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Public Interest Law Initiative

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By I. Vigo. Cumberland College. 2018.

MICRA provides for a sliding scale: a plaintiff attorney keeps 40% of the first $50 buy generic valtrex 1000mg on line antiviral krem,000 of an award but “only” 21% (plus expenses) of a $1 million judgment buy 1000 mg valtrex mastercard hiv infection rates russia. This rules protects patients, allowing more of an award to actually reach the injured patient. A patient with a $1 million award in a state with a contingency fee of 40% must give $400,000 (plus expenses) to his or her attorney as compared to $221,000 (plus expenses) under MICRA. These reforms have reduced California malpractice premiums by 40% in constant dollars since 1975, or less than 3% per year uncorrected for inflation (16). On average, California’s malpractice premiums have risen at a rate of only one-third the national average (Fig. There are considerable data that a $250,000 cap on noneconomic damages reduces malpractice premiums by 25 to 30% (2,28,36), and experience in California, Colorado, and other states is confirmatory. The mirror image of the positive effect of real reform can be seen in the experience of states that had caps on noneconomic damages that were invalidated by their state supreme courts. Ohio enacted MICRA- like reforms in 1975, but the Ohio Supreme Court nullified these in 1985. Malpractice insurance rates fell steadily until 1982, when the law was challenged in the courts. Since 1985, Ohio malpractice premiums have once again increased significantly and the state is dealing with a Chapter 15 / The Case for Legal Reform 215 Fig. In 2003, Ohio approved a new set of reforms in an effort to ameliorate the growing problem. By 2000, malpractice indem- nities in the state had increased 400% compared to 1998 (38). Alabama, Georgia, Illinois, Kansas, New Hampshire, North Dakota, and Washington have also had tort reforms nullified by their state supreme courts (4). Today, Georgia, Illinois, Oregon, and Washington are among the 19 states facing a professional liability crisis (4). New York did so in 1975, 1981, and 1986 with no observable improve- ment in the malpractice insurance situation (33). Florida and Texas have repeated similar experiences (24), and in 2003 both state legis- latures attempted to remedy the deteriorating medical-legal climate in their state with new reforms that do include caps on noneconomic damages. A work group of the American Academy of Actuaries concluded that to be effective, a package of medical malpractice reforms must include a $250,000 per injury limit on noneconomic damages and a collateral source offset (33). They found that reforms worked best when imple- mented together as a comprehensive program. Most significantly, they confirmed that porous caps with built-in exceptions or multipliers and peripheral reforms that do not include the fundamental elements of MICRA are predictably ineffective. States with $250,000 or $350,000 limits on noneconomic damages had average premium increases only one-third as large as those in states without caps between 2000 and 2001 (2,39). California’s experience over the preceding quarter century stands as firm testimony to these data. In 2002, the nonpartisan Congressional Budget Office estimated that the MICRA-based reforms contained in House Resolution 4600 (which failed to pass the Senate) would have lowered malpractice insurance premiums by 25 to 30% (40). Milliman USA analyzed medical malpractice claims in the 15 largest states from 1990 to 2001 and concluded that caps on noneconomic damages reduced medical malpractice loss costs for physicians (41). In this study, reform states like California and Colorado saw loss costs reduced 48 and 31%, respectively. In contrast, New York’s loss cost per physician stood at 300% compared to California, and Pennsylvania’s stood at 328%. In an earlier study, Milliman had estimated that a $250,000 cap on noneconomic damages in New York would reduce premium levels by 29% (32). Perhaps the most comprehensive study of this issue ever undertaken was that delivered by the Governor’s Select Task Force on Healthcare Professional Liability Insurance in Florida in 2002 (22). Testimony ran to 13 volumes and included physicians, lawyers, insurance industry representatives, regulators, legal scholars, professional organizations, and concerned citizens. The final report exceeds 300 pages and contains more than 1300 citations. The report takes note of Florida’s past history of unsuccessful reform and concludes that: “A cap on non-economic damages of $250,000 per incident limited only to healthcare professional liability cases is the only available remedy that can produce a necessary level of predictability... The authors noted that Florida’s unsuccessful previous attempts at reforms that did not include such a cap “are nothing more than a failed litany of alternatives” (22). Chapter 15 / The Case for Legal Reform 217 The National Association of Insurance Commissioners (NAIC) stud- ied the market for medical malpractice insurance to evaluate the current crisis in 2003 (28).

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Thus while it is difficult to characterise the precise receptor subunit involved this provides strong evidence for a neurotransmitter OTHER TRANSMITTERS AND MEDIATORS 267 268 NEUROTRANSMITTERS buy valtrex 1000 mg hiv infection rates in kenya, DRUGS AND BRAIN FUNCTION role for ATP purchase 1000mg valtrex with mastercard antivirus software, although it is not known to what extent blocking P2x2 receptors modifies synaptic transmission when the amino acid receptors are functional. Thus in contrast to NMDA currents, those for ATP are less likely to be involved in the temporal integration of synaptic activity (Gibb and Halliday 1996). This above effect of ATP has also been demonstrated on neurons in lamina II of the dorsal horn in transverse slices of rat cord. Here blockade of glutamate GABA and glycine effects left a current, produced by local tissue or dorsal root stimulation which was again sensitive to the P2x2 antagonist suramin (Bardoni et al. Although only 5% of neurons showed this response, the expression of P2x receptors there and the long established release of ATP from the peripheral terminals of dorsal root ganglia neurons and presumably therefore the central ones, have obviously raised interest in ATP being yet another NT involved in the mediation of afferent painful nociceptive stimuli (Chapter 21). Thus the neurotransmitter role of ATP is well established in the periphary and also in sensory systems but its importance in the CNS remains to be elucidated (see Burnstock 1996). That requires the development of more specific antagonists and methods of mapping its location. The strong linkage of its P2x receptors to calcium currents may also provide a role for ATP in more long-term effects such as plasticity and neuronal development and death. ADENOSINE This is not considered to be a neurotransmitter but it may be an important modulator of neuronal activity through its various receptors, A1,A2 and A3. The normal evoked EPSC of about 160 pA obtained by focal stimulation of nearby tissue was dramatically reduced by addition of a cocktail (CABS) of CNQX 10 mM, D-APV 50 mM, bicuculline 10 mM and strychnine 5 mM to block glutamate, GABAA and glycine receptors. The small residual EPSC shown was blocked by the ATP P2 receptor antagonist suramin and is therefore probably mediated by released ATP. The A receptor appears to be 2 1 negatively linked to adenylate cyclase through Gi and may mediate the presynaptic inhibition of NT release, with the A2 acting positively through Gs. Its basal extracellular level is 2 mM but this can increase rapidly when neuronal firing increases and can rise some twentyfold during seizures. The two enzymes responsible for its breakdown are adenosine kinase (Km ˆ 2 mM) and adenosine deaminase (Km ˆ 50 mM). It will be clear that as more adenosine is released during seizures, it will quickly saturate the kinase and its concentration can therefore only be controlled by deaminase. In fact deaminase but not kinase inhibitors are anticonvulsant as is adenosine and its analogues, while its antagonist theophylline is proconvulsant and a central stimulant. While that may not be realistic, the antiepileptic benzodiazepine drugs, in addition to their effects on GABA receptors, have been shown to increase the efflux of [73H] adenosine from the rat cortex probably by blocking its uptake and adenosine is often considered to be an endogenous limiter of neuronal activity. Despite this it has also been shown to reduce fast inhibitory postsynaptic potentials (IPSPs) in the rat lateral amygdala probably by presynaptic A1 inhibitory effect on GABA release (Henbockel and Pap 1999). Adenosine has also been considered to play a role in sleep induction (Chapter 22). Recently much interest has been shown in the possible neuroproctive effects of adenosine but the responses are complex. Thus A3 agonists can offer some protection given chronically before ischaemic challenge but given acutely post-challenge they can be neurotoxic (see Jacobsen 1998). HISTAMINE The belief that histamine (HT) has a central effect stems from the knowledge that all the classical antihistamines (H1 receptor antagonists) used to treat allergic reaction, such as hay fever, caused marked sedation if, like mepyramine and promethazine, they can cross the blood±brain barrier, but fail to do so if, like terfenedine and cetirizine, they do not. The major problem in establishing histamine as a transmitter in the CNS has been the difficulty in demonstrating its actual presence in neurons rather than just in the invading mast cells, in which it is concentrated and from which it is released in the periphery during allergic reactions. The development of immunohistochemical methods for the visualisation of histamine, and its synthesising enzyme histidine decarboxylase, now show there to be definite histaminergic nerves (see Tohyama et al. These are concentrated in the tuberomammillary nucleus in the posterior hypothalamus, not only in the rat but also in humans, and like the other monoaminergic systems (NA and 5- HT) they give off long highly branched axons which ascend in the medial forebrain bundle projecting to the cerebral cortex and hippocampus. Most histamine neurons also contain other transmitters such as GABA, substance P or enkaphalin. The whole brain concentration of histamine is relatively low (50±70 ng/g) but there is much evidence for its central action (see Schwartz et al. Histidine is a poor substrate for the L-amino- acid decarboxylase responsible for DA and NA synthesis. The synthesis of histamine in the brain can be increased by the administration of histidine, so its decarboxylase is presumably not saturated normally, but it can be inhibited by a fluoromethylhistidine. No high-affinity neuronal uptake has been demonstrated for histamine although after initial metabolism by histamine N-methyl transferase to 3-methylhistamine, it is deaminated by intraneuronal MAOB to 3-methylimidazole acetic acid (Fig. A Ca2‡-dependent KCl-induced release of histamine has been demonstrated by micro- dialysis in the rat hypothalamus (Russell et al.

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Mutations in CYP21A2 generic 500mg valtrex with amex hiv infection through urethra, which encodes 21-hydroxylase generic valtrex 1000 mg on-line antiviral wipes, ac- of Graves’ disease? The antibody titers indicate that the patient has Graves’ dis- associated with excess androgen production. CYP11B1, which encodes 11 -hydroxylase, would also re- Answers to Case Study Questions for Chapter 33 sult in excess adrenal androgen production. Adrenal androgens would be significantly elevated in pa- gest that the patient may be hyperthyroid. However, goiter tients with virilizing forms of congenital adrenal hyperpla- can also occur in hypothyroidism. Adrenal hyperplasia is usually due to defects in cortisol roid disease runs in families, the family history suggests production. Therefore, the serum concentrations of precur- that the thyroiditis might be due to an autoimmune re- sors of cortisol biosythesis such as progesterone, 17 -hy- sponse. The laboratory should determine the blood levels of thyroid In addition, serum ACTH would be elevated as a result of hormones (T4 and T3) and TSH. Thyroid hormones should the lack of negative feedback from the absent cortisol. Genetic defects in the gene for 11 -hydroxylase, resulting in gression of Hashimoto’s disease or decreased if the patient a reduction in the activity of this enzyme, would result in in- has Graves’ disease. The laboratory should measure antibodies to TSH receptor, ylase, which impair the activity of the enzyme, would not thyroid peroxidase, and thyroglobulin. Since 11-deoxy- peroxidase are elevated to the greatest extent in cortisol has significant mineralocorticoid activity, excess Hashimoto’s disease. Antibodies to TSH receptor, thyroid peroxidase, and thy- tension, rather than the volume depletion and hypotension roglobulin can all be elevated in Graves’ disease. Treatment would be directed toward replacement of gluco- 648 PART IX ENDOCRINE PHYSIOLOGY corticoids and mineralocorticoids. Exercise not only helps to control weight, it stimulates glu- place the missing cortisol and also suppress ACTH secre- cose uptake in skeletal muscle, lessening the requirements tion. With less ACTH stimulation of steroid production from for injected insulin. Mineralocorticoids are given to treat the “salt wasting” that CASE STUDY FOR CHAPTER 36 occurs in the absence of aldosterone. Bone Fractures CASE STUDY FOR CHAPTER 35 A 38-year-old Caucasian man recently came to the atten- tion of his physician when he suffered the second of two Type 2 Diabetes bone fractures in the past year and a half. He previously A 65-year-old semi-retired college professor was diag- was in relatively good health, was not a smoker, and used nosed with type 2 diabetes about 4 years ago during a alcohol only moderately. However, his only form of exer- routine physical examination at his family doctor’s of- cise was cutting the lawn on weekends during the sum- fice. He has not required any major surgeries tablet daily of an oral antidiabetic drug of the sulfony- during his lifetime, and had only minor bouts of the typi- lurea class and two daily injections of insulin. However, at age eight he was di- tient’s doctor also recommended modest weight loss agnosed with asthma after he suffered severe respiratory and a regular exercise program. With diligence to the problems during a baseball game on a hot summer day. For The fractures that the patient experienced were to the about one week after the surgery, the patient had to in- left wrist and the right forearm. In both cases, the trauma crease his insulin dosage to maintain normal blood glu- that caused the fracture was relatively minor. He gradually returned to his presurgery in- that there may be an underlying problem, his physician sulin dose. Results of these Because of the surgery, the patient vows to take better studies show that the patient has a considerable reduc- care of himself. He increases his physical activity and be- tion in bone mass compared with other men of the same gins a diet that results in loss of 7 kg in 3 months.

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A coronal T1- weighted (a) and T2- weighted fat-suppress- ed (b) image of the right hip demonstrates the appearance of nor- mal muscle generic valtrex 500mg online hiv infection rate in india. The signal of normal muscle decreases on the T2-weighted image Magnetic Resonance Imaging of Muscle 49 ty infiltration discount valtrex 1000mg fast delivery anti viral ear drops. MR signal alterations are usually seen This middle-aged man pal- pated a mass above his ankle. In A sagittal T1-weighted mag- subacute denervation, the denervated muscle have high netic resonance (MR) image signal intensity on T2-weighted and inversion recovery of the ankle shows an anom- sequences. Typically, the size of the muscle remains nor- alous low-lying soleus mus- mal or is slightly diminished due to concomitant atrophy cle anterior to the Achilles tendon and filling the pre- (Fig. In chronic denervation, the muscle edema re- Achilles fat pad solves, and the involved muscles undergo volume loss fat pad (Fig. Other common accessory muscles include the peroneus quartus muscle, behind the fibula, the accessory abductor digiti minimi, in the wrist, and the anomalous lumbrical muscle, seen in carpal tunnel. Congenital Muscular Disorders There are numerous forms of muscular dystrophy, with Duchenne and Becker muscular dystrophy being the most common. These typically present with progressive proximal muscle weakness in childhood or adoles- cence. The congenital myopathies all involve multiple muscle groups, typically in a symmetrical fashion. In the acute phase of muscle damage, symmetrical mild hyperintensity of the muscles can be seen (Fig. An axial fat-suppressed pro- ton-density (PD)-weighted image of the proximal calf shows a gan- sues remain normal. More advanced disease typically glion adjacent to the proximal tibiofibular joint. Due to compres- shows pseudohypertrophy of lower extremity muscles, sion on the peroneal nerve, denervation changes are apparent in the particularly the calf musculature, due to excessive fat- tibialis anterior muscle Fig. An axial STIR MR image of the thighs shows symmetrical hyperintensity of the quadriceps muscles 50 M. The presence of fatty change implies an Pyomyositis irreversible lesion. Clinical history and the distribution of the muscle abnormalities, which correspond to a specific Deep cellulitis can be associated with septic fasciitis or nerve distribution, allow accurate diagnosis of muscle pyomyositis, an infiltrative deep infection of muscle. Pyomyositis used to be seen most frequently in children and in patients from the tropics. More recently, py- omyositis has been recognized with increasing frequency Atrophy in adult patients with AIDS. Atrophy of muscle is the result or end stage of many mus- The most common causative organism is Staphylococcus cle abnormalities, so it is only a finding, not a diagnosis. Pyomyositis Chronic disuse, denervation, and myopathies are the most is typically limited to one muscle group. Adjacent soft tissue in- flammation may be present, but subcutaneous inflammato- ry changes are minimal compared to those seen in patients Autoimmune Myopathies with cellulitis or fasciitis, and are disproportionately less prominent than the muscular abnormalities. The underlying Polymyositis is the classic autoimmune inflammatory bony cortex and bone marrow are typically not involved. When associated with skin changes, the same On T1-weighted MR, findings are minimal except for syndrome is called dermatomyositis. Numerous other subcutaneous edema and mild enlargement of the affect- forms of autoimmune muscle inflammation are recog- ed muscles due to the increased volume of interstitial flu- id and fluid collections. The autoimmune muscle disorders produce sym- ial in the center of an abscess may show intermediate sig- metrical muscle weakness that primarily involves the nal intensity on T1-weighted images, either diffusely or proximal muscles. High signal intensity is seen within the mus- cle inflammation is the most prominent finding. Adjacent soft-tissue flamed muscles are edematous but the normal muscle ar- inflammation is typically present. Myositis is more often unilateral or asymmetrical in association with collagen vascular disease than it is with idiopathic polymyositis.

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