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Some areas of the skull base-such as the cribriform plate antibiotic 5897 discount 625mg augmentin with visa, olfactory recesses, and petrous ridges-are often very thin. Intracranial Hypotension Intracranial hypotension is a poorly understood, frequently misdiagnosed entity that can present with a wide variety of symptoms. Imaging is key to the diagnosis, sometimes providing the first insight into the cause of often puzzling symptoms. The dura itself typically appears normal without evidence of neoplasia or inflammation. Spinal meningeal diverticula can rupture suddenly and may be responsible for many cases of "spontaneous" intracranial hypotension. Sagittal T1 C+ scan shows severe midbrain "slumping" and downward compression of the pons, flattened internal cerebral veins, thick dural enhancement, and venous sinus distension. Orthostatic or postural headache can have posterior neck pain or stiffness,vomiting, or photophobia. Hyperprolactinemia with stalk effect caused by the infundibular compression may be present. Emergent intrathecal saline infusion may be lifesaving in obtunded, severely encephalopathic patients. Epidural blood patch is often performed on the basis of clinical and brain imaging findings alone. Midbrain "sagging" with the midbrain displaced below the level of the dorsum sellae, decreased angle between the peduncles and pons below 50°, shortened pontomammillary distance below 5. The optic chiasm and hypothalamus are often draped over the sella, effacing the suprasellar cistern. The pituitary gland appears enlarged in at least 50% of all cases (34-46) (34-50C). Midbrain anatomy is distorted with decreased width and increased anteroposterior diameter (34-49C). The lateral ventricles are usually small and distorted, as they are pulled medially and inferiorly by the brain "sagging" (34-48). In cases with severe brain descent, coronal scans may show that the angle between the roof of the lateral ventricles progressively decreases (< 120°) as brain sagging increases (34-48) (34-50). The dural sinuses often appear distended with outwardly convex margins and exaggerated "flow voids" (34-49E). Between 15-50% of cases have subdural fluid collections (hygromas > hematomas) (34-48). The slit-like third ventricle is displaced downward and on axial scans appears almost superimposed on the midbrain and hypothalamus (34-49C). Linear dural thickening may extend into the internal auditory canals, down the clivus, and through the foramen magnum into the upper cervical canal (34-47). On axial imaging the engorged enhancing cervical venous plexuses may appear like a "draped curtain," narrowing the canal and even mimicking sarcoid or metastatic disease. Severe intracranial hypotension often has minimal or no abnormal dura-arachnoid thickening and enhancement. The cerebellar tonsils measured 7 mm below the foramen magnum but are normally shaped. Tearing of bridging veins caused by brain sagging can result in subarachnoid hemorrhage and superficial siderosis. The major differential diagnosis of intracranial hypotension is Chiari 1 malformation. However, in Chiari I the only intracranial abnormality is displaced tonsils, which appear peg-like with vertically oriented folia. Here, we briefly consider normal development of the cerebral hemispheres and cerebellum. We first focus on the basics of neurulation and neural tube closure, then turn our attention to how the neural tube flexes, bends, and evolves into the forebrain, midbrain, and hindbrain. Developmental errors and the resulting malformations that may occur at each stage are briefly summarized. Development of the three major brain commissures (corpus callosum, anterior commissure, and hippocampal commissure) is detailed in Chapter 37 as a prelude to our consideration of callosal anomalies.

There are 2 main forms of gangrene-dry and wet virus united states department of justice 625 mg augmentin sale, and a variant form of wet gangrene called gas gangrene. In all types of gangrene, necrosis undergoes liquefaction by the action of putrefactive bacteria. The typical example is the dry gangrene in the toes and feet of an old patient due to arteriosclerosis. A line of separation is formed at this point between the gangrenous part and the viable part. Grossly, the affected part is dry, shrunken and dark black, resembling the foot of a mummy. The line of separation usually brings about complete separation with eventual falling off of the gangrenous tissue if it is not removed surgically. The gangrenous area is dry, shrunken and dark and is separated from the viable tissue by clear line of Histologically, there is necrosis with smudging of the tissue. Wet Gangrene Wet gangrene occurs in naturally moist tissues and organs such as the mouth, bowel, lung, cervix, vulva etc. Diabetic foot is another example of wet gangrene due to high sugar content in the necrosed tissue which favours growth of bacteria. Bed sores occurring in a bed-ridden patient due to pressure on sites like the sacrum, buttocks and heels are the other important clinical conditions included in wet gangrene. Wet gangrene usually develops rapidly due to blockage of venous, and less commonly, arterial blood flow from thrombosis or embolism. The toxic products formed by bacteria are absorbed causing profound systemic manifestations of septicaemia, and finally death. The spreading wet gangrene generally lacks clear-cut line of demarcation and may spread to peritoneal cavity causing peritonitis. The classic example is gangrene of bowel, commonly due to strangulated hernia, volvulus or intussusception. The line of demarcation between gangrenous segment and viable bowel is generally not clear-cut. It is a special form of wet gangrene caused by gas-forming clostridia (gram-positive anaerobic bacteria) which gain entry into the tissues through open contaminated wounds, especially in the muscles, or as a complication of operation on colon which normally contains clostridia. Grossly, the affected area is swollen, oedematous, painful and crepitant due to accumulation of gas bubbles within the tissues. Microscopy shows coagulative necrosis of the skin, muscle and other soft tissue, and thrombsed vessels. Line of demarcation between gangrenous segment and the viable bowel is not clear-cut. At the periphery, a zone of leucocytic infiltration, oedema and congestion are found. Two distinct types of pathologic calcification are recognised: Dystrophic calcification, which is characterised by deposition of calcium salts in dead or degenerated tissues with normal calcium metabolism and normal serum calcium levels. Histologically, in routine H and E stained sections, calcium salts appear as deeply basophilic, irregular and granular clumps. Calcium deposits can be confirmed by special stains like silver impregnation method of von-Kossa producing black colour, and alizarin red S that produces red staining. Microscopy shows coagulative necrosis of the affected bowel wall and thrombosed vessels while the junction with normal intestine is indistinct and shows an inflammatory infiltrate. Etiopathogenesis the two types of pathologic calcification result from distinctly different etiologies and mechanisms. As apparent from definition, dystrophic calcification may occur due to 2 types of causes: Calcification in dead tissue Calcification of degenerated tissue. Living bacilli may be present even in calcified tuberculous lesions, lymph nodes, lungs, etc. Fat necrosis following acute pancreatitis or traumatic fat necrosis in the breast results in deposition of calcium soaps. Congenital toxoplasmosis involving the central nervous system visualised by calcification in the infant brain. Some tumours show characteristic spherules of calcification called psammoma bodies or calcospherites such as in meningioma, papillary serous cystadenocarcinoma of the ovary and papillary carcinoma of the thyroid.

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Which of the following was most likely a contributing cause of death in these men Beriberi Kwashiorkor Pellagra Pernicious anemia Rickets Scurvy Environmental and Nutritional Diseases 121 53 A 55-year-old woman has been steadily gaining weight for the past 30 years antibiotics for face redness order augmentin 375mg visa. On physical examination, she has decreased range of motion with pain on movement of the knees. Colonic adenocarcinoma Endometrial carcinoma Hepatocellular carcinoma Pulmonary adenocarcinoma Renal cell carcinoma 50 An 18-year-old pregnant woman receives no prenatal care, eats a diet containing mostly carbohydrates and fats, and does not take prenatal vitamins with iron. Laboratory studies show markedly decreased serum ferritin levels in the infant and the mother. Which of the following findings from a nutritional deficiency is most likely to be present in both the infant and the mother Investigators observe that a subset of obese individuals has a consistently high caloric intake because they lack a feeling of satiety when eating. These individuals have diminished responsiveness of a hypothalamic receptor for which of the following molecules Adenosine Glucagon Glucose Insulin Leptin 51 An epidemiologic study evaluates the rate of dental caries and tooth abscesses among children living in communities within a metropolitan area. Investigators discover that the rate is high among children living in an upper middle class community, but low in children living in a community below the poverty level. The levels of trace elements in the water supplies for those communities are measured. A higher level of which of the following minerals in the water is most likely to be associated with a lower rate of dental decay among the children living in the poor community Copper Fluoride Iodine Selenium Zinc 55 It is 1:00 am and a hard-working second-year medical student is intent on finishing her pathology reading assignment. Soon she begins to note that her concentration is fading because 7 hours have passed since she had dinner, and she is feeling famished. Having studied the chapter on ischemic heart disease, she decides to be prudent and forgoes her favorite chocolate cookies, and instead devours two apples, gulping them down with a glass of low-fat milk. Of the following substances, which one was most likely to have increased rapidly when she became hungry and decreased promptly after she finished her healthy snack Which of the following is determined to be the most likely dietary deficiency in this population Calcium Chocolate Folate Iron Vitamin C 56 A clinical study of adults with a body mass index of at least 30 is undertaken. About 8% of these individuals do not have hyperphagia, but are found to have normal levels of leptin and ghrelin, along with a diminished basal metabolic rate. A mutation in which of the following genes is most likely present in these individuals Avoid adding salt to food Drink more water Increase dietary fiber Reduce intake of saturated fat Take vitamin A supplements 57 A case-control study of adult men and women is performed to determine the relationship between obesity and cancer. The data indicate an increased risk for cancers of the esophagus and kidney in subjects with a body mass index above 25. Which of the following substances is most likely to contribute to the development of cancer in these subjects He asks his physician how best to reduce his risk of developing this type of cancer. Consume more beef Drink a glass of red wine Eat more vegetables Have a bowl of ice cream Reduce intake of chocolate 58 A 45-year-old man, whose mother, father, brother, and uncle all had a history of heart disease, asks his physician about ways to reduce his risk of developing coronary artery disease. The patient is 171 cm (5 ft 6 in) tall, weighs 91 kg, and has a blood pressure of 125/80 mm Hg. Biomethylation by environmental microorganisms of inorganic mercury dumped into bodies of water can lead to accumulation of toxic methyl mercury, which can work its way up the food chain to humans. Flavin-containing monooxygenase found in endoplasmic reticulum can oxidize nicotine. Glucuronidation can convert naphthylamine to a carcinogen that causes urinary tract cancers. Reduced glutathione helps to break down free radicals produced by oxygenase systems such as cytochrome P-450; xenobiotic metabolism can deplete glutathione and enhance free radical cellular injury. The peroxidase-dependent cooxidation pathway can metabolize 2-naphthylamine to a carcinogen that causes urinary tract cancers. The saltwater kills the mosquitoes, one advantage of the high tide, so arboviral diseases are less likely. The rise in temperature is not enough to significantly affect the cardiovascular system, except in sporadic but increasingly frequent heat waves. They are generally tolerated by healthy persons, but reduce the quality of life for persons with existing respiratory conditions. Decreasing levels of ozone in the upper atmosphere have been linked to fluorocarbon release (from refrigerants) and increase the risk for skin cancers. Vehicular exhaust is the major contributor to nitrogen dioxide and ozone emissions that react to form smog. Carbon dioxide is a greenhouse gas that is increasingly contributing to global climate change, but more is breathed out than is in the atmosphere. Sulfur dioxide released from industrial processes and burning coal forms acid rain and can contribute to chronic obstructive pulmonary disease. Carbon monoxide binds much more tightly to hemoglobin than does oxygen, resulting in hypoxia. Decreased mental functioning generally begins at carboxyhemoglobin levels greater than 20%, and death is likely at levels greater than 60%.

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Sometimes bladder infection generic augmentin 1000 mg buy on line, the acute inflammatory response may be quite severe and is termed as fulminant acute inflammation. Chronic inflammation is of longer duration and occurs either after the causative agent of acute inflammation persists for a long time, or the stimulus is such that it induces chronic inflammation from the beginning. Intimately linked to these two processes is the release of mediators of acute inflammation, discussed just thereafter. Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is a body defense reaction in order to eliminate or limit the spread of injurious agent, followed by removal of the necrosed cells and tissues. Thus, inflammation is distinct from infection-while inflammation is a protective response by the body to variety of etiologic agents (infectious or non-infectious), while infection is invasion into the body by harmful microbes and their resultant ill-effects by toxins. Though both these processes generally have protective role against injurious agents, inflammation and healing may cause considerable harm to the body as well. As discussed earlier (Chapter 4), "immunity or immune reaction" and "inflammatory response" by the host are both protective mechanisms in the body-inflammation is the visible response to an immune reaction, and activation of immune response is almost essential before inflammatory response appears. This nomenclature had its origin in old times but now we know that burning is only one of the signs of inflammation. Alteration in the microvasculature (arterioles, capillaries and venules) is the earliest response to tissue injury. Haemodynamic Changes the earliest features of inflammatory response result from changes in the vascular flow and calibre of small blood vessels in the injured tissue. Irrespective of the type of injury, immediate vascular response is of transient vasoconstriction of arterioles. With mild form of injury, the blood flow may be re-established in 3-5 seconds while with more severe injury the vasoconstriction may last for about 5 minutes. Vasodilatation results in increased blood volume in microvascular bed of the area, which is responsible for redness and warmth at the site of acute inflammation. Progressive vasodilatation, in turn, may elevate the local hydrostatic pressure resulting in transudation of fluid into the extracellular space. The leucocytes stick to the vascular endothelium briefly, and then move and migrate through the gaps between the endothelial cells into the extravascular space. The features of haemodynamic changes in inflammation are best demonstrated by the Lewis experiment. These features, thus, elicit the classical signs of inflam- 131 mation-redness, heat, swelling and pain. In and around the inflamed tissue, there is accumulation of oedema fluid in the interstitial compartment which comes from blood plasma by its escape through the endothelial wall of peripheral vascular bed. The differences between transudate and exudate, are already summarised in Table 4. In normal circumstances, the fluid balance is maintained by two opposing sets of forces: i) Forces that cause outward movement of fluid from microcirculation are intravascular hydrostatic pressure and colloid osmotic pressure of interstitial fluid. In acute inflammation, normally non-permeable endothelial layer of microvasculature becomes leaky. This is explained by one or more of the following mechanisms which are diagrammatically illustrated in. This is the most common mechanism of increased leakiness that affects venules exclusively while capillaries and arterioles remain unaffected. It is mediated by the release of histamine, bradykinin and other chemical mediators. Example of such immediate transient leakage is mild thermal injury of skin of forearm. In this mechanism, there is structural re-organisation of the cytoskeleton of endothelial cells that causes reversible retraction at the intercellular junctions. The onset of response takes 4-6 hours after injury and lasts for 2-4 hours or more (somewhat delayed and prolonged leakage). Direct injury to the endothelium causes cell necrosis and appearance of physical gaps at the sites of detached endothelial cells.

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The most commonly involved tissues for primary complex are lungs and hilar lymph nodes infection streaking discount augmentin 375mg otc. Microscopically, the lung lesion consists of tuberculous granulomas with caseation necrosis. The lymphatics draining the lung lesion contain phagocytes containing bacilli and may develop beaded, miliary tubercles along the path of hilar lymph nodes. This consists of enlarged hilar and tracheo-bronchial lymph nodes in the area drained. Microscopically, the lesions are characterised by extensive caseation, tuberculous granulomas and fibrosis. In the case of primary tuberculosis of the alimentary tract due to ingestion of tubercle bacilli, a small primary focus is seen in the intestine with enlarged mesenteric lymph nodes producing tabes mesenterica. The lesions of primary tuberculosis of lung commonly do not progress but instead heal by fibrosis, and in time undergo calcification and even ossification. D, Progressive secondary pulmonary tuberculosis from reactivation of dormant primary complex. At times, bacilli may enter the circulation through erosion in a blood vessel and spread to various tissues and organs. This is called primary miliary tuberculosis and the lesions are seen in organs like the liver, spleen, kidney, brain and bone marrow. The bacilli lying dormant in acellular caseous material are activated and cause progressive secondary tuberculosis. It affects children more commonly but adults may also develop this kind of progression. Secondary Tuberculosis the infection of an individual who has been previously infected or sensitised is called secondary, or post-primary or reinfection, or chronic tuberculosis. Other sites and tissues which can be involved are tonsils, pharynx, larynx, small intestine and skin. Secondary Pulmonary Tuberculosis the lesions in secondary pulmonary tuberculosis usually begin as 1-2 cm apical area of consolidation of the lung, which may in time develop a small area of central caseation necrosis and peripheral fibrosis. It occurs by haematogenous spread of infection from primary complex to the apex of the affected lung where the oxygen tension is high and favourable for growth of aerobic tubercle bacilli. Microscopically, the appear- ance is typical of tuberculous granulomas with caseation 155 necrosis. The lesions may coalesce together to form larger area of tuberculous pneumonia and produce progressive secondary pulmonary tuberculosis with the following pulmonary and extrapulmonary involvements: i) Fibrocaseous tuberculosis ii) Tuberculous caseous pneumonia iii) Miliary tuberculosis. The original area of tuberculous pneumonia undergoes massive central caseation necrosis which may: either break into a bronchus from a cavity (cavitary or open fibrocaseous tuberculosis); or remain, as a soft caseous lesion without drainage into a bronchus or bronchiole to produce a non-cavitary lesion (chronic fibrocaseous tuberculosis). The open case of secondary tuberculosis may implant tuberculous lesion on the mucosal lining of air passages producing endobronchial and endotracheal tuberculosis. Ingestion of sputum containing tubercle bacilli from endogenous pulmonary lesions may produce laryngeal and intestinal tuberculosis. Microscopically, the wall of cavity shows eosinophilic, granular, caseous material which may show foci of dystrophic calcification. Complications of cavitary secondary tuberculosis are as follows: a) Aneurysms of patent arteries crossing the cavity producing haemoptysis. The caseous material from a case of secondary tuberculosis in an individual with high degree of hypersensitivity may spread to rest of the lung producing caseous pneumonia. This is lymphohaematogenous spread of tuberculous infection from primary focus or later stages of tuberculosis. The miliary lesions are millet seed-sized (1 mm diameter), yellowish, firm areas without grossly visible caseation necrosis. Microscopically, the lesions show the structure of tubercles with minute areas of caseation necrosis. However, in secondary pulmonary tuberculosis which is the common type, the usual clinical features are as under: 1. Referable to lungs-such as productive cough, may be with haemoptysis, pleural effusion, dyspnoea, orthopnoea etc. Systemic features-such as fever, night sweats, fatigue, loss of weight and appetite.

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• Fisher CM. Occlusion of the internal carotid artery. AMA Arch Neurol Psychiatry 1951;69:346-77.