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Currently symptoms melanoma order 500mg lincocin free shipping, neoplasms of haematopoietic and lymphoid tissues are considered as a unified group and are divided into 3 broad categories: I treatment 6th feb cardiff purchase 500mg lincocin with amex. Myeloid neoplasms: this group includes neoplasms of myeloid cell lineage and therefore includes neoplastic proliferations of red blood cells symptoms kidney pain generic 500mg lincocin with mastercard, platelets treatment 3rd nerve palsy 500mg lincocin amex, granulocytes and monocytes. Histiocytic neoplasms: this group is of interest mainly due to neoplastic proliferations of histiocytes in Langerhans cell histiocytisis. These as well as other classification schemes have been tabulated and discussed later under separate headings of myeloid and lymphoid malignancies. There is evidence to suggest that there is role of family history, occurrence in identical twins and predisposition of these malignancies in certain genetic syndromes: i) Identical twins: There is high concordance rate among identical twins if acute leukaemia develops in the first year of life. Certain environmental factors are known to play a role in the etiology of leukaemias and lymphomas: i) Ionising radiation. Damage due to radiation exposure has been linked to development of leukaemias and lymphomas. Benzene, tobacco smoking, alcohol, use of certain hair dyes and exposure to agriculture chemicals are associated with increased risk of development of haematopoietic malignancies. Long-term exposure to certain drugs such as phenytoin, alkylating agents and other chemotherapeutic agents is associated with increased incidence of leukaemias and lymphomas. Since lymphoid cells are the immune cells of the body, diseases with derangements of the immune system have higher incidence of haematopoietic malignancies: i) Immunodeficiency diseases. Leukaemias and lymphomas arise following malignant transformation of a single clone of cells belonging to myeloid or lymphoid series, followed by proliferation of the transformed clone. The heritable genetic damage may be induced by various etiologic agents listed above. The evolution of leukaemia is multi-step process, and in many cases, acute leukaemia may develop after a pre-existing myelodysplastic or myeloproliferative disorder. A number of cytogenetic abnormalities have been detected in cases of leukaemiaslymphomas, most consistent of which are chromosomal translocations. It needs to be emphasised that it is the maturation defect in leukaemic blasts rather than rapid proliferation of leukaemic cells responsible for causing acute leukaemia. In fact, the generation time of leukaemic blasts is somewhat prolonged rather than shortened. As the leukaemic cells accumulate in the bone marrow, there is suppression of normal haematopoietic stem cells, partly by physically replacing the normal marrow precursors, and partly by inhibiting normal haematopoiesis via cell-mediated or humoral mechanisms. Since myeloid trilineage stem cells further differentiate into 3 series of progenitor cells: erythroid, granulocyte-monocyte, and megakaryocytic series, therefore all examples of myeloid neoplasms fall into these three categories of cell-lines. Acute biphenotypic leukaemia Each of these groups is subclassifed into further types as shown in Table 14. Besides their common stem cell origin, these disorders are closely related, occasionally leading to evolution of one entity into another during the course of the disease. There is reciprocal translocation of the part of the long arms of chromosome 22 to the long arms of chromosome 9 written as t(9;22). Nevertheless, some normal haematopoietic stem cells do remain in the marrow which are capable of proliferating and restoring normal haematopoiesis after effective antileukaemic treatment. The leukaemic cells proliferate primarily in the bone marrow, circulate in the blood and Figure 14. Clinical Features Chronic myeloid (myelogenous, granulocytic) leukaemia comprises about 20% of all leukaemias and its peak incidence is seen in 3rd and 4th decades of life. Symptoms due to hypermetabolism such as weight loss, lassitude, anorexia, night sweats. Bleeding tendencies such as easy bruising, epistaxis, menorrhagia and haematomas may occur. Less common features include gout, visual disturbance, neurologic manifestations and priapism. Other features are frequent infections, haemorrhagic manifestations and facial rash. The group as a whole has slow and insidious onset of clinical features and indolent clinical behaviour. Characteristically, there is marked leucocytosis (approximately 200,000/l or more at the time of presentation). Myeloblasts usually do not exceed 10% of cells in the peripheral blood and bone marrow. Accelerated phase is defined as increasing degree of anaemia, blast count in blood or marrow between 10-20%, marrow basophils 20% or more, and platelet count falling below 1,00,000/l. These blast cells may be myeloid, lymphoid, erythroid or undifferentiated and are established by morphology, cytochemistry, or immunophenotyping. Generally, there is hypercellularity with total or partial replacement of fat spaces by proliferating myeloid cells. The myeloid cells predominate in the bone marrow with increased myeloid-erythroid ratio. The differential counts of myeloid cells in the marrow show similar findings as seen in the peripheral blood with predominance of myelocytes. Complete haematologic remission is achieved for 18 months in 97% cases treated with imatinib. Besides above, other forms of treatment include splenic irradiation, splenectomy and leucopheresis. Secondary polycythaemia or erythrocytosis, on the other hand, may occur secondary to several causes. Clinical features are the result of 359 hyperviscosity, hypervolaemia, hypermetabolism and decreased cerebral perfusion.
Tumour cells express surface antigens which have been seen in animals and in some human tumours treatment alternatives boca raton generic 500 mg lincocin amex. Thus treatment wasp stings discount lincocin 500 mg on line, presently distinction of tumour antigens is based on their recognition by the host immune cells treatment 3 phases malnourished children cheap lincocin 500mg without a prescription, i treatment multiple sclerosis buy generic lincocin 500 mg on-line. Oncoproteins from mutated oncogenes: Protein products derived from mutated oncogenes result in expression of cell surface antigens on tumour cells. In some tumours, protein products of mutated tumour suppressor genes cause expression of tumour antigens on the cell surface. Some tumours are associated with a normal cellular protein but is excessively expressed in tumour cells and incite host immune response. For example, in melanoma the tumour antigen is structurally normal melanocyte specific protein, tyrosinase, which is overexpressed compared with normal cells. Sometimes, a cellular protein is present in some normal cells but is abnormally expressed on the surface of tumour cells of some cancers. As already discussed above, many oncogenic viruses express viral oncoproteins which result in expression of antigens on tumour cells. Various other carcinogens such as chemicals and radiation induce random mutations in the target cells. Normally differentiated cells have cellular antigens which forms the basis of diagnostic immunohistochemistry. Cancers have varying degree of loss of differentiation but particular lineage of the tumour cells can be identified by tumour antigens. The normal cell expresses surface molecules of glycolipids, glycoproteins, mucins and blood group antigens. Although the host immune response to tumour is by both cell-mediated and humoral immunity, the major anti-tumour effector mechanism is cell-mediated. Activated macrophages mediate cytotoxicity by production of oxygen free radicals or by tumour necrosis factor. As such there are no anti-tumour humoral antibodies which are effective against cancer cells in vivo. However, in vitro humoral antibodies may kill tumour cells by complement activation or by antibodydependent cytotoxicity. This is due to some of the following controlling mechanisms: a) During progression of the cancer, immunogenic cells may disappear. Despite the existence of antitumour immune responses, the cancers still progress and eventually cause death of the host. The immune responses to be effective enough must eliminate the cancer cells more rapidly than their rate of proliferation and hence the role of boosting the immune response or immunotherapy. Both benign and malignant tumours cause local effects on the host due to their size or location. Malignant tumours due to rapid and invasive growth potential have more serious effects. Some benign tumours, however, due to their critical location, have more serious consequences. Malignant tumours, both primary and metastatic, infiltrate and destroy the vital structures. Cancers have a greater tendency to undergo infarction, surface ulceration and haemorrhage than the benign tumours. Patients with advanced and disseminated cancers terminally have asthenia (emaciation), and anorexia, together referred to as cancer cachexia (meaning wasting). Exact mechanism of cachexia is not clear but it does not occur due to increased nutritional demands of the tumour. Various other causes include necrosis, ulceration, haemorrhage, infection, malabsorption, anxiety, pain, insomnia, hypermetabolism and pyrexia. The exact mechanism of tumour associated fever is not known but probably the tumour cells themselves elaborate pyrogens. This is a condition caused by extensive destruction of a large number of rapidly proliferating tumour cells. The condition is seen more often in cases of lymphomas and leukaemias than solid tumours and may be due to large tumour burden. It is characterised by hyperuricaemia, hyperkalaemia, 231 hyperphosphataemia and hypocalcaemia, all of which may result in acidosis and renal failure. Hypertrophic osteoarthropathy Clubbing of fingers Lung Lung Not known Not known 4. Nephrotic syndrome Advanced cancers Renal vein thrombosis, systemic amyloidosis 7. Elaboration of hormones or hormone-like substances by cancer cells of non-endocrine origin is called as ectopic hormone production. It occurs from elaboration of parathormone-like substance by tumours such as squamous cell carcinoma of the lung, carcinoma kidney, breast and adult T cell leukaemia lymphoma. Secretion of erythropoietin by certain tumours such as renal cell carcinoma, hepatocellular carcinoma and cerebellar haemangioma may cause polycythaemia. Elaboration of insulin-like substance by fibrosarcomas, islet cell tumours of pancreas and mesothelioma may cause hypoglycaemia. About 5% of cancers are associated with progressive destruction of neurons throughout the nervous system without evidence of metastasis in the brain and spinal cord. The changes are: peripheral neuropathy, cortical cerebellar degeneration, myasthenia gravis syndrome, polymyositis.
Grossly symptoms 24 hour flu discount lincocin 500 mg free shipping, besides the coal macules and nodules of simple pneumoconiosis medicine for pink eye discount lincocin, there are larger symptoms carbon monoxide poisoning 500 mg lincocin free shipping, hard symptoms ketosis buy 500mg lincocin visa, black scattered areas measuring more than 2 cm in diameter and sometimes massive. They are usually bilateral and located more often in the upper parts of the lungs posteriorly. Sometimes, these masses break down centrally due to ischaemic necrosis or due to tuberculosis forming cavities filled with black semifluid resembling India ink. The fibrous lesions are composed almost entirely of dense collagen and carbon pigment. The wall of respiratory bronchioles and pulmonary vessels included in the massive scars are thickened and their lumina obliterated. But bronchogenic carcinoma does not appear to be more common in coal-miners than in other groups. Silicosis is caused by prolonged inhalation of silicon dioxide, commonly called silica. Therefore, a number of occupations engaged in silceous rocks or sand and products manufactured from them are at increased risk. Peculiar to India are the occupational exposure to pencil, slate and agate-grinding industry carrying high risk of silicosis (agate = very hard stone containing silica). According to an Indian Council of Medical Research report, it is estimated that about 3 million workers in India are at high potential risk of silica exposure employed in a variety of occupations including construction workers. An infrequent acute form of silicosis called accelerated silicosis produces irregular fibrosis adjoining the alveoli which is filled with lipoproteinaceous exudate and resembles alveolar proteinosis (page 494). However, if not specified, silicosis refers to the common chronic form of the disease characterised by formation of small collagenous silicotic nodules. Besides, it depends upon a number of other factors such as total dose, duration of exposure, the type of silica inhaled and individual host factors. The mechanisms involved in the formation of silicotic nodules are not clearly understood. The following sequence of events has been proposed and schematically illustrated in. New macrophages engulf the debris and thus a repetitive cycle of phagocytosis and necrosis is set up. Some silica-laden macrophages are carried to the respiratory bronchioles, alveoli and in the interstitial tissue. Some of the silica dust is transported to the subpleural and interlobar lymphatics and into the regional lymph nodes. The cellular aggregates containing silica become associated with lymphocytes, plasma cells, mast cells and fibroblasts. Crystalline form, particularly quartz, is more fibrogenic than non-crystalline form of silica. This results in increased serum levels of immunoglobulins (IgG and IgM), antinuclear antibodies, rheumatoid factor and circulating immune complexes as well as proliferation of T cells. The released silica dust activates viable macrophages leading to secretion of macrophagederived growth factors such as interleukin-1 that favour fibroblast proliferation and collagen synthesis. Coal macules composed of aggregates of dust-laden macrophages and collagens are seen surrounding respiratory bronchioles. The alveoli and respiratory bronchioles surrounding the coal macule are distended. There is scanty inflammatory infiltrate of lymphocytes and plasma cells around the areas of massive scars. Progressive massive fibrosis probably has immunological pathogenetic basis as described above. Grossly, the lungs have rounded, firm nodules with central necrosis, cavitation or calcification. Histologically, the lung lesions are modified rheumatoid nodules with central zone of dust-laden fibrinoid necrosis enclosed by palisading fibroblasts and mononuclear cells. The radiological findings of nodularities in the lungs appear after working for several years in coal-mines. Progressive massive fibrosis is, however, a serious disabling condition manifested by progressive dyspnoea and chronic cough with jet-black sputum. More advanced cases develop pulmonary hypertension and right ventricular hypertrophy (cor pulmonale). Tuberculosis and rheumatoid arthritis are more common in coal miners than the general population. Coal workers have increased risk of developing carcinomas of the stomach, Figure 17. Grossly, the chronic silicotic lung is studded with well-circumscribed, hard, fibrotic nodules, 1 to 5 mm in diameters. They are scattered throughout the lung parenchyma but are initially more often located in the upper zones of the lungs. These nodular lesions frequently have simultaneous deposition of coal-dust and may develop calcification. There may be similar fibrotic nodules on the pleura and within the regional lymph nodes. The lesions may undergo ischaemic necrosis and develop cavitation, or be complicated by tuberculosis and rheumatoid pneumoconiosis. The silicotic nodules are located in the region of respiratory bronchioles, adjacent alveoli, pulmonary arteries, in the pleura and the regional lymph nodes. The silicotic nodules consist of central hyalinised material with scanty cellularity and some amount of dust. The hyalinised centre is surrounded by concentric laminations of collagen which is further enclosed by more cellular connective tissue, dust-filled macrophages and a few lymphocytes and plasma cells.
Syndromes
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Quantitative serum HCG
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Shortness of breath
They are absorbed from intestine in the presence of bile salts and intact pancreatic function medicine 750 dollars cheap 500mg lincocin with visa. Their deficiencies occur more readily due to conditioning factors (secondary deficiency) medicine effexor discount 500mg lincocin with amex. Beside the deficiency syndromes of these vitamins symptoms xanax is prescribed for buy generic lincocin line, a state of hypervitaminosis due to excess of vitamin A and D also occurs medications 5 songs cheap 500 mg lincocin with mastercard. Being water soluble, these vitamins are more easily lost due to cooking or processing of food. It is available in diet in 2 forms: As preformed retinol, the dietary sources of which are animal-derived foods such as yolk of eggs, butter, whole milk, fish, liver, kidney. As provitamin precursor carotenoid, which is derived from -carotene-containing foods such as yellow plants and vegetables. Retinol is stored in the liver cells and released for transport to peripheral tissues after binding to retinol-binding protein found in blood. This involves formation of 2 pigments by oxidation of retinol: rhodopsin, a light sensitive pigment in reduced light synthesised in the rod cells, and iodopsins sensitive in bright light and formed in cone cells of retina. Retinol plays an important role in the synthesis of glycoproteins of the cell membrane of specialised epithelium such as mucus-secreting columnar epithelium in glands and mucosal surfaces, respiratory epithelium and urothelium. Nutritional deficiency of vitamin A is common in countries of South-East Asia, Africa, Central and South America whereas malabsorption syndrome may account for conditioned vitamin A deficiency in developed countries. As a result of replacement metaplasia of mucus-secreting cells by squamous cells, there is dry and scaly scleral conjunctiva (xerophthalmia). This is due to follicular hyperkeratosis and keratin plugging in the sebaceous glands. These are as under: i) Squamous metaplasia of respiratory epithelium of bronchus and trachea may predispose to respiratory infections. Very large doses of vitamin A can produce toxic manifestations in children as well as in adults. The clinical manifestations of chronic vitamin A excess are as under: i) Neurological such as severe headache and disordered vision due to increased intracranial pressure. This fat-soluble vitamin exists in 2 activated sterol forms: Vitamin D2 or calciferol; and Vitamin D3 or cholecalciferol. The material originally described as vitamin D1 was subsequently found to be impure mixture of sterols. Since vitamin D2 and D3 have similar metabolism and functions, they are therefore referred to as vitamin D. The other source of vitamin D is diet such as deep sea fish, fish oil, eggs, butter, milk, some plants and grains. Irrespective of the source of vitamin D, it must be converted to its active metabolites (25-hydroxy vitamin D and 1,25Figure 9. The production of calcitriol by the kidney is regulated by: plasma levels of calcitriol (hormonal feedback); plasma calcium levels (hypocalcaemia stimulates synthesis); and plasma phosphorus levels (hypophosphataemia stimulates synthesis). The main storage site of vitamin D is the adipose tissue rather than the liver which is the case with vitamin A. The main physiologic functions of the most active metabolite of vitamin D, calcitriol, are mediated by its binding to nuclear receptor superfamily, vitamin D receptor, expressed on a wide variety of cells. This is achieved by the following actions of vitamin D: i) Intestinal absorption of calcium and phosphorus is stimulated by vitamin D. Vitamin D is normally required for mineralisation of epiphyseal cartilage and osteoid matrix. However, in hypocalcaemia, vitamin D collaborates with parathyroid hormone and causes osteoclastic resorption of calcium and phosphorus from bone so as to maintain the normal blood levels of calcium and phosphorus. Vitamin D stimulates reabsorption of calcium at distal renal tubular level, though this function is also parathyroid hormone-dependent. Vitamin D receptor is expressed on the parathyroid gland cells by which active form of vitamin D causes antiproliferative action on parathyroid cells and suppresses the parathormone gene. Besides, vitamin D receptor is also expressed on cells of organs which do not have any role in mineral ion homeostasis and has antiproliferative effects on them. Deficiency of vitamin D may result from: i) reduced endogenous synthesis due to inadequate exposure to sunlight; ii) dietary deficiency of vitamin D; iii) malabsorption of lipids due to lack of bile salts such as in intrahepatic biliary obstruction, pancreatic insufficiency and malabsorption syndrome; iv) derangements of vitamin D metabolism as occur in kidney disorders (chronic renal failure, nephrotic syndrome, uraemia), liver disorders (diffuse liver disease) and genetic disorders; and v) resistance of end-organ to respond to vitamin D. Deficiency of vitamin D from any of the above mechanisms results in 3 types of lesions: 1. The primary defects in rickets are: interference with mineralisation of bone; and deranged endochondral and intramembranous bone growth. The pathogenesis of lesions in rickets is better understood by contrasting them with sequence of changes in normal bone growth as outlined in Table 9. These are as under: i) Craniotabes is the earliest bony lesion occurring due to small round unossified areas in the membranous bones of the skull, disappearing within 12 months of birth. Proliferation of cartilage cells at the epiphyses followed by provisional mineralisation ii. Proliferation of cartilage cells at the epiphyses followed by inadequate provisional mineralisation ii. Persistence and overgrowth of epiphyseal cartilage; deposition of osteoid matrix on inadequately mineralised cartilage resulting in enlarged and expanded costochondral junctions iii. Irregular overgrowth of small blood vessels in disorganised and weak bone Mesenchymal cells differentiate into osteoblasts with laying down of osteoid matrix which fails to get mineralised resulting in soft and weak flat bones 250 Biochemical changes. These are as follows: i) Lowered levels of active metabolites of vitamin D (25hydroxy vitamin D and 1, 25-dihydroxy vitamin D). Osteomalacia is the adult counterpart of rickets in which there is failure of mineralisation of the osteoid matrix. It may occur following dietary deficiency, poor endogenous synthesis of vitamin D, or as a result of conditioned deficiency. Due to deficiency of vitamin D, osteoid matrix laid down fails to get mineralised.
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