FF2/9781605475462.jpg' alt='Manual Of Gastroenterology Diagnosis And Therapy 3Rd Edition' title='Manual Of Gastroenterology Diagnosis And Therapy 3Rd Edition' />Constipation Wikipedia. Constipation. Synonyms. Costiveness,1 dyschezia2Constipation in a young child seen on X ray. Circles represent areas of fecal matter stool is white surrounded by black bowel gas. Specialty. Gastroenterology. Symptoms. Infrequent or hard to pass bowel movements, abdominal pain, bloating32Complications. Psychiatry is the medical specialty devoted to the diagnosis, prevention, study, and treatment of mental disorders. These include various abnormalities related to. Essentials of Biostatistics in Public Health, Third Edition provides a fundamental and engaging background for students learning to apply and appropriately interpret. Hemorrhoids, anal fissure, fecal impaction4Causes. Slow movement of stool within the colon, irritable bowel syndrome, celiac disease, non celiac gluten sensitivity, pelvic floor disorders456Risk factors. Hypothyroidism, diabetes, Parkinsons disease, gluten related disorders, colon cancer, diverticulitis, inflammatory bowel disease, certain medications456Treatment. Drinking enough fluids, eating more fiber, exercise4Medication. Laxatives of the bulk forming agent, osmotic agent, stool softener, or lubricant type4Frequency. Constipation refers to bowel movements that are infrequent or hard to pass. The stool is often hard and dry. Other symptoms may include abdominal pain, bloating, and feeling as if one has not completely passed the bowel movement. Complications from constipation may include hemorrhoids, anal fissure or fecal impaction. The normal frequency of bowel movements in adults is between three per day and three per week. Babies often have three to four bowel movements per day while young children typically have two to three per day. Constipation has many causes. Common causes include slow movement of stool within the colon, irritable bowel syndrome, and pelvic floor disorders. Underlying associated diseases include hypothyroidism, diabetes, Parkinsons disease, celiac disease, non celiac gluten sensitivity, colon cancer, diverticulitis, and inflammatory bowel disease. Medications associated with constipation include opioids, certain antacids, calcium channel blockers, and anticholinergics. Of those taking opioids about 9. Constipation is more concerning when there is weight loss or anemia, blood is present in the stool, there is a history of inflammatory bowel disease or colon cancer in a persons family, or it is of new onset in someone who is older. Treatment of constipation depends on the underlying cause and the duration that it has been present. Measures that may help include drinking enough fluids, eating more fiber, and exercise. If this is not effective, laxatives of the bulk forming agent, osmotic agent, stool softener, or lubricant type may be recommended. Stimulant laxatives are generally reserved for when other types are not effective. Other treatments may include biofeedback or in rare cases surgery. In the general population rates of constipation are 23. Among elderly people living in a care home the rate of constipation is 5. People spend, in the United States, more than US2. Definition. Constipation is a symptom, not a disease. Most commonly, constipation is thought of as infrequent bowel movements, usually less than 3 stools per week. However, people may have other complaints as well including 31. Straining with bowel movements. Excessive time needed to pass a bowel movement. Hard stools. Pain with bowel movements secondary to straining. Abdominal pain. Abdominal bloating. The Rome Criteria are a set of symptoms that help standardize the diagnosis of constipation in various age groups. These criteria help physicians to better define constipation in a standardized manner. Causes. The causes of constipation can be divided into congenital, primary, and secondary. The most common kind is primary and not life threatening. It can also be divided by the age group affected such as children and adults. Primary or functional constipation is defined by ongoing symptoms for greater than six months not due to an underlying cause such as medication side effects or an underlying medical condition. It is not associated with abdominal pain, thus distinguishing it from irritable bowel syndrome. It is the most common kind of constipation, and is often multifactorial. In adults, such primary causes include dietary choices such as insufficient dietary fiber or fluid intake, or behavioral causes such as decreased physical activity. In the elderly, common causes have been attributed to insufficient dietary fiber intake, inadequate fluid intake, decreased physical activity, side effects of medications, hypothyroidism, and obstruction by colorectal cancer. Evidence to support these factors however is poor. Secondary causes include side effects of medications such as opiates, endocrine and metabolic disorders such as hypothyroidism, and obstruction such as from colorectal cancer. Celiac disease and non celiac gluten sensitivity may also present with constipation. Diet. Constipation can be caused or exacerbated by a low fiber diet, low liquid intake, or dieting. Dietary fiber helps to decrease colonic transport time, increases stool bulk but simultaneously softens stool. Therefore, diets low in fiber can lead to primary constipation. Medications. Many medications have constipation as a side effect. Some include but are not limited to opioids, diuretics, antidepressants, antihistamines, antispasmodics, anticonvulsants, tricyclic antidepressants, antiarrythmics, beta adrenoceptor antagonists, anti diarrheals, 5 HT3 receptor antagonists such as ondansetron, and aluminum antacids. Certain calcium channel blockers such as nifedipine and verapamil can cause severe constipation due to dysfunction of motility in the rectosigmoid colon. Supplements such as calcium and iron supplements can also have constipation as a notable side effect. Medical conditions. Metabolic and endocrine problems which may lead to constipation include hypercalcemia, hypothyroidism, hyperparathyroidism, porphyria, chronic kidney disease, pan hypopituitarism, diabetes mellitus, and cystic fibrosis. Constipation is also common in individuals with muscular and myotonic dystrophy. Systemic diseases that may present with constipation include celiac disease and systemic sclerosis. Constipation has a number of structural mechanical, morphological, anatomical causes, namely through creating space occupying lesions within the colon that stop the passage of stool, such as colorectal cancer, strictures, rectocoles, anal sphincter damage or malformation and post surgical changes. Extra intestinal masses such as other malignancies can also lead to constipation from external compression. Constipation also has neurological causes, including anismus, descending perineum syndrome, and Hirschsprungs disease. In infants, Hirschsprungs disease is the most common medical disorder associated with constipation. Anismus occurs in a small minority of persons with chronic constipation or obstructed defecation. Spinal cord lesions and neurological disorders such as Parkinsons disease and pelvic floor dysfunction1. Psychological. Voluntary withholding of the stool is a common cause of constipation. The choice to withhold can be due to factors such as fear of pain, fear of public restrooms, or laziness. When a child holds in the stool a combination of encouragement, fluids, fiber, and laxatives may be useful to overcome the problem. Early intervention with withholding is important as this can lead to anal fissures. Programa Para Baixar Videos De Qualquer Sites Da Internet Cafe on this page. Congenital. A number of diseases present at birth can result in constipation in children. British Journal of Medical Practitioners. Authors. Article Citation and PDF Link. Abstract Summary. Despite progress in neurotransmitter identifications and the emergence of novel antipsychotics, the treatment of schizophrenia remains frustrating. There is now a flurry of research trying to figure out the aetiology of schizophrenia and potential etiological models other than neurotransmitter dysfunction deserve consideration. Recent years have witnessed a revival of interest in the viral and immunity based etiological models of schizophrenia. A subset of schizophrenia may have a pure biological aetiology. There are several commonalities between schizophrenia and autoimmune disorders. Coexistence of established autoimmune disorders along with schizophrenia is suggestive that the latter could also have an autoimmune component. Antipsychotics may be working on the principle of immune modulatory and neuro modulatory mechanisms. The well recognized 1 global consistency of the incidence of schizophrenia indicates that the aetiology of schizophrenia involve an evolutionary genetic vulnerability and universally present environmental factors. There may be a genetic predisposition to the hypothetical schizovirus determining the development of schizophrenia in certain individuals. Certain people are genetically vulnerable to microbial infections in the sense that they have a highly sensitive surveillance system to the microbial infection and respond to the microbial adversary in an exaggerated way. Such a vulnerability and anomalous reaction to infection could result in the schizophrenia psycho pathogenesis. Introduction. A clearer understanding of the aetio pathogenesis of schizophrenia would ultimately lead to effective treatment strategies and provide the impetus for elucidation. The autoimmune hypothesis promulgates that it is the auto antibodies that are responsible for schizophrenia and, according to the viral hypothesis, it may be the bodys abnormal response to a slow viral infection or the undefeated viral antigens causing the schizophrenia pathology. The autoimmune and viral hypotheses are interlinked, as autoimmune disorders can be triggered by microbial infection. Viral aetiology is less convincing than the autoimmune model, but from a treatment perspective, the former is more promising than the latter. To gain a detailed understanding of aetiological models of a subset of schizophrenia, herein the author has reported on a review of the literature relating to the immunity and viral based aetiological models of schizophrenia. Genetic vulnerability has been highlighted in the schizophrenia literature alongside environmental factors. The veracity and contestability of the immunity and viral based aetiological hypothesis of schizophrenia merits further investigation. Schizophrenic Syndromes. A prerequisite for incorporating autoimmune and viral aetiology into a scientific discussion would be acceptance of the heterogeneous hypothesis of schizophrenias they may be a cluster of entities with different aetiologies and the end stage of different disease processes. Autoimmune or viral aetiology may account for one subgroup. Schizophrenia has diverse signs and symptoms, and a long history of controversy. Nosologists designate it as polythetic, whereas most other mental illnesses are monothetic, seemingly affecting only one brain system. In the second half of the twentieth century, the psychosocial model gave way to evidence that it is a brain disorder. Schizophrenia has a long history of controversies and there has been much contention over the aetiology, psychopathology, nomenclature, and diagnostic criteria. Schizophrenia is currently seen as a neurodevelopmental encephalopathy, in which the cognitive deficits are produced due to the errors during the normal development of the brain 3 or a neuro degenerative disorder and the cognitive deficits are derived from a degenerative process that goes on unalterably. Modern neuroimaging techniques and an intensification of studies of necropsy tissue have been responsible for this shift. Researchers seem to agree that a neurodevelopmental or degenerative assault precedes the symptoms by several decades. The aetiology of the cognitive deficits is unidentified and several potential factors, genetic and epigenetic, are envisaged. Environmental factorsincluding infectious agents and disturbance in utero through malnutritionaccount for a few cases. Autoimmunity and viral theories would fit in with the neuro developmental and neurodegenerative hypotheses. Proponents of viral aetiology view viruses as acting alongside susceptible genes to initiate a trajectory that manifests as psychotic symptoms. Lessons from Autoimmunity. Disorders of an autoimmune nature are known to occur with increasing frequency in patients with another autoimmune disease. This is somewhat like the coexistence of multiple psychosomatic disorders in a person as per Hallidays psychosomatic formula, association of other psychosomatic afflictions justifies the diagnosis of a new psychosomatic condition. It is well recognised that the central nervous system CNS may be directly affected by autoimmune processes, as in the case of multiple sclerosis MS and autoimmune limbic encephalitis. A physical autoimmune disease, such as systemic lupus erythematosus SLE and antiphospholipid syndrome are also associated with psychiatric morbidity. Paediatric autoimmune neuropsychiatry disorder is a post infection group A Beta haemolytic streptococcal infection autoimmune disorder characterised by abrupt onset of obsessive compulsive disorder OCD and Tourettes syndrome, brought about by molecular mimicry. Nicholson et al observed that 2. OCD patients were positive for anti basal antibodies, considered to be part of a post streptococcal autoimmune reaction. Autoimmunity is a misdirected response occurring when the immune system attacks the body it is the loss of tolerance to self antigens. Immunological tolerance to ones own tissue is probably normally acquired during foetal life, helping to prevent the occurrence of the autoimmune process see Table. Some clones of cells that can produce auto antibodies forbidden clones are thought to be produced throughout life, and are suppressed by large amounts of self antigens or antigen specific T cells. Auto antibodies are produced for a wide variety of antigens some are organ specific and others are non organ specific. Some microorganisms or drugs may trigger changes in individuals who are genetically vulnerable to autoimmunity. Table 1 Mechanisms preventing and causing autoimmunity. Tolerance to self molecules a. Clonal deletion removing any lymphocytes that might react to self molecules b. Clonal anergy decreasing the responsiveness of lymphocytes that recognise self molecules. Receptor editing rearrangement of B cell receptors. Reduction or inhibition of molecules or antigens that may cause self recognition. Failure of self tolerancea. Release of isolated auto antigens tissue trauma or infection may cause breakdown of anatomic barriers and may expose the hidden antigens for recognition of T cells that were not deleted during development. Structural alterations in self peptides Once structurally altered by a trigger such as infection, the self peptides become more antigenic and are subsequently recognised by the undetected T cells evoking immune response.