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STUDENT DIGITAL NEWSLETTER ALAGAPPA INSTITUTIONS |
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Britt C. Smyth, BA, RDMS, RDCS, RVT
A review of the central nervous system pathways activated by leptin and controlling feeding diabetes type 2 uk diet cheap 15mg actos mastercard. A comprehensive series of reviews on the central components of the autonomic nervous system metabolic disease kidney stones 15mg actos. A review of the central nervous system pathways controlling blood pressure and their involvement in neurologic disorders diabetes blindness prevention cheap 45mg actos mastercard. It is axiomatic that patients typically have motor signs before motor symptoms and diabetes mellitus classification buy 45mg actos free shipping, conversely, sensory symptoms before sensory signs. Somewhat paradoxically, patients who complain of "weakness" often do not have confirmatory findings on examination that document the presence of weakness. Weakness, when actually a symptom of neurologic disease, is frequently caused by diseases of the motor unit (see Chapters 468, 497, 505, and 511) and is usually reported by a patient in terms of a loss of specific functions. Symptoms may also reflect the consequences of weakness such as frequent falls or tripping. A patient with leg muscle weakness who is falling even as infrequently as once a month almost invariably has severe weakness of knee extensor muscles and can be shown on examination to have a knee extension lag: the inability to fully lift the leg against gravity and to lock the knee. The symptom of "weakness" without findings of weakness on examination is not usually the result of neuromuscular disease but can be a sign of neurologic disease outside the motor unit or more commonly a symptom of disease outside the nervous system altogether (Table 452-1). The complaints of "fatigue," "tiredness," and "lack of energy" are even less likely than the symptom of "weakness" to reflect definable neurologic disease. With the exception of neuromuscular junction disorders such as myasthenia gravis, fatigue is rarely a complaint of diseases of the motor unit. Fatigue can be a sign of upper motor neuron disease (corticospinal pathways) and is a common complaint of established multiple sclerosis and other multifocal central nervous system disease. Finally, as one would expect, disorders that impair sleep may include fatigue as a complaint. Depression and other psychiatric and behavioral disorders, as well as the medical illnesses associated with a complaint of weakness, are all frequent causes of fatigue. The chronic fatigue syndrome, as well as many cases of fibromyalgia (see Chapter 306), have fatigue as a dominant, disabling symptom. These disorders are defined in part by the absence of consistent neurologic findings and the absence of demonstrable pathology in the nervous system. In general, movements that occur in an entire limb or in more than one muscle group concurrently are caused by central nervous system disease. Those confined to a single muscle are likely to be a reflection of disease of the motor unit (including the motor neurons of the brain stem and spinal cord). When spontaneous movements of a muscle are associated with severe pain, patients often use the term "cramp. Leg cramps are frequent in normal persons and particularly common in older patients. They are occasionally a sign of an underlying disease of the anterior horn cell, nerve roots, or peripheral nerve but are usually benign. When severe, cramps can produce such intense muscle contraction that muscle injury is produced and muscle enzymes. The rare muscle diseases in which an enzyme deficiency interferes with substrate utilization as fuel for exercise. These contractures are electrically silent by electromyography, in contrast to the intense motor unit activity seen with cramps. They must not be confused with the limitation of joint range of motion resulting from long-standing joint disease or long-standing weakness-also termed contractures. Usually a reflection of hypocalcemia, tetany can occasionally be seen without demonstrable electrolyte disturbance. Similarly, in the syndrome of tetanus produced by a clostridial toxin, intensely painful, life-threatening muscle contractions arise from hyperexcitable peripheral nerves. A number of toxic disorders such as strychnine poisoning and black widow spider toxin produce similar neurogenic spasms. Acute muscle pain in the absence of abnormal muscle contractions is an extremely common symptom. When such pain occurs following strenuous exercise or in the context of an acute viral illness. It is uncommon for this frequent and essentially normal sign of muscle injury to be associated with weakness or demonstrable ongoing muscle pathology. Chronic muscle pain is a common symptom but is seldom related to a definable disease of muscle (see Chapter 306). The complaint of attacks of severe weakness or paralysis occurring in a patient with baseline normal strength is an uncommon symptom. Episodic weakness is also seen in patients with neuromuscular junction disorders such as myasthenia gravis and the myasthenic syndrome. Occasionally, patients with narcolepsy complain of intermittent paralysis as a reflection of sleep paralysis (see Chapter 448). When associated with the complaints of dizziness or vertigo, disease of the labyrinth, the vestibular nerve, the brain stem, or the cerebellum is a probable cause. When unsteadiness and loss of balance are unassociated with dizziness, particularly when the unsteadiness appears to be out of proportion to other symptoms of the patient, a widespread disorder of sensation or motor function is likely. The ability to stand and to walk in a well-coordinated, effortless fashion requires the integrity of the entire nervous system. Relatively subtle deficits localized to one part of the central or peripheral nervous system will produce characteristic abnormalities. Disorders of the special senses are considered elsewhere in the text and are not considered further here. Pain and temperature appreciation and aspects of tactile sensation are subserved by one system. The sensory receptors consist of naked nerve endings, from which impulses are conducted by either unmyelinated C fibers (1-2 mum) at a velocity of 0. The cell bodies of these axons are in the dorsal root ganglia, and impulses pass along the central processes of these neurons to the spinal cord, where they synapse in the dorsal horn. Axons of the second-order sensory fibers cross to the contralateral anterior or anterolateral part of the contralateral spinal cord and ascend to the ventral posterolateral nucleus of the thalamus, from which third-order neurons project to the sensorimotor cortex. A second sensory system subserves crude and light touch, position sense, and tactile localization or discrimination. The involved sensory receptors are cutaneous mechanoreceptors and receptors in joints, tendons, and muscles (muscle spindles). The afferent pathways consist of large myelinated fibers that pass to the spinal cord via the dorsal root ganglia and ascend in the ipsilateral posterior and, to a lesser extent, the posterolateral columns of the cord to reach the posterior column nuclei (gracile and cuneate nuclei) in the medulla oblongata, where they synapse with second-order neurons. The fibers from these neurons cross and then ascend in the medial lemniscus to synapse in the contralateral ventral posterolateral nucleus of the thalamus, from which third-order neurons project to the cortex. Negative symptoms are ones in which there is a loss of sensation, such as a feeling of numbness. Positive symptoms, by contrast, consist of sensory phenomena that occur without normal stimulation of receptors and include paresthesias and dysesthesias. Paresthesias may include a feeling of tingling, crawling, itching, compression, tightness, cold, or heat, and are sometimes associated with a feeling of heaviness. The term dysesthesias is used correctly to refer to abnormal sensations, often tingling, painful or uncomfortable, that occur after innocuous stimuli, while allodynia refers to the perception as painful of a stimulus that is not normally painful. Paresthesias and dysesthesias may be difficult to distinguish from pain by some patients. Hypesthesia and hypalgesia denote a loss or impairment of touch or pain sensibility, respectively, and hyperesthesia and hyperalgesia indicate a lowered threshold to tactile or painful stimuli, respectively, so that there is increased sensitivity to such stimuli. With the use of a wisp of cotton, a pin, and a tuning fork, the trunk and extremities are examined for regions of abnormal or absent sensation. Certain instruments are available for quantifying sensory function, such as the computer-assisted sensory examination, which is based on the detection of touch, pressure, vibratory, and thermal sensation thresholds. Alterations in pain and tactile sensibility can generally be detected by clinical examination. It is important to localize the distribution of any such sensory loss in order to distinguish between nerve, root, and central dysfunction.
Diseases
In sum diabetes insipidus nutrition buy actos 30 mg on line, virtually all new fevers in the neutropenic population warrant careful clinical and microbiologic evaluation blood glucose a1c discount 30 mg actos visa, followed by prompt initiation of empirical antibiotic therapy signs diabetes guinea pigs cheap 30 mg actos with mastercard. Conversely blood sugar over 500 best actos 30mg, any clinically evident site of potential infection mandates expeditious broad-spectrum therapy, even in the absence of fever. Because the goal of empirical antibiotic therapy is to protect against the early morbidity and mortality that result from untreated bacterial infections, regimens have been formulated to maximize activity against commonly encountered organisms that are particularly virulent. However, empirical regimens cannot realistically be designed to cover every potential bacterial pathogen. Moreover, no regimen is capable of completely eliminating the risk of subsequent infections in persistently neutropenic patients. Management of Indwelling Intravenous Catheters Although gram-positive bacteria (especially staphylococci) are the most frequent causes of catheter-related infections, other bacterial and non-bacterial species can be encountered, particularly in a neutropenic patient. These species include resistant Corynebacterium, Bacillus species, gram-negative organisms, and fungi. In evaluating a patient with catheter-related infection, it is important to consider the specific type of infection, its location. In general, the vast majority of simple catheter-related bacteremias and exit site infections can be cleared by using appropriate antibiotics and do not require catheter removal. If multilumen devices are used, the antibiotic infusion should be rotated among the ports because infection may be limited to one lumen (failure to do so can be a cause of persistent infection despite antibiotics). If bacteremia persists after 48 hours of appropriate therapy, the catheter should be removed. Failure of therapy is more common when the infections are due to certain organisms such as Bacillus species or C. Infections extending to involve the tunnel of a Hickman catheter also mandate prompt removal of the device because antibiotics alone rarely cure this "closed-space" infection, particularly in a granulocytopenic host. Likewise, infections around the reservoir of an implantable subcutaneous device may be difficult to eradicate without catheter removal. Patients with recurrent catheter infections (despite a history of appropriate therapy) are also candidates for prompt catheter removal. It is unresolved whether a non-neutropenic patient with an indwelling catheter who becomes newly febrile should receive antibiotics empirically. The safest policy is to begin antibiotics (using a 1576 3rd-generation cephalosporin such as ceftriaxone or an aminoglycoside plus vancomycin) and continue them pending culture results and clinical response. This approach protects against rapid progression of undetected yet virulent infections (such as S. If by 72 hours the cultures are negative and the patient is stable, antibiotic therapy can be discontinued. Initial Management of the Neutropenic Patient Who Becomes Febrile Although gram-negative bacteria still predominate at some institutions, in recent years the trend has been toward more gram-positive infections, which now represent the majority of isolates at many centers. In general, gram-negative infections tend to be more virulent, and early empirical regimens have been formulated to provide protection primarily against these organisms while maintaining a broad spectrum of activity against other potential pathogens. Indeed, adequate coverage of these gram-negative organisms is still an essential property of any empirical regimen. Although no single best regimen or recipe is known, a number of options are appropriate. Selection of a specific antibiotic regimen depends on many factors, including institutional sensitivity patterns, individual and institutional experience, and clinical parameters. The standard approach to the empirical management of a febrile neutropenic patient has been to use combination antibiotic regimens. Until recently, combination regimens have been the only way to provide coverage broad enough to encompass the predominant gram-positive and gram-negative organisms. Moreover, some combinations have been thought to provide synergy and to have the potential for decreasing the emergence of resistant isolates. Aminoglycoside-beta-lactam combinations were the first empirical regimens with acceptable efficacy in the setting of fever and neutropenia. Such combination regimens are still widely used and represent a standard against which newer regimens are tested. Many variations have been studied and include aminoglycosides combined with either an extended-spectrum penicillin or a cephalosporin or as a component of a triple-drug regimen. If an aminoglycoside-containing combination regimen is to be used, the choice of specific antibiotics should be based primarily on the institutional antibiotic sensitivity patterns and secondarily on toxicity and cost differences. These regimens have consisted of combinations of two beta-lactam antibiotics, or so-called double beta-lactam regimens, usually consisting of an expanded-spectrum carboxypenicillin or ureidopenicillin plus a 3rd-generation cephalosporin. New or Novel Antibiotics for Neutropenic Patients the advent of beta-lactam antibiotics with broad-spectrum activity that achieve high serum bactericidal levels has made monotherapy another option for the initial empirical treatment of a febrile neutropenic patient (Table 314-3) (Table Not Available). The 3rd-generation and "4th-generation" cephalosporins and the carbapenems are the two classes that include potential candidates for empirical single-agent therapy. Ceftazidime has been the most extensively studied of the 3rd-generation cephalosporins as monotherapy because of its superior activity against P. In this study, patients with fever and granulocytopenia underwent a standard initial evaluation and were then randomized to receive either a combination of antibiotics (cephalothin, gentamicin, and carbenicillin) or ceftazidime as a single agent. The overall results show that monotherapy compared favorably with a standard combination regimen. Approximately two thirds of the episodes in both groups were treated successfully for the entire duration of their granulocytopenia without requiring any changes in their initial regimen. The other third of the episodes required some change or modification (such as the addition of an antibacterial, antifungal, or antiviral drug) to ensure a successful outcome (see indications for modifications below), and an equally low number in both groups (about 5%) died of infection. None of the deaths were attributable to a specific deficiency in one regimen that was not present in the other. The need for modification in these subgroups was identical for episodes treated with monotherapy and those treated with combination therapy. In this study, these modifications did not represent a failure of either regimen per se but instead were reflective of the limitations of any regimen in treating patients who are at high risk for subsequent infections. An international cooperative study that enrolled 676 patients (83% with acute leukemia) with 876 episodes of fever and neutropenia in a recently reported randomized trial comparing ceftazidime monotherapy with the combination of piperacillin and tobramycin demonstrated comparable efficacy with both regimens but less toxicity with ceftazidime monotherapy. Concerns regarding the use of ceftazidime as a single agent for fever and neutropenia include the lack of synergy against documented 1577 gram-negative infections, lack of activity against certain gram-positive isolates, poor antianaerobic activity, and the potential for development of resistance. Cefepime, a "third-generation" cephalosporin, overcomes some of these limitations. In addition to the 3rd-generation cephalosporins, other antibiotics have been evaluated in neutropenic patients. It is formulated in fixed combination with cilastatin, which inhibits a renal enzyme that can degrade imipenem. Of note is its excellent in vitro activity against enterococci and many anaerobes. Interestingly, neither of these studies demonstrate superior efficacy for imipenem. Two potential drawbacks to its use include a relatively high incidence of the development of resistant P. Because of the increasing incidence of gram-positive infections in cancer patients during the 1980s and their increased resistance to beta-lactam antibiotics, some authorities initially recommended that vancomycin be added to empirical regimens. Rather, its use should be guided by institutional microflora and sensitivity patterns. In addition, fluctuations in patterns of infecting microorganisms may occur over time. Furthermore, penicillin-resistant alpha-hemolytic streptococci have recently been identified as particularly virulent pathogens in some centers (perhaps related to the use of high-dose cytosine arabinoside). Clearly, the emergence of new pathogens or pathogens with altered sensitivity profiles may force dramatic changes in how we use antibiotics in the future. The appropriate role for quinolones in a neutropenic patient has yet to be fully defined. Because of their relatively poor activity against certain gram-positive organisms, they should not be used for empirical therapy alone. They may be useful to complete therapy in patients who initially respond to intravenous antibiotics and who have had either an unexplained fever or a susceptible bacterial isolate. A particularly useful feature of the monobactam aztreonam is its apparent lack of cross-reactivity with the other beta-lactams in patients who have penicillin or beta-lactam allergies.
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The rate of progression and the extent to which pelvic girdle and forearm muscles are eventually affected vary considerably between and within different families diabetes mellitus insulin dependent trusted actos 45mg. Some patients experience a late exacerbation of weakness after years of little or slow progression diabetes foundation order actos 15 mg visa. There is no muscle hypertrophy diabetes medicine 30mg actos overnight delivery, although a "trapezius hump" due to an upward movement of the unstable scapula may be mistaken for muscle hypertrophy yahoo diabetic diet soda purchase 45mg actos otc. In addition, the marked biceps/triceps atrophy with relative preservation of the forearm muscles can produce the so-called Popeye arms. The muscle biopsy shows moderate myopathic changes compared to those of other dystrophies. Occasionally a prominent mononuclear inflammatory infiltrate can be present, causing some confusion with polymyositis. Facioscapulohumeral dystrophy has been linked to the telomeric region of chromosome 4q35. Although the gene has not been isolated, a deletion in this region is present in virtually all facioscapulohumeral dystrophy patients. Scapuloperoneal muscular dystrophy is an autosomal dominant disorder that can resemble facioscapulohumeral dystrophy, but without facial weakness. Myotonic dystrophy is an autosomal dominant multisystem disorder that affects skeletal, cardiac, and smooth muscle and other organs, including the eyes, the endocrine system, and the brain. Myotonic dystrophy can occur at any age with the usual onset of symptoms in the late second or third decade. Typical patients exhibit facial weakness with temporalis muscle wasting, frontal balding, ptosis, and neck flexor weakness. Extremity weakness usually begins distally and progresses slowly to affect the limb-girdle muscles proximally. Weakness is a more common symptom than muscle stiffness or myotonia, although patients may complain of the inability to relax the fingers after a hand grip. However, percussion myotonia can be produced on examination in most cases, especially in thenar and wrist extensor muscles. Associated manifestations include posterior subscapular cataracts, testicular atrophy and impotence, intellectual impairment, and hypersomnia due to both central and obstructive sleep apneas. Elevated serum glucose levels occurs as a result of end-organ unresponsiveness to insulin, but frank diabetes mellitus rarely develops. Involvement of the smooth muscle in the gastrointestinal tract can produce dysphagia, reduced gut motility, and chronic pseudo-obstruction. Muscle biopsies show excessive number of central nuclei, type 1 atrophy, and other non-specific myopathic changes. How the gene defect and the abnormal expression of myotonin cause tissue injury and myotonia is not known. Clinical features of this large autosomal family were indistinguishable from those of the 19q-linked disorder. Myotonic dystrophy patients rarely have myotonia that is so symptomatic that it requires treatment. Phenytoin is the safest drug for myotonia, as quinine, tocainide, and mexiletene can exacerbate cardiac arrhythmias and should be avoided. Sedatives and opiates should be used with caution as they can exacerbate ventilatory drive abnormalities. Myotonic dystrophy patients are at risk for pulmonary and cardiac complications during general anesthesia. However, proximal extremity weakness is significant, distal muscles are often normal, and patients usually complain of myotonia and myalagias. Although a number of myopathies can have prominent distal weakness (see Table 505-3) some genetically distinct entities are considered as distal muscular dystrophies. Welander distal dystrophy occurs in Scandinavia and presents between the fourth and sixth decades with selective weakness and atrophy of the forearm extensor and intrinsic hand muscles and then involves the anterior leg and small foot muscles. In patients homozygous for the dominant gene, the onset is earlier and proximal muscles are also affected. Markesbery/Udd distal dystrophy has been observed in English and Finnish patients and initially involves the anterior tibial muscles and later the distal upper extremities. Two varieties of autosomal recessive distal muscular dystrophies with early-adult onset in the late second or early third decade have been described. An autosomal dominant childhood and early-adult-onset distal myopathy has been described by Laing. Muscle biopsy result shows variable degrees of dystrophic changes, and rimmed vacuoles are common in all but Miyoshi myopathy. All of these disorders have progressive courses and over time can involve proximal muscles with the loss of ambulation. Miyoshi myopathy and limb-girdle muscular dystrophy 2B are both associated with a 2p13 mutation in the dysferlin gene. Myofibrillar myopathy (also known as desmin myopathy) is a heterogeneous group of muscular dystrophies that can present with either distal or limb-girdle patterns of weakness. The muscle biopsy findings show vacuoles, cytoplasmic inclusions, and accumulations of desmin and other proteins such as dystrophin and beta-amyloid precursor protein. Myofibrillar myopathy is probably not a single disorder, as some kindreds have a molecular defect in the alphabeta-crystallin chaperone protein on 11q21-23; others have a mutation in the desmin gene on 2q35; and one family has linkage to chromosome 12. The disease oculopharyngeal muscular dystrophy, inherited as an autosomal dominant disorder, presents in the fifth or sixth decade with progressive ptosis followed by dysphagia. Extremity weakness is usually in a limb-girdle pattern, but some variants have significant distal involvement. Death can result from aspiration pneumonia or starvation if adequate nutrition is not addressed. Patients may require surgical correction (cricopharyngeal myotomy) for achalasia or a gastric feeding tube. Muscle biopsy discloses non-specific myopathic changes with rimmed vacuoles in the muscle fibers, and the electron microscopy reveals 8. Oculopharyngeal dystrophy appears to be more common in patients of French-Canadian or Hispanic ancestry. A concise and comprehensive account of what is currently known about the dystrophin gene and dystrophin. Provides data on the frequency of the various sarcoglycan deficiencies in patients with myopathy. Nagano A, Koga R, Ogawa M: Emerin deficiency at the nuclear membrane in patients with Emery-Dreifuss muscular dystrophy. Barohn Congenital myopathies are distinguished from dystrophies in three respects. First, these disorders have characteristic morphologic alterations demonstrated on light and electron microscopy. Second, as the name implies, congenital myopathies usually present at birth with hypotonia and subsequent delayed motor development. Finally, most congenital myopathies are relatively non-progressive with more benign outcomes than occur in the muscular dystrophies. Onset can occur in childhood and even in early adulthood, and some congenital myopathies have a severe course and fatal outcome. Moreover, as the molecular genetic defects of the congenital myopathies become known, distinguishing between these disorders and muscular dystrophies becomes more difficult. The four best recognized congenital myopathies are discussed later, and others are listed in Table 507-1. Common clinical findings in these conditions include reduced muscle bulk (no hypertrophy); slender body build and a long, narrow face, with skeletal abnormalities (high-arched palate, pectus excavatum, kyphoscoliosis, dislocated hips, pes cavus); and absent or reduced muscle stretch reflexes. Most patients have a limb-girdle weakness phenotype, although distal weakness can occur in some families (see Table 505-3). Central core myopathy is characterized by discrete zones (cores) of myofibrillar disruption in the center of muscle fibers. This is demonstrated on the oxidative enzyme stain, which reveals an absence of enzyme within the cores. Electron microscopy confirms the presence of cores along the length of muscle fibers.
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