Massachusetts Agricultural 

Fairs Association

100 years 1920 to 2020


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By: L. Oelk, M.A., M.D.

Co-Director, Stony Brook University School of Medicine

Paraneoplastic disorders can of en be identi ed by the clinical patterns o disease that they produce antibiotic xan cheap ciplox online visa, measurement o speci c autoantibodies quinolone antibiotics for uti buy ciplox 500mg otc, and uncovering the primary cancer; these disorders are of en re ractory to therapy antibiotic for strep throat 500 mg ciplox overnight delivery, but some patients improve ollowing removal o the tumor or immunotherapy (Chap antibiotics e coli ciplox 500mg amex. Ataxia with antigliadin antibodies and gluten-sensitive enteropathy may improve with a gluten- ree diet. Vitamin B1 and B12 levels in serum should be measured, and the vitamins administered to patients having de cient levels. The cerebrospinal uid should be tested or a syphilitic in ection in patients with progressive ataxia and other eatures o tabes dorsalis. Similarly, antibody titers or Lyme disease and Legionella should be measured and appropriate antibiotic therapy should be instituted in antibody-positive patients. Aminoacidopathies, leukodystrophies, urea-cycle abnormalities, and mitochondrial encephalomyopathies may produce ataxia, and some dietary or metabolic therapies are available or these disorders. The deleterious e ects o phenytoin and alcohol on the cerebellum are well known, and these exposures should be avoided in patients with ataxia o any cause. A small preliminary study in a mixed population o patients with di erent inherited ataxias raised the possibility that the glutamate antagonist riluzole may o er modest bene t. Patients with ataxia telangiectasia (A) present in the rst decade o li e with progressive telangiectatic lesions associated with de cits in cerebellar unction and nystagmus. There is a high incidence o recurrent pulmonary in ections and neoplasms o the lymphatic and reticuloendothelial system in patients with A. T ymic hypoplasia with cellular and humoral (IgA and IgG2) immunode ciencies, premature aging, and endocrine disorders such as type 1 diabetes mellitus are described. The most striking neuropathologic changes include loss o Purkinje, granule, and basket cells in the cerebellar cortex as well as o neurons in the deep cerebellar nuclei. There is a loss o anterior horn neurons in the spinal cord and o dorsal root ganglion cells associated with posterior column spinal cord demyelination. Genetic markers are now commercially available to precisely identi y the genetic mutation or correct diagnosis and also or amily planning. Early detection o asymptomatic preclinical disease can reduce or eliminate the inherited orm o ataxia in some amilies on a global, worldwide basis. Ro se n b e rg Ataxias with autosomal dominant, autosomal recessive, X-linked, or mitochondrial orms o inheritance are present on a worldwide basis. Mutation markers are now commercially available to identi y carriers at risk in their amilies, which allows or precise identif cation o the genetic mutation or correct diagnosis and also or amily planning. Identif cation o positive mutation carriers with amily planning has allowed or early detection o asymptomatic preclinical disease to reduce or eliminate the inherited orm o ataxia in specif c amilies on a global, worldwide basis. It is a prime example o a neurodegenerative disease and is arguably the most devastating o the neurodegenerative disorders. In each o these diseases, the a ected motor neurons undergo shrinkage, o en with accumulation o the pigmented lipid (lipo uscin) that normally develops in these cells with advancing age. Focal enlargements are requent in proximal motor axons; ultrastructurally, these "spheroids" are composed o accumulations o neuro laments and other proteins. The death o the peripheral motor neurons in the brainstem and spinal cord leads to denervation and consequent atrophy o the corresponding muscle bers. Histochemical and electrophysiologic evidence indicates that in the early phases o the illness denervated muscle can be reinnervated by sprouting o nearby distal motor nerve terminals, although reinnervation in this disease is considerably less extensive than in most other disorders a ecting motor neurons. As denervation progresses, muscle atrophy is readily recognized in muscle biopsies and on clinical examination. The loss o cortical motor neurons results in thinning o the corticospinal tracts that travel via the internal capsule. The loss o bers in the lateral columns and resulting brillary gliosis impart a particular rmness (lateral sclerosis). By light microscopy, the entire sensory apparatus, the regulatory mechanisms or the control and coordination o movement, remains intact. However, immunostaining indicates that neurons bearing ubiquitin, a marker or degeneration, are also detected in nonmotor systems. Moreover, studies o glucose metabolism in the illness also indicate that there is neuronal dys unction outside o the motor system. T us, motor neurons required or ocular motility remain una ected, as do the parasympathetic neurons in the sacral spinal cord (the nucleus o Onu rowicz, or Onu) that innervate the sphincters o the bowel and bladder. A detailed history o en discloses recent development o cramping with volitional movements, typically in the early hours o the morning. Weakness caused by denervation is associated with progressive wasting and atrophy o muscles and, particularly early in the illness, spontaneous twitching o motor units, or asciculations. When the initial denervation involves bulbar rather than limb muscles, the problem at onset is di culty with chewing, swallowing, and movements o the ace and tongue. Early involvement o the muscles o respiration may lead to death be ore the disease is ar advanced elsewhere. With prominent corticospinal involvement, there is hyperactivity o the muscle-stretch re exes (tendon jerks) and, o en, spastic resistance to passive movements o the af ected limbs. Patients with signi cant re ex hyperactivity complain o muscle stif ness o en out o proportion to weakness. Degeneration o the corticobulbar projections innervating the brainstem results in dysarthria and exaggeration o the motor expressions o emotion. Virtually any muscle group may be the rst to show signs o disease, but, as time passes, more and more muscles become involved until ultimately the disorder takes on a symmetric distribution in all regions.

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If the infant is systemically ill bacterial 2 hybrid purchase ciplox cheap online, do not delay antibiotic therapy to wait for further urine production virus scanner free purchase ciplox online pills. The use of too much suction can draw the bladder mucosa to the needle antibiotic resistance transfer order ciplox 500mg line, obstructing the collection of urine and increasing the risk of injury to the bladder antibiotic uti buy ciplox 500mg with mastercard. Empty bladder as a result of recent void or dehydration A full bladder is essential for success of the procedure and avoidance of complications. Place the tip of a finger in the anus and apply pressure anteriorly in a female infant, or b. The site for needle insertion is 1 to 2 cm above the symphysis pubis in the midline. Clean the suprapubic area (including the area over pubic bone) three times with antiseptic solution. Equipment All equipment must be sterile, except transillumination light or ultrasound equipment. Gauze sponges and cup with iodophor antiseptic solution or 112 Chapter 19 Suprapubic Bladder Aspiration 113. Palpate the symphysis pubis, and insert the needle (with syringe attached) 1 to 2 cm above the pubic symphysis in the midline. Aspirate gently, as the needle is slowly advanced, until urine enters the syringe. B: Midline sagittal section to emphasize the intra-abdominal position of the full bladder in the neonate and its posterior anatomic relations. Use of the portable ultrasound to assist urine collection by suprapubic aspiration. Comparing suprapubic urine aspiration under real time ultrasound guidance with conventional blind aspiration. Does the use of volumetric bladder ultrasound improve the success rate of suprapubic aspiration of urine Pain in infants who are younger than 2 months during suprapubic aspiration and transurethral bladder catheterization: a randomized, controlled trial. Is there bacteremia after suprapubic aspiration in children with urinary tract infection Apply gentle pressure over the puncture site with sterile gauze to stop any bleeding. Remove the needle and place a sterile cap on the syringe or transfer urine to a sterile container to send for culture. Complications Minor transient hematuria is the most commonly reported complication, occurring in <1% to 10% of cases (7). Urethral catheter or suprapubic aspiration to reduce contamination of urine samples in young children Suprapubic aspiration of urine in the diagnosis of urinary tract infection in infants. Is urethral catheterization a successful alternative to suprapubic aspiration in neonates To obtain urine for culture, particularly when suprapubic collection is contraindicated and when clean-catch specimen is unsatisfactory Although suprapubic bladder aspiration is considered the most reliable method of obtaining urine for culture in infants and young children (see Chapter 19), bladder catheterization is an acceptable alternative method. Bladder catheterization has a higher success rate than suprapubic aspiration, especially if the practitioner is inexperienced in bladder aspiration. The diagnosis of urinary tract infection cannot be made reliably by culturing urine collected in a bag (4,12). To instill contrast agent to perform cystourethrography (15) Prepared antiseptic-impregnated swabs Towels for draping Surgical lubricant Cotton-tipped applicators Urinary catheter Silicone urinary drainage catheters are available in 3. Sterile container for specimen collection or collection burette for continuous closed drainage 3. Try to time the procedure for when the infant has not recently voided (1 to 2 hours after the last wet diaper). Portable ultrasound can be helpful in determining when there is sufficient urine present in the bladder, reducing the chance of an unsuccessful attempt (16,17). Avoid separating the labia minora too widely, to prevent tearing of the fourchette. To avoid coiling and knotting, insert the catheter only as far as necessary to obtain urine. If urine is not obtained in a female infant, recheck the location of the catheter by visual inspection or by radiographic examination. Contraindications (1) Contraindications include pelvic fracture, urethral trauma, and blood at the meatus. In the presence of uncorrected bleeding diathesis, potential risks and benefits must be considered. Commercial prepackaged urinary drainage kits, with or without collection burettes for closed drainage, are available. If the infant is uncircumcised, gently retract the foreskin just enough to expose the meatus. The young male infant has physiologic phimosis, and the foreskin cannot be fully retracted (19).

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The amino-terminal domains o each chain orm the antigen-binding elements that antibiotics for esbl uti purchase ciplox 500 mg otc, like the class I molecule antibiotics sinus infection discount 500mg ciplox visa, cradle a bound peptide in a groove bounded by extended -helical loops antibiotic resistance japan order discount ciplox on-line, one encoded by the A (chain) gene and one by the B (chain) gene antibiotics for uti buy buy ciplox 500 mg free shipping. The speci city and tissue distribution o these proteases appear to be an important way in which the immune system regulates access to the peptide-binding groove and cells become exposed to speci c sel -antigens. Di erences in protease expression in the thymus and in the periphery may in part determine which speci c peptide sequences comprise the peripheral repertoire or cell recognition. However, another consequence o diversi cation is that some alleles may become capable o recognition o "innocent bystander" molecules, including drugs, environmental molecules, and tissuederived sel -antigens. In the cases o allogra s in which the host and donor are mismatched at one or more class I loci, host cells can be activated by classic direct alloreactivity, in which the antigen receptors on the host cells react with the oreign class I molecule expressed on the allogra. In the case o class I molecules on allogra s that are shared by the host and the donor, a host cell response may still be triggered because o peptides that are presented by the class I molecules o the gra but not o the host. These loci are termed minor histocompatibility loci, and nonidentical individuals typically di er at many such loci. By comparing allele requencies in patients with any particular disease and in control populations, >100 such associations have been identi ed, some o which are listed in able 2-1. The strength o genetic association is re ected in the term relative risk, which is a statistical odds ratio representing the risk o disease or an individual carrying a particular genetic marker compared with the risk or individuals in that population without that marker. All o the subtypes share a common B pocket in the peptide-binding groove-a deep, negatively charged pocket that shows a strong pre erence or binding the arginine side chain. This may indicate a role or speci c antigenic peptides or cell interactions in the immune response to islet-associated proteins. Precise genetic polymorphisms characteristic o individual alleles dictate the speci city o these interactions and thereby instruct and guide antigen-speci c immune events. Lip sky One o the central eatures o the immune system is the capacity to mount an in ammatory response to potentially harm ul oreign materials while avoiding damage to sel -tissues. Whereas recognition o sel plays an important role in shaping the repertoires o immune receptors on both and B cells and in clearing apoptotic and other tissue debris rom sites throughout the body, the development o potentially harm ul immune responses to sel -antigens is, in general, prohibited. The essential eature o an autoimmune disease is that tissue injury is caused by the immunologic reaction o the organism against its own tissues. Autoimmunity, on the other hand, re ers merely to the presence o antibodies or lymphocytes that react with sel -antigens and does not necessarily imply that the sel -reactivity has pathogenic consequences. Autoimmunity is present in all individuals; however, autoimmune disease occurs only in those individuals in whom the breakdown o one or more o the basic mechanisms regulating immune tolerance results in sel -reactivity that can cause tissue damage. These antibodies are usually o the IgM heavy chain isotype and are encoded by nonmutated germline immunoglobulin variable region genes. When autoimmunity is induced by an inciting event, such as in ection or tissue damage rom trauma or ischemia, the autoreactivity is in general sel -limited. Even in the presence o organ pathology, it may be di cult to determine whether the damage is mediated by autoreactivity. A er an inciting event, the development o sel -reactivity may be the consequence o an ongoing pathologic process, may be nonpathogenic, or may contribute to tissue in ammation and damage. Individuals 60 with autoimmune disease may have numerous autoantibodies, only some or even none o which may be pathogenic. Patients with systemic sclerosis may have a wide array o antinuclear antibodies that are important in disease classi cation but are not clearly pathogenic; patients with pemphigus may also exhibit a wide array o autoantibodies, only one o which (antibody to desmoglein) is known to be pathogenic. These observations indicated that clones o cells capable o responding to autoantigens were present in the repertoire o antigen-reactive cells in normal adults and suggested that mechanisms in addition to clonal deletion were responsible or preventing their activation. In general, these abnormal responses require both an exogenous trigger, such as bacterial or viral in ection or cigarette smoking, and the presence o endogenous abnormalities in the cells o the immune system. Microbial superantigens, such as staphylococcal protein A and staphylococcal enterotoxins, are substances that can stimulate a broad range o and B cells through speci c interactions with selected amilies o immune receptors, irrespective o their antigen speci city. Endocrine abnormalities Alternatively, molecular mimicry or cross-reactivity between a microbial product and a sel -antigen may lead to activation o autoreactive lymphocytes. One o the best examples o autoreactivity and autoimmune disease resulting rom molecular mimicry is rheumatic ever, in which antibodies to the M protein o streptococci cross-react with myosin, laminin, and other matrix proteins as well as with neuronal antigens. Endogenous derangements o the immune system may also contribute to the loss o immunologic tolerance to sel -antigens and the development o autoimmunity (able 3-2). Some autoantigens reside in immunologically privileged sites, such as the brain or the anterior chamber o the eye. Immunologic privilege results rom a number o events, including the limited entry o proteins rom those sites into lymphatics, the local production o immunosuppressive cytokines such as trans orming growth actor, and the local expression o molecules (including Fas ligand) that can induce apoptosis o activated cells. Lymphoid cells remain in a state o immunologic ignorance (neither activated nor anergized) with regard to proteins expressed uniquely in immunologically privileged sites. I the privileged site is damaged by trauma or in lammation or i cells are activated elsewhere, proteins expressed at this site can become immunogenic and also be the targets o immunologic assault. In multiple sclerosis and sympathetic ophthalmia, or example, antigens uniquely expressed in the brain and eye, respectively, become the target o activated cells. Peptide determinants (epitopes) o a sel -antigen that are not routinely presented to lymphocytes may be recognized as a result o altered proteolytic processing o the molecule and the ensuing presentation o novel peptides (cryptic epitopes). When B cells rather than dendritic cells present sel -antigen, they may also present cryptic epitopes that can activate autoreactive cells. These cryptic epitopes will not previously have been available to e ect the silencing o autoreactive lymphocytes. Furthermore, once there is immunologic recognition o one protein component o a multimolecular complex, reactivity may be induced to other components o the complex a er internalization and presentation o all molecules within the complex (epitope spreading).

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It has been rep rted that up t 70% patients with the sepsis syndr me have s me degree neur pathy antibiotic names starting with a buy cheap ciplox 500mg on line, alth ugh ar ewer have a lini al syndr me pr und en ugh t ause severe respirat ry mus le weakness requiring pr l nged me hani al ventilati n r resulting in ailure t wean antibiotics omnicef order ciplox 500mg on-line. Critical illness myopathy is an verall term that des ribes several di erent dis rete mus le dis rders that may ur in riti ally ill patients antibiotic mechanism of action order ciplox 500mg fast delivery. This less mm n acute necrotizing intensive care myopathy is hara terized lini ally by weakness pr gressing t a pr und level ver just a ew days pcr antibiotic resistance purchase ciplox 500mg with visa. Clini ally this syndr me is m st en re gnized when a patient ails t wean r m me hani al ventilati n despite res luti n the primary pulm nary pr ess. I patients survive their underlying riti al illness, the my pathy invariably impr ves and m st patients return t n rmal. H wever, be ause this syndr me is a result true mus le damage, n t just pr l nged bl kade at the neur mus ular jun ti n, this pr ess may take weeks r m nths, and tra he t my with pr l nged ventilat ry supp rt may be ne essary. H wever, this is m re likely t prevent the mpli ati n pr l nged neur mus ular jun ti n bl kade than it is t prevent this my pathy. Other auses in lude bleeding r m a vas ular mal rmati n (arteri ven us mal rmati n r dural arteri ven us stula) and extensi n int the subara hn id spa e r m a primary intra erebral hem rrhage. O th se wh survive, m re than hal are le with maj r neur l gi de its as a result the initial hemrrhage, erebral vas spasm with in ar ti n, r hydr ephalus. I the patient survives but the aneurysm is n t bliterated, the rate rebleeding is ab ut 20% in the rst 2 weeks, 30% in the rst m nth, and ab ut 3% per year a erward. Be ause the l nger length exp sure t risk rupture, y unger patients with aneurysms >10 mm in size may bene t r m pr phyla ti treatment. As with the treatment asympt mati ar tid sten sis, this risk-bene t rati str ngly depends n the mpli ati n rate treatment. M st result r m in e ted emb li due t ba terial end arditis ausing septi degenerati n arteries and subsequent dilati n and rupture. Whether these lesi ns sh uld be s ught and repaired pri r t rupture r le t heal sp ntane usly with antibi ti treatment is ntr versial. Pa th o p hysio lo gy Sa ular aneurysms ur at the bi ur ati ns the large- t medium-sized intra ranial arteries; rupture is int the subara hn id spa e in the basal isterns and en int the paren hyma the adja ent brain. The length the ne k and the size the d me vary greatly and are imp rtant a t rs in planning neur surgi al bliterati n r end vasular emb lizati n. T se >7 mm in diameter and th se at the t p the basilar artery and at the rigin the p steri r mmuni ating artery are at greater risk rupture. Sudden l ss ns i usness may be pre eded by a brie m ment ex ru iating heada he, but m st patients rst mplain heada he up n regaining ns i usness. The patient en alls the heada he "the w rst heada he my li e"; h wever, the m st imp rtant hara teristi is sudden nset. Alth ugh sudden heada he in the absen e al neur l gi sympt ms is the hallmark aneurysmal rupture, al neur l gi de its may ur. A third ranial nerve palsy, parti ularly when ass iated with pupillary dilati n, l ss ipsilateral (but retained ntralateral) light re ex, and al pain ab ve r behind the eye, may ur with an expanding aneurysm at the jun ti n the p steri r mmuni ating artery and the internal ar tid artery. A sixth nerve palsy may indi ate an aneurysm in the avern us sinus, and visual eld de e ts an ur with an expanding supra lin id ar tid r anteri r erebral artery aneurysm. O ipital and p steri r ervi al pain may signal a p steri r in eri r erebellar artery r anteri r in eri r erebellar artery aneurysm (Chap. Be re n luding that a patient with sudden, severe heada he has thunder lap migraine, a de nitive w rkup r aneurysm r ther intra ranial path l gy is required. Aneurysms an underg small ruptures and leaks bl d int the subara hn id spa e, s - alled sentinel bleeds. F r example, it is unusual r a Hunt-Hess grade 1 patient t die i the aneurysm is treated, but the m rtality rate r grade 4 and 5 patients may be as high as 80%. Dela ye d n eu ro lo g ic d ef cits There are ur maj r auses delayed neur l gi de its: rerupture, hydr ephalus, vas spasm, and hyp natremia. A ute hydr ephalus an ause stup r and ma and an be mitigated by pla ement an external ventri ular drain. M re en, suba ute hydr ephalus may devel p ver a ew days r weeks and auses pr gressive dr wsiness r sl wed mentati n (abulia) with in ntinen. Delayed vas spasm is believed t result r m dire t e e ts l tted bl d and its breakd wn pr du ts n the arteries within the subara hn id spa. Vas spasm an be dete ted reliably with nventi nal x-ray angi graphy, but this invasive pr edure is expensive and arries the risk str ke and ther mpli ati ns. B th atrial natriureti peptide and brain natriureti peptide have a r le in pr du ing this " erebral salt-wasting syndr me. M re than 95% ases have en ugh bl d t be visualized n a high-quality n n ntrast C s an btained within 72 h. The extent and l ati n subara hn id bl d n a n n ntrast C s an help l ate the underlying aneurysm, identi y the ause any neur l gi de it, and predi t delayed vas spasm. E h ardi graphy reveals a pattern regi nal wall m ti n abn rmalities that ll w the distributi n sympatheti nerves rather than the maj r r nary arteries, with relative sparing the ventri ular wall apex. The sympatheti nerves themselves appear t be injured by dire t t xi ity r m the ex essive ate h lamine release. Conventional anteropos terior x ray angiogram o the right vertebral and basilar artery showing the large aneurysm. Conventional angiogram ollow ing coil embolization o the aneurysm, whereby the aneurysm body is lled with platinum coils delivered through a microcath eter navigated rom the emoral artery into the aneurysm neck.

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The anticonvulsants that are predominantly used in bromyalgia are those that are ligands o the -2- subunit o voltage-gated calcium channels antibiotic yogurt after effective 500 mg ciplox. They have no e cacy in treating bromyalgia and may induce hyperalgesia that can worsen both pain and unction antibiotics nerve damage discount ciplox 500 mg mastercard. Clubbing can be a benign amilial condition and is also associated with a variety o other disorders 600 mg antibiotic buy cheapest ciplox and ciplox, including cyanotic congenital heart disease antibiotics running out order generic ciplox from india, subacute bacterial endocarditis, Crohn disease, ulcerative colitis, celiac disease, and cancer o the esophagus, liver, small bowel, and large bowel. In untreated hyperthyroidism, clubbing can occur in association with periostitis in a condition called thyroid acropachy. Although these numerous clinical associations have been described or many centuries, the cause o clubbing remains unknown. The arthropathy is an osteoarthritis-like disorder af ecting the small joints o the hands and later the larger joints, such as knees, ankles, shoulders, and hips. The second and third metacarpophalangeal joints o both hands are o en the rst and most prominent joints af ected; this clinical picture may provide an important clue to the possibility o hemochromatosis because these joints are not predominantly af ected by "routine" osteoarthritis. Radiographs show narrowing o the joint space, subchondral sclerosis, subchondral cysts, and juxta-articular proli eration o bone. Hooklike osteophytes are seen in up to 20% o patients; although they are regarded as a characteristic eature o hemochromatosis, they can also occur in osteoarthritis and are not disease speci c. In approximately hal o patients, there is evidence o calcium pyrophosphate deposition disease, and some patients experience episodes o acute pseudogout late in the course o disease (Chap. Un ortunately, this treatment has little ef ect on established arthritis, which, along with chondrocalcinosis, may progress. Although the pathogenesis is not clear, there are associations with disturbed sleep and abnormal pain perception. Fibromyalgia is diagnosed by the presence o widespread pain, a history o widespread musculoskeletal pain that has been present or more than 3 months, and presence o neuropsychological dys unction (atigue, waking unre reshed, or cognitive symptoms). In the prior diagnostic criteria, it was required to demonstrate pain on palpation at 11 o 18 tender point sites. However, this was abandoned in the updated criteria because it was elt that strict application o a threshold o pain could lead to underdiagnosis o the disorder. Besides pain on palpation, the neurologic and musculoskeletal examinations are normal in patients with bromyalgia. Psychiatric illnesses, particularly depression and anxiety disorders, are common comorbidities in these patients but do not help satis y any diagnostic criteria. Clubbing occurs in the distal portions o the digits and is characterized by widening o the ngertips, convexity o the nail contour, and loss o the normal 15-degree angle between the proximal nail and cuticle. One approach to the diagnosis o clubbing is to measure the diameter o the nger at the base o the nail and at the tip o the nger in all 10 ngers. A simpler approach is to have an individual place the dorsal sur aces o the distal ourth digits rom each hand together. Clubbing most commonly occurs in advanced lung disease, especially bronchiectasis, cystic brosis, and interstitial lung diseases like sarcoidosis or idiopathic pulmonary brosis. Clubbing was originally described in individuals with empyema and can occur in chronic lung in ections, including lung abscess, tuberculosis, or ungal in ections. However, R eview and Self-A ssessment Hip or knee total joint replacement has been success ul in advanced disease. Bursae lie throughout the body with the purpose o acilitating movement o tendons and muscles over bony prominences. Direct palpation over the posterior aspect o the greater trochanter reproduces the pain, and o en sleeping on the af ected side is pain ul. Other causes o hip pain include osteoarthritis, avascular necrosis, meralgia paresthetica, septic arthritis, occult hip racture, and re erred pain rom lumbar spine disease. In patients with true disorders o the hip joint such as osteoarthritis, avascular necrosis, and occult hip racture, the pain is most commonly localized to the groin area. Meralgia paresthetica (lateral emoral nerve entrapment syndrome) causes a neuropathic pain in the upper outer thigh with symptoms ranging rom tingling sensations to a burning pain. When degenerative spinal disease is the cause o re erred hip pain, there is typically back pain as well. When this band becomes tightened or in amed, pain most commonly occurs where the band passes over the lateral emoral condyle o the knee, leading to a burning or aching pain in this area that can radiate toward the outer thigh. This overuse injury is most o en seen in runners and can be caused by improperly tted shoes, running on uneven sur aces, and excessive running. Glucocorticoid injection at the lateral emoral condyle may alleviate pain, but running must strictly be avoided or 2 weeks ollowing injection. Because every individual has the right to determine what happens to his or her own body, the individual must ultimately make decisions about which medical procedures he or she will undergo. In the context of neonates, the notion of personal autonomy is more attenuated, but the requirements of informed consent are no less stringent. The presumption, then, is that parents or legal guardians will make treatment decisions based on the information provided by the treating physician. If the information disclosed is inadequate, inaccurate, or unclear, the parent or guardian is not placed in an optimal position to make a treatment decision. A priority physician duty is to explain disease process, prognosis, and the range of possible treatments with their individual risks and benefits. Although a treating physician may 18 delegate the responsibility for obtaining informed consent, he or she needs to keep in mind that when the treating physician fails to ensure that parents or guardians are provided with all the information that they require to make a decision, in a language and manner that the parents or guardians fully understand, the treating physician fails to fulfill his or her duty to the patient. If injury results that was not covered in the informed consent process, the treating physician may be liable for this injury, as may other members of the health care team who were involved in the performance of the procedure (8,9). A plaintiff may (alternatively or additionally) make a medical malpractice claim for failure to provide adequate disclosure. Medical malpractice is a type of negligence, so the elements required for a prima facie case are the same.

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