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Diabetes mellitus presenting symptoms

TDDM, also called Type 1 diabetes, generally presents in persons by the age of 30 years, and accounts for only 5-10% of all persons with diabetes mellitus- The symptoms of IDDM occur somewhat abruptly and require prompt treatment- The disease results in the loss of T-cells of the pancreas and the consequent absence of the insulin that is synthesized by the p-cells, IDDM is an autoimmune disease. This means that the body produces antibodies that recognize and bind to various proteins of the [i-cells. This is followed by the infiltration of the p-ce s with white blood cells. The white blood cells destroy the p-cells gradually over the course of several years. IDDM makes the patient feel sick only after most of the pcommercially available, and persons with the disease can easily learn to administer the injections at home Bach, 1994, 1997 Tisch and McDevitt, 1996),... [Pg.172]

The underlying causes of the nervous changes that can occur in patients with diabetes mellitus present a challenge that is still with us. Symptoms of diabetic neuropathy may develop in mild, severe and controlled states of the disease, and with or without accompanying arteriosclerotic lesions. [Pg.8]

Differential diagnoses include diabetes mellitus and metabolic syndrome because patients with these conditions share several similar characteristics with Cushing s syndrome patients (e.g., obesity, hypertension, hyperlipidemia, hyperglycemia, and insulin resistance). In women, the presentations of hirsutism, menstrual abnormalities, and insulin resistance are similar to those of polycystic ovary syndrome. Cushing s syndrome can be differentiated from these conditions by identifying the classic signs and symptoms of truncal obesity, "moon faces" with facial plethora, a "buffalo hump" and supraclavicular fat pads, red-purple skin striae, and proximal muscle weakness. [Pg.694]

Onset of type 1 diabetes mellitus usually occurs within the first two decades of life presenting symptoms Include hyperglycemia, polyuria, polydipsia, and polyphagia (excessive urination, thirst, and appetite, respectively), often with serious ketoacidosis in response to a stressor such as a viral infection. [Pg.65]

The clinical manifestations of PAD are associated with reduction in functional capacity and quality of life, but because of the systemic nature of the atherosclerotic process there is a strong association with coronary and carotid artery disease. Consequently, patients with PAD have an increased risk of cardiovascular and cerebrovascular ischemic events [myocardial infarction (Ml), ischemic stroke, and death] compared to the general population (4,5). In addition, these cardiovascular ischemic events are more frequent than ischemic limb events in any lower extremity PAD cohort, whether individuals present without symptoms or with atypical leg pain, classic claudication, or critical limb ischemia (6). Therefore, aggressive treatment of known risk factors for progression of atherosclerosis is warranted. In addition to tobacco cessation, encouragement of daily exercise and use of a low cholesterol, low salt diet, PAD patients should be offered therapies to reduce lipid levels, control blood pressure, control blood glucose in patients with diabetes mellitus, and offer other effective antiatherosclerotic strategies. A recent position paper... [Pg.515]

Diabetes mellitus is a major cause of blindness, renal failure, and cause for surgical amputation of legs or feet- The risk of cardiovascular disease is doubled in a person with diabetes mellitus. Thus, diabetes is a serious health hazard. How dt>es diabetes first present itself The initial symptoms of the disease include excessive thirst, excessive food consumption, excessive urination, weight loss, and blurred vision.. Diabetes often results in neuropathies leading to impotence (in males) and numb feet. Foot ulcers may occur, and in extreme cases, the foot must be amputated-Diabeles is a leading cause of blindness in adults. Diabetes often accelerates the development of cardiovascular disease, but the mechanism of this acceleration is not clear. [Pg.171]

Approximately 5% to 10% of aU cases of diabetes mellitus are in this category. Patients usually have abrupt onset of symptoms (e.g., polyuria, polydipsia, and rapid weight loss). Patients have insulinopenia (a deficiency of insulin) caused by loss of pancreatic islet (3-ceUs and are dependent on insulin to sustain life and prevent ketosis. Most patients have antibodies that identify an autoimmune process (see later discussion) some patients have no evidence of autoimmunity and are classified as type 1 idiopathic. The peak incidence is in childliood and adolescence. Approximately 75% acquire the disease before age 30 years, but the onset in the remainder may occur at any age. Age at presentation is not a criterion for classification. [Pg.854]

This patient presents with many of the classic findings of Cushing syndrome. Adrenal hyperplasia can be caused by excessive stimulation from ACTH (pituitary or ectopic production) or from a primary adrenal problem such as adenomas/ carcinomas. In addition to above symptoms, patients with Cushing syndrome are also at risk for osteoporosis and diabetes mellitus (DM). The diagnosis is confirmed with elevated cortisol levels after a dexamethasone suppression test. Treatment depends on the underlying etiology and is often surgical. [Pg.444]

Frohne et al. (1984) described the clinical course of a man who presented with severe gastroenteritis after ingesting a powder made from jequirity beans. He developed acute pancreatitis, leucocytosis, bloody ascites, increased serum amylase and lipase activities, hypocalcaemia and diabetes mellitus. Moreover, in addition to delirium, hallucinations, reduced consciousness and generalized seizures, he also developed a hemi-paresis. Respiratory depression necessitated ventilation for 10 days but all symptoms improved gradually over the following three weeks. Neurological recovery was complete. [Pg.624]


See other pages where Diabetes mellitus presenting symptoms is mentioned: [Pg.38]    [Pg.213]    [Pg.237]    [Pg.267]    [Pg.98]    [Pg.55]    [Pg.346]    [Pg.589]    [Pg.1064]    [Pg.1689]    [Pg.266]    [Pg.456]    [Pg.1127]    [Pg.1341]    [Pg.1416]    [Pg.65]    [Pg.169]    [Pg.1276]    [Pg.55]    [Pg.357]    [Pg.110]    [Pg.314]    [Pg.123]    [Pg.226]    [Pg.541]    [Pg.545]    [Pg.357]   
See also in sourсe #XX -- [ Pg.401 , Pg.402 ]




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