Crohn’s Disease

Crohn’s disease is a recurrent segmental inflammatory disorder that may affect the any location in the gastrointestinal tract from the mouth to the anus. Crohn’s disease is of unknown etiology. Fifty percent of patients have involvement of both the small intestine and colon, whereas one third have disease limited to their small intestine and the remaining 20% have inflammation in the colon only. Perianal lesions and inflammatory conditions involving the skin, eyes, joints, and liver are common. The transmural inflammatory process and variable anatomic extent of disease contribute to diverse clinical presentations with unpredictable spontaneous exacerbations and remissions.

Multiple Myeloma - TREATMENT

About 10 percent of patients with myeloma will have an indolent course demonstrating only very slow progression of disease over many years. Such patients only require antitumor therapy when the serum myeloma protein level rises above 50 g/L (5 g/dL) or progressive bone lesions develop. Patients with solitary bone plasmacytomas and extramedullary plasmacytomas may be expected to enjoy prolonged disease-free survival after local radiation therapy to a dose of around 40 Gy. There is a low incidence of occult marrow involvement in patients with solitary bone plasmacytoma. Such patients are usually detected because their serum M component falls slowly or disappears initially only to return after a few months. These patients respond well to systemic chemotherapy.

The vast majority of patients with myeloma require therapeutic intervention. In general, such therapy is of two sorts: systemic chemotherapy to control the progression of myeloma, and symptomatic supportive care to prevent serious morbidity from the complications of the disease. All patients with stage II or III disease and stage I patients exhibiting Bence Jones proteinuria, progressive lytic bone lesions, vertebral compression fractures, recurrent infections, or rising serum M component should be treated with systemic combination chemotherapy. Therapy can prolong and improve the quality of life for myeloma patients.

Read the rest of this entry »

Multiple Myeloma

Multiple myeloma is a malignant proliferation of plasma cells. The tumor, its products, and the host response to it result in a number of organ dysfunctions and symptoms of bone pain or fracture, renal failure, susceptibility to infection, anemia, hypercalcemia, and occasionally clotting abnormalities, neurologic symptoms, and vascular manifestations of hyperviscosity.

Etiology The cause of myeloma is not known. Myeloma occurred with increased frequency in those exposed to the radiation of nuclear warheads in World War II after a 20-year latency. In contrast to most other B cell tumors, consistent chromosomal alterations have not been found in patients with myeloma, though cytogenetic abnormalities are noted in a substantial fraction of cases. Overexpression of myc or ras genes has been noted in some cases. Mutations in p53 and Rb-1 have also been described, but no common molecular pathogenesis has yet emerged. The murine plasmacytoma models suggest that the induction of plasmacytomas (e.g., with mineral oil injection) may require exposure to foreign antigens as well as a cellular event. Thus chronic antigenic stimulation may play a role in the transformation of a particular B cell clone. This is supported by evidence that M proteins from different persons sometimes share idiotypes. There is also some evidence for a genetic predisposition to myeloma in humans. Myeloma has been seen more commonly than expected among farmers, wood workers, leather workers, and those exposed to petroleum products. The neoplastic event in myeloma may involve cells earlier in B cell differentiation than the plasma cell. Circulating B cells bearing surface immunoglobulin that share the idiotype of the M component are present in myeloma patients. It is possible that the malignant clone escapes normal control mechanisms at a pre-plasma cell stage of differentiation and the chronic exposure to a particular antigenic stimulus drives the cell to terminal differentiation. Interleukin (IL) 6 may play a role in driving myeloma cell proliferation; a large fraction of myeloma cells exposed to IL-6 in vitro respond by proliferating. It remains difficult to distinguish benign from malignant plasma cells on the basis of morphologic criteria in all but a few cases.

Read the rest of this entry »

Polyarteritis Nodosa

Definition

Classic polyarteritis nodosa (PAN) is a multisystem, necrotizing vasculitis of small and medium-sized muscular arteries in which involvement of the renal and visceral arteries is characteristic. PAN does not involve pulmonary arteries, although bronchial vessels may be involved; granulomas, significant eosinophilia, and an allergic diathesis are not part of the classic syndrome. The term microscopic polyangiitis (microscopic polyarteritis) discribes the necrotizing vasculitis with few or no immune complexes (pauci-immune) affecting small vessels (capillaries, venules, or arterioles). Since necrotizing arteritis involving small and medium-sized arteries may also be present, it shares features with classic PAN except that glomerulonephritis is very common in microscopic polyangiitis, and pulmonary capillaritis often occurs.

Incidence And Prevalence

Pan is an uncommon disorder. The mean age at onset in reports of PAN is 48 years, and the male-to-female ratio is 1.6:1.

Pathophysiology And Pathogenesis

The vascular lesion in classic PAN is a necrotizing inflammation of small and medium-sized muscular arteries. The lesions are segmental and tend to involve bifurcations and branchings of arteries. They may spread circumferentially to involve adjacent veins. However, involvement of venules is not seen in classic PAN and, if present, suggests microscopic polyangiitis or the polyangiitis overlap syndrome (see below). In the acute stages of disease, polymorphonuclear neutrophils infiltrate all layers of the vessel wall and perivascular areas, which results in intimal proliferation and degeneration of the vessel wall. Mononuclear cells infiltrate the area as the lesions progress to the subacute and chronic stages. Fibrinoid necrosis of the vessels ensues with compromise of the lumen, thrombosis, infarction of the tissues supplied by the involved vessel, and, in some cases, hemorrhage. As the lesions heal, there is collagen deposition, which may lead to further occlusion of the vessel lumen. Aneurysmal dilatations up to 1 cm in size along the involved arteries are characteristic of classic PAN. Granulomas and substantial eosinophilia with eosinophilic tissue infiltrations are not characteristically found and suggest allergic angiitis and granulomatosis (see below). online canadian pharmacy

Read the rest of this entry »

Huntington’s Disease

Huntington’s disease is a movement disorder characterized by chorea and dementia. It is inherited in an autosomal dominant manner and occurs throughout the world, in all ethnic groups, with a prevalence rate of about 5 per 100,000. The gene responsible for the disease has been located on the short arm of chromosome No. 4. At 4p16.3 there is an expanded and unstable CAG trinucleotide repeat. Symptoms do not usually develop until after 30 years of age, by which time the patient has usually had children, and so the disease continues from one generation to the next. The cause of Huntington’s disease is unknown. Online Trusted Pharmacy

Clinical Findings

Clinical onset is usually between 30 and 50 years of age. The disease is progressive and usually leads to a fatal outcome within 15–20 years. The initial symptoms may consist of either abnormal movements or intellectual changes, but ultimately both occur. The earliest mental changes are often behavioral, with irritability, moodiness, antisocial behavior, or a psychiatric disturbance, but a more obvious dementia subsequently develops. The dyskinesia may initially be no more than an apparent fidgetiness or restlessness, but eventually choreiform movements and some dystonic posturing occur. Progressive rigidity and akinesia (rather than chorea) sometimes occur in association with dementia, especially in cases with childhood onset. CT scanning usually demonstrates cerebral atrophy and atrophy of the caudate nucleus in established cases. MRI and positron emission tomography (PET) have shown reduced glucose utilization in an anatomically normal caudate nucleus. Buy Cheap Antibiotics pills

Chorea developing with no family history of choreoathetosis should not be attributed to Huntington’s disease, at least not until other causes of chorea have been excluded clinically and by appropriate laboratory studies. In younger patients, self-limiting Sydenham’s chorea develops after group A streptococcal infections on rare occasions. If a patient presents solely with progressive intellectual failure, it may not be possible to distinguish Huntington’s disease from other causes of dementia unless there is a characteristic family history or a dyskinesia develops. Canadian Prescriptions Drugs Read the rest of this entry »