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By: U. Alima, M.S., Ph.D.

Professor, Albany Medical College

The cystic change is seen to extend into renal parenchyma medications gabapentin buy online duphalac, compressing the cortex as a thin rim at the periphery medications quotes order 100 ml duphalac fast delivery. Hydronephrosis develops if one or both the pelviureteric sphincters are incompetent medications 4 times a day duphalac 100ml cheap. Renal infarcts are already described in Chapter 4 (page 113); other conditions are discussed here. With this background knowledge, we next turn to the mechanisms involved in the two forms of hypertension (Table 20. The evidences in support are the familial aggregation, occurrence of hypertension in twins, epidemiologic data, experimental animal studies and identification of hypertension susceptibility gene (angiotensinogen gene). In either case, renal hypertension can be produced by one of the following 3 inter-related pathogenetic mechanisms: a) Activation of renin-angiotensin system Renin is a proteolytic enzyme produced and stored in the granules of the juxtaglomerular cells surrounding the afferent arterioles of glomerulus (page 638). The release of renin is stimulated by renal ischaemia, sympathetic nervous system stimulation, depressed sodium concentration, fluid depletion and decreased potassium intake. Benign Nephrosclerosis Benign nephrosclerosis is the term used to describe the kidney of benign phase of hypertension. The surface of the kidney is finely granular and shows V-shaped areas of scarring. The capsule is adherent to the cortex and has granular depressed scars on the surface. Microscopically, there are primarily diffuse vascular changes which produce parenchymal changes secondarily as a result of ischaemia. There are 2 types of changes in these blood vessels: a) Hyaline arteriolosclerosis that results in homogeneous and eosinophilic thickening of the wall of small blood vessels. In long-standing cases, there may be mild proteinuria with some hyaline or granular casts. The presence of papilloedema distinguishes malignant from benign phase of hypertension. The vascular changes are necrotising arteriolitis and hyperplastic intimal sclerosis or onion-skin proliferation. The parenchymal changes are tubular loss, fine interstitial fibrosis and foci of infarction necrosis. Causes of thrombotic microangiopathy of renal microvasculature are listed in Table 20. The injured endothelial surface causes the following effects: i) Passage of plasma constituents to the subendothelial zone of microvasculature. Clinically, hypertension may be benign (moderate and slow elevation of blood pressure 90/140 mmHg) or malignant hypertension in which there is marked and sudden increase of blood pressure (200/140 mmHg) in a known case of hypertension. Main mechanisms of essential hypertension are activation of renin-angiotensin pathway while secondary hypertension may be due to endocrine, aortic coarctation or neurogenic causes. Oncocytoma Oncocytoma is a benign epithelial tumour arising from collecting ducts. Adenocarcinoma of Kidney (Synonyms: Renal Cell Carcinoma, Hypernephroma, Grawitz Tumour) Hypernephroma is an old misnomer under the mistaken belief that the tumour arises from adrenal rests because of the resemblance of the tumour cells with clear cells of the adrenal cortex. Microscopically, the tumour cells are plump with abundant, finely granular, acidophilic cytoplasm and round nuclei. Other Benign Tumours Angiomyolipoma is a hamartoma of the kidney that contains differentiated tissue element derived from blood vessels, smooth muscle and fat. Granular cell type Chromophobe type Sarcomatoid type Collecting duct type 8% 5% 1. The clear cytoplasm of tumour cells is due to removal of glycogen and lipid from the cytoplasm during processing of tissues. The upper pole of the kidney shows a large and tan mass while rest of the kidney has reniform contour. Sectioned surface shows irregular, circumscribed, yellowish mass with areas of haemorrhages and necrosis. Clear cells predominate in the tumour while the stroma is composed of fine and delicate fibrous tissue. These tumours have more marked nuclear pleomorphism, hyperchromatism and cellular atypia. The classical clinical evidence for diagnosis of renal cell carcinoma is the triad of gross haematuria, flank plain and palpable abdominal mass. Systemic symptoms of fatiguability, weight loss, cachexia and intermittent fever unassociated with evidence of infection are found in many cases at presentation.

Routes of Metastasis Cancers may spread to distant sites by following pathways: 1 medicine hat lodge buy 100 ml duphalac. The involvement of lymph nodes by malignant cells may be of two forms: i) Lymphatic permeation the walls of lymphatics are readily invaded by cancer cells and may form a continuous growth in the lymphatic channels called lymphatic permeation medications related to the female reproductive system order duphalac with amex. The tumour emboli enter the lymph node at its convex surface and are lodged in the subcapsular sinus where they start growing symptoms joint pain and tiredness duphalac 100 ml with visa. Later, of course, the whole lymph node may be replaced and enlarged by the metastatic tumour. A few characteristics of lymphatic spread of malignant tumors are as follows: Generally, regional lymph nodes draining the tumour are invariably involved producing regional nodal metastasis. Sometimes lymphatic metastases do not develop first in the lymph node nearest to the tumour because of venouslymphatic anastomoses or due to obliteration of lymphatics by inflammation or radiation, so called skip metastasis. Sectioned surface shows merging capsules of lymph nodes and replacement of grey brown tissue of nodes by large grey white areas of tumour. In general, only a proportion of cancer cells are capable of clonal proliferation in the proper environment; others die without establishing a metastasis. Nevertheless, arterial spread may occur when tumour cells pass through pulmonary capillary bed or through pulmonary arterial branches which have thin walls. However, cancers of the kidneys, adrenals, bones, limbs and uterus, which are drained by systemic veins, spread to the lungs via pulmonary artery. At times, metastatic deposits may come to attention first without an evident primary tumour. Metastatic deposits just like primary tumour may cause further dissemination via lymphatics and blood vessels. However, the same primary tumour on metastasis at different sites may show varying grades of differentiation, apparently due to the influence of local environment surrounding the tumour for its growth. A few examples of transcoelomic spread are as follows: a) Carcinoma of the stomach seeding to both ovaries (Krukenberg tumour). The following sequential steps are involved which are schematically illustrated in. Aggressive clonal proliferation and angiogenesis the first step in the spread of cancer cells is the development of rapidly proliferating clone of cancer cells. Tumour angiogenesis plays a very significant role in metastasis since the new vessels formed as part of growing tumour are more vulnerable to invasion because these evolving vessels are directly in contact with cancer cells. This attachment is facilitated due to profoundness of receptors on the cancer cells for both these proteins. There is also loss of integrins, the transmembrane receptors, further favouring invasion. Thrombus formation the tumour cells protruding in the lumen of the capillary are now covered with constituents of the circulating blood and form the thrombus. In fact, normally a large number of tumour cells are released into circulation but they are attacked by the host immune cells. Extravasation of tumour cells Tumour cells in the circulation (capillaries, venules, lymphatics) may mechanically block these vascular channels and attach to vascular endothelium and then extravasate to the extravascular space. In this way, the sequence similar to local invasion is repeated and the basement membrane is exposed. Recent evidence has shown that in metastatic tumours, survival of host is correlated with some clinical and molecular features of tumours which act as prognostic markers. Grading is defined as the gross appearance and microscopic degree of differentiation of the tumour, while staging means extent of spread of the tumour within the patient. Gross features like exophytic or fungating appearance are indicative of less malignant growth than diffusely infiltrating tumours. More objective criteria for histologic grading include use of flow cytometry for mitotic cell counts, cell proliferation markers by immunohistochemistry, and by applying image morphometry for cancer cell and nuclear parameters. In general, most common cancers in the developed and developing countries are as under: Developed countries: lung, breast, prostate and colorectal. Overall, there has been a declining trend in incidence of some of the cancers due to cancer screening programmes. Carriers of such genetic composition have 10,000 times higher risk of developing retinoblastoma which is often bilateral.

Fibroma durum is a benign medicine effects purchase duphalac overnight, often pedunculated and well-circumscribed tumour occurring on the body surfaces and mucous membranes treatment centers for depression generic duphalac 100ml visa. Fibroma molle or fibrolipoma medications 2 times a day duphalac 100 ml with amex, also termed soft fibroma, is similar type of benign growth composed of mixture of mature fibrous connective tissue and adult-type fat. It is characterised by association of collagen bundles and branching elastic fibres. Soft tissue tumours are defined as tumours arising from non-epithelial extra-skeletal tissues of the body except the reticuloendothelial system, the glia and the supporting tissues of specific organs and viscera. Based on histologic features, they are divided into low-, intermediate- and high-grade. The appearance is sufficiently atypical to suggest osteosarcoma but osteosarcoma lacks maturation phenomena seen in myositis ossificans. These lesions may, therefore, be regarded as non-metastasising fibroblastic tumours which tend to invade locally and recur after surgical excision. The circumscribed lesion is composed of mature collagenised fibrous connective tissue. Grossly, the keloid is a firm, smooth, pink, raised patch from which extend claw-like processes (keloid-claw). Grossly, the lesion appears as a solitary well-circumscribed nodule (true to its name) in the superficial fascia. The individual cells are spindle-shaped, plump fibroblasts showing mild nuclear atypia. The pathogenesis of these lesions is not known but among the factors implicated are the role of antecedent trauma, genetic influences and relationship to oestrogen as obsereved by occurrence of these lesions in pregnancy. Extra-abdominal desmoids, on the other hand, are more common in men and are widely distributed such as in the upper and lower extremities, chest wall, back, buttocks, and head and neck region. Grossly, desmoids are solitary, large, grey-white, firm and unencapsulated tumours infiltrating the muscle locally. Histologically, the tumour is composed of uniform, spindleshaped fibroblasts arranged in intersecting fascicles. Poorlydifferentiated fibrosarcoma, however, has highly pleomorphic appearance with frequent mitoses and bizarre cells. The group includes full spectrum of lesions varying from benign (benign fibrous histiocytoma) to malignant (malignant fibrous histiocytoma), with dermatofibrosarcoma protuberans occupying the intermediate (low-grade malignancy) position. All these tumours have mixed composition of benign fibroblastic and histiocytic pattern of cells and have been described in relevant sections already. The tumour recurs locally, and in rare instances gives rise to distant metastases. It is the most common soft tissue sarcoma and is the most frequent sarcoma associated with radiotherapy. It begins as a painless, enlarging mass, generally in relation to skeletal muscle, deep fascia or subcutaneous tissue. The tumour is believed to arise from primitive mesenchymal cells which are capable of differentiating towards both fibroblastic and histiocytic cell lines. Currently, this is termed as undifferentiated pleomorphic sarcoma with prominent inflammation. Benign fibrous histiocytomas include dermatofibroma, sclerosing haemangioma, fibroxanthoma, xanthogranuloma, giant cell tumour of tendon sheath and pigmented villonodular synovitis. Dermatofibrosarcoma protuberans is a low-grade malignant cutaneous tumour of fibrohistiocytic origin. Malignant fibrous histiocytoma or pleomophic sarcoma is the most common soft tissue sarcoma and has a few variants such as pleomorphic, inflammatory, giant cell type and myxoid. It appears as a solitary, soft, movable and painless mass which may remain stationary or grow slowly. They may be found at different locations in the body but most common sites are the subcutaneous tissues in the neck, back and shoulder. Grossly, a subcutaneous lipoma is usually small, round to oval and encapsulated mass. Histologically, the tumour is composed of lobules of mature adipose cells separated by delicate fibrous septa.

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