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Two types of metaplasia are commonly associated with atrophic gastritis: i) Intestinal metaplasia spasms medication 400mg carbamazepine sale. Characteristic histologic feature is the presence of intestinal type mucus-goblet cells; Paneth cells and endocrine cells may also be present spasms meaning in telugu 200mg carbamazepine with amex. A few other types of gastritis which do not fit into the description of the types of gastritis described above are as under: i) Eosinophilic gastritis muscle relaxant id purchase carbamazepine canada. This condition is characterised by diffuse thickening of the pyloric antrum due to oedema and extensive infiltration by eosinophils in all the layers of the wall of antrum muscle relaxant in india order cheap carbamazepine on-line. This is a variant of chronic atrophic gastritis in which numerous lymphoid follicles are present in the mucosa and submucosa of the stomach. In this condition, there are superficial erosions and mucosal haemorrhages, usually following severe haematemesis. Though they can occur at any level of the alimentary tract that is exposed to hydrochloric acid and pepsin, they occur most commonly (98-99%) in either the duodenum or the stomach in the ratio of 4:1. Intestinal metaplasia, focal or extensive, in atrophic gastritis is significant because its incidence is high in populations having high prevalence rate of gastric cancer like in Japan. It involves the body glands which are replaced by proliferated mucus neck cells, conforming in appearance to normal pyloric glands. In this, there is thinning of the gastric mucosa with loss of glands but no inflammation though lymphoid aggregates may be present. This is an uncommon condition characterised pathologically by enormous thickening of gastric rugal folds resembling cerebral convolutions, affecting mainly the region of fundic-body mucosa and characteristically sparing antral mucosa. The patients present with dyspepsia, haematemesis, melaena or protein-losing enteropathy. There is marked gastric atrophy with disappearance of gastric glands and appearance of goblet cells (intestinal metaplasia). In these conditions, the possible hypotheses for genesis of stress ulcers are as under: 1. Grossly, acute stress ulcers are multiple (more than three ulcers in 75% of cases). They are more common anywhere in the stomach, followed in decreasing frequency by occurrence in the first part of duodenum. Microscopically, the stress ulcers are shallow and do not invade the muscular layer. The margins and base may show some inflammatory reaction depending upon the duration of the ulcers. These ulcers commonly heal by complete re-epithelialisation without leaving any scars. Peptic ulcers are common in the present-day life of the industrialised and civilised world. Gastric and duodenal ulcers represent two distinct diseases as far as their etiology, pathogenesis and clinical features are concerned. The features of gastric and duodenal peptic ulcers are described together below while their contrasting features are presented in Table 20. The peak incidence for duodenal ulcer is 5th decade, while for gastric ulcer it is a decade later (6th decade). Duodenal ulcer is almost four times more common than gastric ulcer; the overall incidence of gastroduodenal ulcers being approximately 10% of the male population. However, in contrast to duodenal ulcers, the patients of gastric ulcer have low-to-normal gastric acid secretions, though true achlorhydria in response to stimulants never occurs in benign gastric ulcer. Besides, 10-20% patients of gastric ulcer may have coexistent duodenal ulcer as well. Thus, the etiology of peptic ulcers possibly may not be explained on the basis of a single factor but is multifactorial. Non-steroidal antiinflammatory drugs are most commonly used medications in the developed countries and are responsible for direct toxicity, endothelial damage and epithelial injury to both gastric as well as duodenal mucosa. There is conclusive evidence that some level of acid-pepsin secretion is essential for the development of duodenal as well as gastric ulcer. Peptic ulcers never occur in association with pernicious anaemia in which there are no acid and pepsin-secreting parietal and chief cells respectively. Some degree of gastritis is always present in the region of gastric ulcer, though it is not clear whether it is the cause or the effect of ulcer. Besides, the population distribution pattern of gastric ulcer is similar to that of chronic gastritis. Pyloric antrum and lesser curvature of the stomach are the sites most exposed for longer periods to local irritants and thus are the common sites for occurrence of gastric ulcers. Some of the local irritating substances implicated in the etiology of peptic ulcers are heavily spiced foods, alcohol, cigarette smoking, unbuffered aspirin. Nutritional deficiencies have been regarded as etiologic factors in peptic ulcers. However, malnutrition does not appear to have any causative role in peptic ulceration in European countries and the U. Duodenal Ulcer i) Four times more common than gastric ulcers ii) Usual age 25-50 years iii) More common in males than in females (4:1) Gastric Ulcer Less common than duodenal ulcers Usually beyond 6th decade More common in males than in females (3. Association with gastritis, bile reflux, drugs, alcohol, tobacco Usually normal-to-low acid levels; hyperacidity if present is due to high serum gastrin Damage to mucus barrier significant factor Most common along the lesser curvature and pyloric antrum Grossly similar to duodenal ulcer 551 Feature 1. Pathologic changes i) Most common in the first part of duodenum ii) Often solitary, 1-2. Clinical features the Gastrointestinal Tract Vomiting common Haematemesis more common Significant loss of weight Patients choose bland diet devoid of fried foods, curries etc. Deep tenderness in the midline in epigastrium No seasonal variation More often in labouring groups vii) Deep tenderness in the right hypochondrium viii) Marked seasonal variation ix) Occurs more commonly in people at greater stress 7. Psychological stress, anxiety, fatigue and ulcer-type personality may exacerbate as well as predispose to peptic ulcer disease.
The causes are as under: i) Luminal occlusion in microvasculature: a) By red cells spasms right before falling asleep carbamazepine 100 mg low price. The extent of damage produced by ischaemia due to occlusion of arterial or venous blood vessels depends upon a number of factors spasms vhs 200mg carbamazepine otc. The extent of injury by ischaemia depends upon the anatomic pattern of arterial blood supply of the organ or tissue affected spasms in back purchase carbamazepine 400 mg amex. There are 4 different patterns of arterial blood supply: i) Single arterial supply without anastomosis muscle relaxant magnesium purchase 400mg carbamazepine mastercard. Some organs receive blood supply from arteries which do not have significant anastomosis and are thus functional end-arteries. Arterial supply to some organs has rich interarterial anastomoses so that blockage of one vessel can re-establish blood supply bypassing the blocked arterial branch, and hence the infarction is less common in such circumstances. Interarterial anastomoses in the 3 main trunks of the 125 coronary arterial system. Blood supply to some organs and tissues is such that the vitality of the tissue is maintained by alternative blood supply in case of occlusion of one. The effect of occlusion of one set of vessels is modified if an organ has dual blood supply. For example: Lungs are perfused by bronchial circulation as well as by pulmonary arterial branches. However, collateral circulation is of little value if the vessels are severely affected with spasm, atheroma or any other such condition. The general status of an individual as regards cardiovascular function is an important determinant to assess the effect of ischaemia. Some of the factors which render the tissues more vulnerable to the effects of ischaemia are as under: i) Anaemias (sickle cell anaemia, in particular) ii) Lowered oxygenation of blood (hypoxaemia) iii) Senility with marked coronary atherosclerosis iv) Cardiac failure v) Blood loss vi) Shock. The mesenchymal tissues are quite resistant to the effect of ischaemia as compared to parenchymal cells of the organs. The following tissues are more vulnerable to ischaemia: i) Brain (cerebral cortical neurons, in particular). Sudden vascular obstruction results in more severe effects of ischaemia than if it is gradual since there is less time for collaterals to develop. Complete vascular obstruction results in more severe ischaemic injury than the partial occlusion. No effects on the tissues, if the collateral channels develop adequately so that the effect of ischaemia fails to occur. These result when collateral channels are able to supply blood during normal activity but the supply is not adequate to withstand the effect of exertion. Infarction results when the deprivation of blood supply is complete so as to cause necrosis of tissue affected. Some general morphological features of infarcts are common to infarcts of all organ sites. Grossly, infarcts of solid organs are usually wedgeshaped, the apex pointing towards the occluded artery and the wide base on the surface of the organ. Infarcts due to arterial occlusion are generally pale while those due to venous obstruction are haemorrhagic. Most infarcts become pale later as the red cells are lysed but pulmonary infarcts never become pale due to extensive amount of blood. Recent infarcts are generally slightly elevated over the surface while the old infarcts are shrunken and depressed under the surface of the organ. Microscopically, the pathognomonic cytologic change in all infarcts is coagulative (ischaemic) necrosis of the affected area of tissue or organ. Initially, neutrophils predominate but subsequently macrophages and fibroblasts appear. Eventually, the necrotic area is replaced by fibrous scar tissue, which at times may show dystrophic calcification. A few representative examples of infarction of some organs (lungs, kidney, liver and spleen) are discussed below. Myocardial infarction (Chapter 16), cerebral infarction (Chapter 30) and infarction of the small intestines (Chapter 20) are covered in detail later in respective chapters of Systemic Pathology. Embolism of the pulmonary arteries may produce pulmonary infarction, though not always. This is because lungs receive blood supply from bronchial arteries as well, and thus occlusion of pulmonary artery ordinarily does not produce infarcts. The cause of sudden death from ischaemia is usually myocardial and cerebral infarction. The most important and common outcome of ischaemia is infarction which is discussed below. Infarction is the process of tissue necrosis resulting from some form of circulatory insufficiency; the localised area of necrosis so developed is called an infarct. There are a few other noteworthy features in infarction: Most commonly, infarcts are caused by interruption in arterial blood supply, called ischaemic necrosis. According to their colour: Pale or anaemic, due to arterial occlusion and are seen in compact organs. Red or haemorrhagic, seen in soft loose tissues and are caused either by pulmonary arterial obstruction.
Tumours arising from cerumen-secreting apocrine sweat glands of the external auditory canal are cerumen-gland adenomas or cerumengland adenocarcinomas and are counter-parts of sweat gland tumours (hideradenoma and adenocarcinoma) of the skin discussed in Chapter 26 spasms in 7 month old discount carbamazepine 200mg visa. The usual source of infection is via the eustachian tube and the common causative organisms are Streptococcus pneumoniae spasms in 6 month old baby generic carbamazepine 200mg visa, Haemophilus influenzae and -Streptococcus haemolyticus muscle relaxant cephalon cheap carbamazepine 200 mg without prescription. Serous or mucoid otitis media refers to nonsuppurative accumulation of serous or thick viscid fluid in the middle ear muscle relaxant with ibuprofen purchase carbamazepine discount. These collections of fluid are encountered more often in children causing hearing problems and occur due to obstruction of the eustachian tube. This is an uncommon autoimmune disease characterised by complete loss of glycosaminoglycans resulting in destruction of cartilage of the ear, nose, eustachian tube, larynx and lower respiratory tract. Histologically, the perichondral areas show acute inflammatory cell infiltrate and destruction and vascularisation of the cartilage. The skin in this location is in direct contact with the cartilage without protective subcutaneous layer. On the lateral wall of the nasal cavity, there is a system of 3 ridges on each side known as conchae or turbinates-the inferior, middle and superior. The nasal accessory sinuses are air spaces in the bones of the skull and communicate with the nasal cavity. They are the frontal air sinus, maxillary air sinus and the anterior ethmoid air cells, comprising the anterior group, while posterior ethmoidal cells and sphenoidal sinus form the posterior group. The anterior group drains into the middle meatus while the posterior group drains into the superior meatus and the sphenoethmoidal recess. Nasal mucous membranes as well as the lining of the nasal sinus are lined by respiratory epithelium (pseudostratified columnar ciliated cells). Besides, the upper and middle turbinate processes and the upper third of the septum are covered with olfactory mucous membrane. The main physiologic functions of the nose are smell, filtration, humidification and warming of the air being breathed. Acute rhinitis or common cold is the common inflammatory disorder of the nasal cavities that may extend into the nasal sinuses. Initially, the nasal discharge is watery, but later it becomes thick and purulent. Microscopically, there are numerous neutrophils, lymphocytes, plasma cells and some eosinophils with abundant oedema. It is an IgE-mediated immune response consisting of an early acute response due to degranulation of mast cells, and a delayed prolonged response in which there is infiltration by leucocytes such as eosinophils, basophils, neutrophils and macrophages accompanied with oedema. Acute sinusitis is generally a complication of acute or allergic rhinitis and rarely secondary to dental sepsis. Acute sinusitis may become chronic due to incomplete resolution of acute inflammation and from damage to the mucous membrane. There is chronic inflammatory granulation tissue and foreign body giant cells around the cholesterol clefts and some pink keratinous material. Rarely, it may be a primary lesion arising from embryonal rests of squamous epithelium in the temporal bone. Histologically, the lesion consists of cyst containing abundant keratin material admixed with cholesterol crystals and large number of histiocytes. The one arising from glomus jugulare bodies of the middle ear (jugulotympanic bodies) is called jugular paraganglioma or chemodectoma or nonchromaffin paraganglioma and is the most common benign tumour of the middle ear. Histologically similar tumours are seen in the carotid bodies and vagus (Chapter 27). Microscopically, the tumour cells containing neurosecretory granules are arranged in typical organoid pattern or nests. The tumour may extend locally to involve the skull and brain but may rarely metastasise. It is a benign tumour similar to other schwannomas but by virtue of its location and large size, may produce compression of the important neighbouring tissues leading to deafness, tinnitus, paralysis of 5th and 7th nerves, compression of the brainstem and hydrocephalus. Typically it occurs in a nasal polyp but may be found in other locations like nasopharynx, larynx and conjunctiva. The disease is common in India and Sri Lanka and sporadic in other parts of the world. Microscopically, besides the structure of inflammatory or allergic polyp, large number of organisms of the size of erythrocytes with chitinous wall are seen in the thickwalled sporangia. On rupture of a sporangium, the spores are discharged into the submucosa or on to the surface of the mucosa. The intervening tissue consists of inflammatory granulation tissue (plasma cells, lymphocytes, histiocytes, neutrophils) while the overlying epithelium shows hyperplasia, focal thinning and occasional ulceration. This is a chronic destructive inflammatory lesion of the nose and upper respiratory airways caused by diplobacilli, Klebsiella rhinoscleromatis. The condition is endemic in parts of Africa, America, South Asia and Eastern Europe. The condition begins as a common cold and progresses to atrophic stage, and then into the nodular stage characterised by small tumour-like submucosal masses. Histologically, there is extensive infiltration by foamy histiocytes containing the organisms (Mikulicz cells) and other chronic inflammatory cells like lymphocytes and plasma cells. The overlying mucosa is covered partly by respiratory and partly by squamous metaplastic epithelium. The underlying stroma is oedematous and contains inflammatory cells with prominence of eosinophils. Antrochoanal polyps originate from the mucosa of the maxillary sinus and appear in the nasal cavity. Microscopically, they are composed of loose oedematous connective tissue containing some mucous glands and varying number of inflammatory cells like lymphocytes, plasma cells and eosinophils.
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