By T. Brontobb. Park College.

The olfactory buy discount apcalis sx 20 mg on-line erectile dysfunction drug approved to treat bph symptoms, optic 20mg apcalis sx with amex erectile dysfunction treatment san diego, and (a) There are four plexuses of spinal (c) The lumbar plexus and the sacral vestibulocochlear cranial nerves nerves: the cervical, the brachial, the plexus are collectively referred to as are sensory only; the trigeminal, lumbar, and the sacral. Peripheral Nervous © The McGraw−Hill Anatomy, Sixth Edition Coordination System Companies, 2001 Chapter 12 Peripheral Nervous System 433 Reflex Arc and Reflexes (pp. A reflex arc is the simplest type of nerve (a) The stretch reflex is a monosynaptic motor neuron and its innervation in the pathway. Visceral reflexes cause smooth or cardiac (b) The flexor reflex is a polysynaptic more association neurons in the CNS. The reflex arc enables a rapid, automatic Review Activities Objective Questions 7. A person with quadriplegia from a spinal (b) It contains components of the (e) the sacral plexus cord injury at the level of C5 can speak, autonomic nervous system. Roots, trunks, divisions, and cords are digest food, breath, and regulate his or her (c) Sensory receptors, nerves, ganglia, characteristic of heartbeat, yet the person cannot move and plexuses are all part of the PNS. Which cranial nerve innervates the (c) axillary/brachial appointment with the company doctor muscle that raises the upper eyelid? Following a routine physical exam, (b) the oculomotor nerve ligament is tapped is an example of the physician scheduled the man for a (c) the abducens nerve (a) a visceral reflex. Discuss (b) the facial nerve Essay Questions the possible treatment of this condition. Explain the structural and functional (You may have to refer to medical (d) the vagus nerve relationships between the central nervous textbooks in your library to find the system, the autonomic nervous system, answer. Which cranial nerve passes through the and the peripheral nervous system. List the cranial nerves and describe the punch during the world featherweight (a) the facial nerve major function(s) of each. How is each championship fight, the ringside (b) the glossopharyngeal nerve cranial nerve tested for dysfunction? List the roots of each of the spinal damage when his right zygomatic bone 6. Describe where each plexus is located and state the nerves that originate symptoms might the boxer have displayed fibers? Autonomic Nervous © The McGraw−Hill Anatomy, Sixth Edition Coordination System Companies, 2001 Autonomic Nervous System 13 Introduction to the Autonomic Nervous System 435 Structure of the Autonomic Nervous System 438 Functions of the Autonomic Nervous System 444 Control of the Autonomic Nervous System by Higher Brain Centers 448 CLINICAL CONSIDERATIONS 450 Clinical Case Study Answer 451 Chapter Summary 451 Review Activities 452 Clinical Case Study A low-flying crop duster sprays a field worker. Within the hour, he develops blurry vision, ex- cessive salivation, and a runny nose. As the minutes pass, he begins to experience nausea, vom- iting, abdominal cramping, and coughing up of copious mucus. An observant paramedic called to the scene makes a diagnosis of organophosphate poisoning and promptly initiates therapy. Can you account for each of the symptoms this man suffered by describing the normal response of individual organs to parasympathetic stimuli? What effect would this drug have on the eyes, salivary glands, and nose? FIGURE: Because many pesticides are neurotoxins that can be readily absorbed through the skin and mucous membranes, caution must always be taken when using these poisons. Autonomic Nervous © The McGraw−Hill Anatomy, Sixth Edition Coordination System Companies, 2001 Chapter 13 Autonomic Nervous System 435 Autonomic motor nerves innervate organs whose functions INTRODUCTION TO THE are not usually under voluntary control. The effectors that re- AUTONOMIC NERVOUS SYSTEM spond to autonomic regulation include cardiac muscle tissue (within the heart), smooth muscle tissue (within the viscera), The action of effectors (muscle tissue and glandular epithelium) is and glandular epithelium. These effectors are part of the organs controlled to a large extent by motor neuron impulses. Skeletal of the viscera, of blood vessels, and of specialized structures muscles, which are the voluntary effectors, are regulated by so- within other organs. The involuntary effectors (smooth muscle vation contrast with the voluntary control of skeletal muscles by tissue, cardiac muscle tissue, and glandular epithelium) are regu- way of somatic motor innervation.

The latter requires physician advocacy beyond the welfare of indi- vidual patients to “promote justice in the health care system” (23) quality apcalis sx 20 mg impotence mayo clinic. Commitment to honesty with patients order 20mg apcalis sx otc impotence in the sun also rises, emphasizing both informed con- sent, and prompt reporting and analysis of medical error. Commitment to maintaining appropriate relations with patients such as the avoidance of patient exploitation for sexual advantage, financial gain, or other private purpose. Commitment to professional responsibilities emphasizing the indi- vidual and collective obligations to participate in processes to improve patient care (23). Nonetheless, every constitu- ency in our society agrees on the critical nature of medical services and all want more, not less, access. Ultimately, the practice of medicine is too important, and the men and women who undertake it too estimable, for the system not to balance itself. This book is offered as a look at the problems, some solutions that are available today, and more that are possible in the future. Doctor discon- tent—a comparison of physician satisfaction in different delivery system settings, 1986 and 1997. Changes in career satisfaction among primary care and specialist physicians, 1997–2001. Results from CMA’s huge 1998 physician survey point to a dispirited profession. Changing nature of physician satis- faction with health maintenance organization and fee-for-service practices. Subcommit- tee on Health, Committee on Energy and Commerce, US House of Representatives. The Harris Poll #6, Confidence in leadership of nation’s institutions remains relatively high: www. Confronting the New Health Care Crisis: Improving Health Care Quality and Lowering Costs by Fixing Our Medical Liability System. LEGAL 2 What Every Doctor Should Know About Litigation: A Primer on How to Win Medical Malpractice Lawsuits......................................................................... ANDERSON, MD, FACP • Chairman and Chief Executive Officer, The Doctors Company, Napa, CA; former Chief of Medicine, Scripps Memorial Hospital, LaJolla CA, and former Clinical Professor of Medicine, University of California, San Diego, CA TROYEN A. BRENNAN, MD, JD, MPH • Department of Health Policy and Management, Harvard School of Public Health, Brigham and Women’s Hospital, Boston, MA MICHAEL JAY BRESLER, MD, FACEP • Clinical Professor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, CA; Medical Director, Department of Emergency Medicine, Mills-Peninsula Health System, Burlingame, CA JONATHAN I. EPSTEIN, MD • Professor, Departments of Pathology, Urology, and Oncology; the Reinhard Professor of Urologic Pathology; and Director of Surgical Pathology, Johns Hopkins Medical Institutions, Baltimore, MD EDWARD FOTSCH, MD • Medem Inc. HIESTAND, JD • Counselor at Law; General Counsel to the Civil Justice Association of California (1978–Present); CEO and General Counsel to Californians Allied for Patient Protection, Sacramento, CA DAVID WM. LOFSKY, MD • Anesthesiologist, Saint John’s Hospital, Santa Monica, CA; Member, Board of Governors, The Doctors Company, Napa, CA JOEL A. MATTISON, MD, FACS • Department of Utilization Management and Quality Assurance, St. Joseph’s Hospital, Tampa, FL; former Clinical Professor of Surgery, University of South Florida, Tampa, FL xix xx Contributors MICHELLE M. MELLO, JD, PhD, MPhil • Assistant Professor of Health Policy and Law, Department of Health Policy and Management, Harvard School of Public Health, Boston, MA WILLIAM M. SAGE, MD, JD • Professor of Law, Columbia Law School, New York, NY JACK M. SCHNEIDER, MD • Chief Medical Officer, Sharp Mary Birch Hospital for Women, San Diego, CA DAVID M. STUDDERT, LLB, ScD, MPH • Department of Health Policy and Management, Harvard School of Public Health, Boston, MA DAVID B. TROXEL, MD, FCAP • Member, Board of Governors, The Doctors Company, Napa, CA; Clinical Professor, Health and Medical Sciences, University of California, Berkeley, CA MALCOLM H. WEISS, MD • Clinical Professor, Department of Family and Community Medicine, University of Nevada School of Medicine, Reno, NV Chapter 1 / Insuring the Practice of Medicine 1 I INSURANCE 2 Gorney and Anderson Chapter 1 / Insuring the Practice of Medicine 3 1 Insuring the Practice of Medicine Mark Gorney, MD and Richard E. Anderson, MD, FACP SUMMARY Although all physicians are aware that practicing medicine in the United States is virtually impossible without some form of liabil- ity insurance, many have only a limited understanding of how the American system of professional assurance really works. It is important for the practicing physician to understand not only some of the technical language regarding insurance but also the various forms in which it is available.

Cytochrome P450scc purchase apcalis sx 20 mg with amex erectile dysfunction treatment in lucknow, the specific hydroxylase needed for cleavage of the cholesterol side-chain to give PREG buy apcalis sx 20mg mastercard erectile dysfunction shake drink, has been found widely in white matter and in myelinating oligodendrocytes, but not in neurons. Enzymes are present for the conversion of PREG to PROG and both are reduced in glia and neurons. This does not occur with DHEA and very little is known of either its synthesis or metabolism. Neurosteroids are widely and fairly evenly distributed in the brain with few note- worthy localisations but the concentration of the conjugated forms (sulphated and reduced) of PREG and DHEA can exceed that of the parent compounds. By contrast, although the concentration of progesterone rises some twelvefold in plasma and eight times in hippocampus of animals and humans as they pass from the follicular to luteal phase of the ovarian cycle, it increases by 300 in the cortex, suggesting a considerable variation in the ability of different brain regions to concentrate it. In considering the neurosteroids as possible NTs it should be remembered that neither specific steroid neurons nor an evoked neuronal release of steroids have been demonstrated. There are, however, receptors for them in the CNS and no shortage of actions attributed to them. Given clinically in the therapy of inflammatory conditions, the glucocorticoids are considered to produce euphoria, followed after prolonged or higher dosing by depression and, of course, when we are stressed the corticocosteroids pumped out by the adrenal cortex easily enter the brain and may initiate some of the behavioural response. In women the premenstrual syn- drome (irritability, depression and anxiety) is thought to be associated in some way with progesterone since not only does its concentration rise then fall during that time but in post-menopausal women the use of sequential oestrogen and progestogen hormone replacement therapy (HRT) shows that similar mood changes accompany only the addition of progestogen. More specifically, in women with epilepsy while the incidence of seizures decreases when plasma progesterone is high, it increases during the immediate premenstrual period as progesterone levels fall, rather as with withdrawing 274 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION Figure 13. Pregnenolone (PREG) (1) is synthesised from cholesterol and is then either metabolised, reduced to 20a dihydropregnenolone (7) or sulphated (6), or converted by 3b-hydroxysteroid dehydrogenase to progesterone (PROG) (2) or to dehydroepiandrosterone (DHEA) (3). The former (PROG) can then be reduced to allopregnanolone (3a5aThPROG) (4) and DHEA sulphated to dehydroepiandrosterone sulphate (5). The structures of alphaxalone, a steroid anaesthetic and tetrahydrodeoxy- corticosterone, which is formed in the brain from deoxycorticosterone of peripheral origin, are also shown OTHER TRANSMITTERS AND MEDIATORS 275 an antiepileptic drug. Of course, it cannot be assumed that plasma levels are reflected in the brain but in rats stressed by insertion in the Morris water maze, so that they have to swim to a safe platform (see Chapter 18), there is still some increase in the concen- tration of brain PROG and in particular its reduced metabolic (ThPROG), even after adrenalectomy (Purdy et al. The aggressiveness of castrated male mice exposed to lactating females in a cage can also be reduced by DHEA administration. These observations, while implicating steroids in brain function and behaviour, cannot be taken as a reliable indicator of their actual effect on neuronal function. Nevertheless, some neurosteroids produce CNS depression with a rapid inhibition of neuronal excitability and one progesterone derivative, alphaxalone (3a-hydroxy- 5a pregnane-11, 20 dione, see Fig. Intracellular steroid receptors, which alter gene expression, exist for corticosteroids, oestrogens and progesterone in the brain, as in the periphery but they cannot account for the relatively rapid depression of CNS function induced by some steroids. This was explained when Harrison and Simmonds (1984) discovered that alphaxalone (the steroid anaesthetic) potentiated the duration of GABA-induced currents at the GABAA receptor in slices of rat cuneate nucleus just like the barbiturates (Fig. Depolarisations recorded extracellularly from dorsal funiculus fibres and terminals in the rat cuneate brain slice after superfusion for 2 min with muscimol 2. In the presence of alphaxalone (1 mM), responses to GABA and the GABAA agonist muscimol, but not those to glycine, were substantially enhanced. The effect was reversible with responses slowly returning to normal after 3 h. The sulphated metabolite of PREG is similarly active at low (nM) concentrations. These allosteric effects are still seen after maximal barbiturate potentiation and are not affected by benzodiazepine antagonists suggesting a specific and separate modulating site for the steroids (see Paul and Purdy 1992) although it has not been found. Also while their activity changes with the subunit composition of recombinent GABAA receptors no specific configuration has been established for their effectiveness but expression of a2 with a1 ‡ B1 or a2 ‡ B1 gives a more responsive receptor than the inclusion of a3 (Shingai, Sutherland and Barnard 1991). The GABA potentiation seen with low concentrations of PREG sulphate changes to antagonism at higher strengths and both this compound and sulphated DHEA, which also inhibits GABAA receptors, are proconvulsant. There is also evidence that the sulphates of PREG and DHEA potentiate NMDA receptors while glucocorticoids reduce seizure threshold without affecting GABA receptors. Thus even without considering reports of effects on glycine sigma and ACh nicotinic receptors, the electrophysiology of the steroids is complex. In practice, although steriods modulate GABAA receptors at realistic nM concentrations, unphysiological mM amounts are required at other ligand-gated ion channels (see Rupprecht and Holsboer 1999).

Although OSA is diagnosable through formal sleep studies buy discount apcalis sx 20 mg line erectile dysfunction wellbutrin xl, it also has clinical hallmarks order 20 mg apcalis sx impotence doctor. These include loud snoring—often requiring couples to sleep in separate rooms; obstruction noted by the sleeping partner, including episodes of gasping and choking while asleep; and exces- sive daytime somnolence with an uncontrollable sleepiness interfer- ing with professional or private life (15). Patients who exhibit these symptoms might not all have OSA if evaluated by formal sleep stud- ies, but it might be safer to treat them as if they did until proven otherwise (11). Children with obstruction secondary to adenotonsillar hypertrophy may also have clinical sleep apnea presenting with the same clinical signs. They can also be at risk post-tonsillectomies if medicated with parenteral narcotics. Risk-management suggestions include finding ways to monitor OSA patients appropriately postoperatively. Pulse oximetry currently has the ability to detect hypoxic episodes early, but oximeter alarms must be audible to hospital personnel if arrests are to be prevented. This can be accomplished in intensive care units or on wards that are staffed for this purpose. The administration of narcotics to OSA patients needs to be closely monitored. Pain medication orders for any given patient might be written by different individuals (e. Red-flagging the charts of OSA patients can warn all physicians and caregivers of the increased risk of narcotic administration. Patients who use continuous positive airway pressure masks at home should be advised in advance to bring them to the hospital and should use them postoperatively where appropriate. As pain is treated more aggressively, the tragic complication of respiratory arrest in patients with OSA may be seen more frequently. Anesthesiologists should be alert to signs of OSA and should consider routinely asking questions to identify those patients at risk (11). When Bad Claims Happen to Good Anesthesiologists Much has been written about the stress of being named in a malprac- tice lawsuit. Anesthesiologists may be particularly vulnerable in this circumstance because they do not have a consistent and loyal patient base and have only transient relationships with the other physicians with whom they work. As one anesthesiologist explained, “It’s like you’re only as good as your last case. The legal admonition not to speak to other physicians about the details of cases facing pos- sible litigation can leave an anesthesiologist feeling isolated and alone. However, in being sued, anesthesiologists are actually joining the ranks of the majority of their colleagues. One’s partners are more likely than not to have been involved in malpractice cases themselves, but this is not a topic that comes up frequently for discussion in the operating room. Malpractice lawsuits are an unpleasant but real part of life for most anesthesiologists with busy practices. Those who manage to avoid litigation entirely are just as likely to be lucky as unusually skilled. With 4% of anesthesiology claims generated solely by surgical complications, avoiding those is really a matter of luck. Naturally, physicians tend to dwell on the facts of cases with adverse outcomes. In retrospect, it can be frustrating how simple the steps that would have avoided a complication might seem. However, any one anesthetic may be acceptably accomplished in many different ways, so there will always be a number of alternatives to whatever choices a physician makes. From a medical-legal standpoint, the standard of care does not depend on 20/20 hindsight but rather on what a similarly trained physician might have chosen to do given similar circumstances. Errors in judgment or tech- nique will be made, and sometimes patients will have ill effects that could possibly have been avoided. Anesthesia is certainly not risk- free, even in the best of hands, and complications will arise in every practice. As those who have lived through malpractice litigation attest, life goes on and operating room conversation ultimately shifts to more interesting topics.