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Disorders of red cell interior Introduction to Haematopoietic System and Disorders of Erythroid Series Disorders of haemoglobin (Haemoglobinopathies) i) ii) investigations of a patient suspected to have haemolytic anaemia should provide answers to 3 vital questions: 1 bacteria 400x magnification buy discount tolchicine 0.5 mg line. Heinz bodies Traumatic damage to red cell membrane Polymerisation of HbS Abnormality in membrane lipids Precipitated Hb 312 anaemia) antibiotic not working purchase tolchicine discount, mechanical factors (microangiopathic haemolytic anaemia) virus removal software buy tolchicine with american express, direct toxic effect (in malaria, clostridial infection etc), splenomegaly, and certain acquired membrane abnormalities (paroxysmal nocturnal haemoglobinuria). Immune haemolysis in these cases may be induced by one of the following three types of antibodies: 1. Isoimmune haemolytic anaemia in which the antibodies are acquired by blood transfusions, pregnancies and haemolytic disease of the newborn. Warm antibodies reactive at body temperature and coating the red cells are generally IgG class antibodies and occasionally they are IgA. A part of the coated cell membrane is lost resulting in spherical transformation of the red cells (acquired spherocytosis). Red cells coated with IgG along with C3 on the surface further promote this red cell-leucocyte interaction, accounting for more severe haemolysis. The spleen is particularly efficient in trapping red cells coated with IgG antibodies. Cold agglutinin disease a) Acute: Mycoplasma infection, infectious mononucleosis b) Chronic: Idiopathic, lymphomas 2. Treatment of these cases consists of removal of the cause whenever present, corticosteroid therapy, and in severe cases blood transfusions. These cold antibodies are usually directed against the I antigen on the red cell surface. Haemolytic effect is mediated through fixation of C3 to the red blood cell surface and not by agglutination alone. Cyanosis affecting the cold exposed regions such as tips of nose, ears, fingers and toes. Drug-induced Immunohaemolytic Anaemia Drugs may cause immunohaemolytic anaemia by 3 different mechanisms: 1. Patients receiving large doses of penicillin or penicillin-type antibiotics develop antibodies against the red blood cell-drug complex which induces haemolysis. Drugs such as quinidine form a complex with plasma proteins to which an antibody forms. This drug-plasma protein-antibody complex may induce lysis of bystanding red blood cells or platelets. In each type of drug-induced immunohaemolytic 313 anaemia, discontinuation of the drug results in gradual disappearance of haemolysis. Isoimmune Haemolytic Anaemia Isoimmune haemolytic anaemias are caused by acquiring isoantibodies or alloantibodies by blood transfusions, pregnancies and in haemolytic disease of the newborn. These antibodies produced by one individual are directed against red blood cells of the other. It is generally due to mechanical trauma to the red cells in circulation and is characterised by red cell fragmentation (schistocytosis). There are 3 different ways by which microangiopathic haemolytic anaemia results: 1. Direct external trauma to red blood cells when they pass through microcirculation, especially over the bony prominences, may cause haemolysis during various activities.
A number of other predisposing factors contributing to formation of calcium stones are alkaline urinary pH antibiotic you cant drink alcohol purchase 0.5 mg tolchicine mastercard, decreased urinary volume and increased excretion of oxalate and uric acid bacterial cell wall order genuine tolchicine online. Calcium stones are usually small (less than a centimeter) antibiotics vs surgery appendicitis discount tolchicine 0.5mg online, ovoid, hard, with granular rough surface. They are dark brown due to old blood pigment deposited in them as a result of repeated trauma caused to the urinary tract by these sharp-edged stones. Struvite stones are formed as a result of infection of the urinary tract with urea-splitting organisms that produce urease such as by species of Proteus, and occasionally Klebsiella, Pseudomonas and Enterobacter. Types of Urinary Calculi There are 4 main types of urinary calculi-calcium containing, mixed (struvite), uric acid and cystine stones, and a few rare types (Table 22. They may be pure stones of calcium oxalate (50%) or calcium phosphate (5%), or mixture of calcium oxalate and calcium phosphate (45%). Sectioned surface shows dilated pelvicalyceal system with atrophied and thin peripheral cortex. The pelvis of the kidney contains a single, large, sof t yellow white stone t aking the contour of the pelvi-calyceal system (arrow). Type Calcium stones Incidence 75% Etiology Hypercalciuria with or without hypercalcaemia; idiopathic Urinary infection with ureasplitting organisms like Proteus Hyperuricosuria with or without hyperuricaemia. Uric acid stones are frequently formed in cases with hyperuricaemia and hyperuricosuria such as due to primary gout or secondary gout due to myeloproliferative disorders. Other factors contributing to their formation are acidic urinary pH (below 6) and low urinary volume. Thus, as the urine becomes more acidic, the solubility of uric acid in urine decreases and precipitation of uric acid crystals increases favouring the formation of uric acid stones. Hyperuricosuria is the most important factor in the production of uric acid stones, while hyperuricaemia is found in about half the cases. Cystine stones are associated with cystinuria due to a genetically-determined defect in the transport of cystine and other amino acids across the cell membrane of the renal tubules and the small intestinal mucosa. The resultant excessive excretion of cystine which is least soluble of the naturally-occurring amino acids leads to formation of crystals and eventually cystine calculi. Less than 2% of urinary calculi consist of other rare types such as due to inherited abnormality of enzyme metabolism. Hydronephrosis develops if one or both the pelviureteric sphincters are incompetent, as otherwise there will be dilatation and hypertrophy of the urinary bladder but no hydronephrosis. Bilateral Hydronephrosis this is generally the result of some form of urethral obstruction but can occur from the various causes listed above if the lesions involve both sides. The pathologic changes vary depending upon whether the obstruction is sudden and complete, or incomplete and intermittent. Initially, there is extrarenal hydronephrosis characterised by dilatation of renal pelvis medially in the form of a sac. On cut section, the renal pelvis and calyces are dilated and cystic and contain a large stone in the pelvis of the kidney (arrow). The cystic change is seen to extend into renal p arenchyma, compressing the cortex as a thin rim at the periphery. Unlike polycystic kidney, however, these cysts are communicating with the pelvi-calyceal system. Eventually, the dilated pelvi-calyceal system extends deep into the renal cortex so that a thin rim of renal cortex is stretched over the dilated calyces and the external surface assumes lobulated appearance. An important point of distinction between the sectioned surface of advanced hydronephrosis and polycystic kidney disease (page 657) is the direct continuity of dilated cystic spaces.
Age 50 60 30 47 58 25 11 38 56 22 39 48 Sex M F M F F M f F M M M F Histology Glioblastoma Glioblastoma Chondrosarcoma Meningioma Meningioma An antibiotics for sinus and respiratory infection buy tolchicine 0.5mg without a prescription. Twelve patients (four glioblastomas and four anaplastic astrocytomas three meningioma antibiotic ointment over the counter order tolchicine 0.5 mg, one chondrosarcoma) lived more than 10 years antibiotic 2014 discount tolchicine 0.5mg mastercard. There were two patients with glioblastoma, 10 patients with anaplastic astrocytoma and one with low grade astrocytoma. As prognostic factors, grading of the tumour, ages of the patients and target depth were proved as important 246 factors. However, the most important factor was tumour volume radiation dose demonstrated by boron n-alpha reaction. Nine of the 14 had neurological deficits such as motor weakness and speech disturbance. The patients were treated with a high dose of steroid therapy (Dexamethasone 32-64mg/day was tapered for one to two weeks and changed to prednisolone 10-30mg / day per os). The remaining five patients had only radiographic change without neurological deterioration. Vascular radiation dose was calculated according to the report by Kitao and Rydin. Only one-third of the 10 B (n, a)7 Li radiation occurring in vascular lumen will be absorbed by the vascular endothelium. Age 50 15 4 44 37 Sex M F F M M Histology Glioblastoma Rhabdomiosarcoma Pontine glioma An. Radiation necrosis and related factors Necrosis (+) Age Radiation time B-10 in blood Neutron fluences Maximum Vascular dose 21. Surgical procedures and making a cavity played an important role not only to irradiate with sufficient neutron fluence, but also to avoid radiation side effect. The factors related to radiation necrosis were maximum thermal neutron fluence on the brain surface and vascular dose. Therefore, we decided the maximum thermal neutron fluence on the surface of the brain should be below 2. Vascular dose in the brain tissue near the surface of the brain or maximum vascular dose must be controlled below 15 Gy. To improve the neutron penetration, we decided to utilize epithermal neutron beams. Both reactors have the capacity to yield thermal neutron beam, epithermal neutron beam and 248 mixed beams. We compared the neutron fluences at the target point and on the surface of the cavity between a case treated by thermal neutron and one by mixed beam. The new combination of surgical procedure and irradiation using epithermal neutrons should remarkably improve the target volume dose compared to the radiation dose treated by thermal neutrons, seven times without cavity and 3. Wolbers Department of Neurosurgery, University Hospital "Vrije Universiteit", Amsterdam, Netherlands K.
The veins of other parts of the body which are affected are the lower oesophagus (oesophageal varices antibiotic associated diarrhea buy 0.5 mg tolchicine, Chapter 19) bacteria jokes humor order 0.5mg tolchicine with amex, the anal region (haemorrhoids music infection buy tolchicine toronto, Chapter 20) and the spermatic cord (varicocele, Chapter 23). About 10-12% of the general population develops varicose veins of lower legs, with the peak incidence in 4th and 5th decades of life. Adult females are affected more commonly than the males, especially during pregnancy. This is attributed to venous stasis in the lower legs because of compression on the iliac veins by pregnant uterus. A number of etiologic and pathogenetic factors are involved in causing varicose veins. These are as follows: i) Familial weakness of vein walls and valves is the most common cause. Other systemic manifestations include bacteraemia and septic embolisation to brain, meninges, liver etc. Special Types of Phlebothrombosis A few special variants of phlebothrombosis are considered below: 1. The condition is not a morphologic entity but a clinical one, seen most often in disseminated visceral cancers. It occurs most often in women during late pregnancy or following delivery when the pregnant uterus causes pressure on the iliofemoral veins, or after extensive pelvic surgery. Development of pulmonary embolism may occur due to involvement of inferior vena cava. It is a serious complication of massive iliofemoral venous thrombosis and decreased arterial blood flow. Some of the common causes of superior vena caval syndrome are malignancy (especially lung cancer and lymphoma), syphilitic aortic aneurysm and tuberculous mediastinitis. Clinical features include dilated veins of neck and thorax, oedema of the face, neck and upper chest, visual disturbances and disturbed sensorium. Most often, obstruction results from thrombosis by extension from iliofemoral veins. Clinical features are oedema of lower extremities, dilated leg veins and collateral venous channels in the lower abdomen layer of endothelium have thin muscle in their walls than in veins of the same size and the valves are more numerous. The walls of lymphatic capillaries are permeable to tissue fluid, proteins and particulate matter. Microscopically, the dilated lumen contains acute inflammatory exudate, cell debris and clotted lymph. There is inflammatory infiltration into the perilymphatic tissues alongwith hyperaemia and oedema. Chronic lymphangitis occurs due to persistent and recurrent acute lymphangitis or from chronic infections like tuberculosis, syphilis and actinomycosis. Histologically, there is permanent obstruction due to fibrosis of affected lymphatics called chronic lymphoedema. Lymphoedema occurring without underlying secondary cause is called primary or idiopathic lymphoedema. The disease is inherited as an autosomal dominant trait and is often associated with other congenital anomalies. The condition results from developmental defect of lymphatic channels so that the affected tissue shows abnormally dilated lymphatics and the area shows honey-combed appearance. Recurrent infection of the tissue causes cellulitis and fibrosis of lymphatic vessels. Lymphatic capillaries resemble blood capillaries, and larger lymphatics are identical to veins. However, lymphatics lined by a single begins in the foot and progresses slowly upwards to involve the whole extremity.
Changes of epithelial dysplasia are often present in the surrounding areas of the lesion antibiotics for sinus infection over the counter buy tolchicine cheap online. Carcinoma of the lip and intraoral squamous carcinoma are usually always welldifferentiated antibiotics for pet birds order 0.5mg tolchicine with visa. Carcinoma of the lip has a more favourable prognosis due to visible and easily accessible location and less frequent metastasis to the regional lymph nodes antibiotics for acne south africa buy 0.5mg tolchicine with visa. However, intraoral squamous carcinomas have poor prognosis because they are detected late and metastasis to regional lymph nodes occur early, especially in the case of carcinoma of tongue and soft palate. Verrucous carcinoma, on the other hand, is composed of very well-differentiated squamous epithelium with minimal atypia and hence has very good prognosis. The teeth are peculiar than other calcified tissues of the body by being surrounded by Figure 19. There is keratosis, irregular stratification, cellular pleomorphism, increased and abnormal mitotic figures and individual cell keratinisation, while a few areas show superficial invasive islands of malignant cells in the subepithelial soft tissues. Nests of odontogenic epithelium are normally present in the jaw and may develop into cysts and tumours. Dental caries is essentially a disease of modern society, associated with diet containing high proportion of refined carbohydrates. It has been known for almost 100 years that mixture of sugar or bread with saliva in the presence of acidogenic bacteria of the mouth, especially streptococci, produces organic acids which can decalcify enamel and dentin. Bacteria present in the oral cavity cause proteolysis of the remaining organic material of dentin, completing the process of destruction. Diets rich in carbohydrates do not require much chewing and thus the soft and sticky food gets clung to the teeth rather than being cleared away, particularly in the areas of occlusal pits and fissures. If these plaques are not removed by brushing or by vigorous chewing of fibrous foods, the process of tooth decay begins. There is evidence that consumption of water containing one part per million (ppm) fluoride is sufficient to reduce the rate of tooth decay in children. Caries occurs chiefly in the areas of pits and fissures, mainly of the molars and premolars, where food retention occurs, and in the cervical part of the tooth. Grossly, the earliest change is the appearance of a small, chalky-white spot on the enamel which subsequently enlarges and often becomes yellow or brown and breaks down to form carious cavity. Embryologically, odontogenic development takes place from primitive structure, the dental lamina or primitive oral cavity, as follows: Inner epithelial layer of the dental lamina is ectodermderived columnar to cuboidal oral epithelium called ameloblasts which secrete enamel matrix, also called enamel organ. Mesoderm-derived connective tissue gives rise to structures in the dental papilla. Outer margin of the dental papilla differentiates into odontoblasts, which continue with ameloblastsic epithelium; odontoblasts secrete dentin. It is composed of organic material in the form of collagen fibrils as well as inorganic material in the form of calcium phosphates as in bone. Dentin is composed of odontoblasts or dentin cells which are counterparts of osteocytes in bone but differ from the latter in having odontoblast processes. There is complete destruction of enamel, deposition of secondary dentine and evidence of pulpitis. There is evidence of reaction of the tooth to the carious process in the form of secondary dentin, which is a layer of odontoblasts laid down under the original dentine. Carious destruction of dental hard tissues frequently produces pulpitis and other inflammatory lesions like apical granuloma and apical abscess. Less common causes of these lesions are fracture of tooth and accidental exposure of pulp by the dentist. Acute pulpitis is accompanied by severe pain which may be continuous, throbbing or dull, and is accentuated by heat or cold.
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