to the number of Sertoli which FSH stimulates inhibin secretion and inhibin sup- cells. At puberty, the capacity of Sertoli cells to bind FSH presses FSH release. Inhibin also functions as a paracrine 654 PART X REPRODUCTIVE PHYSIOLOGY agent in the testes. Follistatin, an activin-binding protein, reduces FSH secre- Leydig cell tion induced by activin. Basement membrane surrounding seminiferous tubule Leydig Cells Produce Testosterone Spermatogonium Leydig cells are large polyhedral cells that are often found in clusters near blood vessels in the interstitium between Basal compartment seminiferous tubules. They are equipped to produce Tight junction steroids because they have numerous mitochondria, a Adluminal compartment prominent smooth ER, and conspicuous lipid droplets. Spermatocyte Leydig cells undergo significant changes in quantity and activity throughout life. This mechanism may depend on a nuclear transcription factor, steroidogenic factor-1 (SF-1), that recognizes a sequence in the promoter of all genes en- Spermatid Nucleus coding CYP enzymes. In the human fetus, the period from weeks 8 to 18 is marked by active steroidogenesis, which is Nucleus obligatory for differentiation of the male genital ducts. Ley- dig cells at this time are prominent and very active, reach- Intercellular space ing their maximal steroidogenic activity at about 14 weeks, when they constitute more than 50% of the testicular vol- Spermatozoon ume. Because the fetal hypothalamic-pituitary axis is still underdeveloped, steroidogenesis is controlled by human chorionic gonadotropin (hCG) from the placenta, rather Sertoli cell Sertoli cell than by LH from the fetal pituitary (see Chapter 39); LH and hCG bind the same receptor. At about 2 to 3 months of postnatal Lumen life, male infants have a significant rise in testosterone pro- duction (infantile testosterone surge), the regulation and FIGURE 37. Leydig cells remain quies- tight junctions, which divide the intercellular cent throughout childhood but increase in number and ac- space into a basal compartment and an adluminal compart- tivity at the onset of puberty. Spermatogonia are located in the basal compartment and maturing sperm in the adluminal compartment. Spermatocytes are Leydig cells do not have FSH receptors, but FSH can in- formed from the spermatogonia and cross the tight junctions into crease the number of developing Leydig cells by stimulat- the adluminal compartment, where they mature into spermatozoa. Molecular Biol- that subsequently enhance the growth of the Leydig cells. Estrogen receptors are present on Ley- dig cells, and they reduce the proliferation and activity of these cells. Leydig cell Sertoli cell Lumen of seminiferous Cholesterol tubule cAMP ABP LH ATP T-ABP Pregnenolone T T Testosterone (T) ATP cAMP FSH E T Estradiol Regulation, (E) FIGURE 37. ABP, androgen-binding protein; E, estradiol; T, testos- Proteins Proteins terone; R, receptor. CHAPTER 37 The Male Reproductive System 655 Leydig cells have LH receptors, and the major effect of vasodilation of the arterioles and corpora cavernosa. The LH is to stimulate androgen secretion via a cAMP-depend- smooth muscles in those structures relax, and the blood ent mechanism (see Fig. The main product of Leydig vessels dilate and begin to engorge with blood. The thin- cells is testosterone, but two other androgens of less bio- walled veins become compressed by the swelling of the logical activity, dehydroepiandrosterone (DHEA) and an- blood-filled arterioles and cavernosa, restricting blood drostenedione, are also produced. The result is a reduction in the outflow of blood from There are bidirectional interactions between Sertoli and the penis, and blood is trapped in the surrounding erectile Leydig cells (see Fig. The Sertoli cell is incapable of tissue, leading to engorgement, rigidity, and elongation of producing testosterone but contains testosterone receptors the penis in an erect position. The Leydig cell does Semen, consisting of sperm and the associated fluids, not produce estradiol but contains receptors for it, and is expelled by a neuromuscular reflex that is divided into estradiol can suppress the response of the Leydig cell to two sequential phases: emission and ejaculation. Testosterone diffuses from the Leydig cells, crosses the sion moves sperm and associated fluids from the cauda basement membrane, enters the Sertoli cell, and binds to epididymis and vas deferens into the urethra. As a result, androgen levels can reach high local con- process involves efferent stimuli originating in the lum- centrations in the seminiferous tubules. Testosterone is bar areas (L1 and L2) of the spinal cord and is mediated obligatory for spermatogenesis and the proper functioning by adrenergic sympathetic (hypogastric) nerves that in- of Sertoli cells. In Sertoli cells, testosterone also serves as a duce contraction of smooth muscles of the epididymis precursor for estradiol production. This action propels sperm through the diol in the functioning of Leydig cells is unclear, but it may ejaculatory ducts and into the urethra. Ejaculation is the expulsion of the semen from the penile The Duct System Functions in Sperm Maturation, urethra; it is initiated after emission. The filling of the Storage, and Transport urethra with sperm initiates sensory signals via the pu- After formation in the seminiferous tubules, spermatozoa dendal nerves that travel to the sacrospinal region of the are transported to the rete testes and from there through cord. A spinal reflex mechanism that induces rhythmic the efferent ductules to the epididymis.

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In a resting individual order midamor 45 mg with amex pulse pressure of 30, the heart ejects Bulk Flow and Diffusion Are Influenced by blood into the aorta about once every second (i discount 45mg midamor otc peripheral neuropathy. The phase during The aorta has the largest diameter of any artery, and the which cardiac muscle contracts is called systole, from subsequent branches become progressively smaller the Greek for “a drawing together. Although the capillaries are the the pressures in the atria increase and push blood into smallest blood vessels, there are several billion of them. During ventricular systole, pressures in For this reason, the total cross-sectional area of the lu- the ventricles rise and the blood is pushed into the pul- mens of all systemic capillaries (approximately 2,000 monary artery or aorta. During diastole (“a drawing 2 cm ) greatly exceeds that of the lumen of the aorta (7 apart”), the cardiac muscle relaxes and the chambers fill 2 cm ). In a steady state, the blood flow is equal at any two from the venous side. Because of the pulsatile nature of cross sections in series along the circulation. For exam- the cardiac pump, pressure in the arterial system rises ple, the flow through the aorta is the same as the total and falls with each heartbeat. The large arteries are dis- flow through all of the systemic capillaries. Because the tended when the pressure within them is increased (dur- combined cross-sectional area of the capillaries is much ing systole), and they recoil when the ejection of blood greater and the total flow is the same, the velocity of falls during the latter phase of systole and ceases entirely flow in the capillaries is much lower. This recoil of the arteries sustains the ment of blood through the capillaries provides maximum flow of blood into the distal vasculature when there is no opportunity for diffusional exchanges of substances be- ventricular input of blood into the arterial system. In contrast, blood peak in systemic arterial pressure occurs during ventric- moves quickly in the aorta, where bulk flow, not diffu- ular systole and is called systolic pressure. The difference between systolic pressure and diastolic pressure is the pulse pressure. We will discuss these THE LYMPHATIC CIRCULATION three pressure types thoroughly in Chapter 15. This fluid eventually returns from the interstitial space to the TRANSPORT IN THE CARDIOVASCULAR systemic circulation via another set of vessels, the lym- SYSTEM phatic vessels. This movement of fluid from the systemic The cardiovascular system depends on the energy provided and pulmonary circulation into the interstitial space and by hemodynamic pressure gradients to move materials over then back to the systemic circulation via the lymphatic ves- long distances (bulk flow) and the energy provided by con- sels is referred to as the lymphatic circulation (see Chapter centration gradients to move material over short distances 16). Both types of movement are the result of differ- mulates in the interstitial space. Diffusion occurs be- CONTROL OF THE CIRCULATION cause of differences in chemical concentration. The healthy cardiovascular system is capable of providing appropriate blood flow to each of the organs and tissues of the body under a wide range of conditions. This is done by Hemodynamic Pressure Gradients Drive Bulk • Maintaining arterial blood pressure within normal limits Flow; Concentration Gradients Drive Diffusion • Adjusting the output of the heart to the appropriate level Blood circulation is an example of transport by bulk flow. Diffusion is The regulation of arterial pressure, cardiac output, and accomplished by the random movement of individual mol- regional blood flow and capillary exchange is achieved by ecules and is an effective transport mechanism over short using a variety of neural, hormonal, and local mecha- distances. Select the (E) Hydrostatic pressure JS, Sheriff DD, Robotham JL, Wise, ONE lettered answer or completion that is 4. Exercise: Regulation and the (C) Blood vessel diameter exceeds a Integration of Multiple Systems. New (A) Square of the radius certain value (B) Square root of the length York: Oxford University Press, (D) Reynolds number exceeds a certain (C) Fourth power of the radius 1996;649–704. The volume of an aorta is increased by (E) Square root of the radius NJ: Humana Press, 2000. New York: Oxford University (A) Can only be caused by changes in compliance of the aorta is Press, 1993. In the tube in the of the blood vessel diagram to the right, the inlet pressure is 75 mm (D) Cause proportional changes in Hg and the outlet blood flow pressure at A and B is 25 (E) Are proportional to the length of a mm Hg. The pressure measured in either the (A) 2 PRU 5 mL/min arterial or the venous circulation when (B) 0. Electrical activity spreads across the atria, through the atri- lective opening and closing of plasma membrane channels oventricular (AV) node, through the Purkinje system, and for sodium, potassium, and calcium ions. Norepinephrine increases pacemaker activity and the calcium channels and the closing of potassium channels. Acetylcholine decreases pacemaker activity and the speed channels and the closing of sodium and calcium of action potential conduction. Pacemaker potentials are achieved by the opening of chan- regions of the heart are recorded by an electrocardiogram nels for sodium and calcium ions and the closing of chan- (ECG). Electrical activity is normally initiated in the sinoatrial (SA) rhythm, pattern of depolarization, and mass of electrically node where pacemaker cells reach threshold first. After initia- potential; phase 3 is the repolarization to the resting mem- tion, the electrical activity spreads throughout the heart, brane potential; and phase 4 is the resting membrane po- reaching every cardiac cell rapidly with the correct timing. In resting ventricular muscle The electrical activity of cardiac cells depends on the ionic cells, the potential inside the membrane is stable at approx- gradients across their plasma membranes and changes in per- imately 90 mV relative to the outside of the cell (see meability to selected ions brought about by the opening and phase 4, Fig. This chapter describes how these an action potential occurs (see Chapter 3).

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Since 1975 buy midamor 45 mg with visa arrhythmia life threatening, we have had direct experience with various legal reforms and clear knowledge of which of these are effective and which are not order 45mg midamor overnight delivery blood pressure and diabetes. It is best to effectuate legal reform as part of a comprehensive package based on California’s MICRA experience. A $250,000 cap on noneco- nomic damages is most important, but collateral source reform, a peri- odic payments rule, and control of attorney contingency fees are also important. Other reforms may be appropriate and useful, but a quarter century of experience indicates they will have much less impact than the MICRA statutes. In the absence of these reforms, it is predictable that the cost of malpractice insurance will continue to rise, as will the cost of medical care in general, defensive medicine will increase, and access to funda- mental health care will be increasingly imperiled. Confronting the New Health Care Crisis: Improving Health Care Quality and Lowering Costs by Fixing Our Medical Liability System. Medical Malpractice: Implications of Rising Premiums on Access to Health Care. Subcom- mittee on Health, Committee on Energy and Commerce, US House of Represen- tatives. Straight Talk on Medical Malpractice: American Trial Law- yers Association, 1994:20. Governor’s Select Task Force on Healthcare Professional Liability Insurance. Medical Malpractice Insurance: Mul- tiple Factors Have Contributed to Increased Premium Rates. Relation between negligent adverse events in the outcomes of medical malpractice litigation. Medical Malpractice Insur- ance: A Study of Market Conditions, 2003, pp. National Association of Insurance Commissioners 1999 Profitability Study, 1999. An Analysis of Harvey Rosenfield’s Report: “California’s MICRA”: LECG, 1997, p. Medical Liability Mutual Insurance Company Projected Effect on New York Professional Liability Costs of Capping Noneconomic Dam- ages: Milliman & Robertson, 1995. California’s medical malpractice crisis: Health Care Liability Alliance, 2003, pp. Excerpts of Reports Received by the American Tort Reform Association on the Crisis in Medical Liability: American Medical Association, 2002. Trends in 2002 Rates for Physicians’ Medical Profes- sional Liability Insurance. Milliman USA Analysis Sees Savings for Professional Medical Malpractice Costs. Sued and non-sued physicians’ self-reported reactions to malpractice litigation. Influence of cardiac-surgery performance reports on re- ferral practices and access to care. The Impact of State Laws Limiting Malpractice Awards on the Geographic Distribution of Physicians: Agency for Healthcare Research and Quality, US Department of Health and Human Services, 2003. How the MICRA Cap Influences Health Care Costs for Safety Net Providers and Medi-Cal: LECG, 1999;1–13. Americans Believe Access to Health Care Threatened by Medical Liability Crisis. Chapter 16 / Health Policy Review 227 16 Health Policy Review Medical Malpractice David M. Brennan, MD, JD, MPH SUMMARY Since the 1980s, empirical analyses of the system of medical malpractice have revealed that it largely fails to provide reason- able compensation for injured individuals, or to provide appro- priate incentive for safety and prevention. The most promising approaches for reform involve fundamental system changes rather than tinkering with tort doctrine. Key Words: Standard of care; Harvard Medical Practice Study; patient safety; tort reform; system reform. INTRODUCTION Few issues in health care spark ire and angst like medical malprac- tice litigation. Physicians revile malpractice claims as random events that visit unwarranted expense and emotional pain on competent, hardworking practitioners. Commentators lament the “lawsuit lottery” that provides windfalls for some patients but no compensation for From: Medical Malpractice: A Physician’s Sourcebook Edited by: R. Within the health care industry, there is a near-universal belief that malpractice litigation has long since surpassed sensible levels and major tort reform is overdue. Plaintiff attorneys and some con- sumer groups interpret providers’ grievances as little more than pre- dictable chafing from a profession unaccustomed to external policing. They view litigation as an indispensable form of protection against medical carelessness. Trial attorneys’ responses to recent research on medical errors illustrates their self-image as champions of patient safety: new knowledge of the burden of medical error is seen as vin- dication of the battles fought on behalf of patients, and the imperative such findings announce is clear—more litigation (3). With a malpractice crisis now spreading across the United States, it is timely to review the current situation in light of the liability system’s goals, previous crises, and available evidence on system performance.

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