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Prevaience Prevalence of delayed sleep phase type in the general population is approximately 0 medications starting with p purchase cheap triamcinolone on line. Although the prevalence of familial de layed sleep phase type has not been established treatment mononucleosis purchase triamcinolone 15 mg without a prescription, a family history of delayed sleep phase is present in individuals with delayed sleep phase type treatment skin cancer buy triamcinolone mastercard. Development and Course Course is persistent 4 medications at target buy generic triamcinolone 15 mg online, lasting longer than 3 months, with intermittent exacerbations through out adulthood. Although age at onset is variable, symptoms begin typically in adolescence and early adulthood and persist for several months to years before diagnosis is estab lished. Exacerbation is usually triggered by a change in work or school schedule that requires an early rise time. Individuals who can alter their work schedules to accommo date the delayed circadian sleep and wake timing can experience remission of symptoms. Increased prevalence in adolescence may be a consequence of both physiological and be havioral factors. Hormonal changes may be involved specifically, as delayed sleep phase is as sociated with the onset of puberty. Thus, delayed sleep phase type in adolescents should be differentiated from the common delay in the timing of circadian rhythms in this age group. In the familial form, the course is persistent and may not improve sig^iificantly with age. Predisposing factors may include a longer than average cir cadian period, changes in light sensitivity, and impaired homeostatic sleep drive. Some in dividuals with delayed sleep phase type may be hypersensitive to evening light, which can serve as a delay signal to the circadian clock, or they may be hyposensitive to morning light such that its phase-advancing effects are reduced. Genetic factors may play a role in the pathogenesis of familial and sporadic forms of delayed sleep phase type, including mutations in circadian genes. Diagnostic i/larl(ers Confirmation of the diagnosis includes a complete history and use of a sleep diary or actigra phy. The period covered should include weekends, when social and occupational obligations are less strict, to ensure that the individual exhibits a consistently delayed sleep-wake pattern. Biomarkers such as salivary dim light melatonin onset should be obtained only when the diagnosis is unclear. Functional Consequences of Delayed Sleep Phase Type Excessive early day sleepiness is prominent. The severity of insomnia and excessive sleepiness symptoms varies substantially among individuals and largely de pends on the occupational and social demands on the individual. Delayed sleep phase type must be distinguished from "normal" sleep patterns in which an individual has a late schedule that does not cause personal, social, or occupational distress (most commonly seen in adolescents and young adults). Insomnia disorder and other circadian rhythm sleep-wake dis orders should be included in the differential. Excessive sleepiness may also be caused by other sleep disturbances, such as breathing-related sleep disorders, insomnias, sleep related movement disorders, and medical, neurological, and mental disorders. Overnight polysomnography may help in evaluating for other comorbid sleep disorders, such as sleep apnea. The circadian nature of delayed sleep phase type, however, should differen tiate it from other disorders with similar complaints. Comorbidity Delayed sleep phase type is strongly associated with depression, personality disorder, and somatic symptom disorder or illness anxiety disorder. In addition, comorbid sleep disor ders, such as insomnia disorder, restless legs syndrome, and sleep apnea, as well as depres sive and bipolar disorders and anxiety disorders, can exacerbate symptoms of insomnia and excessive sleepiness. Delayed sleep phase type may overlap with another circadian rhythm sleep-wake disorder, non-24-hour sleep-wake type. Sighted individuals with non 24-hour sleep-wake type disorder commonly also have a history of delayed circadian sleep phase. Advanced Sleep Phase Type Specifiers Advanced sleep phase type may be documented with the specified "famihal. In this type, specific mutations demonstrate an autosomal dominant mode of inheritance. In the familial form, onset of symptoms may occur earlier (during childhood and early adulthood), the course is persistent, and the severity of symptoms may increase with age. Diagnostic Features Advanced sleep phase type is characterized by sleep-wake times that are several hours earlier than desired or conventional times. Diagnosis is based primarily on a history of an advance in the timing of the major sleep period (usually more than 2hours) in relation to the desired sleep and wake-up time, with symptoms of early morning insomnia and ex cessive daytime sleepiness. When allowed to set their schedule, individuals with ad vanced sleep phase type will exhibit normal sleep quality and duration for age. Associated Features Supporting Diagnosis Individuals with advanced sleep phase type are "morning types," having earlier sleep wake times, with the timing of circadian biomarkers such as melatonin and core body tem perature rhythms occurring 2-A hours earlier than normal. When required to keep a con ventional schedule requiring a delay of bedtime, these individuals will continue to have an early rise time, leading to persistent sleep deprivation and daytime sleepiness. Use of hyp notics or alcohol to combat sleep-maintenance insomnia and stimulants to reduce daytime sleepiness may lead to substance abuse in these individuals. Prevaience the estimated prevalence of advanced sleep phase type is approximately 1% in middle age adults. Sleep-wake times and circadian phase advance in older individuals, probably accounting for increased prevalence in this population. The course is typ ically persistent, lasting more than 3 months, but the severity may increase depending on work and social schedules. Individuals who can alter their work schedules to accommodate the advanced circadian sleep and wake timing can experience remission of symptoms. Increasing age tends to advance the sleep phase, however, it is unclear whether the common age-associ ated advanced sleep phase type is due solely to a change in circadian timing (as seen in the familial form) or also to age-related changes in the homeostatic regulation of sleep, result ing in earlier awakening. Severity, remission, and relapse of symptoms suggest lack of ad herence to behavioral and environmental treatments designed to control sleep and wake structure and light exposure. Decreased late aftemoon/early evening exposure to light and/or expo sure to early morning light due to early morning awakening can increase the risk of ad vanced sleep phase type by advancing circadian rhythms. By going to bed early, these individuals are not exposed to light in the phase delay region of the curve, resulting in per petuation of advanced phase. In familial advanced sleep phase type, a shortening of the endogenous circadian period can result in an advanced sleep phase, although circadian pe riod does not appear to systematically decrease with age. Diagnostic iVlaricers A sleep diary and actigraphy may be used as diagnostic markers, as described earlier for delayed sleep phase type. Functionai Consequences of Advanced Sieep Pliase Type Excessive sleepiness associated with advanced sleep phase can have a negative effect on cognitive performance, social interaction, and safety. Use of wake-promoting agents to combat sleepiness or sedatives for early morning awakening may increase potential for substance abuse. Behavioral factors such as irregular sleep schedules, voluntary early awakening, and exposure to light in the early morning should be considered, partic ularly in older adults. Careful attention should be paid to rule out other sleep-wake dis orders, such as insomnia disorder, and other mental disorders and medical conditions that can cause early morning awakening. Because early morning awakening, fatigue, and sleep iness are prominent features of major depressive disorder, depressive and bipolar disor ders must also be considered. Comorbidity Medical conditions and mental disorders with the symptom of early morning awakening, such as insomnia, can co-occur with the advance sleep phase type. Irregular Sleep-Wake Type Diagnostic Features the diagnosis of irregular sleep-wake type is based primarily on a history of symptoms of insomnia at night (during the usual sleep period) and excessive sleepiness (napping) dur ing the day. Irregular sleep-wake type is characterized by a lack of discernable sleep-wake circadian rhythm. There is no major sleep period, and sleep is fragmented into at least three periods diring the 24-hour day. Associated Features Supporting Diagnosis Individuals with irregular sleep-wake type typically present with insomnia or excessive sleepiness, depending on the time of day. Sleep and wake periods across 24 hours are frag mented, although the longest sleep period tends to occur between 2:00 A. A history of isolation or reclusion may occur in association with the disorder and contribute to the symptoms via a lack of external stimuli to help en train a normal pattern. Irregular sleep-wake type is most commonly associated with neurodegenerative dis orders, such as major neurocognitive disorder, and many neurodevelopmental disorders in children.

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In addi the test and control treatments were performed at tion symptoms indigestion discount triamcinolone 4mg with visa, a suspensory suture was placed in the periosteum the same surgical appointment symptoms 14 days after iui buy genuine triamcinolone on line. The first surgery was apical to medicine nausea buy triamcinolone 15 mg free shipping the graft and looped around the neck of the always performed on the left side with the recession tooth to medications xyzal cheap triamcinolone 10mg overnight delivery provide a secure adaptation of the graft to defect treated either with the test or control procedure the root surface. The fiap was then coronally advanced according to a computer generated randomization list. Patients were instructed not to brush Surgical protocol for test treatment with coronally the teeth in the treated areas but to use 0. After this period, Parameters patients were instructed in a brushing technique that minimized apically directed trauma to the soft tissue of the treated teeth. Calculations at 5% sig nificance level show that 20 patients were sufficient to Control 0. One patient moved out of the Alveolar bone level country, one had a change in job and could not com Control 6. Test sites were found to be significantly of follow-up, and complete data for 19 were available superior in healing after 1 week compared to control for 6 months of follow-up. The only significant dif 6-month follow-up, we had 70% power to detect a ferences between test and control groups over the time 10% difference in root coverage after 6 months. Repeated measures of ously exposed root surfaces was achieved with both analysis of variance revealed no significant differences treatment groups. Repeated measures for analysis of between test and control sites over time for plaque covariance, while controlling for subject were per scores, root dentin hypersensitivity, infiammation score, formed. Similarly, in recession depth between the test and control groups Wilcoxon signed rank tests at each time point demon at 12 months (P = 0. However, test sites had sig strated no statistically significant differences between nificantly less recession than control sites at 4 weeks test and control sites at any time point for any of these (P = 0. In addi 12 months demonstrated no statistically significant dif tion, the trend in Figure 3 shows that test sites tended ference in the change in clinical attachment level to have less recession over time than control sites, between test and control groups (P = 0. Healing was evaluated 1 week following surgery Percentage of root coverage obtained for control based on a visual analog scale as much worse than and test sites was evaluated. Analysis of covariance expected, expected, and much better than with adjustment for differences in baseline depth and expected. No significant difference in the percentage of week, in nine (45%) subjects, the healing at the test root coverage was found between the test group and site was superior to the healing at the control site, the control group (P = 0. Heal advanced fiap plus subepithelial connective tissue graft ing at 1 week was tested using a chi-squared test of were covered, whereas 95. Figure 4 refers to adjusted mean changes in probing pocket depth over time with 95% confidence intervals as obtained from repeated measures of analysis of covariance with the baseline clinical parameter by treat ment group. A) Baseline appearance of the maxillary lateral incisors which were randomized to receive the test (left) or control (right) treatment. B) At 1 week following treatment, the test (left) treatment exhibits fewer clinical signs of infiammation as compared to the control (right) tooth. C)Test (left) and control (right) teeth at 4 weeks, the test treatment continues to exhibit superior wound healing. D) At 12 months postsurgery, the recreation of a functional and esthetic morphology of the mucogingival complex is clinically demonstrated. Figure 5 shows the change in the amount of kera for the test group demonstrated statistically significant tinized tissue over time up to 12 months between test differences in the amount of keratinized tissue relative and control groups. Following treatment, Figure 6 depicts the results of the patient question there was a statistically significant difference in the naire regarding discomfort levels over time between the amount of keratinized tissue between the control and two treatment groups. Control sites yielded more severe adverse and clearly demonstrate the recreation of a functional and observations including self-reported patient discom esthetic morphology of the mucogingival complex. The purpose of this randomized, controlled, single the only reported adverse events included pain, center, split-mouth design study was to compare the 1116 J Periodontol August 2003 McGuire, Nunn Figure 4. The summary second paper in this series19 addresses the requirement of the evidence indicates that both procedures are of regeneration of the lost attachment apparatus. This paper tive tissue graft is clearly the preferred treatment of has demonstrated that test and control treatments both choice in most mucogingival recession defects. A) Preoperative photograph of a maxillary cuspid in patient #20 randomized to receive a subeptithelial connective tissue graft (control). They reported no sig an effort to improve root coverage and to eliminate the nificant differences in percentage of root coverage or need for a secondary surgical site to harvest the con prevalence of 100% root coverage between the two nective tissue. In that same year, Siervo and Corani29 reported a G) Probing depth measurements on the test tooth at 12 months. Fourteen gen membrane treated sites produced mean root cov pairs of comparable defects were included in this study erage of 73% 26% (average baseline recession depth from 12 patients. It is also interesting to note that the cor for the control group and a mean root coverage of responding data for the coronally advanced fiap alone 95. They want to know how often they can expect grafts with and without citric acid root conditioning for the treatment of recession defects, Bouchard et al. At 12 months, the average gain in kera root coverage in 62% of his subpedicle connective tis tinized tissue was 4. Furthermore, the amount of keratinized similar mean root coverage results: Trombelli et al. In their study, the kera tinized tissue width seemed to be related to the presurgical dimensions of the keratinized tissue and the amount of connective tissue left exposed coronal to the fiap margin at the end of the surgical procedure. B) Clinical appearance of the control tooth at there is not a certain amount of ker 12 months. All of the test sites exceeded those dimensions at all time periods following baseline. Since most root coverage grafts are performed in response to esthetic concerns of the patient, the overall esthetic outcome should be evalu ated as the clinician decides which surgical procedure will best meet the needs of the patient (Fig. Note not only the root coverage, but also increase should recreate the normal the increase in keratinized tissue as compared to the preoperative photograph A. One hundred percent root Many teeth that require root coverage grafts have coverage was obtained 89. There not only in covering the denuded root surface, but were no statistically significant differences in clinical also in reestablishing the proper emergence profile attachment gain, root hypersensitivity, probing depth, as the tooth surface emerges from the free gingival or any of the other evaluated parameters with the margin. The connective tissue is trimmed to fit into exception of healing at 1 week, self reported the abraded root surface in an inlay fashion and the discomfort, and width of keratinized gingiva. Within thickness of the graft provides the bulk necessary the limitations of this paper, the results indicate that to recreate a natural looking root eminence (Figs. Nancy Whitley for At 1 week there was a notable difference, statisti their assistance with the manuscript. In addition, almost half (45%) lateral bridging fiap for coverage of denuded root sur of the patients reported great discomfort with the face: Longitudinal study and clinical evaluation after 5 subepithelial connective tissue grafting procedure as to 8 years. The coronally positioned pedicle the significance of less patient-reported discomfort graft with inlaid margins: A predictable method to obtain ing root coverage of shallow defects. Increased gingival dimen site to harvest the connective tissue would obviously sions. A significant factor for successful outcome of root lead to more discomfort associated with the control coverage proceduresfi Fibrin important, is that procuring the connective tissue can glue application in conjunction with tetracycline root be challenging for the clinician especially in patients conditioning and coronally positioned fiap procedure in with thin palatal tissue, with shallow palatal vaults, and the treatment of mucogingival defects. Coronally eration in a buccal fenestration model of monkeys after advanced fiap procedure for root coverage. Covering localized areas of root exposure ing of recession type defects following treatment with employing the envelope technique. Mucogingival and regenerative ther obtained with guided tissue regeneration utilizing a bioab apy with amelogenins. J Periodontol of a new bioabsorbable barrier for recession therapy: A 1997;68:779-790. J Clin Periodontol 2002;29 cessful and predictable procedure in areas of deep-wide (Suppl. J Clin Periodontol 1997;24(Part 2): denuded root surface with a one-stage gingival graft. Guided tissue regeneration versus mucogin derivative in one human experimental defect.

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The promise of intimacy and the fear of our the limitations-and moral courageimplicated in caring own understanding symptoms xanax withdrawal quality triamcinolone 15 mg. Unclaimed experience: trauma treatment e coli buy triamcinolone 10mg with visa, narrative treatment jiggers order triamcinolone on line amex, and limit nurses ability to medications just for anxiety generic 15 mg triamcinolone fast delivery interact in a meaningful and safe history. Mediating positive moods: the impact of experienc ing and absorbing of unmanageable emotions may lead ing compassion at work. Compassion fatigue within tional culture, clinical supervision, and ongoing educa nursing practice: A concept analysis. Nursing & Health Sciences, tion may protect health care professionals from secondary 12(2), 235243. Journal of Psychiatric and Journal of Respiratory and Critical Care Medicine, 175(7), Mental Health Nursing, 10, 1727. Coping while caring for systems as a defenses against anxiety: A report of nursing the dying child: nurses experiences in an acute care setting. A proposed model of health professionals secondary traumatic stress among emergency nurses. International Journal disorder and the social usefulness of a psychiatric category. The prevalence of compassion fatigue secondary traumatization: Provider self care on intensive care and burnout among healthcare professionals in intensive units for children. For another continuing education article related to secondary traumatic stress, go to NursingCenter. Apart from any use as permitted under the Copyright Act 1968, no part may be reproduced by any process without prior written permission from Phoenix Australia Centre for Posttraumatic Mental Health. Requests and inquiries concerning reproduction and rights should be addressed to Phoenix Australia Centre for Posttraumatic Mental Health (phoenix-info@unimelb. Copies of the full guidelines, and brief guides for practitioners and the public are available online: Australian Guidelines for the Treatment of Acute Stress Disorder and Posttraumatic Stress Disorder. In recognition of the pace of advances in the feld, it is recommended that the guidelines be reviewed and updated in fve years time. Australian Guidelines for the Treatment of Acute Stress Disorder & Posttraumatic Stress Disorder Endorsed by the Australian Psychological Society the Royal Australian College of General Practitioners the Royal Australian and New Zealand College of Psychiatrists Acknowledgments Funding bodies We gratefully acknowledge the fnancial contribution of the Department of Veterans Affairs, the Department of Defence and beyondblue in the development of these Guidelines. Importantly, the Guidelines are intended to guide practice rather than be used prescriptively. Each persons unique circumstances and their overall mental healthcare needs must be considered. These psychological treatments involve confronting the memory of the traumatic event and coming to terms with the experience. However this should be appropriately tailored to the developmental stage of the individual child or adolescent. The groups include Aboriginal and Torres Strait Islander peoples, refugees and asylum seekers, military and ex-military personnel, emergency service personnel and older people and the types of traumatic events include motor vehicle accidents, crime, sexual assault, natural disasters and terrorism. The most signifcant change has been an expansion of the Guidelines to cover treatment recommendations for children and adolescents, as well as adults. Chapter 1 Introduction provides an overview of the Guideline development process and details their objectives and scope. The work of the Guideline Development Group was overseen by a steering committee and supported by an independent methodologist, an independent systematic review of the literature and a project team from Phoenix Australia Centre for Posttraumatic Mental Health. Practitioners should use their experience and expertise in applying Guideline recommendations in routine clinical practice and all clinical interventions should be provided with compassion and sensitivity. Naturally, this varies depending on the nature of the particular incident that the individual is exposed to. Typical clinical presentations in children and adolescents, as well as issues of screening, assessment and treatment in this group are detailed in Chapter 3. Protocols that have been designed specifcally for children and adolescents should be used in preference to attempting to modify an adult treatment protocol. Psychological interventions for children and adolescents Grade B For children exposed to a potentially traumatic event, psychological debriefng should not be offered. The complete list of Guideline recommendations is provided at the end of this executive summary. A comprehensive economic evaluation of the implications of key Guideline recommendations has been undertaken and is available in a separate companion document to the main Guidelines. The categories of traumatic event covered in the chapter are: Motor vehicle accidents Crime Sexual assault Natural disasters Terrorism. The grading system for each recommendation is fully explained later in the document (see Chapter 5). The working party then generated the recommendations and gave each a grade to indicate the strength of the recommendation in order to assist users in making clinical judgments. The grade is based on, but not necessarily a direct translation of, the strength of evidence. Grade A recommendations indicate that the body of evidence can be trusted to guide practice. Grade C indicates that the body of evidence provides some support for the recommendation but care should be taken in its application. Grade D indicates that the body of evidence is weak and the recommendation must be applied with caution. As explained in Chapter 1, the recommendations are not intended to be used prescriptively, but as a guide to appropriate interventions in the context of each persons unique circumstances and their overall mental healthcare needs. When adequate progress in treatment is not being made, the practitioner should revisit the case formulation, reassess potential treatment obstacles, and implement appropriate strategies, or refer to another practitioner. Effective inter-professional collaboration and communication is essential at such times. This requires specialist training, over and above basic mental health or counselling qualifcations. This includes maintaining a balanced and healthy lifestyle and responding early to signs of stress. Where assessment involves very young children (aged 0-3) this should include an evaluation of the behaviour of the child with particular reference to developmental stage, and attachment status. In doing this the practitioner should keep in mind the potential adverse effects of excessive ventilation in those who are very distressed. This would involve ongoing monitoring of people who are more distressed and/or at heightened risk of adverse mental health impact, with targeted assessment and intervention when indicated. In the interim, supportive psychotherapy with a substantial psychoeducational component should be offered. Information following traumatic events may also include a recognition of the role of, and impact on, caregivers, siblings and teachers. The purpose of this chapter is to describe the revised Guideline aims, scope, development process and implementation strategy. Although the basic approach to guideline development is the same for this version as it was for the 2007 Guidelines, there are minor differences. Membership of both the working party and the multidisciplinary panel was broader for the current Guidelines, refecting the addition of people with expertise in child and adolescent trauma. The number and range of questions was broader on this occasion, predominantly refecting the addition of evidence around children and adolescents. The approach to conducting the systematic review was the same, although the manner in which the data was summarised is slightly different; notably, evidence statement matrices appear in this version, but were not used in the 2007 Guidelines. This requirement did not exist for the 2007 Guidelines, and explains why some recommendations are lower on this occasion than in the earlier version, despite the evidence base being the same or comparable. They should not limit treatment innovation and development that is based upon scientifc evidence, expert consensus, practitioner judgment of the needs of the person, and the persons preferences. The Guidelines are intended to infuence the care of all Australian men, women and children, across the full range of populations, who develop, or are at risk of developing, these forms of distress following traumatic events. The Guideline developers recognise that there are a number of interventions that are widely used in clinical practice that have not been adequately tested, and it is important to acknowledge that the absence of evidence does not necessarily mean that these interventions are ineffective. The gap between evidence-based interventions and clinical practice should help defne the research agenda into the future. The Guidelines have been formulated with the assumption that treatment will be provided by qualifed professionals who are skilled in the relevant psychosocial and medical interventions, as assessed against the prevailing professional standards. The Guidelines do not substitute for the knowledge and skill of competent individual practitioners.

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Bone tissue forms in rings (lamellae) around these canals treatment 4s syndrome buy 15mg triamcinolone, creating a structure called an osteon symptoms lymphoma buy triamcinolone discount. Examine the bone tissue slide medicine shoppe order triamcinolone 10 mg otc, noting the osteons with their lamellae and bulls-eye like central canals medications and mothers milk order triamcinolone overnight delivery. The lacunae, which contain the bone cells, are visible as small dark patches in the lamellae. The skeletal muscle fibers are long and cylindrical, with multiple peripherally located nuclei. Cells are striated, but the striations are much less obvious than in skeletal muscle tissue. The cells are shorter than skeletal muscle fibers, have a single nucleus and are often branched. These cellular connections are visible under the microscope as dark bands called intercalated disks. These cellular communication junctions are necessary for the coordinated beating of the heart. Smooth muscle (muscle composite slide & artery/vein/nerve slide) Smooth muscle tissue is found in the walls of hollow organs, such as the gastrointestinal tract, blood vessels, and the urinary bladder. Smooth muscle cells are not striated (hence the name smooth muscle); they have a single nucleus, and have tapered ends. Nervous Tissue Nervous tissue is specialized for communication and composes the brain, spinal cord, and peripheral nerves. They have nucleated cell bodies and two types of elongated cellular processes: dendrites which receive signals, and axons which send signals. There are several different types with various functions, including maintaining proper ion concentrations in the fluid surrounding neurons, generating myelin (an insulating material that surrounds some axons), and cleaning up debris. The incidence and prevalence of rheumatoid arthritis in developing countries is thought to be lower, but is difficult to quantify. Although joint disease is the main presentation, there are a number of extra-articular manifestations including subcutaneous nodule formation, vasculitis, inflammatory eye disease and lung disease. Of these manifestations, lung disease is a major contributor to morbidity and mortality. These changes may reflect chronic immune activation, increased susceptibility to infection (often related to immunomodulatory medications) or direct toxicity from disease modifying or biological therapy. Herein, we review the various manifestations of rheumatoid arthritis-associated lung disease, as well as the recent advances in treatment. Types of pulmonary involvement Respiratory symptoms in rheumatoid arthritis can be due to a variety of conditions that affect the parenchyma, pleura, airways or vasculature (table 1). Respiratory symptoms may precede onset of articular symptoms in 1020% of cases [2]. The exact mechanism for this has not been elucidated, but may involve formation of circulating immune complexes [14]. Cigarette smoking may play a role in inducing antibody formation and has been linked to higher titres of rheumatoid factor [20, 21]. Smoking is also a risk factor for rheumatoid arthritis alone and results in repeated injuries to the alveolar epithelium and alterations in the cytokine milieu. While knowledge of the specific histopathological patterns of interstitial pneumonias may clarify histopathological diagnosis and be of prognostic value, this knowledge is usually not essential to determining a treatment regimen, which is invariably made up of immune modulating agents. Subpleural and basilar predominant reticulations, minimal ground-glass opacities, honeycombing (arrow) and pleural thickening (arrowhead) are visible, as well as traction bronchiectasis. Management Treatment with anti-inflammatory and/or immunosuppressive agents is recommended regardless of the pattern of fibrosis. To date, there have been no randomised controlled trials comparing medications for the treatment of rheumatoid arthritis lung disease. This suggests that methotrexate use may not be associated with poorer outcomes than other disease modifying anti-rheumatic drugs [44]. Studies evaluating this issue tend to be confounded by older age and prior use of methotrexate among participants. In the absence of active rheumatoid arthritis, patients with rheumatoid arthritis lung disease who fail to respond to therapy should be considered for lung transplant. Pleural disease Pleural involvement is a common pulmonary manifestation of rheumatoid arthritis, with small pleural effusions noted in up to 70% on autopsy studies [50, 51]. Most effusions are unilateral, although occasionally bilateral effusions are found [50, 52]. Fever and pleuritic chest pain are common, but cough is generally absent unless there is comorbid parenchymal lung disease. Pathogenesis A variety of mechanisms have been postulated for pleural effusions occurring in rheumatoid arthritis patients. Imaging Most cases of rheumatoid pleural disease can be diagnosed on chest radiography, with blunting of the costophrenic angles in the upright position. Fluid can also be detected on chest ultrasonograpy or computed tomography, with the latter being more useful if there is concern for comorbid parenchymal pathology (fig. Fluid glucose levels may be similar to serum glucose levels in acute disease, but typically fall quite low in chronic effusions. Characteristic elongated multinucleated macrophages, ragocytes (polymorphonuclear phagocytes with intracellular inclusions of IgG and/or rheumatoid factor), or necrotic background debris may be seen. An analysis of 29 cases of rheumatoid pleural effusion for which fluid studies were reported noted predominance of neutrophils, lymphocytes and eosinophils in 56%, 37% and 15% of cases, respectively. Interestingly, all patients with eosinophil-predominant fluid lacked a preceding diagnosis of rheumatoid arthritis; this was either diagnosed concurrently or at a later time [54]. Infection should always be ruled out, particularly as the low pH, low glucose and high lactate dehydrogenase seen in rheumatoid effusions is also typical for empyema. Sterile empyematous effusions may be the result of a ruptured necrotic subpleural rheumatoid nodule into the pleural space and subsequent bronchopleural fistula. Although not necessary for the diagnosis of rheumatoid pleural effusion, video-assisted thorascopy with pleural biopsy is undertaken when the diagnosis is unclear. On histology, there is replacement of the normal mesothelial lining with multinucleated giant cells and foci of palisading fibroblasts and lymphocytes surrounding necrotic centres, similar to rheumatoid nodules [52, 53]. Management Most cases of rheumatoid pleuritis improve with treatment of the underlying rheumatoid arthritis; effusions that are small and asymptomatic do not require specific intervention [50]. No specific treatment was used other than therapeutic thoracentesis when indicated [53]. This would argue that patients with large or persistent effusions should be treated to avoid similar complications. Airway disease Conditions affecting both the upper and lower airways can occur in patients with rheumatoid arthritis. Manifestations include rheumatoid nodules on the vocal cords, vasculitis affecting the recurrent laryngeal or vagus nerves leading to vocal cord paralysis, or arthritis of the cricoarytenoid joint. In the latter condition, synovial thickening and build-up of excess synovial fluid leads to progressive cartilage erosion and subluxation of the joint. For more severe obstruction, surgical intervention may be required in addition to immediate airway management [56, 60]. Lower airway involvement Lower airway disease may include bronchial hyperresponsiveness, bronchiolitis or bronchiectasis. For more severe or symptomatic disease, corticosteroids and macrolide antibiotics have been used [65]. In contrast to other rheumatoid lung manifestations, obliterative bronchiolitis presents acutely with rapidly progressive dyspnoea, cough and bronchorrhea in the absence of other systemic symptoms. The mainstay of treatment is to discontinue the offending agent, which will occasionally result in the regression of symptoms. Azathioprine and cyclophosphamide have been used, although it is unclear whether these agents have any efficacy [68, 69]. Macrolide antibiotics, in particular erythromycin, may also be effective [65, 68]. Various hypotheses exist regarding the association between bronchietasis and rheumatoid arthritis, including: chronic suppurative infections leading to bronchiectasis, which is perhaps enhanced in the setting of rheumatoid arthritis; or treatment with disease modifying anti-rheumatic drugs, or alternatively that chronic infections in a bronchiectasis patient provide additional antigenic stimuli that then triggers rheumatoid arthritis [72, 73]. A French study found that patients with rheumatoid arthritis and symptomatic bronchiectasis were more likely to be heterozygous for the fiF508 mutation, compared to those with rheumatoid arthritis without bronchiectasis and those with bronchiectasis of unknown aetiology [74].

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