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Although initially it can seem like things will only get worse purchase precose 50 mg without a prescription, the vast majority of physicians report that the negative feelings pass with time and life does return to normal generic 25 mg precose fast delivery. Spend- ing time on outside activities they enjoy and avoiding overwork and sleep deprivation can only have positive effects on anesthesiologists’ mental state and job function (16) order precose 50mg with mastercard. Guidelines for Risk Management in Anesthesiology 50 mg precose amex, TDC Anesthesia Handbook purchase 25 mg precose mastercard, 1999. Lofsky AS: Labor and Delivery Disaster Claims, TDC Risk Management Bulletin, 2004. Anesthesiology: A Claims Review Panel on Epidural Anesthesia, TDC Anesthesia Handbook, 1999. Sleep Apnea and Narcotic Postoperative Pain Medication: A Morbid- ity and Mortality Risk, TDC Risk Management Bulletin, 2001. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Chapter 11 / Obstetrics and Gynecology 139 11 Malpractice and Medical Practice Obstetrics and Gynecology Jack M. Schneider, MD SUMMARY This chapter presents general and specialty-specific issues leading to malpractice litigation. Strategies for decreasing medical error and preventing malpractice litigation are outlined with emphasis on accurate documentation, review of clinical information, selec- tion and appropriate use of consultants, and above all, communi- cation to the patient and family. The need to continue learning from national care guidelines and specialty-specific publications is emphasized. Key Words: Labor; delivery; informed consent; maternal health care; Cesarean section; American College of Obstetrics and Gyne- cology Guidelines. INTRODUCTION Most cases of medical malpractice in obstetrics or gynecology follow from negligent performance of physician obligations that are not unique to this specialty. The physician must have the degree of learning and skill ordinarily possessed by reputable specialists practicing in the same field in the same or similar locality. Failure to meet these duties consti- tutes negligence, that is, the failure to meet the standard of care. Meeting the standard of care requires knowl- edge and application of national professional (e. With the exception of the emergency situation, informed consent must be obtained from the patient or legal guardian prior to providing treatment or performing a procedure. Appropriate alternatives must be disclosed and the risks of the proposed intervention discussed in detail. Although possible death or serious bodily harm must be addressed, it is wise to discuss more common complications of the specific treat- ment and to present them in terms of expected frequency of occurrence. One is failure to document the specific complications covered in the discussion (e. For example, the patient with pelvic pain often has the implied expectation of relief from the pain, but the physician knows this is possible but not certain. Refusal by the patient to consent to a plan of treatment must be made on an informed basis. The physician should thoroughly docu- ment the advice provided, the patient’s refusal to embrace the plan of care, and the potential consequences. It is extremely important that the practitioner not reflect his or her frustration or anger regarding the patient’s expression of her right to refuse care. It is also important to have the patient sign in the medical record what specific aspect, or aspects, of the treatment is being refused. When death or bodily harm results from a physician’s failure to meet the standard of care, causation is established. If no harm inures from a standard-of-care issue, then there is typically no basis for suit. On the other hand, death or serious injury often leads to a malpractice suit even when negligence is not evident. The failure to communicate and to thoroughly document those conversations is the most frequent cause of litigation in obstetrics and gynecology. Communication is a two-way process, and the physician must be a good listener as well as presenter. I ascribe over 35 years of an active clinical practice of maternal and fetal medicine without litigation to open communication with my patients, their families, staff, and colleagues.

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All muscarinic receptors have seven transmembrane domains and the major difference between them is within the long cytoplasmic linkage connecting the fifth and sixth domains generic precose 25mg without a prescription. Some possibilities are shown although the position of the M1 and M2 boxes is not intended to indicate their precise structural differences within the loop ACETYLCHOLINE 125 mamalian nAChR subunits have been selectively deleted (see Cordero-Erausquin et al generic precose 50mg overnight delivery. While only those mice lackingsubunits found mainly in peripheral nicotinic receptors (e generic 25 mg precose otc. Muscarinic Despite the wide variety of effects associated with the activation of muscarinic receptors on different peripheral organs it appeared that they were either identical or very similar because known antagonists generic 25 mg precose with visa, like atropine order precose 50mg free shipping, were equally effective against all muscarinic responses. A decade ago, one drug, pirenzepine, was found to be a hundredfold more active against ACh-induced gastric acid secretion than against other peripheral muscarinic effects. The receptors blocked by pirenzapine became known as M1 and all the others as M2. Recently some differences between muscarinic M2 receptors on heart (inhibitory) and those on exocrine glands (generally excitatory) became apparent through slight (fivefold) differences in the binding of some antagonist drugs (tools) such as AF-DX- 116 and 4-DAMP. The former was more active on the receptors in the heart, accepted as M2 receptors, while the glandular ones, blocked preferentially by 4-DAMP, became M3. Molecular biology has since confirmed the existence of these three receptors and revealed (at the time of printing) two more Ð M4 and M5. The M1 receptor mediates most of the central postsynaptic muscarinic effects of ACh while the M2 is pre- dominantly a presynaptic autoreceptor. The structure of the muscarinic receptor is very different from that of the nicotinic. They are single-subunit proteins which belong to the group of seven transmembrane receptors (like adreno and dopamine receptors) typically associated with second messenger systems. The major difference between muscarinic receptors is in the long cytoplasmic linkage connecting the fifth and sixth transmembrane domain, suggesting different G-protein connections and functions. Thus M1,M 3 and M5 receptors are structurally similar and their activation causes stimulation of guanylate cyclase and an increase in cyclic GMP as well as inosotal triphosphate hydrolysis through an increase in G-protein (Gp) (Fig. Through G-protein (G1) they inhibit cyclic AMP production and open K‡ channels while activation of another G-protein (G ) closes Ca2‡ channels. The latter effect will cause membrane hyper- 0 polarisation as will the G -induced increase in K‡ efflux. The reduction in cAMP 1 production, although possibly leading to depolarisation, is more likely to explain the presynaptic reduction in ACh release associated with the M2 receptor. DISTRIBUTION Cholinergic receptors should obviously be found where ACh is concentrated and cholinergic pathways terminate. Autoradiography with appropriately labelled ligands does in fact show M1 receptors to be predominantly in the neocortex and hippocampus (where pathways terminate) and in the striatum where ACh is released from intrinsic neurons. By contrast, M2 receptors are found more in the basal forebrain where ascending cholinergic pathways originate. Such a distribution is in keeping with the postsynaptic action of the M1 receptor and the presynaptic cell body (autoinhibition) mediated effects of its M2 counterpart. Unfortunately the ligands available for labelling 126 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION are not sufficiently specific to use this technique to reliably distinguish M1 from M3 and M5 receptors or M2 from M4. In situ hybridisation studies of receptor mRNA, which detects cell body receptors, is more sensitive and confirms the M1 dominance in the neocortex, hippocampus and striatum with M2 again in subcortical areas. Receptor mRNA for the M3 is, like that for M1, in the cortex and hippocampus but not in the striatum while that for M4 is highest in the striatum and low in the cortex. Elucidation of the precise functional significance of such a distribution awaits the arrival of much more specific ligands for the receptor subsets. In their absence a more detailed analysis of the distribution of muscarinic and nicotinic receptors is not justified here but see Hersch et al. Nicotinic receptors have been found and studied predominantly in the hippocampus, cerebral cortex and viatral tegmented area (VTA). FUNCTION Activation of nicotinic receptors causes the rapid openingof Na‡ channels and membrane depolarisation. This is a feature of cholinergic transmission at peripheral neuromuscular junctions and autonomic ganglia but while it is found in the CNS, it is not widely observed. Exogenously applied nicotinic agonists have been shown to directly excite neurons through somato-dendritic receptors in various brain regions while the excitatory response of GABA interneurons in the hippocampus and dopamine neurons in the VTA followingsome afferent stimulation is reduced by nicotinic antagonists (see Jones, Sudweeks and Yakel 1999). Nicotinic receptors also mediate the fast response of ACh released at the endings of collaterals from motoneuron axons to adjacent inhibitory interneurons (Renshaw cells) in the ventral horn of the spinal cord (see below). More recently much interest has been directed towards presynaptic nicotinic receptors that have been shown to enhance the release of a number of NTs, i. ACh, DA, NA, glutamate and GABA, in perfused synaptosomes or slices from various brain regions, as well as DA into microdialysates of the striatum in vivo.

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Therefore buy generic precose 25 mg line, at the time of fertilization purchase 25 mg precose fast delivery, chromosomal programming 50 mg precose sale, the inner medullary tissue will become the sex or genetic sex is determined order precose 25mg mastercard. Sexual differentiation is testicular components buy precose 50mg with mastercard, and the outer cortical tissue will de- controlled by gonadal hormones that act at critical times velop into an ovary. In an XY fetus, the testes differ- culinization, whereas feminization does not require (fe- entiate first. Between weeks 6 and 8 of gestation, the cortex male) hormonal intervention. The process of sexual devel- regresses, the medulla enlarges, and the seminiferous opment is incomplete at birth; the secondary sex tubules become distinguishable. Sertoli cells line the base- characteristics and a functional reproductive system are not ment membrane of the tubules, and Leydig cells undergo fully developed until puberty. Development of the ovary begins at Human somatic cells have 44 autosomes and 2 sex chro- weeks 9 to 10. The female is homogametic (having two X chro- surrounded by a single layer of granulosa cells, are dis- mosomes) and produces similar X-bearing ova. The male is cernible in the cortex between weeks 11 and 12 and reach heterogametic (having one X and one Y chromosome) and maximal development by weeks 20 to 25. The X chromosome is large, containing 80 to 90 genes responsi- Differentiation of the Genital Ducts Is ble for many vital functions. The Y chromosome is much Determined by Hormones smaller, carrying only few genes responsible for testicular development and normal spermatogenesis. Gene mutation During the indifferent stage, the primordial genital ducts of genes on an X chromosome results in the transmission of are the paired mesonephric (wolffian) ducts and the paired X-linked traits, such as hemophilia and color-blindness, to paramesonephric (müllerian) ducts. In the normal male fe- male offspring, which, unlike females, cannot compensate tus, the wolffian ducts give rise to the epididymis, vas def- with an unaffected allele. In the normal female fe- male has an advantage over the male, who has only one. The domly inactivates either the paternally or the maternally mesonephros is the embryonic kidney. Leydig cells, either autonomously or under regu- nized cytologically as the sex chromatin or Barr body. Sertoli cells males, with more than one X chromosome, or in females, produce two nonsteroidal compounds. One is the antimül- with more than two extra X chromosomes are inactivated lerian hormone (AMH), also known as müllerian inhibit- and only one remains functional. This does not apply to the ing substance, a large glycoprotein with a sequence ho- germ cells. The single active X chromosome of the sper- mologous to inhibin and transforming growth factor , matogonium becomes inactivated during meiosis, and a which inhibits cell division of the müllerian ducts. The sec- functional X chromosome is not necessary for the forma- ond is androgen-binding protein (ABP), which binds tion of fertile sperm. Peak production of these compounds occurs its second X chromosome, and both are functional in between weeks 9 and 12, coinciding with the time of dif- oocytes and important for normal oocyte development. Testicular differentiation requires a Y chromosome and The ovary, which differentiates later, does not produce occurs even in the presence of two or more X chromo- hormones and has a passive role. Gonadal sex determination is regulated by a testis- The primordial external genitalia include the genital tu- determining gene designated SRY (sex-determining region, bercle, genital swellings, urethral folds, and urogenital si- Y chromosome). Differentiation of the external genitalia also occurs mosome, SRY encodes a DNA-binding protein, which between weeks 8 and 12 and is determined by the presence binds to the target DNA in a sequence-specific manner. Differentiation along The presence or absence of SRY in the genome determines the male line requires active 5 -reductase, the enzyme whether male or female gonadal differentiation takes place. Without DHT, re- Thus, in normal XX (female) fetuses, which lack a Y chro- gardless of the genetic, gonadal, or hormonal sex, the ex- mosome, ovaries, rather than testes, develop. The Whether possessing the XX or the XY karyotype, every structures that develop from the primordial structures are embryo goes initially through an ambisexual stage and has illustrated in Figure 39. A 4- to 6-week-old human embryo possesses in- gen-dependent differentiation occurs only during fetal life different gonads, and undifferentiated pituitary, hypothal- and is thereafter irreversible.

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