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A consistent theme is that people who contribute their own information to public databases want to be asked for permission buy 5 mg clarinex with amex allergy forecast yonkers ny, to have a clear explanation of how the data will be used cheap clarinex 5 mg fast delivery allergy symptoms throat, and to be treated as true partners in the research process (Damschroder et al cheap clarinex 5mg amex allergy testing on a two year old. Although privacy concerns remain discount clarinex 5mg on line allergy medicine 911, there is little evidence that the public has the extreme sensitivity toward genetic data that many researchers anticipated 25 years ago. The Proposed Knowledge Network of Disease Could Catalyze Changes in Biology, Information Technology, Medicine, and Society The powerful forces affecting basic biological research, information technology, clinical medicine, and public attitudes toward the privacy of health records and personal genetic information create an unprecedented opportunity to change how biomedical research is conducted and to improve health outcomes. The development of the proposed Knowledge Network of Disease and its associated New Taxonomy could take advantage of these forces to inspire revolutionary change. This Committee regards commitment to the development of these resources as a powerful unifying idea that could harness—and, to an appropriate degree, redirect—the creative energies of the key constituencies to achieve the full potential of biology to improve health outcomes. Toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease 3 What Would a Knowledge Network and New Taxonomy Look Like? In the previous chapter, the Committee outlined the reasons it concluded that the time is right to develop a Knowledge Network of Disease and New Taxonomy. But what would these resources look like and what implications would they have for disease classification, basic research, clinical care and the health-care system? This chapter describes the Committee’s vision of a comprehensive Knowledge Network of Disease and New Taxonomy that would unite the biomedical-research, public-health, and health-care-delivery communities around the related goals of advancing our understanding of disease pathogenesis and improving health. The Committee envisions that the proposed resources would have several key features: x They would drive development of a disease taxonomy that describes and defines diseases based on their intrinsic biology in addition to traditional physical “signs and symptoms”. The Knowledge Network of Disease Would Incorporate Multiple Parameters and Enable a Taxonomy Heavily Rooted in the Intrinsic Biology of Disease Physical signs and symptoms are the overt manifestations of disease observed by physicians and patients. Physical signs and symptoms are generally also difficult to measure quantitatively. Indeed, in a strict sense, all diseases are presumably asymptomatic for some “latent period” following the initiation of pathological processes. As a consequence, diagnosis based on traditional “signs and symptoms” alone carries the risk of missing opportunities for prevention, or early intervention can readily misdiagnose patients altogether. Toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease 36 diseases become clinically evident, obtaining optimal diagnostic results can depend on supplementing standard histology with ancillary genetic or immunohistochemical testing to identify specific mutations or marker proteins. Biology-based indicators of disease such as genetic mutations, marker-protein molecules, and other metabolites have the potential to be precise descriptors of disease. They can be measured accurately and precisely–be it in the form of a standardized biochemical assay or a genetic sequence—thus enabling comparison across datasets obtained from independent studies. Particularly when multiple molecular indicators are used in combination with conventional clinical, histological, and laboratory findings, they offer the opportunity for a more accurate and precise description and classification of disease, particularly. Numerous molecularly-based disease markers are already available, and the number will grow rapidly in the future. Amongst the most prominent parameters of disease are an individual’s: x Genome x Transcriptome x Proteome x Metabolome x Lipidome x Epigenome As discussed in Chapter 2, it is increasingly feasible to obtain substantial information about these biological features for each individual patient. The cost of sequencing an individual’s genome is rapidly dropping, and significant advances in the ability to globally and affordably characterize proteomes, metabolomes, lipidomes, epigenomes, and microbiomes of individual subjects will continue, creating the potential for an increasingly rich molecular characterization of individuals in the future. Eventually, it is likely that extensive molecular characterization of individuals will occur routinely as a normal part of health care – even prior to appearance of disease thereby allowing the collection of data on both sick and healthy individuals on a scale vastly exceeding current practice. In addition to providing a new resource for research on disease processes, these data would provide a far more flexible and useful definition of the “normal” state, in all its diversity, than now exists. The ability to make such measurements on both non-affected tissues and in sites altered by disease would allow monitoring of the development and natural history of many disorders about which even the most basic information is presently unavailable. Gene- environment interactions have been implicated in a diverse group of diseases and pathological processes, including some psychological illnesses (Caspi et al. Toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease 37 2009), and cardiovascular reactivity (Williams et al. Therefore, data added to the Information Commons should not be limited to molecular parameters as they are currently understood: patient-related data on environmental, behavioral, and socioeconomic factors will need to be considered as well in a 7 thorough description of disease features (see Box 3-1: The Exposome). Despite the focus on the individual patient in the creation of the Information Commons, the Committee expects that the inclusion of patients from diverse populations coupled with the incorporation of various types of information contained in the exposome will result in a Knowledge Network that could also inform the identification of population level interventions and the improvement of population health. For example, a better understanding of the impact of a sedentary lifestyle at the molecular level could conceivably facilitate the development of new approaches to physical education in early childhood. In addition, findings from the Knowledge Network and the New Taxonomy could reveal yet unidentified behavioral, social, and environmental factors that are associated with particular diseases or sub-classifications of diseases in certain populations and are amenable to public health interventions. While molecular variables are often more easily measured and more directly tied to disease outcomes, if the modifiable factors that have contributed to the signature are known, we will be better able to prevent disease and to phenotype, genotype, and treat patients. A long-range goal is to ascertain the combined effects of these exposures by assessing the biomarkers and diseases they influence. In its broadest definition, the exposome encompasses all exposures—internal (such as the microbiome, described elsewhere in this report) and external—across the lifespan. Toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease 38 Zanobetti et al. However, the concept of the exposome extends beyond these factors to include social factors, such as socioeconomic status, quality of housing, neighborhood, social relationships, access to services, and experience of discrimination that can contribute to psychological stress and contribute to poor health and health inequities (Epel et al. By incorporating data derived from multi-level assessments, a Knowledge Network of Disease could lead to better understanding of the variables and mechanisms underlying disease and health disparities, thereby helping to reveal a truer picture of the ecology of human health and facilitating a more holistic approach to health promotion and disease prevention. Asthma illustrates the interplay of social, behavioral, environmental, and genetic factors in disease classification. It is estimated that various types of asthma affect more than 300 million people worldwide. The term “asthma” is now used to refer to a set of “signs and symptoms” including reversible airway narrowing (“wheezing”), airway inflammation and remodeling, and airway hyper-reactivity. These various “signs and symptoms” likely reflect distinct etiologies in different patients. Many subjects with asthma have an allergic component, while in other cases, no clear allergic contributor can be defined (Hill et al. In some patients, asthma attacks are precipitated by exercise or aspirin (Cheong et al. Some patients, particularly those with severe asthma, may be resistant to treatment with corticosteroids (Searing et al. This phenomenological approach to asthma diagnosis has led to a plethora of asthma sub-types such as “allergic asthma,” “exercise-induced asthma,” and “steroid-resistant asthma” that may be clinically useful but provide little insight into underlying etiologies. Over the years, linkage-analysis, candidate-gene, and genome-wide-association approaches have been applied to the study of the genetic underpinnings of asthma, leading to the identification of several associated genes and sub-phenotypes (Lee et al. However, these findings still leave most of the genetic influences of asthma unexplained (Li et al. Moreover, pediatric asthma research, in particular, has focused on a broad range of social and environmental, as well as genetic, contributors to the increased prevalence and severity of illness (Hill et al. Since the burden of asthma disproportionately affects children living in socioeconomically disadvantaged neighborhoods (D. A knowledge- network-derived-taxonomy based on the biology of disease may help to divide patients with asthma—as well as many other diseases— into subtypes in which the different etiologies of the disorder can be better understood, and for which appropriate, subtype-specific approaches to treatment and prevention can be devised and tested. Toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease 39 The Proposed Knowledge Network of Disease Would Include Information about Pathogens and Other Microbes Particularly because of advances in genomics, the proposed Knowledge Network of Disease has unprecedented potential to incorporate information about disease-causing and disease-associated microbial agents. Thousands of microbial genomes have been sequenced, providing a wealth of data on pathogenic and non-pathogenic organisms, and there has been an associated renaissance in studies of the molecular mechanisms of host-pathogen interactions.
Fasching and coworkers (1996) reported no difference in insulin secretion or sensitivity in men who con- sumed a 33 percent saturated cheap clarinex american express allergy panel, monounsaturated discount clarinex master card allergy treatment nz, or polyunsaturated fatty acid diet cheap 5 mg clarinex otc allergy symptoms for alcohol. There was no difference in postprandial glucose or insulin con- centration when healthy adults were fed butter or olive oil (Thomsen et al order clarinex now allergy shots in pregnancy. Louheranta and colleagues (1998) found no difference in glucose tolerance and insulin sensitivity in healthy women fed either a high oleic or stearic acid diet. It is neither possible nor advisable to achieve 0 percent of energy from satu- rated fatty acids in typical whole-food diets. This is because all fat and oil sources are mixtures of fatty acids, and consuming 0 percent of energy would require extraordinary changes in patterns of dietary intake, such as the inclusion of fats and oils devoid of saturated fatty acids, which are presently unavailable. It is possible to consume a diet low in saturated fatty acids by following the dietary guidance provided in Chapter 11. Within the range of usual intake, there are no clearly established adverse effects of n-9 monounsaturated fatty acids in humans. There is some preliminary evidence that a meal providing 50 g of fat from olive oil reduced brachial artery flow-mediated vasodilation by 31 percent in 10 healthy, normolipidemic individuals versus canola oil or salmon (Vogel et al. Dietary mono- unsaturated fatty acids induce atherogenesis due to greater hepatic lipid concentrations (i. Overconsumption of energy related to a high n-9 mono- unsaturated fatty acid and high fat diet is another potential risk associated with excess consumption of monounsaturated fatty acids. While most epidemiological studies indicate that mono- unsaturated fatty acid intake is not associated with increased risk of most cancers (Holmes et al. There is some epidemiological evidence for a positive association between oleic acid intake and breast cancer risk in women with no history of benign breast disease (Velie et al. In addition, one study reported that women with a family history of colorectal cancer who consumed a diet high in mono- and polyunsaturated fatty acids were at greater risk of colon cancer than women without a family history (Slattery et al. Giovannucci and coworkers (1993) reported a positive association between monounsaturated fatty acid intake and risk of advanced prostate cancer, while two studies observed increased risk of lung cancer (De Stefani et al. Numerous studies have shown suppression of various aspects of human immune function in vitro or ex vivo in peripheral blood mononuclear cells, or in isolated neutrophils or monocytes in individuals provided n-3 polyunsaturated fatty acids as a supplement or as an experimental diet compared with baseline values before the intervention (Table 8-8). This diminished ability, however, is also associated with suppression of inflammatory responses, suggesting benefits for individuals suffering from autoimmune diseases such as rheumatoid arthritis. It seems that the same doses of n-3 fatty acids that may be beneficial in chronic disease preven- tion are doses that are also immunosuppressive. These data support a lack of long-term adverse effect of fish-oil supplementation on cytokine activity. Differences in study design (single treatment versus multitreatment parallel designs) seem to be quite significant in determin- ing whether n-3 fatty acid supplementation exerts immunosuppression or not. For example, the difference in results between Caughey and colleagues (1996) (a baseline comparison study) and Blok and colleagues (1997) (a group comparison study) is not accounted for by greater variability in measurements by the latter group. Therefore, the study by Mølvig and colleagues (1991) showed some concurrence with that of Blok and colleagues (1997) and Caughey and colleagues (1996). Another alternative is to extrapolate from animal studies using model species that are known to have similar immune system components and responsiveness compared to humans. Detailed characterization of appro- priateness of animal models for extrapolation to humans with respect to immunosuppression has not been done. A few animal studies have shown the effects of dietary n-3 fatty acids on response to infection (Chang et al. The platelet count can decline by as much as 35 percent; however, the count does not usually fall below the lower limit of normal (Goodnight et al. Although prolonged bleeding times have been shown to be beneficial in preventing heart disease, bleed- ing times can become prolonged enough to result in excessive bleeding and bruising. Intervention studies that have examined the effects of n-3 fatty acids on bleeding time are mixed. None of the above studies reported excessive bleeding times, bleeding episodes, or bruising. Excessive cutaneous bleed- ing time and reduced in vitro platelet aggregability have been reported in Greenland Eskimos (Dyerberg and Bang, 1979; Dyerberg et al. A tendency to bleed from the nose and urinary tract was observed among the Greenland Eskimos (Bang and Dyerberg, 1980). Furthermore, ecologi- cal studies have suggested an increased risk of hemorrhagic stroke among Greenland Eskimos (Kristensen, 1983; Kromann and Green, 1980). A recent prospective study in the United States showed no association between intake of n-3 fatty acids and risk of hemorrhagic stroke (Iso et al. The median intake levels for the quintiles of n-3 polyunsaturated fat intake, however, ranged from only 0. The oxidative damage was shown to be reduced or prevented with the coconsumption of vitamin E (Ando et al. Studies on immune function were done in vitro and it is difficult, if not impossible, to know how well these artificial condi- tions simulate human immune cell response in vivo. Special Considerations A few special populations have been reported to exhibit adverse effects from consuming n-3 polyunsaturated fatty acids. Despite the favorable effects of n-3 fatty acids on glucose homeostasis, caution has been sug- gested for the use of n-3 fatty acids in those individuals who already exhibit glucose intolerance or diabetic conditions (Glauber et al. Increased episodes of nose bleeds have been observed in individuals with familial hypercholes- terolemia during fish-oil supplementation (Clarke et al. Anticoagu- lants, such as aspirin, warfarin, and coumadin, will prolong bleeding times and the simultaneous ingestion of n-3 fatty acids by individuals may exces- sively prolong bleeding times (Thorngren and Gustafson, 1981). During the early 1980s studies showed a hypercholesterolemic effect of trans fatty acids in rabbits (Kritchevsky, 1982; Ruttenberg et al. Renewed interest in the topic of hydrogenated fat in human diets, or more precisely trans fatty acid intake, started in the early 1990s. The availability of a methodology to distinguish the responses of individual lipoprotein classes to dietary modification expanded the depth to which the topic could be readdressed. Lipoprotein(a) (Lp(a)) concentrations in plasma have been associated with increased risk for developing cardiovascular and cerebrovascular disease, possibly via inhibition of plasminogen activity (Lippi and Guidi, 1999; Nielsen, 1999; Wild et al. Lp(a) concentrations have been reported by some investigators to be increased after the consumption of diets enriched in hydrogenated fat/trans fatty acids (Tables 8-9, 8-10, and 8-11) (Almendingen et al. The magnitude of the mean increases in Lp(a) concentrations reported to date that is associated with trans fatty acid intake for the most part would not be predicted to have a physiologically significant effect on cardiovascular disease risk. How- ever, an unresolved issue at this time is the potential effect of relatively high levels of trans fatty acids in individuals with initially high concentra- tions of Lp(a). The effect of trans fatty acids on hemostatic factors has been assessed by a number of investigators (Almendingen et al. In general, these researchers have concluded that hydrogenated fat/trans fatty acids had little effect on a variety of hemostatic variables. Similarly, Müller and colleagues (1998) reported that hemostatic variables were unaffected by the substitution of a vegetable oil- based margarine relatively high in saturated fatty acids when compared with a hydrogenated fish oil-based margarine.
They are less likely to recommend certain tests or treatments clarinex 5mg overnight delivery allergy symptoms cough dry, thinking that their patient would not want to take the risk associated with the test or therapy generic clarinex 5 mg free shipping allergy testing pros and cons, but will be willing to take the risk associated with an error of omission in the process of diagnosis or treatment purchase clarinex with visa allergy medicine mold spores. The test minimizer projects that the patient is willing to take the risk of missing an unlikely diagnosis and would not want any additional tests performed buy discount clarinex 5 mg on-line allergy testing ashby de la zouch. Additionally, use the communica- tions techniques discussed in Chapter 18 to maximize understanding, informed consent, and shared decision making with the patient. If things aren’t working right because of personal issues, such as a ﬁght with your spouse, kids, or partners, problems paying your bills, or other issues, don’t take it out on patients. Physicians must learn to overcome their own feelings and not let them get in the way of good and empathic com- munications with patients. The examinee Biologic variation in the system being examined The main source of random error in medicine is biologic variation. People are complex biological organisms and all physiological responses vary from per- son to person, or from time to time in the same person. For example, some patients with chronic bronchitis will have audible wheezes and rhonchi while others won’t have wheezes and will only have a cough on forced expiration. Some people with heart attacks have typical crushing substantial chest pain while oth- ers have a fainting spell, weakness, or shortness of breath as their only symptom. Understanding this will lead to better appreciation of subtle variations in the his- tory and physical examination. Effects of illness and medication Ignoring the effect of medication or illness on the physiologic response of the patient may result in an inaccurate examination. For instance, patients who take beta-blocker drugs for hypertension will have a slowing of the pulse, so they may not have the expected physical exam ﬁndings like tachycardia even if they are in a condition such as shock. Memory and rumination Patients may remember their medical history differently at different times, which results in a form of recall bias. This explains the commonly observed 238 Essential Evidence-Based Medicine phenomenon that the attending seems to obtain the most accurate history. The intern or medical student will usually obtain the ﬁrst history from a patient. When the attending gets the history later, the patient will have had time to recon- sider their answers to the questions and may give a different and more accurate history. They may have recalled things they did not remember or thought were not important during the ﬁrst questioning. A way to reduce this is by summariz- ing the history obtained several times during the initial encounter. Filling in Sometimes patients will invent parts of the history because they cannot recall what actually happened. In some instances, otherwise oriented patients will be unable to recall an event because they were brieﬂy impaired and actually don’t know what happened. These patients may ﬁll in a plausible explanation for their fall such as “I must have tripped. Toss-ups Some questions can be answered correctly in many different ways, and because of this, the way a question is worded may result in the patient giving apparently contradictory answers. Descriptors of pain and discomfort are notoriously vague in their presentation and will change from telling to telling by the patient. Ask- ing “do you have pain” could be answered no by the patient who describes their pain as pressure and doesn’t equate that with pain. The examiner will not ﬁnd out that this person has chest pain without asking more speciﬁc questions using other common descriptors of chest pain such as aching, burning, pressure, or discomfort. Patient ignorance The patient may not be able to give accurate and correct answers due to lack of understanding of the examiner’s questions. The average patient understands at the level of a tenth-grade student, meaning that half of patients are below the tenth-grade level. They may not understand the meaning of a word as simple as congestion, and answer no, when they have a cough and stuffed nose. This is especially important because patients who do not speak English are more likely to be admitted to the hospital from the Emergency Department, and to have additional and often unnecessary diagnostic testing performed. Patient embarrassment Patients will not usually volunteer sensitive information although they may be very anxious to discuss these same topics when asked directly. This includes questions about sexual problems, domestic violence, and alcohol or drug abuse. For example, even though teenagers are engaged in sexual activity, they may not know how to ask about protection from pregnancy or sexually transmitted dis- eases. It is better to assume that most patients will not feel comfortable asking questions about these awkward subjects, thus the physician should ask about these issues directly in an empathetic and non-judgmental manner. Denial Some patients will minimize certain complaints because they are afraid of ﬁnd- ing out they have a bad disease. They may say that their pain is really not so bad and that the tests or treatments the physician is proposing are not necessary. The physician’s job is to determine the patient’s fear, educate the patient about the nature of the illness, and help him or her make an informed decision. Patient assessment of risk and level of risk taking Some patients will reject the physician’s interpretation of the nature of their com- plaint because of their own risk-taking behavior. They may be more willing or less willing to take a risk than the physician thinks is reasonable. The physician’s job is to educate the patient about the nature of their illness and the level of risk they are assuming by their behavior, and then help them make an informed decision. In the end, if the patient decides to refuse the physician’s suggestions for evaluation and treat- ment after being fully informed of the risks and beneﬁts, they have the capacity to refuse care and should be treated with therapies that they will accept. Ques- tions about alcohol or drug abuse, child abuse, and sexual activity are common areas where this occurs. The physician may detect inconsistencies in the history or pick up secondary clues that give an idea that this may be happening. The best way to handle this situation is to get corroborating evidence from the family, current and previous physicians, and medical records. The environment Disruptive environments for the examination Excess noise or interruptions, including background noise or children in the examination room, make it hard to be accurate in examination. This may be unavoidable in some circumstances like in the Emergency Department with its chaotic environment and constant noise from disruptive patients. If it is impos- sible to remove the noise, make sure it is compensated for in some other way. It may take longer to gather information in these circumstances, but the physician will be rewarded with increased accuracy. Disruptive interactions between the examiner and the examined Patients who are uncooperative, delirious, agitated, or in severe pain, as well as crying children are in this category. In this circumstance, the physician must sim- ply try his or her best to do a competent examination over the interruptions.
It may provoke fear of imminent death over the infarction with resulting risk of embolism 5 mg clarinex with amex allergy blood test. It is often associated with restlessness order generic clarinex online dust allergy symptoms uk, breath- r Recurrent ischaemia or myocardial infarction may oc- lessness buy 5mg clarinex free shipping allergy shots and anxiety, sweating order clarinex paypal milk allergy symptoms 12 month old, nausea and vomiting. Signs may in- cur due to thrombus formation within the same or clude pallor, sweating, hypotension, tachycardia, raised other coronary arteries. Macroscopy/microscopy r Ventricular aneurysms may form as the collagen scar In the infarct-related artery, there is nearly always evi- that replaces the infarcted tissue formation does not dence of plaque rupture/erosion and thrombotic occlu- contract and is non-elastic. In the infarct zone a sequence of changes occurs: frequently complicated by thrombus formation but r 0–12hours:Notvisiblemacroscopically,thereislossof embolism is rare. The development of tion, hypotension or in patients previously exposed persistent Q waves usually denotes a more substantial in- to streptokinase. It is now available as These should be given to all patients without evidence abedside test. They reduce mortality, reduce the number who de- Myoglobin velop cardiac failure and slow progression of the in- farct, by improving the remodelling of myocardium postinfarct. All di- Days after onset of acute Ml abetic patients should be treated with subcutaneous insulin for 3 months after discharge rather than oral Figure 2. Primary percu- Arrhythmiasmayoccurintheischaemicepisode(usually taneous coronary intervention (i. It is of particular value in patients with contraindica- Investigations tions to thrombolysis. Management Full mobilisation should be achieved after about 3 days r Nitrates and calcium antagonists are useful as pro- and discharge at 5 days, if there are no complications. The patient Prognosis may return to work after 2–3 months, depending on the The prognosis in patients with angina without underly- typeofwork. Rheumatic fever Prognosis Deﬁnition 50% 30-day mortality; 25% die before reaching hospital. Recurrent inﬂammatory disease affecting the heart; it Of those who leave hospital alive, 15–25% die within the occurs following a streptococcal infection. Incidence 1in100,000 United Kingdom/United States population peryear; incidence has declined over the last 100 years. Variant/Prinzmetal’s angina Deﬁnition Age Angina of no obvious provocation not as a direct result First attack usually 5–15 years. Sex Aetiology/pathophysiology M = F Causedbyspasmofacoronaryarterymostoftenwithout atheroma or in association with a mild eccentric lesion. Common in Middle and Far East, South America and Central Africa, declining in the West. Clinical features Pain is usually more severe and more prolonged than Aetiology classical angina occurring at rest particularly in the early Cell-mediated autoimmune reaction following a pha- morning. Risk fac- centre over the trunk and limbs, which appear and tors forstreptococcalinfectionincludepovertyandover- disappear over a matter of hours. Non-speciﬁc symptoms include It appears that antistreptococcal antibodies crossre- malaise and loss of appetite. Macroscopy r Pericarditis: Nodules are seen within the pericardium Fibrinous vegetations form on the edges of the valve associated with an inﬂammatory pericardial effusion. Valve leaﬂets may fuse r Myocarditis:Nodulesdevelopwithinthemyocardium and scar, particularly affecting the mitral and aortic associated with inﬂammation. These may result in an acute disturbance thesecellsarereplacedbyhistiocytes,whichmaybemult- of valve function. Complications Clinical features More than 50% of patients with acute rheumatic cardi- There may be a history of pharyngitis in up to 50% of tis will develop chronic rheumatic valve disease 10–20 patients. The diagnosis is made on two or more major years later, particularly mitral and aortic stenosis. These manifestations or one major plus two or more minor may be complicated by atrial ﬁbrillation, heart failure, manifestations (Duckett Jones criteria). A pericardial friction r Cultures of blood and tissues are sterile by the time rubmay be audible due to pericarditis. Management Pathophysiology r Patients with a clinical diagnosis of rheumatic fever Inacutemitralregurgitation,retrogradebloodﬂowfrom should be treated with benzylpenicillin regardless of the left ventricle into the left atrium causes the left atrial culture results. There is an increase in the pul- r Pain, fever and inﬂammation are treated with high- monary venous pressure and there may be pulmonary dose aspirin. This allows the r Patients may require treatment for heart failure (see increased volume of atrial blood to be compensated for page 63) and chorea may respond to haloperidol. The left ventricu- r Following recovery patients should receive prophy- lar stroke volume increases due to volume overload and lactic penicillin for at least 5 years after the last at- over time this results in left ventricular hypertrophy. In Although symptomatic improvement occurs with treat- most cases mitral regurgitation is chronic and is asymp- ment, therapy does not appear to prevent subsequent tomatic for many years. On examination the pulse is normal volume, but may be ir- Mitral regurgitation regular due to atrial ﬁbrillation. On aus- Flow of blood from the left ventricle to the left atrium cultation the ﬁrst heart sound is soft due to incomplete during systole through an incompetent mitral valve. There may be a prominent third heart sound due to the Aetiology sudden rush of blood back into the dilated left ventricle In developing countries rheumatic disease accounts for in early diastole. In developed countries other causes predomi- Complications nate: Patients develop left ventricular failure due to chronic r Prolapsing mitral valve. Atrial ﬁbrillation is common due r Myocardial infarction may lead to papillary muscle to atrial dilation, with an increased risk of throm- dysfunction or rupture. Other complications include pulmonary r Any disease that causes dilation of the left ventricle, oedema and infective endocarditis. Congestive heart fail- ure may also cause mitral regurgitation due to down- Investigations ward displacement of the papillary muscle. This leads r The chest X-ray shows cardiomegaly due to left atrial to a failure of the valve cusps to meet and regurgita- and left ventricular enlargement. Valve calciﬁcation tion ranging in severity according to the degree of left may be seen in cases due to rheumatic fever. It is thought to be due to progressive stretching of the The clinical effect of the valve lesion is however best valve leaﬂets. The normal anatomy of the mitral valve prevents pro- lapse thus one or more anomalies must be present: ex- Management cessively large mitral valve leaﬂets, an enlarged mitral r Mild mitral regurgitation in the absence of symptoms annulus, abnormally long chordae or disordered pap- is managed conservatively, more severe disease with illary muscle contraction. During systole one of the evidence of progressive cardiac enlargement is treated valve leaﬂets (usually the posterior) balloons up into surgically. In some cases this causes retraction at the of choice, but valve replacement may be required for normal point of contact of the valve cusps and hence severely diseased valves. The condition does not often cause and chordal rupture may require emergency valve re- signiﬁcant regurgitation. Mitral valve prolase Deﬁnition Complications Prolapsing mitral valve is a condition in which the valve Rupture of one of the chordae may occur leading to se- cusps prolapse into the left atrium during systole.
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