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Marc A. Bjurlin, DO, MSc

  • Assistant Professor, Urology
  • New York University

Then erectile dysfunction caused by diabetes quality 80mg top avana, by means of a snarelike cutting instrument erectile dysfunction and pregnancy buy 80 mg top avana free shipping, pieces of the enlarged prostate are shaved off and removed erectile dysfunction causes treatment buy discount top avana line. The lining of the urethra covering the enlarged prostate is removed along with the obstructing part of the gland erectile dysfunction in young men buy 80mg top avana, but the epithelial lining soon regenerates and the continuity of the urethral lining is restored erectile dysfunction causes uk cheap top avana 80 mg with visa. The incidence of prostate cancer varies widely with geographic region fast facts erectile dysfunction buy 80 mg top avana overnight delivery, being highest in North America and Europe and much lower in southeastern and south central Asia. The disease in rare under the age of forty; however, detailed histopathology studies of prostate glands removed at autopsy detect cancer in about 20 percent of glands from men in their forties and 80 percent of glands taken from persons of age eighty. In contrast to benign prostatic hyperplasia, which involves the inner group of glands, the tumor usually originates in the outer group of prostatic glands (peripheral zone). Multiple sites within the prostate are sampled to increase the chances of detection. In the absence of early detection, the first manifestations may appear when the growing tumor partially obstructs the bladder neck, causing symptoms similar to those of patients with benign prostatic hyperplasia. The tumor may eventually infiltrate the tissues surrounding the prostate and metastasize to the bones of the spine and pelvis. Diagnostic screening of asymptomatic individuals by digital rectal examination and the use of prostatic-specific antigen testing has led to an increase in the diagnosis of prostate cancer. Somewhat controversially, statistical studies have questioned the utility of such screening programs because most studies have shown no significant reduction in prostate cancer specific deaths as a result of screening. These results suggest that prostate cancer is relatively benign (or slow growing) in many men and that men are far more likely to die of other causes. Screening may lead to overdiagnosis and overtreatment, including anxiety, infection, and bleeding associated with biopsy procedures. Currently the American Cancer Society suggests starting screening at age fifty for individuals with a ten-year expected life expectancy and at forty to forty-five years for high-risk individuals and African Americans. Preventative Service Task Force has (controversially) recommended against any routine screening using current technology. What is not controversial is that better, more predictive screening for prostate cancer is necessary to detect those cases most likely to progress to life-threatening disease. Treatment depends on the degree of differentiation of the tumor, the age of the patient, and most important, on whether the tumor has spread beyond the prostate gland. A well-differentiated localized tumor in an elderly man may progress slowly and may not produce symptoms for as long as ten years. In contrast, a less welldifferentiated tumor in a younger man requires more aggressive treatment. A small, localized prostatic carcinoma can be treated by removing the entire prostate and surrounding tissues. Although this operation may eradicate the tumor, it usually also disrupts the nerve supply to the penis, which leads to permanent inability to achieve an erection of the penis (impotence) and also urinary incontinence. Radical prostatectomy alone or combined with radiation therapy appears to improve survival in many patients. There is considerable controversy, however, about the effectiveness of radical surgery or radiation therapy in older men with localized well-differentiated carcinoma of the prostate. Many physicians believe that treatment does not improve survival in this group of patients, that the treatment causes more disability and complications than the tumor, and that a slowly growing prostatic carcinoma in an older man is best left alone. When a prostatic carcinoma has advanced to the stage that it has spread beyond the prostate, it is often possible to induce regression of the tumor by altering the level of male sex hormones in the body. Most prostatic carcinomas are initially dependent on the male sex hormone for their continued growth. Therefore, many advanced prostatic tumors can be treated effectively by surgical removal of the testes, eliminating the source of the male sex hormone. Alternatively, drugs that suppress output of pituitary gonadotropic hormone can be administered, thereby inhibiting testicular testosterone secretion. Either surgical or hormone-induced castration or hormone treatment usually causes a temporary regression of the tumor. Widespread metastatic disease to lymph nodes, bones, liver, and lungs is often accompanied by hormone independent tumor growth, and traditional chemotherapy and local radiation are used palliatively. Testicular tumors are rare in prepubertal males (but both benign and malignant tumors occur infrequently). Most tumors arise from the germinal epithelium of the testicular tubules and are malignant. Some testicular tumors are derived from undifferentiated embryonal cells and are called embryonal carcinomas. More differentiated embryonal cells give rise to teratocarcinomas (malignant teratomas), which are composed of many different types of malignant tissues, some of which demonstrate the characteristics of a variety of somatic or extraembryonic cells of the developing embryo (described in the discussion on neoplastic disease). An example is choriocarcinoma, which is the same kind of tumor that arises from trophoblastic tissue in the uterus (described in the discussion on prenatal development and diseases associated with pregnancy). Consequently, a pregnancy test given to a man with testicular cancer may be positive. If a testicular carcinoma produces these substances, the concentrations fall after successful treatment of the tumor and rise again if the tumor recurs. Nonseminoma tumors are not as sensitive to radiation and often require the use of chemotherapy in management. Teratocarcinomas/ malignant teratomas A malignant testicular tumor composed of many different types of malignant tissues. The same hormone is made by neoplastic cells in some types of malignant testicular tumors. It is possible that the secretions that accumulate under the foreskin of the penis are carcinogenic and that this accumulation is prevented by circumcision. However, other factors also may account for the low incidence of carcinoma in circumcised males. Carcinogenic strains of the papilloma virus, the same virus that appears related to cervical dysplasia and carcinoma in women, may play a major role in causing penile cancer. The papilloma virus may grow well beneath an intact foreskin but does not grow if the foreskin has been removed. Obstructions to the lower urinary tract are not uncommon developmental abnormalities in neonatal males. During gonadogenesis, the defect occurs when an embryological structure that normally recedes during male development leaves a remnant in the prostatic urethra, termed the verumontanum; when this occurs, it can partially or completely block the fetal urethra. This can lead to failure of normal development of the fetal kidney, which may lead to chronic renal failure, end stage renal disease, and the necessity for renal transplantation. Severe cases may lead to total renal dysplasia, failure of pulmonary development (dependent on fetal renal function), and death in utero or shortly after birth. The abnormal location of the urethra may occur near the tip (leading to an abnormal urethral meatus) or further down the shaft (more proximal) near the scrotum. The defect results from abnormal fusion of the genital folds, which during the twelfth to sixteenth week of development form the shaft of the penis, and labioscrotal folds, which fuse to form the scrotum. Epispadias, opening of the urethra on the dorsum of the penis, is far less common (about 1 in 25,000 births) and also occurs in females (as a bifid clitoris). The condition is most often associated with serious malformations of the bladder (extrophy, eversion of part of the bladder onto the abdominal wall). Phimosis, the inability to retract the prepuce (foreskin) over the glans of the penis, is a physiologic condition occurring normally in newborn males. The condition is the result of adhesion between the epithelium of the foreskin and the glans and usually disappears with continued retraction and erection. The condition may persist in a small percentage of males over the age of sixteen and occasional requires corrective surgery, usually circumcision. Infection of the prepuce and head of the penis (balanitis) can also result in a secondary form of phimosis. Most commonly the undescended testes is located in the inguinal or upper scrotal region. Surgical repair of the condition (orchioplexy) is critical because the condition is associated with oligospermia (a low sperm count), if one testis is affected, and complete lack of sperm (azoospermia), if both testes are undescended. Abnormalities of testicular development begin as early as two years of age, and early repair (between six months and one year) is recommended. In addition to infertility, a twenty to fortyfold increase in the rate of testicular cancer is associated with cryptorchidism. Surprisingly, a contralateral, normally descended testis is also at a fourfold increased risk. The large clusters of cells between the hyaline atrophic tubules (arrows) are interstitial cells, which function normally at body temperature. The condition may occur in the neonatal period (either in the fetus or soon after birth) where it is not associated with an anatomic defect. A testicular torsion is characterized by an acute onset of severe testicular pain associated with swelling of the involved testis and is an acute surgical emergency. If the torsion can be untwisted and the testis is properly anchored in the scrotum within a few hours after onset of the torsion, the testis probably can be salvaged. The longer the delay, the less likely is the possibility that the testis will survive. Adult testicular torsion is associated with bell-clapper defect, an anatomic abnormality responsible for increased testicular mobility. Because the abnormal mobility of the testis within the scrotum that caused the torsion is likely to be present in the other testis as well, the other testis generally is surgically anchored in the scrotum so that it cannot undergo torsion. Bell-clapper defect Anatomic abnormality responsible for increased testicular mobility. Normally, the epididymis is located along the posterior surface of the testis, but the torsion has rotated the testis and also rotated the epididymis anteriorly. The condition may be congenital or result from trauma, infection, or other causes. Although this usually does not require therapy, the scrotal swelling may be uncomfortable. Long-standing hydrocele can cause testicular atrophy and may require surgical excision of the sac. When a physician examines a patient believed to have a hydrocele, a careful examination of the testis and scrotum is also performed, which may be supplemented by an ultrasound examination to exclude the possibility of a testicular tumor or some other condition associated with the hydrocele. Varicose veins form in a similar fashion in other locations, as described in the cardiovascular system. When the scrotum is examined while the patient is standing, the scrotal varicose veins located above the testis are sometimes described as "feeling like a bag full of worms. However, varicoceles may occasionally reduce fertility by impairing spermatogenesis, possibly as result of the higher scrotal temperature caused by warm venous blood pooling in the varicose scrotal veins. A varicocele can be treated surgically if it causes scrotal discomfort or impairs fertility. Each cylinder, surrounded by a thick fibrous tissue capsule, is composed of a spongy meshwork of endothelium-lined blood sinuses supported by trabeculae (partitions) composed of connective tissue and smooth muscle. The blood sinuses of the erectile tissue are supplied by arteries and drained by veins. Normally, the arteries are constricted and very little blood flows into the cavernous bodies, and the vascular sinuses are collapsed. As a result, the penile arteries dilate, and the sinuses in the cavernous bodies expand. Blood enters under arterial pressure into the blood sinuses within the cavernous bodies. The greatly increased arterial blood flow and rising pressure within the blood sinuses compresses the draining veins, which retards outflow of blood from the penis and contributes to the engorgement of the blood sinuses. Erectile Dysfunction 551 Erectile dysfunction is an inability to achieve and maintain a penile erection of sufficient rigidity to penetrate the vagina and maintain the erection during sexual intercourse. This is a relatively common problem that increases in frequency with advancing age. First, sexual desire is required to initiate the physiologic events that increase blood flow to the penis. Second, the arteries supplying the cavernous bodies must dilate enough to deliver a large volume of blood to the penis. Third, the pressure of the blood within the cavernous bodies must be sufficiently high to compress the draining veins. Blood must flow into the penis faster than it drains out, or an erection cannot be maintained. One well-known treatment involves the use of drugs that inhibit phosphodiesterase and promote increased blood flow to the penis. Several phosphodiesterase inhibiting drugs are available (sildenafil, vardenafil, tadalafil) and differ primarily in their duration of action. They are relatively safe drugs when used properly, but rarely may be associated with serious complications. The best known of these drugs is sildenafil, better known by its trade name Viagra. She has noted bilateral enlargement of his breasts and is concerned that he might have breast cancer. The patient states that he has had mild dyspnea (shortness of breath) for about a month. On questioning he notes that he has had a painless mass in the right testis in the last several months. His history is also pertinent; he had cryptorchidism that was surgically repaired at twenty-four months.

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Acting systemically they are responsible for the fever and malaise associated with inflammation and the increased synthesis of acute-phase reactants previously mentioned erectile dysfunction treatment in kolkata buy 80mg top avana overnight delivery. Mediators from Blood Plasma Blood plasma contains various protein substances that circulate as inactive compounds and leak from the permeable capillaries into the area of tissue damage where they become transformed (activated) by a complex process into chemical mediators erectile dysfunction foods to eat proven 80 mg top avana. One important group of mediators formed in this way is called bradykinins (or simply kinins) erectile dysfunction chicago order top avana 80 mg fast delivery. The series of reactions that leads to the formation of bradykinins is triggered by one of the proteins concerned with blood coagulation erectile dysfunction drugs medications purchase top avana 80mg, which is activated by tissue injury impotence yoga postures order generic top avana from india. Kinins are important in producing vasodilation erectile dysfunction pills that work buy top avana no prescription, help recruit neutrophils to injured sites, and are responsible for much of the pain associated with inflammation. Mediators of inflammation are also formed from another group of blood proteins called complement. Complement consists of at least fifty protein components, some of the best known of which are numbered as C1 through C9, the proteins interact in a regular sequence to yield a series of by-products, some of which function as mediators of inflammation. Complement (abbreviated as C) participates in both the nonspecific and specific responses to cell injury. The various functions of the complement system are considered in connection with immunity, hypersensitivity, allergy, and autoimmune diseases. The release of mediators from any source not only initiates the inflammatory process but also induces release of more mediators from other sources, setting off a "chain reaction" that intensifies the inflammatory process. Cytokine Small protein released by cells that modulate the production of mediators of inflammation. Complement Group of proteins interact to produce by-products, some of which act as mediators of inflammation. Activation of mediators from any source also leads to the formation of mediators from other sources, which intensifies the inflammatory reaction. Lysosomes contain potent enzymes that are capable of digesting the material brought into the cytoplasm of the cells by phagocytosis. In addition to lysosomal-mediated destruction, potent oxidizing agents such as hydrogen peroxide and hypochlorous acid (laundry bleach) are synthesized by neutrophils and discharged into phagocytic vacuoles where they are important in destroying bacteria and fungi. Much of the tissue injury in an area of inflammation is a result of the destructive effect of the lysosomal enzymes released from leukocytes. In the course of any inflammatory reaction, lysosomal enzymes are released from damaged neutrophils and monocytes. Some lysosomal enzymes and oxidizing agents also escape from intact leukocytes during phagocytosis. The tissue injury in turn generates more mediators, and this induces further inflammatory changes. Lack of oxidative killing of pathogens is associated with a serious inherited disease (chronic granulomatous disease) in which patients suffer from life-long and repeated infections by bacteria and fungi. Oxidizing agents Chemicals synthesized by neutrophils that help destroy bacteria and fungi. Chronic granulomatous disease Disease caused by lack of oxidative killing of pathogens. Phagolysosome (C2) Within the phagolysosome, the bacterial cell is killed and digested through the activity of lysosomal enzymes and other toxic products. Lysosomes Bacterial debris Receptor (D) Egestion Microbial fragment the process concludes with the elimination of bacterial debris as microbial fragments are placed on membrane receptor proteins. In most cases, the inflammatory process is self-limited and subsides when the harmful agent has been eliminated. At times, however, an inflammatory process may persist and cause extensive, progressive tissue injury. If this occurs, the inflammatory process may need suppression by administering adrenal corticosteroid hormones (steroids) to reduce the tissue damage that would result if the inflammatory process were not restrained. The term virulence refers to the ease with which a pathogenic organism can overcome the defenses of the body. A highly virulent organism is one that is likely to produce progressive disease in the majority of susceptible individuals. In contrast, an organism of low virulence is capable only of producing disease in a highly susceptible individual under favorable circumstances. The outcome of any infection depends on two factors: the virulence of the organism combined with the numbers ("dosage") of the invading organisms and the resistance of the infected individual (often called the host). When large numbers of organisms of high virulence are introduced into the body, especially when host resistance is lowered, the balance is tipped in favor of the invader and progressive or fatal disease develops. Role of Inflammatory Cells in Antimicrobial Defense Neutrophils and macrophage-like cells (monocytes when in the blood) internalize and digest foreign material including pathogenic microorganisms by a process termed phagocytosis. There is some specialization as to which cells deal with particular types of pathogens. Viral and fungal disease most commonly presents as chronic inflammation without a preliminary acute inflammatory phase. Hence, the response to these pathogens is characterized by "mononuclear" cells including macrophage-like cells and lymphocytes. For this reason, a physician noting a higher than normal level of neutrophils in the blood suspects a bacterial etiology. Both neutrophils and macrophages are attracted to the foreign material (undergo chemotaxis) when it is coated with plasma proteins collectively called opsonins, which are either derived from complement or are immunoglobulins produced as part of the adaptive host response. The role of inflammatory cells is crucial in degrading microbes but also contributes to further cell damage and inflammation as a result of release of lysosomal enzymes and oxidizing agents into tissue. The importance of these cells in antimicrobial defense is further emphasized by the frequency and severity of infections when these cells are decreased due to the neutropenia resulting from cancer chemotherapy or congenital diseases or when cells are incapable of killing the phagocytosed material. Generally, the ending -itis is appended to the name of the tissue or organ to indicate an infection or inflammatory process. For example, the terms appendicitis, hepatitis, colitis, and pneumonitis refer to inflammation of the appendix, liver, colon, and lung, respectively. Usually, this term is used to refer to an acute infection of the skin and deeper tissues. If a localized infection spreads into the lymphatic channels draining the site of inflammation, the term lymphangitis is used. Lymphadenitis refers to infection in the regional lymph nodes draining the primary site of infection. The term septicemia is used to refer to an overwhelming infection in which pathogenic bacteria gain access to the bloodstream. Clinically, this results in a chronic infection, characterized by a relatively quiet, smoldering inflammation that is usually associated with continued attempts at healing on the part of the host. The infection may flare up at times when the pathogen obtains a temporary advantage, or it may become quiescent at other times when the defenses of the host gain the upper hand. Lymphocytes, plasma cells, and monocytes are the predominant cells in chronic inflammatory processes. She lands on a broken beer bottle and suffers a laceration on the dorsal surface of her thigh. Her friends suggest that she visit student health, but she has an examination in the afternoon. The mass is composed of granulation tissue, an excessive amount of what is a normal part of the healing process. However, because of the infection and large mass of granulation tissue, the physician debrides the wound. He explains that because she did not immediately seek medical attention and have the wound sutured she is likely to be left with a large scar. Discussion During wound healing, granulation tissue is the matrix in which new blood vessels form and in which fibroblasts proliferate to produce collagen, a process termed fibrosis (scar formation). In addition, many mononuclear inflammatory cells and the elongated nuclei of fibroblasts are present. In cases where wound healing is delayed (as it was by infection in Case 5-1), cytokine production by inflammatory cells may promote the growth of excessive granulation tissue that can gape above the wound (sometimes termed proud flesh). Sutured wounds oppose the injured surfaces, leaving little space for granulation tissue to form. Plastic and reconstructive surgeons go to great effort to carefully suture wounds to minimize scarring and to produce esthetically satisfactory results. Etiology and Pathogenesis the etiology is traumatic injury (laceration) resulting in superficial bacterial infection. The pathogenesis demonstrates healing of a wound by secondary union combined with excess production of granulation tissue. Granulation tissue consists of mononuclear inflammatory cells, fibroblasts, and new Laceration An irregular jagged wound. Detailed discussion of the aspects of inflammation and repair are of importance in undergraduate medical education. Hence, medical textbooks are the best source for concise and timely discussion of these complex areas. Current understanding of molecular and cellular mechanisms in fibroplasia and angiogenesis during acute wound healing. This article provides an up-to-date review of molecular and cellular aspects of wound healing. List the five classes of antibodies, and explain how they differ from one another. Describe the pathogenesis of allergic manifestations and the role of IgE in allergy. Explain why it is sometimes necessary to suppress the immune response, and describe how this is accomplished. Compare and contrast tolerance and autoimmune disease, including the clinical manifestations and the methods of treatment. The innate immune response is limited to specific challenges that have frequently occurred during human evolution. Unlike us, many pathogens have the ability to quickly evolve to counter our host defenses. Even during the course of an infection, organisms may develop mechanisms to thwart our innate defenses mechanisms. In addition, the movement of populations and changes in the environment constantly exposes us to new challenges with which innate immunity may be unable to cope. First found in lower vertebrates with jaws (cartilaginous fish such as sharks), adaptive immunity-comprised of cell-mediated immunity and humoral immunity- provides us with the ability to detect and adaptively respond essentially to any molecular structure foreign to us (even one never before encountered). The aspects of adaptive recognition and response to foreign structures and immune memory define adaptive immunity and differentiate it from innate immunity. Innate immunity can only adapt to new challenges with evolution, whereas adaptive immunity can cope with previously unrecognized agents nearly in "real time. Courtesy of Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill Innate immunity Preprogrammed immune response. Adaptive immunity Immune response with the ability to respond to almost any foreign molecule. Although low levels of cells, such as neutrophils, or a defect in one of the chemical mediators may result in disease, the many overlapping mechanisms of the innate immune system ensure that broad immunodeficiency to a wide array of opportunistic pathogens does not occur. Several sets of these receptors are found on the surface of cells, within membrane bound vesicles, or free in the cytoplasm. All of the receptors of a given type are identical and invariant, and can cope with only a limited array of pathogen structures. In summary, innate immunity is a rapidly acting first line of defense that often slows the infectious process but cannot eliminate it. Innate immunity primes the adaptive immune system, buying time for the adaptive system to respond as a second line and highly effective mechanism for host defense. Adaptive Immunity Adaptive immunity can be divided into two tightly interrelated systems: humoral immunity and cell-mediated (or cellular) immunity. Lack of either system will result in susceptibility to pathogens (albeit of a somewhat different nature) and can result in life-threatening disease. Humoral immunity absolutely requires an intact cellular immune system to function effectively. Humoral immunity is associated with the production of antibodies, soluble proteins of the immunoglobulin class. Antibodies circulate in the blood and body fluids and function by binding to and eliminating foreign material. Cell-mediated immunity is characterized by the formation of a population of lymphocytes (T lymphocytes or simply T cells) that can attack and destroy the foreign material. Cell-mediated immunity is the main defense against viruses, fungi, parasites, and some bacteria (particularly those that are intracellular). When activated, B cells form memory cells and plasma cells, which produce antibodies to these antigens. Comparison of Humoral and Cell-Mediated Immunity Cell-mediated Principal cellular agent is the T cell. T cell responds to cancer cells, virus-infected cells, single-cell fungi, parasites, and foreign cells in an organ transplant. When activated, T cells differentiate into memory cells, cytotoxic cells, suppressor cells, and helper cells; cytotoxic T cells attack the antigen directly. However, the functioning of adaptive immunity can also lead to disease (autoimmunity) resulting from a failure of our immune systems to distinguish the self (the host) from foreign material. Autoimmune diseases tend to be chronic, debilitating, and difficult to control (short of making the patient immunodeficient to some degree). Certain damaging aspects of adaptive immunity are termed hypersensitivity reactions, implying excessive immunity. More often inappropriate immunity, such as occurs in allergic responses, is the cause. The plant products that result in "hay fever" allergies are foreign to us and recognized as such by our adaptive immune system.

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Elderly patients may acquire a Zenker diverticulum erectile dysfunction caffeine top avana 80 mg generic, which is an outpouching in the upper portion of the esophagus that traps food and causes regurgitation erectile dysfunction korean red ginseng buy cheap top avana. Diseases of the Esophagus 611 Achalasia Sometimes the cardiac sphincter fails to open properly zyrtec impotence purchase top avana, caused by a malfunction of the nerve plexuses in the esophagus that control its functions erectile dysfunction kit cheap top avana 80mg overnight delivery. As a result erectile dysfunction drugs pictures purchase top avana 80mg visa, food cannot pass normally into the stomach best erectile dysfunction pills at gnc purchase 80 mg top avana fast delivery, and the smooth muscle in the wall of the esophagus must contract more vigorously to force the food past the constricted sphincter. Eventually the esophageal muscle undergoes marked hypertrophy, and the esophagus becomes dilated proximal to the constricted sphincter because of food retention. A number of drugs are useful in helping to relax the muscle, including endoscopic injection of botulinum toxin, which blocks the transmission of nerve impulses from the nerve plexuses to the muscle fibers for several months. More permanent therapy consists of periodic stretching of the sphincter or by surgically cutting the muscle fibers in the constricted area. Incompetent Cardiac Sphincter and Its Complications In this relatively common condition, acid gastric juice leaks back into the esophagus through the improperly closed, incompetent lower esophageal sphincter. The squamous epithelial lining of the esophagus, which was not "designed" to tolerate high-acid secretions, becomes irritated and inflamed, leading to reflux esophagitis. The condition is most commonly found in people after the age of forty and is associated with obesity, smoking, and alcohol consumption. In some patients, the squamous mucosal lining may actually become ulcerated and scarred. Sometimes the squamous lining responds to the acidity by undergoing a change (metaplasia) into a more acid-resistant columnar gastric type mucosa. This condition is called Barrett esophagus after the person who first described it. Patients with a significant degree of Barrett esophagus require periodic endoscopic monitoring and biopsy to detect early cancer. The condition may be treated endoscopically by using radiofrequency-induced heating to ablate affected areas. Treatment of reflux esophagitis to prevent progression to Barrett esophagus consists of avoiding lying down soon after eating because the recumbent position promotes reflux, sleeping with the head of the bed elevated to minimize reflux, Barrett esophagus Squamous lining changes to a more acid-resistant columnar mucosa. The area between them demonstrates mucosal metaplasia where the squamous epithelium has been replaced by columnar epithelium. Drugs that reduce secretion of gastric acid and antacids that neutralize gastric acid are helpful. The repetitive, intermittent, vigorous contractions of the abdominal muscles associated with vomiting raise intragastric pressure while lowering the intrathoracic pressure and lead to distension and extremely forceful ejection of stomach contents through the esophagus. The additional stresses resulting from vigorous contractions of the muscular walls of the stomach and esophagus associated with vomiting probably place additional stress on the mucosa, which also plays a role in causing the laceration. This vomiting-related complication is not uncommon and is responsible for up to 10 percent of cases of bloody vomiting (hematemesis) and often follows the retching and vomiting related to excess alcohol intake, but it may follow vomiting from any cause, including self-induced vomiting to control weight. The opaque mucosa in the upper part of the photograph is the normal stratified squamous mucosa of the esophagus. The 2 cm long tear extends distally from the gastroesophageal junction and caused a fatal gastric hemorrhage. Worldwide, squamous cell carcinoma is the more common although frequency varies in different geographic areas. However, adenocarcinoma has rapidly increased in frequency in the United States, possibly in relation to the increased frequency of Barrett esophagus related to changes in dietary habits, and it is now more common than squamous cell carcinoma. In either case, the tumor gradually narrows the lumen of the esophagus, frequently infiltrates the surrounding tissues, and may invade the trachea. Necrosis of the tumor extending between the esophagus and trachea may lead to the formation of an abnormal communication between these two structures called a tracheoesophageal fistula (fistula = tube). The tumor is often discovered at an advanced stage, requiring esophagectomy, chemotherapy, and radiation. Food Impaction Obstruction of the esophagus may be caused by impaction of poorly chewed meat in the distal part of the esophagus. This is sometimes encountered in people who are unable to chew their food properly because they have poor teeth or improperly fitting dentures or who have poor eating habits. Reflux esophagitis with ulceration and scarring is the most common cause of stricture. Esophageal scarring also may result from accidentally or deliberately swallowing a corrosive chemical that causes necrosis and inflammation. A common cause of esophageal stricture in children is accidental swallowing of commercial lye solutions (used for cleaning clogged drains). Ingestion of other household cleaning agents and disc batteries also are frequent causes. Diseases of the Stomach Diseases of the stomach include acute and chronic gastritis, peptic ulcer, carcinoma of the stomach, and gastroenteritis. Many patients with gastritis have few symptoms, but some experience abdominal discomfort and nausea. However, acute gastritis may be severe enough to result in life-threatening hemorrhage. Acute Gastritis In most cases, acute gastritis is a self-limited inflammation of short duration. However, at times, the acute inflammation may be quite severe and may be complicated by ulceration of the mucosa with bleeding from the ulcerated areas. These drugs are widely used to treat symptoms of arthritis and related musculoskeletal pain problems. The drugs act by inhibiting an enzyme called cyclooxygenase, which is required for the synthesis of prostaglandins (potent mediators discussed in the inflammation and repair section). Prostaglandins are produced by many different cells and have many different functions. Those produced by gastric epithelial cells help protect the stomach from the damaging effects of gastric acid by promoting the secretion not only of sodium bicarbonate to counteract the acid but also of mucin to coat and protect the stomach lining. Excess ingestion of alcoholic beverages is another common cause of acute gastritis because the alcohol is a gastric irritant and also stimulates gastric acid secretion. In addition, any type of stress (such as burns, surgery, or serious systemic infections) may compromise the circulation to the stomach and contribute to the formation of acute gastritis, erosion of the stomach wall, and, if severe, stress ulcers. Chronic Gastritis and Its Complications: the Role of Helicobacter Pylori Many cases of chronic gastritis are related to growth (colonization) of a small, curved, gram-negative organism called Helicobacter pylori on the surface of the gastric mucosa. This unique organism grows in the layer of mucus covering the epithelial cells lining the stomach, where it can be identified by special bacterial stains, by culture, or by other specialized tests. The organism produces an enzyme called urease, which decomposes urea, a normal by-product of protein metabolism present in small amounts in blood and body fluids. Decomposition of urea yields ammonia, a substance that neutralizes the gastric acid and allows the organism to flourish in an acid environment that would destroy other bacteria. Helicobacter also produces enzymes that can break down the layer of protective mucus that covers the epithelial surface. Presumably, the chronic gastritis is caused by the ammonia and other products produced by the organism that damage the gastric mucosa of susceptible individuals. By age fifty, the proportion increases to about 50 percent and may be as high as 65 percent in people older Diseases of the Stomach 615 than age sixty-five. There are also some uncommon but important long-term harmful effects of Helicobacter infection. The gastric carcinoma risk occurs because the gastritis often leads to atrophy of the gastric mucosa and causes the gastric epithelium to change into an abnormal intestinal-type epithelium (a process called intestinal metaplasia). It is these cellular changes in the gastric mucosa that predispose to gastric carcinoma. The lymphoma risk probably results because the gastritis overstimulates the mucosaassociated lymphoid tissue, which may lead to unregulated growth of lymphocytes that eventually progresses to gastric lymphoma. People who secrete large volumes of acidic gastric juice and who are infected with H. The bacteria is present in nearly all patients with duodenal ulcer disease but is not, in itself, sufficient to cause the disease; many people harboring the agent do not develop ulcers. The initial event is probably a small, superficial erosion of the gastric or duodenal mucosa. Gastric acid and pepsin begin to digest the deeper tissues, which have been denuded of covering epithelium. Attempts at healing in the presence of continuing digestion eventually lead to considerable scarring at the base of the ulcer. Clinically, ulcers produce pain that is usually relieved by ingestion of food or antacids that neutralize the gastric acid. An ulcer may erode into a large blood vessel, causing severe hemorrhage, or erode completely through the wall of the stomach or duodenum, causing a perforation through which gastric and duodenal contents leak into the peritoneal cavity, resulting in a generalized inflammation of the peritoneum (peritonitis). Sometimes the scarring that follows healing of a gastric ulcer may be so severe as to cause obstruction of the outlet of the stomach, called the pylorus, preventing the stomach from emptying properly. Peptic ulcer is generally treated by antacids, which neutralize the excess gastric acid, or by drugs that block the secretion of acid by the gastric epithelial cells (histamine receptor blockers and proton pump inhibitors). This may be related to the decreased consumption of smoked and cured meat products with the advent of refrigerators for the preservation of fresh foods. Sometimes the first manifestation is an iron deficiency anemia, the result of chronic blood loss from the ulcerated surface of the tumor. Unfortunately, a gastric carcinoma is often far advanced and has metastasized by the time it causes symptoms; consequently, long-term survival of patients with stomach carcinoma is relatively poor. Some cases of gastric carcinoma may be restricted to the mucosa or submucosa (termed early gastric cancer). This may be a unique form of the disease and appears to have a much better surgical outcome. Sometimes gastric carcinoma may produce symptoms similar to those of a benign peptic ulcer. The distinction usually can be made by endoscopic techniques (gastroscopy) and, if necessary, via examination of biopsy material. Diseases of the Small Intestine Diseases of the intestine can be divided into those that predominantly affect the small bowel or the large (colon) although there is some overlap. Acute viral and bacterial enteritis predominantly affect the small intestine (and in some cases the stomach, so the term gastroenteritis is sometimes used). The condition is characterized by an abrupt onset of nausea, vomiting, abdominal cramps, and profuse diarrhea, which may affect only a few people or may occur as an epidemic affecting large numbers of people. Severely affected people may require intravenous fluids to replace depleted body fluids and electrolytes resulting from the diarrhea. Rotavirus primarily affects infants and young children, most commonly in the winter and spring. Outbreaks occur in the day care setting and occasionally as widespread epidemics related to contaminated food or water. Norovirus is extremely contagious and is now the leading cause of illness from contaminated food in the United States. Contaminated leaf greens, fresh fruits, and shellfish are the most common sources. The illness is also spread from person to person, stool and vomitus being viral sources. Outbreaks tend to occur in closed places such as day care centers, nursing homes, and on cruise ships. Unlike the case with rotavirus, no vaccine is available and proper sanitary techniques (including frequent hand washing and washing contaminated clothing) is critical for prevention. They are generally of short duration and may subside without specific treatment, or may respond to appropriate antibiotics or other agents. Clinical manifestations include nausea, vomiting, abdominal discomfort, and passage of many loose stools. In severe infections, the bowel mucosa may be ulcerated, and the diarrheal stools may be bloody. Bacterial diarrhea (commonly caused by Escherichia coli and Vibrio species) are a major cause of death in young children, accounting for more than three-quarters of the deaths of children in developing countries in Africa and Asia. Cholera, caused by ingestion of the bacteria Vibrio cholerae from contaminated water, remains a common and in some regions endemic cause of severe and potentially fatal diarrhea. Following the 2010 earthquake in Haiti, cholera has become a continuing problem, with 700,000 suspected cases and 8,500 deaths to date. The bacteria does not invade the mucosa of the small bowel but rather multiply in the mucous layer where they secrete a cholera toxin that causes the intestinal cells to secrete large amounts of water and sodium ion into the intestinal lumen, which results in profound diarrhea and salt loss leading to dehydration shock and death if untreated. Replacement of lost fluids and salt with oral rehydration fluid consisting of water, salt, and glucose is a simple and highly effective therapy. These include atresia and stenosis (complete and partial blockage of the lumen, respectively). The most common is Meckel diverticulum, an abnormal retention of the vitelline duct (vitellus = yolk) that connects the yolk sac to the developing embryo during embryogenesis. Most Meckel diverticula are asymptomatic, but sometimes the diverticulum becomes infected, causing the same symptoms and complications as an acute appendicitis. If a Meckel diverticulum contains misplaced (ectopic) gastric mucosa, the acidic "gastric juice" secreted by the diverticulum may cause a peptic ulcer of the diverticulum, which is at times complicated by bleeding or perforation. Hence, the surgeon searches for a Meckel diverticulum in cases of suspected appendicitis or other abdominal surgery. Vitelline duct Duct connecting the yolk sac to the developing embryo during embryogenesis. Disturbances of Bowel Function: Food Intolerance Some patients manifest crampy abdominal pain, abdominal distention, flatulence (excessive gas in the intestinal tract), and frequent loose stools as a result of food intolerance. During digestion, lactose must be split into its two component monosaccharides, glucose and galactose, before it can be absorbed. This process is accomplished by an enzyme called lactase, which is present on the mucosal surface of the epithelial cells in the small intestine. In many populations, however, the concentration of lactase gradually declines to very low levels during adolescence and early adult life. However, some populations tend to have persistent levels of lactase into adulthood.

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Shock results from a disproportion between the volume of blood in the circulatory system and the capacity of the vascular system that carries the blood erectile dysfunction drugs market share buy generic top avana 80 mg. Blood pressure falls if the volume of blood filling the circulatory system falls or if marked dilation of blood vessels expands the capacity of the vascular system to such an extent that the existing blood volume is insufficient to fill the vessels adequately impotence from blood pressure medication cheap 80 mg top avana with mastercard. Hypovolemic shock is caused by low blood volume erectile dysfunction pump rings buy 80mg top avana otc, leading to a corresponding drop in blood pressure impotence over 60 generic 80 mg top avana overnight delivery. Most cases result from a large hemorrhage that significantly reduces the circulating blood volume erectile dysfunction injection drugs buy cheap top avana 80 mg, but any excessive depletion of body fluids such as fluid losses from a severe burn erectile dysfunction by country buy top avana with a visa, from severe diarrhea, or from excessive fluid loss in urine resulting from diuretics can also reduce blood volume as fluid shifts from the vascular compartment into the depleted extravascular body fluids. Cardiogenic shock is caused by inadequate or impaired cardiac pumping function, which reduces cardiac output. Cardiogenic shock usually is a complication of a myocardial infarction, but the pumping function of the heart can also be impaired if the heart is compressed by accumulation of blood or fluid within the pericardial sac, which prevents filling of the heart in diastole, or by other conditions that cause acute heart failure. Septic shock results from the release of inflammatory mediators in response to infection (often by gram-negative organisms that release endotoxin, a potent inflammatory mediator). These mediators can increase capillary permeability, resulting in the decrease of plasma oncotic pressure and fluid loss. The infection also can result in endothelial cell injury and vasodilation as a result of endothelial cell stimulation. Anaphylactic shock (described in the discussion on immunity, hypersensitivity, allergy, and autoimmune diseases) also results from excessive vasodilation caused by the widespread release of mediators of inflammation from mast cells and basophils, which is often followed by circulatory collapse. Treatment consists of administering drugs that raise blood pressure by constricting blood vessels, restoring blood volume by intravenous fluids or blood if the shock is caused by a severe hemorrhage, and treating the underlying condition that leads to the shock. Unfortunately, septic shock or cardiogenic shock in an elderly patient with other medical problems has a very poor prognosis. The main cause of arterial thrombosis is injury to the wall of the vessel, usually secondary to atherosclerosis. Blockage of a coronary artery frequently causes infarction of the heart muscle and consequent "heart attack. Thrombi may form within the atrial appendages when heart function is abnormal, as in heart failure, or when the atria are not contracting normally. Thrombi may also form on the surfaces of heart valves that have been damaged as a result of disease. Occasionally, thrombi may form on the internal lining of the ventricle adjacent to an area where the heart muscle is infarcted. Intracardiac thrombi may become dislodged and may be carried into the systemic circulation, resulting in infarction of the spleen, kidneys, brain, or other organs. A normal heart valve (the mitral valve) and its components are seen at the top of the photo. This tendency results from the release of thromboplastic materials into the circulation from the tumor. The same basic mechanism induces hemorrhage in patients with a disseminated intravascular coagulation syndrome (discussed in abnormalities of blood coagulation). The disease is believed to be triggered by endothelial injury and is associated with the gradual accumulation of cells, connective tissue, and lipid (mostly free cholesterol and cholesterol esterified to long-chain fatty acids) within the intima of the vessel wall. The nonthrombogenic single layer of endothelial cells (the endothelium) lining the lumen overlays the tunica intima, which is predominantly collagenous in nature and contains few fibroblasts or smooth muscle cells. Under this is the tunica media, composed of multiple concentric layers of smooth muscle cells that are rich in elastin in an elastic artery. During the process of atherosclerosis, inflammatory and immune cells accumulate in the intima as do smooth muscle cells, which migrate from the media in response to cytokines liberated by inflammatory and immune cells. The artery shown here consists of three major layers: tunica intima, tunica media, and tunica adventitia. In addition (and critical to the process), damaged endothelial cells express cell surface molecules that facilitate adherence of blood monocytes/macrophages to the damaged endothelium and migration of these inflammatory cells into the arterial wall. These macrophages carry lipids (as a component of low-density lipoprotein) from the blood into the intima where they accumulate as foamy macrophages. The macrophages release cytokines and growth factors, which stimulate smooth muscle cell, connective tissue, and additional inflammatory cell accumulation. The inflammatory cells and damaged endothelium promote oxidation of the deposited lipid carried by lipoproteins, and these oxidized lipids are a further source of tissue damage and inflammation. With time the hallmark lesion of atherosclerosis, the raised atheroma (athere = porridge), forms in the intima. The atheroma is a plaque with a necrotic core rich in lipid (and in particular cholesterol, which often deposits as crystals). The core is covered by a fibrous cap tissue containing immune and inflammatory cells (often foamy macrophages), smooth muscle cells, and other connective tissue. The gradual growth of the atheroma (likely over decades) leads it to encroach into the lumen of the artery where it compromises blood flow. The artery can initially remodel to enlarge the lumen, but this is a limited process that will ultimately result in arterial stenosis (narrowing) and reduced oxygenation to adjacent tissue. As the atheroma enlarges, the surface of the vessel over the atheroma becomes increasingly damaged and fibrotic (termed complicated plaque). Turbulent hemodynamic flow over the stenosed area will result in endothelial damage and possibly ulceration and plaque rupture, releasing thrombotic lipids and calcified damaged cellular debris into the circulation. Hemorrhage into the plaque may occur suddenly, increasing the size and totally blocking blood flow. Atherosclerosis 311 increasingly prothrombotic as the endothelium is lost and the fibrous cap is exposed, leading to platelet adhesion and the formation of an adherent thrombus blocking arterial flow. However, the blood supply may become inadequate under exertion when the heart requires more blood to satisfy the increased demands. If the reduction in blood flow is sudden and sufficiently severe, a myocardial infarct (heart attack) will occur. In cerebral vessels, a thrombotic stroke leading to brain ischemia will result in damage and death of neural tissue. Atherosclerosis of the arteries supplying the legs results in vascular claudication with severe cramping leg pain, impaired mobility, and potentially gangrene of the lower limb. Atherosclerosis of the renal arteries can lead to loss of kidney function; in the mesenteric vessels atherosclerosis can result in lethal necrosis of the gut. These fatty streak lesions are accumulations of lipid-rich foam cells within the intima. The lesions are often elongated (hence the term "streak") and parallel to the direction of blood flow. Fatty streaks first appear in the thoracic aorta, but the distribution of these lesions does not mirror the location of atheromas in adults (which are not frequent in this location). Somewhat later in life, fatty streaks begin to appear in coronary vessels in locations where fibrofatty atheromas become common with age, suggesting the fatty streaks are a precursor lesion of atherosclerosis. This occurs at sites where endothelial injury occurs, a process in which blood flow dynamics plays a role. Initially the atheroma may be stabile, but as it begins to grow in size, it becomes clinically significant and causes luminal stenosis and reduced blood flow. This results in a cramping chest pain (cardiac angina) that can be relieved using vasodilators to increase the luminal diameter of the vessels (discussed in cardiovascular system, coronary vascular disease). As the process continues, changes to the plaque destabilize it and render it prothrombotic. Eventually (possibly in the late sixth or seventh decade) an acute change to a complicated lesion results in clinically evident (and possibly catastrophic) disease. Prevention of atherosclerosis requires modification of risk factors and recognition that some risk factors may not be changed and require positive therapeutic intervention. Risk Factors for Atherosclerotic Disease: Introduction A number of modifiable factors are known to increase the risk of developing atherosclerotic vascular disease and its associated complications. Of the four major risk factors (elevated blood lipids, high blood pressure, cigarette smoking, and diabetes), the most important is elevated blood lipids (hyperlipidemia), and specifically hypercholesterolemia, which even in the absence of other risk factors can promote atheroma development. The remaining major modifiable risk factors include high blood pressure, cigarette smoking, and diabetes. If one risk factor is present, the likelihood of coronary heart disease and heart attacks is twice that of an individual lacking risk factors. If two risk factors are present, the risk increases fourfold, and if three factors are present, the risk of heart attack is seven times that for an individual with none. Low-density lipoprotein (L) promotes atherosclerosis by transporting cholesterol into the arterial wall. High-density lipoprotein (H) protects against atherosclerosis by transporting cholesterol to the liver for excretion. It is uncertain whether dietary therapy using B vitamins and folic acid reduce the incidence of cardiovascular disease. Likewise, an elevated level of the acute phase reactant C-reactive protein, associated with inflammation, is an independent risk factor for atherosclerosis; it is uncertain whether modification by drug therapy is effective in reducing this risk. A number of genetic diseases, including familial hypercholesterolemia and homocystinuria, an uncommon autosomal recessive condition related to defects in the metabolism of the amino acid methionine associated with grossly elevated plasma homocysteine, are associated with increased risk for atherosclerosis. Cholesterol is found in nutrients of animal origin (eggs, meats, and dairy products). Currently, it is unclear whether dietary cholesterol intake is associated with cardiovascular disease. Although prudence suggests some caution in excessive consumption, butter and eggs have lost much of their evil repute. Nevertheless, the American Heart Association recommends limiting saturated fat consumption to 5 to 6 percent of caloric intake. Examples of foods with saturated fats include tropical oils (such as coconut or palm kernel oil), beef fat, lard and cream, and many other meat and dairy products. Trans fats are solid fats chemically synthesized from unsaturated fats to improve shelf life and baking characteristics. Recognizing Wall Cholesterol Risk Factors for Atherosclerotic Disease: Introduction 315 the risks, several governments have either banned or soon will ban trans fats from all food products (the "no trans fat" label is already common in the United States). Triglyceride levels are best reduced by losing weight, cutting back on calories, and lifestyle modifications. The omega 3 and 6 indicate the position of an unsaturated double bond in the long carbon chain. Therapeutic Approaches to Hyperlipidemia the decision to actively lower blood lipid levels, and in particular cholesterol levels, is clinically based on the overall risk of cardiovascular disease. Individuals with known cardiovascular disease (including deposits in coronary arteries and also in other areas of the vasculature) or with genetic diseases that elevate cholesterol levels clearly benefit from drug-based therapy using a class of agents termed statins (although other generally less effective agents are available). Even individuals without known cardiovascular disease are likely to show reduced risk of developing disease (or exacerbation of undiagnosed early disease). Clinicians use risk calculation estimators (one is available online from the American Heart Association) to estimate the risk of a myocardial infarct in the next decade and base suggested intervention on the degree of future risk. Lifestyle modification-including weight loss, exercise, and diet modification-is often suggested in an initial attempt to improve cholesterol levels in individuals without current disease. These interventions provide an overall health benefit, but they have little if any effect on overall mortality from cardiovascular disease. Serum cholesterol levels depend on genetic factors, and once body mass is elevated, those levels respond poorly to dietary modification. For these reasons, the use of drug therapy with statins to lower serum cholesterol levels is clearly of benefit. Potential side effects of statin use include muscle pain and (rarely) serious damage to muscles; drug cost is a potential problem for some. The decision of when to treat otherwise healthy individuals and how aggressively to attempt to lower cholesterol levels is complex and still not fully settled. More aggressive drug use is also suggested for individuals between the ages of forty and seventy-five. Homocysteine is then metabolized by other biochemical pathways in which vitamin B6, vitamin B12, and folic acid are required. Blood concentrations of homocysteine are higher in men than in premenopausal women but increase in women after the menopause. Renal function also influences homocysteine blood levels, which are elevated in people with kidney disease. Abnormal homocysteine metabolism is characteristic of a rare hereditary disease called homocystinuria. The disease results from a gene mutation leading to an enzyme defect that impairs the normal metabolism of homocysteine. Affected individuals have an extremely high concentration of homocysteine in their blood and excrete the amino acid in their urine. Those affected show evidence of marked vascular disease, which has its onset at a very young age. These manifestations include atherosclerosis of coronary arteries and other major arteries, strokes, and blood clots in arteries and veins. Clinical studies have demonstrated that many people with cardiovascular disease, strokes, and peripheral vascular disease have elevated homocysteine blood levels, and a high homocysteine blood level is a risk factor for atherosclerosis, comparable to the increased risk associated with hypercholesterolemia, smoking, and hypertension. In most people in whom renal function is normal, the elevated homocysteine level may be related to a deficiency of B vitamins and folic acid; however, it is unclear whether dietary supplementation reduces the risk of cardiovascular disease in individuals who do not have hereditary homocytinuria. Traditionally, normal blood pressure is considered to be below 120/80 (systolic/diastolic). A pressure consistently higher than 140/90 is called hypertension, whereas in-between values are considered to be "prehypertensive" and indicate a potential problem. Normal blood pressures are defined on the basis of population studies and vary depending on age and sex among normal individuals. Rather than defining "normal," current guidelines set "blood pressure goals" above which antihypertensive therapy should be considered. Individuals of any age with diabetes or chronic renal disease have a goal of 140/90. Ninety-five percent of cases of hypertension (so-called essential hypertension) have no easily identifiable cause but rather are multifactorial with genetics, salt intake, and vascular tone all playing a role. In the case of vascular tone, increased sympathetic activity can result in excessive vasoconstriction of the small arterioles throughout the body, which raises the diastolic pressure.

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John is unaware of any history of colorectal cancer in his large number of relatives erectile dysfunction lyrics 80mg top avana fast delivery. John undergoes successful colonoscopy during which several small polyps are found in the descending colon and removed erectile dysfunction treatment cream buy discount top avana 80mg line. However facts on erectile dysfunction generic 80 mg top avana mastercard, the endoscopist is unable to fully examine the colon because the lumen of the colon is stenosed (constricted) in the ascending portion erectile dysfunction kidney top avana 80mg otc, preventing further passage of the scope erectile dysfunction herbal treatment options purchase 80mg top avana with mastercard. The stenosed area appears to be associated with a large tumor that cannot be removed using the endoscope muse erectile dysfunction wiki cheapest generic top avana uk. The endoscopist tattoos the area with ink to note the area of concern and refers the patient for surgery. The surgeon notes a suspicious lesion of the right (ascending colon) and performs a right hemicolectomy, removing the lesion and the right colon, reattaching the small intestine to the transverse colon to preserve bowel function. It is extremely likely that John would never have had colon cancer had he followed routine cancer screening guidelines. Hence, screening for polyps in the colon and rectum should start at age fifty (in the absence of other risk factors such as a strong family history or a defined hereditary disease). Because most colon cancer starts as a detectable precancerous lesion, removal of these lesions (colon and rectal adenomatous polyps) via endoscopy prevents colon cancer from occurring. Even removal of lesions showing marked dysplasia or localized cancer is likely to be curative. Because colon cancer progresses slowly, screening tests need not be undertaken frequently if no suspicious lesions are found. Colonoscopy at ten-year intervals allows examination of the entire colon and cecum and is considered to be the most sensitive screening test. This procedure (unlike colonoscopy) generally does not require anesthesia and is often done by a trained physician rather than a gastroenterologist. It is less costly than colonoscopy and requires less patient preparation (generally two disposable enemas as opposed to the thorough bowel cleaning needed for colonoscopy). However, proctosigmoidoscopy (as the name implies) can examine only the descending colon. Detection of multiple polyps in this region suggests the presence of additional undetected polyps in the transverse or ascending colon, necessitating colonoscopy. None of these techniques allow for removal of lesions, and suspicious findings require follow-up colonoscopy. There is dispute over the cost effectiveness of colonoscopy versus proctosigmoidoscopy. What factors should be taken into account in establishing the procedure that should be recommended How does the body defend itself against abnormal cells that arise spontaneously in the course of cell division The second entry provides a detailed text on all aspects of neoplastc disease; strong on experimental concepts. The third entry contains a very readable overview of cancer genetics and cell cycle control in Chapter 13, Molecular Genetics of the Cell Cycle and Cancer. One of the most exciting and recent advances in cancer immunotherapy is the concept of checkpoint blockade. The approach has resulted in a major advance in concepts of cancer therapy (and some striking clinical results). The other three present additional details of current experimental and clinical applications. However, the recognition of specific molecular defects not only may serve as a biomarker for cancer but also as an important therapeutic target. A thorough overview that presents a molecular overview of the case in this chapter. Describe the mechanism by which antibiotics inhibit the growth and metabolism of bacteria. Introduction Of the wide spectrum of microorganisms found in nature, only a relatively small proportion cause disease in humans. These pathogenic microorganisms are classified into several large groups: bacteria, viruses, chlamydiae, rickettsiae/ehrlichiae, mycoplasmas, and fungi. In addition, humans serve as host to a number of animal parasites capable of causing illness or disability. Porins Unique proteins on bacteria outer membrane contributing to resistance to antimicrobial agents. Cocci may grow in clusters (staphylococci), in pairs (diplococci), or in chains (streptococci). A dried, fixed suspension of bacteria, prepared on a microscope slide, is stained first with a purple dye (hematoxylin) and then with an iodine solution. Next, the slide is decolorized with alcohol or another solvent and is then stained with a red dye (eosin). Each type of bacterium contains a large number of antigens associated with the cell body, the capsule of the bacterium, and the flagella (in the case of motile organisms). The antigenic structure can be determined by special methods, defining a system of antigens unique for each group of bacteria. Some bacteria are quite fastidious and can be grown only on enriched media under carefully controlled conditions of temperature and acidity (pH). Other bacteria are hardy and capable of growing on relatively simple culture media under a wide variety of conditions. Some bacteria are able to grow only in the absence of oxygen or under extremely low oxygen tension. Flagella give a bacterium its motility; organisms that lack flagella are nonmotile. Some bacteria form spores, spherical structures found within the bacterial cell that can survive under conditions. Spores may be considered as a dormant, extremely resistant bacterial modification that forms under adverse conditions. Spores can germinate and give rise to actively growing bacteria under favorable conditions. Some types of bacteria are capable of fermenting carbohydrates and can promote many different biochemical reactions under suitable cultural conditions. Gram-negative bacteria are also unique in having lipid A (a lipopolysaccharide important in bacterial virulence) and unique proteins called porins in the outer membrane that contribute to the resistance of this class of bacteria to certain antimicrobial agents. Genetic probes Preparations of nucleic acid devised to identify specific sequences in bacteria. This biochemical profile can be determined by growing the bacteria on different media. For example, an organism has been isolated from the blood of a patient with a febrile illness. The organism is a gram-negative bacillus that is not fastidious and not anaerobic. At this point, the number of possible organisms consistent with these characteristics has been reduced to relatively few gram-negative bacteria. The number of possibilities is narrowed still further by testing with various biochemical tests that indicate the bacterium does not ferment lactose but is able to ferment glucose and certain other sugars. These and other biochemical and immunological tests support the conclusion that the organism is a type of pathogenic bacterium called Salmonella, which is found in the gastrointestinal tract and is capable of causing a typhoid-like febrile illness. Once the organism has been identified, the clinician can select appropriate antibiotics and, if necessary, institute proper isolation and control procedures. In addition to the classic identification methods of culture and visualization, microorganisms today may be identified by molecular methods that detect the presence of specific nucleic acid. These methods can demonstrate the organisms in patient specimens as well as identify isolated organisms. This is particularly useful for microorganisms such as mycobacteria that are difficult to culture. Commercially available genetic probes can detect specific nucleic acid sequences in bacteria, mycobacteria, and fungi. One potential drawback of molecular methods are that they detect dead as well as living organisms. Hence, this test may be inappropriate for measuring the effects of antibiotic therapy on bacteria. Staphylococci Staphylococci, normal inhabitants of the skin and nasal cavity, are generally not pathogenic. Pathogens usually can be distinguished from nonpathogenic staphylococci by the appearance of their colonies on media containing blood (blood agar plates). Occasionally, staphylococci cause serious pulmonary infections and other types of systemic infections. Some strains of staphylococci are highly resistant to antibiotics, and infections caused by antibiotic-resistant staphylococci are extremely difficult to treat. Streptococci Streptococci are classified on the basis of their serologic group designated by a capital letter, and on the type of hemolysis the organism produces when grown on a solid medium containing blood. Generally, both the letter group and the type of hemolysis are specified when describing a streptococcus. The serologic classification, called the Lancefield system, divides the streptococci into twenty major groups based on differences in the carbohydrate antigens present in their cell walls. These groups are designated A through H and K through V, with most of the streptococci of medical importance in groups A, B, and D. Loss of normal intestinal flora caused by antibiotics allows overgrowth of Clostridia. Febrile illness from contact with infected animals or consumption of raw milk from infected animals. Febrile illness acquired from flesh of infected animals, usually wild rabbits, or transmitted to humans by bite of infected ticks or deer flies. Organisms live in water and cause pulmonary infection in persons who inhale aerosolized droplets from showers, air conditioners, or other water sources. Humans infected from contaminated water, undercooked meat or poultry, or contact with infected animals. Some strains (0157:H7) produce toxins that cause hemolytic anemia and kidney damage. Enzymes produced by the bacteria break down (hemolyze) the blood cells in the culture medium, which causes the clear zones surrounding the colonies. Rheumatic fever Inflammatory disease that occurs following a Streptococcus pyogenes infection that can involve the heart, joints, skin, and brain. Glomerulonephritis An inflammation of the glomeruli caused by either antigen-antibody complexes trapped in the glomeruli or by antiglomerular basement membrane antibodies. Usually, both the Lancefield group and the type of hemolysis are specified when describing a streptococcus. Alpha hemolytic streptococci (or simply alpha streptococci) produce green discoloration of the blood immediately around the colony and are often called Streptococcus viridans because of this growth characteristic (viridans = green). These organisms are normal inhabitants of the mouth and throat and usually are not pathogenic. They cannot be classified in the Lancefield system because they lack the carbohydrate antigen possessed by other streptococci. Beta hemolytic streptococci (or simply beta streptococci) produce a narrow zone of complete hemolysis around the growing colony. One of the most important beta streptococci is in Lancefield group A and is called a group A beta streptococcus. Many group A beta streptococci are extremely pathogenic, causing streptococcal sore throat, scarlet fever, serious skin infections, and infections of the uterus after childbirth. Some produce a toxin that causes a toxic shock syndrome similar to that caused by toxin-producing staphylococci. One particularly virulent toxin-producing group A beta streptococcal strain causes a rapidly progressive, destructive infection of the subcutaneous tissues and the fibrous tissue (fascia) covering the adjacent muscles. This condition, called necrotizing fasciitis, may be complicated by necrosis (gangrene) of the overlying skin and by necrosis of the muscles in the infected area (streptococcal myositis). In addition to causing infections in various tissues, some strains of group A beta streptococci are capable of inducing a state of hypersensitivity in susceptible individuals, leading to development of rheumatic fever or a type of kidney disease called glomerulonephritis. These diseases are considered in greater detail in the sections on the circulatory system (discussion on the cardiovascular system) and kidneys (discussion on the urinary system). Fortunately, group A beta streptococci still remain quite sensitive to penicillin and other antibiotics. Group B beta streptococci may cause urinary tract and wound infections, but they are of greatest importance as a cause of serious infections in newborn infants. They often inhabit (colonize) the rectum and vagina of pregnant women, and the infant may become infected during labor and delivery. Because of the potential hazard of a life-threatening infection in an infant born to a mother colonized by group B beta streptococci, routine rectal and vaginal cultures to detect the organism are recommended for all pregnant women late in pregnancy. Those women who are colonized are treated with intravenous antibiotics during labor to reduce the risk of a serious group B beta streptococcal infection in the infant. Group D streptococci and streptococci of other Lancefield groups may also cause various types of infections, but it is the group A beta streptococcus that is responsible for almost all of the late immunologic complications: rheumatic fever and glomerulonephritis. Closely related to group D streptococci but classified separately are organisms that inhabit the intestinal tract called enterococci (enteron = bowel). Consequently, a wound or urinary tract infection caused by an enterococcus may be very difficult to treat. Pneumococci Pneumococci (Streptococcus pneumoniae) are gram-positive cocci and are classified with the streptococci. They grow in pairs and short chains and have certain biochemical characteristics setting them apart from other streptococci. Bacteria 187 Gram-Negative Cocci Most gram-negative cocci are nonpathogenic members of the genus Neisseria and are normal inhabitants of the upper respiratory passages.

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Técnica

Operario Portuario

Formar técnicos que desarrollen competencias para desempeñarse en la operación de los puertos, que son unos nodos de las redes mundiales de producción y distribución de mercancías, que se ubican en puntos en los que se genera transbordo de carga entre modos acuáticos (marítimo o fluvial) o transferencias de cargas entre estos modos acuáticos y otros modos

3 semestres

17 módulos

Presencial

Inversión semestre

$1.200.000

Técnica

Funcionarios de Aduanas e Impuestos

Formar técnicos para que colaboren en Gestión de Aduanas, Comercio Exterior e impuestos, enfocándose para el apoyo de procesos de diseño, administración y realización de operaciones, gestiones y trámites legales propios del comercio exterior y su respectiva tributación.

3 semestres

15 módulos

Presencial

Inversión semestre

$1.200.000

Técnica

Almacenmaiento y Bodegaje

Formar técnicos para que desarrollen habilidades que faciliten y agilicen todas las actividades que demandan las empresas en el área de almacén, almacenamiento y bodegaje, operación de equipos de carga, movilización y descarga de materias primas, materiales e insumos…

3 semestres

17 módulos

Presencial

Inversión semestre

$1.200.000

Técnica

Auxiliar en TIC

Formar Técnicos que comprendan la complejidad de la gestión de tecnologías de la información y comunicaciones, atendiendo de forma integrada sus procesos, manejando los sistemas de información a desarrollar de acuerdo con las particularidades del modelo de negocio, en cada empresa, organización y/o institución, Identificando la tecnología y las herramientas informáticas del cliente.

4 semestres

17 módulos

Presencial

Inversión semestre

$800.000

Técnica

Auxiliar de Seguridad y Salud en el Trabajo

Formar Técnicos para que administren el Sistema de Gestión de la Seguridad y la Salud en el trabajo, bajo la normatividad vigente.

4 semestres

17 módulos

Presencial

Inversión semestre

$800.000

Técnica

Auxiliar de Recursos Humanos

Formar Técnicos con competencias como auxiliar de recursos humanos para que apoyen la gestión organizacional en los temas de reclutamiento, transformación, contratación y actividades de bienestar laboral, asesoramiento laboral, gestión y apoyo al personal y organización del trabajo, tanto en el sector privado como público.

4 semestres

22 módulos

Presencial

Inversión semestre

$800.000

Técnica

Auxiliar de Enfermería

Formar Técnicos en habilidades para el manejo de cuidados clínicos y domiciliarios a los diferentes grupos etarios, manejo de los documentos requeridos para la admisión a los servicios de salud de una persona, el reporte físico o electrónico de comprobación de derechos de las personas aseguradas o no aseguradas, ejecución del diagrama sobre el proceso de admisión, medicamentos listos para ser administrados según prescripción realizada, y manejo de los registros institucionales.

4 semestres

32 módulos

Presencial y virtual

Inversión semestre

$1500.000

Técnica

Auxiliar Contable y Financiero

Formar Técnicos con habilidad para la contabilización de los recursos de operación y presentación de la información contable, cumpliendo con la normatividad y legislación vigente, con capacidad de organizar la documentación contable y financiera, aplicando las tecnologías vigentes y que desarrollen competencias en el uso de aplicaciones informáticas y de comunicación para apoyar el proceso contable y financiero.

4 semestres

17 módulos

Presencial

Inversión semestre

$800.000