Medical Instructor, A. T. Still University Kirksville College of Osteopathic Medicine
In contrast to the other types of gallstones asthma 1cd 10 buy fluticasone 250mcg low cost, brown pigment stones are found more frequently in the intrahepatic and extrahepatic bile ducts than in the gallbladder asthma symptoms and joint pain purchase fluticasone master card. Rare or uncommon in Western countries asthma no inhaler order 500 mcg fluticasone fast delivery, brown stones are not infrequent in Asia asthma symptoms in children coughing cheap fluticasone 500mcg overnight delivery, where they are almost entirely restricted to persons infested with Ascaris lumbricoides or Clonorchis sinensis, helminths that may invade the biliary tract. The pathogenesis of brown pigment stones also relates to an increased concentration of unconjugated bilirubin in the bile. Conjugated bilirubin is hydrolyzed to unconjugated bilirubin by the action of bacterial -glucuronidase or other hydrolytic enzymes. Increasing age Obesity Membership in certain ethnic groups Familial predisposition Diet high in calories and cholesterol Certain metabolic abnormalities associated with high blood cholesterol levels Treatment of gallstones is today most commonly accomplished by laparoscopic cholecystectomy. Most of the complications of cholelithiasis relate to the obstruction of the cystic duct or common bile duct by gallstones. Passage of a stone into the cystic duct often, but not invariably, causes severe biliary colic and may lead to acute cholecystitis. Gallstones may pass into the common duct (choledocholithiasis), where they may produce obstructive jaundice, cholangitis and pancreatitis. In fact, in populations in whom alcoholism is not a factor, gallstones are the most common cause of acute pancreatitis. In obstruction of the cystic duct, with or without acute cholecystitis, the bile in the gallbladder is reabsorbed, to be replaced by a clear mucinous fluid secreted by the gallbladder epithelium. The term hydrops of the gallbladder (mucocele) is applied to the distended and palpable gallbladder, which may become secondarily infected. Decreased secretion of bile salts and lecithin occurs in nonobese whites who develop gallstones. Gastrointestinal absorptive disorders that interfere with the enterohepatic circulation of bile acids Black stones contain calcium bilirubinate, bilirubin polymers, calcium salts and mucin. Chronic hemolysis, such as occurs with sickle cell anemia and thalassemia, predisposes to the development of black pigment stones. Cirrhosis, either because it leads to increased hemolysis or because of damage to liver cells, is also associated with Acute Cholecystitis Acute cholecystitis is a diffuse inflammation of the gallbladder, usually secondary to obstruction of the gallbladder outlet. The remaining cases (acalculous cholecystitis) occur in conjunction with sepsis, severe trauma, infection of the gallbladder with Salmonella typhosa and polyarteritis nodosa. Bacterial infection is usually secondary to biliary obstruction, rather than a primary event. Tumors der in acute cholecystitis is congested and layered with a fibrinous exudate. Gallstones are usually found within the lumen, and a stone is often seen obstructing the cystic duct. On rare occasions, when obstruction of the cystic duct is complete and bacteria have invaded the gallbladder, the cavity may be distended by cloudy, purulent fluid, a condition termed empyema of the gallbladder. Microscopically, edema and hemorrhage in the wall are striking, with accompanying acute and chronic inflammation. The mucosa shows focal ulcerations or, in severe cases, widespread necrosis, in which case the term gangrenous cholecystitis is applied. Gallbladder perforation is a dreaded complication that may follow secondary bacterial infection, most commonly of the fundus. More often, inflammatory adhesions form a pericholecystic abscess and limit spread of gallbladder contents after perforation. In most cases, the acute illness subsides within a week, but persistent pain, fever, leukocytosis and shaking chills indicate progression of acute cholecystitis and the need for cholecystectomy. As the inflammatory process resolves, the gallbladder wall becomes fibrotic and the mucosa heals. Because this cancer is usually associated with cholelithiasis and chronic cholecystitis, it is considerably more common in women than in men. In addition, populations that have a high incidence of cholelithiasis, such as Native Americans, have a higher risk of carcinoma of the gallbladder. Chronic Cholecystitis Chronic cholecystitis, the most common disease of the gallbladder, is a persistent inflammation of the gallbladder wall that is almost invariably associated with gallstones. Chronic cholecystitis may also result from repeated attacks of acute cholecystitis. In the latter case, the pathogenesis probably relates to chronic irritation and chemical injury to the gallbladder epithelium. Gallstones are usually found within the lumen, and the bile often contains gravel or sludge. Microscopically, the wall is fibrotic and often penetrated by sinuses of RokitanskyAschoff. In long-standing chronic cholecystitis, the wall of the gallbladder may become calcified (porcelain gallbladder). It may occur anywhere along the length of the bile duct, including the location where the right and left hepatic ducts join to form the common hepatic duct. The tumor is less common than gallbladder cancer, and the female predominance of gallbladder cancer is not evident. Gallstones are frequently found in those affected, and there is an association with inflammatory disease of the colon. In Asia, bile duct carcinoma is associated with biliary infestation by the fluke Clonorchis sinensis. The prognosis is poor, but because symptoms arise early in the course of the disease, the outcome is somewhat better than that of gallbladder carcinoma.
Patients with encephalitis present with paresis asthma definition 6 studio order cheapest fluticasone and fluticasone, seizures asthma treatment yoga discount 250 mcg fluticasone with visa, alterations in visual acuity and changes in mentation asthmatic bronchitis medscape buy generic fluticasone on-line. Toxoplasma encephalitis in immunocompromised patients is fatal if not treated with effective antiprotozoal agents asthmatic bronchitis journal article cheap 250 mcg fluticasone. The exudate raises the undermined mucosa, producing chronic amebic ulcers, with a shape that has been described as resembling a flask or a bottle neck. Trophozoites are found on the surface of the ulcer, in the exudate and in the crater They are also frequent in the submucosa, muscularis propria, serosa and small veins of the submucosa. Early amebic ulcers display little inflammatory response, but as the ulcers enlarge, acute and chronic inflammatory cells accumulate. Intestinal amebiasis ranges from a completely asymptomatic to a severe dysenteric disease. Nausea, vomiting, malodorous flatus and intermittent constipation are typical features. Liquid stools (up to 25 a day) contain bloody mucus, but diarrhea is rarely prolonged enough to cause dehydration. Amebic colitis often persists for months or years, and patients may become emaciated and anemic. Transmission of disease is by cystic forms of the organism, which are spread in stool and persist in the environment. Therapy for symptomatic intestinal amebiasis includes metronidazole or tinidazole, which act against trophozoites, followed by diloxanide, paromomycin or iodoquinol-drugs that are effective against cysts. Amebic liver abscess is a major complication of amebiasis that occurs when trophozoites invade the submucosal veins of the colon, enter the portal circulation and reach the liver. Here, the organisms kill hepatocytes, producing a slowly expanding necrotic cavity filled with a dark brown, odorless, semisolid material. Neutrophils are rare within the cavity, and trophozoites are found along the edges adjacent to hepatocytes. An amebic liver abscess may expand and rupture through the capsule, extending into the peritoneum, diaphragm, pleural cavity, lungs or pericardium. The infection varies from a self-limited gastrointestinal infection in immunocompetent persons to a potentially life-threatening illness in the immunocompromised. It is acquired by ingesting Cryptosporidium oocysts, which are shed in the feces of infected humans and animals. Many domesticated animals harbor the parasite and are a large reservoir for human infection. Intestinal infection ranges from asymptomatic colonization to severe invasive infections with bloody diarrhea. In the United States, the disease is uncommon and is associated with travelers, immigrants and male homosexuals. The organism kills the target cell by elaborating a lytic protein that breaches the cell membrane. Progressive death of mucosal cells produces small foci of necrosis that progress to ulcers. Undermining tremely stable in the environment, survive passage through the stomach and release forms that attach to the microvillous surface of the small bowel. In that location, they form a complex structure involving both the host and parasite cell membranes. The organisms reproduce on the luminal surface of the gut, from stomach to rectum, forming progeny that also attach to the epithelium. In the small intestine (the most common site of infection), there may be moderate or severe chronic inflammation in the lamina propria and some villous atrophy directly related to the density of the parasites. In immunologically competent persons, infection is terminated by immune responses. Amebiasis results from the ingestion of food or water contaminated with amebic cysts. In the colon, the amebae penetrate the mucosa and produce flask-shaped ulcers of the mucosa and submucosa. The organisms may invade submucosal venules, thereby disseminating the infection to the liver and other organs. The colonic mucosa shows superficial ulceration beneath a cluster of trophozoites of Entamoeba histolytica. The lamina propria contains excess acute and chronic inflammatory cells, including eosinophils. B Cryptosporidiosis presents as profuse, watery diarrhea, sometimes accompanied by cramping abdominal pain or low-grade fever. Extraordinary volumes of fluid can be lost as diarrhea, and intensive fluid replacement is required. In immunologically competent individuals, diarrhea resolves spontaneously in 1 to 2 weeks. In immunocompromised patients, diarrhea persists indefinitely and may contribute to death. Giardiasis is acquired by ingesting infectious cyst forms of the organism, which are shed in the feces of infected humans and animals. Infection spreads directly from person to person and also in contaminated water or food. Microscopic examination shows Giardia trophozoites on the surface of villi and within crypts, with minimal associated mucosal changes. Acute giardiasis occurs with the abrupt onset of abdominal cramping and frequent foul-smelling stools.
Common goitrogenic drugs include lithium (which is used to manage bipolar disorders) asthmatic bronchitis and pneumonia order 500 mcg fluticasone with amex, phenylbutazone and p-aminosalicylic acid asthma definition republic buy fluticasone from india. Certain cruciferous vegetables (turnips asthma treatment mask generic 500mcg fluticasone fast delivery, rutabaga asthma brochure buy generic fluticasone canada, cassava) contain goitrogens, and their ingestion can potentiate an iodine-deficient diet to produce goitrous hypothyroidism. Under this continued stimulation, the thyroid becomes diffusely hyperplastic and excessively vascular. Graves autoantibodies are heterogeneous, and those that stimulate thyroid hormone secretion represent only one component. Other antibodi es seem to be cytotoxic and may cause the thyroid failure that often follows long-standing Graves disease. In endemic areas, the large majority of cases reflect dietary deficiency of iodine, especially in inland and mountain areas (see above). By the age of 6 months, the clinical syndrome of congenital hypothyroidism is well developed. Mental retardation, stunted growth (due to defective osseous maturation) and characteristic facies are evident. Prompt thyroid hormone replacement therapy is needed to prevent mental retardation and stunted growth. Although treatment may prevent dwarfism, its effects on mental development are more variable. Children in whom hypothyroidism is detected early with neonatal screening respond well to thyroid hormone treatment and are apparently normal mentally. Hyperthyroidism Hyperthyroidism refers to the clinical consequences of excessive circulating thyroid hormone. Patients with Graves disease and their relatives have a considerably higher incidence of other autoimmune diseases, including pernicious anemia and Hashimoto thyroiditis. Both T and B lymphocytes are sensitized to antigens shared by thyroid follicular cells and orbital fibroblasts. These cells stimulate orbital fibroblasts to proliferate and produce collagen and glycosaminoglycans, either by cytokine synthesis or by antibody-mediated receptor activation. Physical examination reveals a symmetrically enlarged thyroid, often with an audible bruit and a palpable thrill. Proptosis and retraction of the eyelids expose the sclera above the superior margin of the limbus. The skin is warm and moist, and some patients exhibit Graves dermopathy, a peculiar pretibial edema caused by fluid accumulation and glycosaminoglycans. They are intolerant of heat, seek cooler environments, tend to sweat profusely and may report palpitations. Excess thyroid hormone reduces systemic vascular resistance, enhances cardiac contractility and increases the heart rate. The tan translucence of normal thyroid, reflecting stored colloid, is notably absent. The epithelial cells are tall and columnar and are often arranged as papillae that project into the lumen of the follicles. The colloid tends to be depleted and appears scalloped or "moth-eaten" where it abuts the epithelial cells. Scattered B and T lymphocytes and plasma cells infiltrate the interstitial tissue and may even aggregate to form germinal follicles. Exophthalmos is caused by enlargement of the orbital extraocular muscles by mucinous edema, accumulation of fibroblasts and lymphocyte infiltration. Unfortunately, despite successful relief of hyperthyroidism, exophthalmos often persists and may even worsen. Thyroiditis Thyroiditis describes a heterogeneous group of inflammatory disorders of the thyroid gland, including those that are caused by autoimmune mechanisms and infectious agents. Like its precursor disease, toxic goiter is 10 times more frequent in women than in men. Patients present with diffuse thyroid enlargement accompanied by either mild hyperthyroidism or hypothyroidism. The disease can affect several family members, who often also suffer from other autoimmune conditions, such as systemic lupus erythematosus, Graves disease, arteritis and scleroderma. In some patients, iodine uptake is diffuse and not affected by the administration of thyroid hormone. Microscopically, the thyroid shows groups of small hyperplastic follicles mixed with other nodules of varying size that appear to be inactive. A second pattern is characterized by focal accumulation of radiolabeled iodine in one or more nodules. Hyperfunction of these nodules suppresses the function of the rest of the thyroid. The functional nodules are clearly demarcated from the inactive areas histologically, contain large hyperplastic follicles and thus resemble adenomas. Because patients with toxic goiter tend to be older, cardiac complications, including atrial fibrillation and congestive heart failure, may dominate the clinical presentation. Serum T4 and T3 levels are frequently only minimally elevated, and the uptake of radiolabeled iodine may be normal or only slightly elevated. Radiolabeled iodine following a course of antithyroid therapy is the most common treatment. Hyperfunction of a toxic adenoma eventually suppresses the remainder of the thyroid, which then atrophies. Under these circumstances, a 131I scintiscan shows a solitary focus of iodine uptake ("hot nodule") in a background of minimal uptake. Because the normal thyroid tissue is suppressed, toxic adenoma is treated effectively with radiolabeled iodine.
The abscess expands into the cartilage and stimulates reactive bone formation by the periosteum asthma treatment singulair buy generic fluticasone from india. The abscess asthma symptoms from anxiety cheap fluticasone, which continues to expand through the cortex into the subperiosteal tissue asthma symptoms and causes buy fluticasone uk, shears off the perforating arteries that supply the cortex with blood asthma symptoms hay fever cheap fluticasone 500mcg overnight delivery, thereby leading to necrosis of the cortex. The extension of this process into the joint space, the epiphysis, and the skin produces a draining sinus. In this patient with chronic osteomyelitis, the skin overlying the infected bone is ulcerated, and a draining sinus (dark area) is evident over the heel. After amputation of the foot, a sagittal section shows a draining sinus (straight arrow) that connects the infected bone with the surface of the ulcerated skin. The white tissue (curved arrow) is invasive squamous cell carcinoma, which arose in the skin. Thus, this family of diseases should be viewed in the context of failure of the remodeling cycle to replace all the resorbed bone. Primary osteoporosis, by far the more common variety, is of uncertain origin and occurs principally in postmenopausal women (type 1) and elderly persons of both sexes (type 2). Secondary osteoporosis is a disorder associated with a defined cause, including a variety of endocrine and genetic abnormalities (see below). Because there is little or no reactive bone formation, affected vertebrae usually collapse, leading to kyphosis and scoliosis. The intervertebral disk is crushed and destroyed by the compression fracture, rather than by invasion of organisms. Metabolic Bone Diseases Metabolic bone diseases are defined as disorders of metabolism that result in secondary structural effects on the skeleton, including diminished bone mass (due to decreased synthesis or increased destruction), reduced bone mineralization or both. Because metabolic bone diseases are systemic, a biopsy of any bone should reveal the abnormality, although the severity may differ in various parts of the skeleton. Bone loss and eventually fractures are the hallmarks of osteoporosis, regardless of the underlying causes. The etiology of bone loss is diverse but includes smoking, vitamin D deficiency, low body mass index, hypogonadism, a sedentary lifestyle and glucocorticoid therapy. In healthy persons of both sexes, bone mass peaks between the ages of 25 and 35 years and begins to decline in the fifth or sixth decade. Bone loss with age occurs in all races, but because of higher peak bone mass, blacks are less prone to osteoporosis than are Asians and whites. Bone loss in women has been divided into two phases: one due to menopause and the other associated with aging. At a certain point, the loss of bone suffices to justify the label osteoporosis and renders weight-bearing bones susceptible to fractures. Women have twice the risk of hip fracture as men, although among blacks and some Asian populations, the incidence is equal among the sexes. A subset of women in their early postmenopausal years is at particular risk of vertebral fractures, which are rare in middle-aged men. Type 1 primary osteoporosis is due to an absolute increase in osteoclast activity. In the early postmenopausal period, estrogen withdrawal leads to the secretion of cytokines by cells derived from the marrow stroma, which recruit and activate osteoclasts. Type 2 primary osteoporosis, also called senile osteoporosis, has a more complex pathogenesis than does type 1. It generally appears after age 70 years and reflects decreased osteoblast function rather than increased osteoclast activity. Primary osteoporosis has been linked to a number of factors that influence peak bone mass and the rate of bone loss. Genetic factors: the development of clinically significant osteoporosis is related, in largest part, to the maximal amount of bone in a given person, referred to as the peak bone mass. In general, peak bone mass is greater in men than in women and in blacks than in whites or Asians. However, whether this apparent shortfall contributes to development of osteoporosis is controversial, in view of a number of studies to the contrary. Nevertheless, it has been recommended that both premenopausal and postmenopausal women increase the intake of calcium and vitamin D. The trabeculae of the lamellar bone have abnormal amounts of nonmineralized bone (osteoid). These osteoid seams are thickened and cover a larger than normal area of the trabecular bone surface. The lamellar bone trabeculae are actively resorbed by numerous osteoclasts that bore into each trabecula. The appearance of osteoclasts dissecting into the trabeculae, a process termed dissecting osteitis, is diagnostic of hyperparathyroidism. The morphologic appearance is similar to that of primary hyperparathyroidism, except that prominent osteoid covers the trabeculae. Osteoclasts do not resorb osteoid, and wherever an osteoid seam is lacking, osteoclasts bore into the trabeculae. Current guidelines suggest exercise as being helpful in maintaining bone strength in the elderly. Environmental factors: Cigarette smoking in women has been correlated with an increased incidence of osteoporosis. It is possible that the decreased level of active estrogens produced by smoking (see Chapter 8) is responsible for this effect.
