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But I must explain to you how all this mistaken idea of denouncing pleasure and praising pain was born and will give you a complete account of the system and expound the actual teachings of the great explore

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    Jeremy Greene, M.A., M.D., Ph.D.

    • Elizabeth Treide and A. McGehee Harvey Chair in the History of Medicine
    • Professor of History of Medicine

    https://www.hopkinsmedicine.org/profiles/results/directory/profile/9622265/jeremy-greene

    Cross References Allodynia; Dysaesthesia; Hyperalgesia Hyperphagia Hyperphagia is increased or excessive eating muscle relaxant cephalon generic tizanidine 4mg without prescription. Cross References Cover tests; Heterophoria; Hypophoria Hyperpilaphesie the name given to the augmentation of tactile faculties in response to other sensory deprivation muscle relaxant drugs z buy tizanidine 2 mg otc, for example muscle relaxant radiolab purchase 2 mg tizanidine amex, touch sensation in the blind muscle relaxant hamstring buy genuine tizanidine online. This may be physiological in an anxious patient (refiexes often denoted ++) spasms near heart generic 4 mg tizanidine with mastercard, or pathological in the context of corticospinal pathway pathology (upper motor neurone syndrome quetiapine spasms purchase tizanidine 4 mg without prescription, often denoted +++). It is sometimes difficult to distinguish normally brisk refiexes from pathologically brisk refiexes. Hyperrefiexia (including a jaw jerk) in isolation cannot be used to diagnose an upper motor neurone syndrome, and asymmetry of refiexes is a soft sign. Hyper-refiexia without spasticity after unilateral infarct of the medullary pyramid. In the context of refractory epilepsy, it has been associated with reduced volume of the right hippocampus, but not right amygdala. Cross References Hypergraphia; Hyposexuality Hypersexuality Hypersexuality is a pathological increase in sexual drive and activity. Sexual disinhibition may be a feature of frontal lobe syndromes, particularly of the orbitofrontal cortex. Clinical signs may include a bounding hyperdynamic circulation and sometimes papilloedema, as well as features of any underlying neuromuscular disease. Cross References Akinesia; Bradykinesia; Dysmetria; Fatigue; Hypokinesia; Parkinsonism; Saccades Hypomimia Hypomimia, or amimia, is a deficit or absence of expression by gesture or mimicry. This may be physiological, as with the diminution of the ankle jerks with normal ageing; or pathological, most usually as a feature of peripheral lesions such as radiculopathy or neuropathy. Cross Reference Hyperthermia Hypotonia, Hypotonus Hypotonia (hypotonus) is a diminution or loss of normal muscular tone, causing fioppiness of the limbs. Cross References Ataxia; Flaccidity; Hemiballismus; Hypertonia Hypotropia Hypotropia is a variety of heterotropia in which there is manifest downward vertical deviation of the visual axis of one eye. Improvement of ptosis is said to be specific for myasthenia gravis, perhaps because cold improves transmission at the neuromuscular junction (myasthenic patients often improve in cold as opposed to hot weather). This phenomenon is generally not observed in other causes of ptosis, although it has been reported in Miller Fisher syndrome. A pooled analysis of several studies gave a test sensitivity of 89% and specificity of 100% with correspondingly high positive and negative likelihood ratios. There may be accompanying primitive refiexes, particularly the grasp refiex, and sometimes utilization behaviour. Imitation behaviour occurs with frontal lobe damage; originally mediobasal disease was thought the anatomical correlate, but more recent studies suggest upper medial and lateral frontal cortex. Part I: imitation and utilization behaviour: a neuropsychological study of 75 patients. However, other signs may be absent in disease of the frontal lobe or cauda equina. Intermanual confiict is more characteristic of the callosal, rather than the frontal, subtype of anterior or motor alien hand. Intrusions are thought to refiect inattention and may be seen in dementing disorders or delirium. Intrusions as a sign of Alzheimer dementia: chemical and pathological verification. The finding of inverted refiexes may refiect dual pathology, but more usually refiects a single lesion which simultaneously affects a root or roots, interrupting the local refiex arc, and the spinal cord, damaging corticospinal (pyramidal tract) pathways which supply segments below the refiex arc. Hence, an inverted supinator jerk is indicative of a lesion at C5/6, paradoxical triceps refiex occurs with C7 lesions; and an inverted knee jerk indicates interruption of the L2/3/4 refiex arcs, with concurrent damage to pathways descending to levels below these segments. The pathophysiological implication is of electrical disturbance spreading through the homunculus of the motor cortex. It may also be used to refer to the restlessness seen in acute illness, high fever, and exhaustion, though differing from the restlessness implied by akathisia. Cross References Akathisia; Myoclonus; Seizures Jamais Entendu A sensation of unfamiliarity akin to jamais vu but referring to auditory experiences. This is suggestive of seizure onset in the limbic system, but is not lateralizing (cf. Both the afferent and efferent limbs of the arc run in the mandibular division of the trigeminal (V) nerve, connecting centrally with the mesencephalic (motor) nucleus of the trigeminal nerve. The refiex is highly reproducible; there is a linear correlation between age and refiex latency and a negative correlation between age and refiex amplitude. Facilitation of monosynaptic refiexes by voluntary contractions of muscle in remote parts of the body. This may be confused in neonates with clonic seizures, but in the former there is stimulus sensitivity and an absence of associated ocular movements. However, both may occur in hypoxicfiischaemic or metabolic encephalopathies or with drug withdrawal. This observation helped to promote the idea that tics were due to neurological disease rather than being psychogenic, for example, in Tourette syndrome. It is due to rapid rhythmic contractions of the leg muscles on standing, which dampen or subside on walking, leaning against a wall, or being lifted off the ground, with disappearance of the knee tremor; hence this is a task-specific tremor. Auscultation with the diaphragm of a stethoscope over the lower limb muscles reveals a regular thumping sound, likened to the sound of a distant helicopter. Duchenne muscular dystrophy Stiff person syndrome may produce a characteristic hyperlordotic spine. The test may be positive with disc protrusion, intraspinal tumour, or infiammatory radiculopathy. A positive straight leg raising test is reported to be a sensitive indicator of nerve root irritation, proving positive in 95% of those with surgically proven disc herniation. Crossed straight leg raising, when the complaint of pain on the affected side occurs with raising of the contralateral leg, is said to be less sensitive but highly specific. Infarction due to vertebral artery occlusion (occasionally posterior inferior cerebellar artery) or dissection is the most common cause of lateral medullary syndrome, although tumour, demyelination, and trauma are also recognized causes. This spinal refiex manifests as fiexion of the arms at the elbow, adduction of the shoulders, lifting of the arms, dystonic posturing of the hands, and crossing of the hands. Causes include retinoblastoma, retinal detachment, toxocara infection, congenital cataract, and benign retinal hypopigmentation. Pathophysiologically, this movement-induced symptom may refiect the exquisite mechanosensitivity of axons which are demyelinated or damaged in some other way. Conduction properties of central demyelinated axons: the generation of symptoms in demyelinating disease. Ectropion may also be seen with lower lid tumour or chalazion, trauma with scarring, and ageing. The locked-in syndrome may be mistaken for abulia, akinetic mutism, coma, and catatonia. The locked-in syndrome: what is it like to be conscious but paralyzed and voicelessfi Cross Reference Aphasia Logorrhoea Logorrhoea is literally a fiow of speech, or pressure of speech, denoting an excessive verbal output, an abnormal number of words produced during each utterance. The term may be used for the output in the Wernicke/posterior/sensory type of aphasia or for an output which superficially resembles Wernicke aphasia but in which syntax and morphology are intact, rhythm and articulation are usually normal, and paraphasias and neologisms are few. Patients may be unaware of their impaired output (anosognosia) due to a failure of self-monitoring. Logorrhoea may be observed in subcortical (thalamic) aphasia, usually following recovery from lesions (usually haemorrhage) to the anterolateral nuclei. It is often possible to draw a clinical distinction between motor symptoms resulting from lower or upper motor neurone pathology and hence to formulate a differential diagnosis and direct investigations accordingly. Cortical blindness due to bilateral (sequential or simultaneous) posterior cerebral artery occlusion may leave a small central field around the fixation point intact, also known as macula sparing. Macula splitting, a homonymous hemianopia which cuts through the vertical meridian of the macula, occurs with lesions of the optic radiation. Hence, macula sparing and macula splitting have localizing value when assessing homonymous hemianopia. Cross References Flail arm; Quadriparesis, Quadriplegia Marche a Petit Pas Marche a petit pas is a disorder of gait characterized by impairments of balance, gait ignition, and locomotion. Particularly there is shortened stride (literally marche a petit pas) and a variably wide base. This gait disorder is often associated with dementia, frontal release signs, and urinary incontinence, and sometimes with apraxia, parkinsonism, and pyramidal signs. This constellation of clinical signs refiects underlying pathology in the frontal lobe and subjacent white matter, most usually of vascular origin, and is often associated with a subcortical vascular dementia.

    Diseases

    • Arachnodactyly ataxia cataract aminoaciduria mental retardation
    • Fetal prostaglandin syndrome
    • Mental retardation macrocephaly coarse facies hypotonia
    • McCallum Macadam Johnston syndrome
    • Hyperostosis corticalis generalisata
    • Marchiafava Micheli disease
    • Congenital absence of the uterus and vagina

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    Correlation of changes in quality of life after lung volume reduction surgery with changes in lung function spasms quadriceps buy tizanidine 4mg line, exercise muscle relaxant tablets generic tizanidine 2 mg overnight delivery, and gas exchange muscle relaxer kick in order 4mg tizanidine with visa. Prospective randomized trial comparing bilateral lung volume reduction surgery to pulmonary rehabilitation in severe chronic obstructive pulmonary disease spasms in stomach order tizanidine 2mg with visa. Serial lung function and elastic recoil 2 years after lung volume reduction surgery for emphysema muscle relaxant agents generic tizanidine 4mg free shipping. Functional results of single-lung transplantation for chronic obstructive lung disease spasms after hysterectomy buy tizanidine 4mg cheap. Comparison of outcomes of double and single lung transplantation for obstructive lung disease. Comparison of outcomes after single and bilateral lung transplantation for obstructive lung disease. Cardiopulmonary exercise testing following allogeneic lung transplantation for different underlying disease states. Long-term health status and quality of life outcomes of lung transplant recipients. The Registry of the International Society for Heart and Lung Transplantation: eighteenth Official Report-2001. Listing for lung transplantation: life expectancy and transplant effect, stratified by type of end-stage lung disease, the Eurotransplant experience. Lung transplant waiting list: differential outcome of type of end-stage lung disease, one year after registration. Effect of diagnosis on survival benefit of lung transplantation for end-stage lung disease. Bronchiolitis obliterans syndrome: incidence, natural history, prognosis, and risk factors. Risk of anesthesia and surgery in patients with chronic bronchitis and chronic obstructive pulmonary disease. Minimal complications in a surgical population with severe asthma receiving prophylactic corticosteroids. Prevention of postoperative pulmonary complications through respiratory rehabilitation: a controlled clinical study. Anaesthesia and postoperative analgesia in older patients with chronic obstructive pulmonary disease. Residual neuromuscular block is a risk factor for postoperative pulmonary complications. A prospective, randomised, and blinded study of postoperative pulmonary complications after atracurium, vecuronium and pancuronium. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results from overview of randomised trials. Epidural anasesthesia and analgesia and outcome of major surgery: a randomised trial. Thoracic epidural anesthesia combined with general anesthesia: the preferred anesthetic technique for thoracic surgery. Lung function under high thoracic segmental epidural anesthesia with ropivacaine or bupivacaine in patients with severe obstructive pulmonary disease undergoing breast surgery. The effect of incentive spirometry on postoperative pulmonary complications: a systematic review. Continuous thoracic epidural analgesia for postoperative pain relief following thoracotomy: a randomized prospective study. A randomized, double-blind comparison of lumbar epidural and intravenous fentanyl infusions for postthoracotomy pain relief. Background Sleep has effects on breathing that include changes in central respiratory control, airways resistance and muscle contractility. Sleep disturbance is probably a consequence of the underlying lung disease, although adverse effects of drug therapy may also contribute. Sleep disturbance probably contributes to the nonspecific daytime symptoms of chronic fatigue, lethargy and overall impairment in quality of life described by these patients [7, 8]. There is a close relationship between the awake arterial oxygen tension (Pa,O2) and nocturnal arterial oxygen saturation (Sa,O2) levels [2, 11], although hypercapnia is associated with more pronounced nocturnal oxygen desaturation than normocapnia for any given level of awake Sa,O2 in some studies [11, 12] but not in others [2]. However, some patients with awake Pa,O2 levels in the mildly hypoxaemic range can also develop clinically significant nocturnal oxygen desaturation, which may predispose to pulmonary hypertension [13]. Furthermore, there is a normal circadian change in airway calibre resulting in mild nocturnal bronchoconstriction. This contributes to worsening ventilation/perfusion relationships, which also aggravates hypoxaemia. There is evidence that nocturnal oxygen desaturation contributes to mortality, particularly during acute exacerbations. Two studies have demonstrated a significant relationship between nocturnal desaturation and long-term survival, although the data are less clear on whether the relationship is independent of other factors such as lung function or awake blood gases [11, 16]. Furthermore, there is no clear evidence that correction of nocturnal oxygen desaturation improves survival [16]. However, there is evidence that patients with exacerbations are more likely to die at night, particularly those with hypercapnia [5]. Therefore, they are particularly prone to the complications of chronic hypoxaemia, such as cor pulmonale and polycythaemia. Measures to improve sleep quality should focus on minimising symptoms such as cough and dyspnoea that may disturb sleep patterns by arousal. Nocturnal oxygen therapy is not recommended for isolated nocturnal hypoxaemia except in special circumstances, such as the presence of complications of hypoxaemia, i. A number of pharmaceutical agents have been shown to benefit nocturnal Sa,O2, including theophylline [18] and anticholinergic agents [19, 20], and ipratropium has been shown to improve sleep quality [19]. Nocturnal hypoxemia and associated electrocardiographic changes in patients with chronic obstructive airways disease. Pulmonary vascular hemodynamics in chronic lung disease patients with and without oxyhemoglobin desaturation during sleep. Prevalence of reported sleep disturbances in a general population and their relationship to obstructive airways diseases. Nocturnal hypoxaemia and quality of sleep in patients with chronic obstructive lung disease. Contribution of hypoventilation to sleep oxygen desaturation in chronic obstructive pulmonary disease. Do sleep studies contribute to the management of patients with severe chronic obstructive pulmonary diseasefi Sleep and Sleep-disordered Breathing in Adults with Predominantly Mild Obstructive Airway Disease. Theophylline improves gas exchange during rest, exercise and sleep in severe chronic obstructive pulmonary disease. Effects of Zolpidem and Triazolam on sleep and respiration in mild to moderate chronic obstructive pulmonary disease. Since sea-level Pa,O2 values are on the steep portion of the O2-haemoglobin dissociation curve, the corresponding fall in arterial O2 saturation (Sa,O2) may be quite severe. During flights, patients may develop dyspnoea, wheezing, chest pain, cyanosis and right heart failure, leading to urgent requests for O2 [2]. Even light physical exertion during a flight can increase the risk of an exacerbation of symptoms [3]. Although death due to a purely 159 of 222 160 of 222 respiratory cause rarely occurs during flight, the frequency of less-morbid events, including worsening symptoms after exiting the plane, may be underreported. Air travel in small aircraft with pressurised and unpressurised cabins, including commuter planes, can also result in significant hypobaric exposure. If specific information concerning cabin altitude is known in advance, it should be integrated into decision-making processes. Co-morbidities Recent literature has suggested that pulmonary embolism is a risk factor for many airline travellers. This seems to be related to the duration of flight and underlying predisposing factors [5]. Pre-flight assessment the pre-flight assessment should incorporate the following steps in many cases: 1) estimate the expected degree of hypoxaemia at altitude; 2) identify co-morbid disease conditions; and 3) prescribe O2 if necessary. Counselling the patient and documenting recent clinical condition and laboratory tests are also desirable elements of pre-flight patient care, particularly if the patient is travelling abroad. At present, the two most widespread means of estimating the degree of hypoxaemia at altitude consist of the hypoxia inhalation test [6, 7] and the use of regression formulae [1]. Pulse oximetry tends to underestimate the degree of acute hypobaric hypoxia and should not be used alone to decide if significant hypoxaemia has occurred [10]. Pulse oximetry can be used to titrate O2 supplementation and avoid multiple needle sticks for blood gas testing. Regression equations Regression equations offer the opportunity to compare an individual to a group of patients with similar clinical characteristics who have been previously studied during exposure to hypobaric hypoxia [1]. Furthermore, the alveolar/arterial gradient at sea level should not be assumed constant at altitude. Assessments within 2 h of flight have greater accuracy but less practicality [11]. Oxygen supplementation It is currently recommended that the Pa,O2 during air travel should be maintained above 50 mmHg (6. Patients will also require additional O2 supplementation if the elevation at the destination is significantly greater than at home. O2 conserving devices have been demonstrated to be effective at altitude and may be practical for long-duration flights. All carriers provided nasal cannulas with a wide variation in other devices, O2 flow rates and prices. Hypoxemia during air travel in patients with chronic obstructive pulmonary disease. Development of severe hypoxaemia in chronic obstructive pulmonary disease patients at 2438 m (8000 ft) altitude. Hemodynamic effects of altitude exposure and oxygen administration in chronic obstructive pulmonary disease. The preflight evaluation: a comparison of the hypoxia inhalation test with hypobaric exposure. Accuracy of oxyhemoglobin saturation monitors during simulated altitude exposure of men with chronic obstructive pulmonary disease. Is normobaric simulation of hypobaric hypoxia accurate in chronic airflow limitationfi Oxygen supplementation during air travel in patients with chronic obstructive pulmonary disease. A comparative analysis of arranging in-flight oxygen aboard commercial air carriers. Despite aggressive medical treatment, approximately one third of patients discharged from the emergency department with acute exacerbations have recurrent symptoms within 14 days [10], and 17% relapse and require hospitalisation [11]. These end-points have been used to evaluate new drugs but may lack clinical relevance. Other end-points, such as an exacerbation-free interval, resource utilisation (hospitalisation, clinic 166 of 222 167 of 222 visits, medication use, lost work days, etc. The following operational classification of severity can help rank the clinical relevance of the episode and its outcome. Assessment Several clinical elements must be considered when evaluating patients with exacerbations. The physical examination should evaluate the effect of the episode on the haemodynamic and respiratory systems. The diagnostic procedures to be performed depend on the setting of the evaluation [22, 23]. Table 1 shows the elements of the clinical evaluation and diagnostic procedures that are usually informative in patients with exacerbations according to the severity of the episode. Treatment the treatment of exacerbation has to be based on the clinical presentation of the patient, as shown in table 2 for Level I. Hospitalisation Traditionally, the decision to admit derives from subjective interpretation of clinical features, such as the severity of dyspnoea, determination of respiratory failure, short-term response to emergency room therapy, degree of cor pulmonale and the presence of complicating features, such as severe bronchitis, pneumonia or other comorbid conditions. General consensus supports the need for hospitalisation in patients with severe acute hypoxaemia or acute hypercarbia. Less extreme arterial blood gas abnormalities, however, do not assist decision analysis. Indications Table 3 below provides reasonable guidelines for patient hospitalisation.

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    It is important to distinguish between severe asthma and asthma that is uncontrolled muscle relaxant images buy tizanidine 2mg with visa. Assess symptom control from the frequency of daytime and night-time asthma symptoms and reliever use spasms under breastbone buy tizanidine cheap, and from activity limitation muscle relaxant for back pain purchase tizanidine online. Symptom control tools include Asthma Control Test and Asthma Control Questionnaire spasms colon purchase tizanidine 4mg without prescription. Identified risk factors for exacerbations that are independent of symptom control include a history of fi1 exacerbations in the previous year spasms and pain under right rib cage purchase tizanidine 4 mg mastercard, poor adherence spasms above ear purchase tizanidine 4 mg online, incorrect inhaler technique, low lung function, smoking, and blood eosinophilia. Discordance between symptoms and lung function should prompt further investigation. The level of asthma control is the extent to which the manifestations of asthma can be observed in the patient, or have 14,58 been reduced or removed by treatment. He also has several additional risk factors for future exacerbations including low lung function, current smoking, and poor medication adherence. Poor symptom control is also strongly associated with 60-62 an increased risk of asthma exacerbations. Asthma symptom control should be assessed at every opportunity, including during routine prescribing or dispensing. Directed questioning is important, as the frequency or severity of symptoms that patients regard as unacceptable or bothersome may vary from current recommendations about the goals of asthma treatment, and differs from patient to patient. For example, despite having low lung function, a person with a sedentary lifestyle may not experience bothersome symptoms and so may appear to have good symptom control. In general, do not include reliever taken before exercise, since this is often routine. Asthma symptom control tools for adults and adolescents Simple screening tools: these can be used in primary care to quickly identify patients who need more detailed assessment. This classification 63,64 correlates with assessments made using numerical asthma control scores. It can be used, together with a risk assessment (Box 2-2B), to guide treatment decisions (Box 3-5, p. This assessment is linked to a care algorithm for identifying problems and adjusting treatment up or down. These scores may be useful for assessing patient progress; they are commonly used in clinical research, but may be subject to copyright restrictions. When different systems are used for assessing asthma symptom control, the results correlate broadly with each other, but are not identical. Respiratory symptoms may be non-specific so, when assessing changes in symptom control, it is important to clarify that symptoms are due to asthma. Many children with poorly controlled asthma avoid strenuous exercise so their asthma may appear to be well controlled. Children vary considerably in the degree of airflow limitation observed before they complain of dyspnea or use their reliever therapy, and marked reduction in lung function is often seen before it is recognized by the parents. Risk factors for poor asthma outcomes Assess risk factors at diagnosis and periodically, particularly for patients experiencing exacerbations. Poor symptom control and exacerbation risk should not be simply combined numerically, as they may have different causes and may need different treatment strategies. Level of activity What sports/hobbies/interests does the child have, at school and in their spare timefi Persistent 98 bronchodilator reversibility is a risk factor for exacerbations, even if the child has few symptoms. Treatment factors Inhaler technique Ask the child to show how they use their inhaler. Goals/concerns Does the child or their parent/carer have any concerns about their asthma. Other investigations (if needed) 2-week diary If no clear assessment can be made based on the above questions, ask the child or parent/carer to keep a daily diary of asthma symptoms, reliever use and peak expiratory flow (best of three) for 2 weeks (Appendix Chapter 4). Exercise challenge Provides information about airway hyperresponsiveness and fitness (Box 1-2, p. Only (laboratory) undertake a challenge if it is otherwise difficult to assess asthma control. Asthma symptom control and exacerbation risk should not be simply combined numerically, as poor control of symptoms and of exacerbations may have different causes and may need different treatment approaches. Risk factors for exacerbations 60-62 Poor asthma symptom control itself substantially increases the risk of exacerbations. These risk factors (Box 2-2B) include a history of fi1 exacerbations in the previous year, poor 115 adherence, incorrect inhaler technique, chronic sinusitis and smoking, all of which can be assessed in primary care. People with asthma may have an accelerated decline in lung function and develop airflow limitation that is not fully reversible. Children with persistent asthma may have reduced growth in lung function, and some 117 are at risk of accelerated decline in lung function in early adult life. Risk factors for medication side-effects Choices with any medication are based on the balance of benefit and risk. The risk of side-effects increases with higher doses of medications, but these are needed in few patients. In some asthma control tools, 69,120 lung function is numerically averaged or added with symptoms, but if the tool includes several symptom items, 121 these can outweigh clinically important differences in lung function. For example, in most adult patients, lung function should be recorded at least every 1-2 years, but more frequently in higher risk patients including those with exacerbations and 2. Lung function should also be recorded more frequently in children based on asthma severity and clinical course (Evidence D). Once the diagnosis of asthma has been confirmed, it is not generally necessary to ask patients to withhold their regular 14 or as-needed medications before visits, but preferably the same conditions should apply at each visit. In children, spirometry cannot be reliably obtained until age 5 years or more, and it is less useful than in adults. Many children with uncontrolled asthma have normal lung function between flare-ups (exacerbations). While many patients with uncontrolled asthma may be difficult to treat due to inadequate or inappropriate treatment, or persistent problems with adherence or comorbidities such as chronic rhinosinusitis or obesity, the European Respiratory Society/American Thoracic Society Task Force on Severe Asthma considered that the definition of severe asthma should be reserved for patients with refractory asthma and those in whom response to treatment 136 of comorbidities is incomplete. This approach is based on the assumption that patients are receiving appropriate treatment, and that those prescribed more intense treatment are likely to have more severe underlying disease. However, this is only a surrogate measure, and it causes confusion since most studies also require participants to have uncontrolled symptoms at entry. For epidemiological studies or clinical trials, it is preferable to categorize patients by the type of treatment that they are prescribed, without inferring severity. This category corresponds to other classifications of uncontrolled asthma in patients not taking controller treatment. In older asthma literature, many different severity classifications have been used; many of 58 these were similar to current concepts of asthma control. How to distinguish between uncontrolled and severe asthma Although most asthma patients can achieve good symptom control and minimal exacerbations with regular controller 120 treatment, some patients will not achieve one or both of these goals even with maximal therapy. In some patients this is due to truly refractory severe asthma, but in many others, it is due to comorbidities, persistent environmental exposures, or psychosocial factors. Assessment of asthma 35 It is important to distinguish between severe asthma and uncontrolled asthma, as the latter is a much more common reason for persistent symptoms and exacerbations, and may be more easily improved. Box 2-4 shows the initial steps that can be carried out to identify common causes of uncontrolled asthma. Investigating a patient with poor symptom control and/or exacerbations despite treatment 36 2. Treating asthma to control symptoms and minimize risk this chapter is divided into five parts: Part A. Difficult-to-treat and severe asthma in adults and adolescents (including decision tree) Management of worsening and acute asthma is described in Chapter 4 (p. Shared goals for asthma management can be achieved in various ways, taking into account differing health care systems, medication availability, and cultural and personal preferences. This should enable the person with asthma to gain the knowledge, confidence and skills to assume a major role in the management of their asthma. Self-management education reduces 140 141 asthma morbidity in both adults (Evidence A) and children (Evidence A). Patients should be encouraged to participate in decisions about their treatment, and given the opportunity to express their expectations and concerns. Good communication 143-145 Good communication by health care providers is essential as the basis for good outcomes (Evidence B). Teaching health care providers to improve their communication skills (Box 3-1) can result in increased patient satisfaction, better 143-145 146 health outcomes, and reduced use of health care resources without lengthening consultation times. Training patients to give information clearly, seek information, and check their 146 understanding of information provided is also associated with improved adherence with treatment recommendations. Health literacy and asthma 147,148 There is increasing recognition of the impact of low health literacy on health outcomes, including in asthma. Low 149 health literacy is associated with reduced knowledge and worse asthma control. In one study, low numeracy among 148 parents of children with asthma was associated with higher risk of exacerbations.

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