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By H. Jaroll. University of Minnesota-Twin Cities.

The technical/nursing staff prepares the trolley and assists the surgeon during the procedure discount zetia 10mg with amex cholesterol ratio 1.9 is that good. Referral criteria:- The criterion for referral remains order zetia 10 mg with amex cholesterol hdl ratio formula, lack of appropriate infrastructure and expertise at primary level zetia 10mg without prescription cholesterol lowering drugs. The indications for referral to tertiary care centre in managing stones disease are:-! The treatment of small non obstructing calyceal calculi in patients with symptoms order 10mg zetia visa ldl cholesterol diet chart. The role of ureteral stent placement in the Prevention of steinstrasse J Endourol 1999;13(3):151-5. A prospective multivariate analysis of factors predicting stone disintegration by extracorporeal shock wave lithotripsy: The value of high resolution non contrast computed tomography Eur Urol 2007; 51(6):1688-93. Air pockets trapped during routine coupling in dry head lithotripsy can significantly decrease the delivery of shock wave energy. Lower pole I A prospective randomized trial of extracorporeal shock wave lithotripsy and percutaneous nephrolithotomy for lower pole nephrolithiassis-initial results J Urol 2001;166(6):2072-80. Perioperative antibiotic prophylaxis in ureteroscopic stone removal Eur Urol 2003; 44(1):115-8. Flexible ureterorenoscopy for the treatment of lower pole calyx stones; influence of different lithotripsy probes and stone extraction tools on scope deflection 37 and irrigation flow. Ureteroscopic management Of ureteral calculi:Electrohydraulic versus holmium Yag lithotripsy J Urol 1997;158(4):1357-61. A systematic review of the best available evidence and the strength of that evidence. If necessary relevant focused questions can be framed in order to exactly define the purview of the exercise. The authors should be clearly mentioned in the published version ( we understand this is not desirable in a document for peer review). Introduction Line 17 – 20 : ”However, a significant proportion, particularly in rural areas tend to disregard symptoms till complications develop and this segment requires a more proactive and individualized approach. The lack of access to effective health care in rural areas will make a proactive and individualized approach difficult. It is important for guidelines to be applicable to the entire populations of the country. Metaanalysis of the recent evidence showed screening to have no significant impact on either overall mortality or death from prostate cancer with significant overdiagnosis and overtreatment and is unlikely to save lives. Ultrasound evaluation should be restricted to the bladder and post void residual urine as an optional test. Blood urea – Blood urea estimation is superfluous when creatinine is being measured. Urethrography – An uroflowmerty is a non invasive test which can indicate a possible urethral stricture. An urethrography is invasive and will require prior urine culture sensitivity before its performance. Indications for surgery “Patients presenting with chronic low pressure require catheterization and urodynamic evaluation” – Catheterization is not required unless the patient has acute on chronic retention, overflow incontinence or obstructive uropathy with raised creatinine. Surgical (endoscopic and open) procedures • “Open prostatectomy is still an acceptable procedure for glands exceeding 100 gms in wt. Screening for prostate cancer: systematic review and meta-analysis of randomised controlled trials. A meta-analysis of the vascular-related safety profile and efficacyof a-adrenergic blockers for symptoms related to benign prostatic hyperplasia. In 2010, an estimated 58,240 Americans were diagnosed with renal malignancies and 3 13,040 deaths were estimated. Surgical excision remains the only curative treatment as this tumor is remarkably resistant to radiotherapy and chemotherapy. Currently, it may be considered in case of equivocal findings on conventional imaging, where detection of metastatic disease will influence management decision. Acceptable in the following indications: h) Considering inflammatory mass / lymphoma / metastasis, vague Radiology, multiple masses, associated significant lymphadenopathy i) Considering non-surgical therapy (e. Stage I Preferred – nephron-sparing surgery if technically feasible Optional – radical nephrectomy* Others 51 9. Ablative therapies (cryotherapy, radiofrequency ablation, microwave thermotherapy, high frequency focussed ultrasound, etc. A mere sampling of the renal hilar lymph nodes is insufficient for pathologic staging. For right sided tumor, paracaval and interaortocaval lymph nodes and for left sided tumor para-aortic and interaortocaval lymph nodes should be removed from the crus of the diaphragm to the common iliac artery. Socio-economic and facility issues – Advanced – • staging tools • surgical facility • follow up facility • socio-economic support may not be available everywhere. A substantial improvement in progression-free survival and overall survival has been 54 achieved in large randomized controlled trials, when compared to Interferon-α. Sarcomatoid variant is associated with poor prognosis, and a modest response with doxorubicin & gemcitabine is observed. Renal cell carcinoma with retroperitoneal lymph nodes: role of lymph node dissection. Lack of retroperitoneal lymphadenopathy predicts survival of patients with metastatic renal cell carcinoma. Lymph Node Dissection at the Time of Radical Nephrectomy for High-Risk Clear Cell Renal Cell Carcinoma: Indications and Recommendations for Surgical Templates. Risk group assessment and clinical outcome algorithm to predict the natural history of patients with surgically resected renal cell carcinoma. Invasive bladder cancer: Bladder cancer that histologically invades the muscularis propria. This may be partially attributed due to better detection and improved health care. Detailed evaluation of all patients with gross hematuria and elderly patients (>40 years) with microscopic hematuria and associated risk factors like smoking 15. Prompt referral of men with advanced bladder cancer to higher centers for further evaluation V. Diagnosis –The diagnosis mainly depends on the cystoscopic examination of the bladder, biopsy, and urine cytology. The management algorithm is based on the diagnosis of invasion of muscularis propria or not. Biopsy of the apical prostatic urethra when there is a bladder neck tumour or when abnormalities of prostatic urethra are visible. Pelvic examination (Bimanual examination) under anaesthesia: Helpful in assessment of local staging in muscle invasive bladder cancer and advanced cases. Bone scan –Indicated in patients with raised alkaline phosphatase and with bone pain. Stage T1 tumours originate from the urothelium but penetrate the basement membrane which separates the urothelium from the deeper layers. T1 tumours invade into the lamina propria, but are not so deep that they reach the detrusor muscle. Carcinoma in situ (Tis) is a high-grade (anaplastic) carcinoma confined to the urothelium, but with a flat non-papillary configuration. Unlike a papillary tumour, Tis appears as reddened and velvety mucosa and is slightly elevated but sometimes not visible. Three types of Tis are distinguishable;  Primary Tis (no previous or concurrent papillary tumours);  Secondary Tis (with a history of papillary tumours);  Concurrent Tis (in the presence of papillary tumours). Predicting recurrence and progression of tumours [15,16]: TaT1 tumours The pattern of recurrence and progression depends on the following clinical and pathological factors: 1. Larger tumours should be resected in fractions, which include the exophytic part, the underlying bladder wall and the edges of resection area.

If there is no improvement in the level of consciousness or excessive cough continues to accumulate in the lungs cheap zetia 10mg line cholesterol free diet foods; doctors usually decide to perform tracheostomy 10 mg zetia for sale cholesterol ratio us. In this procedure a small hole is made in front of the neck on the windpipe and a plastic or metal tube is inserted into it zetia 10mg mastercard cholesterol medication with the least side effects, so as to facilitate the breathing process generic zetia 10mg with amex less cholesterol in eggs. The secretions accumulated in the respiratory tract can be easily removed through suction and the risk of pneumonia is minimised. When breathing starts improving, level of consciousness improves and secretions decrease, then gradually the diameter of the tube can be decreased, thus decreasing the size of the hole. In order to avoid secretions from accumulating and thereby preventing hypostatic pneumonia and maintain normal breathing, chest physiotherapy should be initiated early. Predictions about the patient’s disease, whether the medicines given to the patient are proper, whether the doctors are good- etc topics should be avoided. Due to this the patient and the relatives can become confused, which can create, a problem in patient’s treatment and health. Things like offering fruits, flowers, books, get well soon cards for the patient can be done to convey well wishes. Prayers for the patient can be done at a holy place or home; the patient can also be convinced to pray. In a situation where the patient is not insured and financially not in a good condition and requires financial support for the treatment, the doctor’s attention should definitely be drawn towards this. With the doctor’s guidance medicines can be obtained at subsidized- rates from various social organizations. Liberty Cinema Toll Free: 540-433-7686, Fax: 540-432-0206 Marine Lines, Mumbai-400020 Email : maainfo@shentel. It is for this reason that we emphasize the basic components of cells and their matrices during the early portion of the course. With an understanding of the nature of the relationship between cells and their matrices, we can proceed to the study of the organization of these two components into the basic tissues of the body. In turn, the four basic tissues are organized into the various organs of the body, and these generally exist as interrelated functional units termed organ systems. The four basic tissues of the body are: 1) Epithelium 2) Connective tissue 3) Muscle 4) Nervous tissue Again, we emphasize: All of the organs of the body are composed of varying proportions of the four basic tissues, and each of the four basic tissues consists of cells and extracellular matrices. Note: The images were scanned from the Histology Slide Collection, which is listed at the end of this manual. In the online version, there are low power thumbnail images of the microscopic slides that have been scanned. Ross and Wojciech Pawlina, Lippincott Williams & Wilkins, 2016 th Junquiera’s Basic Histology, Text and Atlas, 13 ed. Whichever of these you choose, it is advisable to read the appropriate material in preparation for lab and bring the histology text to lab. This book includes some images that are not in the online lab manual and supplements the basic material. Understand and be able to describe how the most common dye combination, hematoxylin and eosin (H&E), stains various components of cells and tissues. Note: There is a more complete description of methods for preparation of histological samples at the end of this laboratory manual (p. The specimen on the microscope slide is a thin section (usually 5 micrometers) of the fixed tissue or organ. Components of the specimen generally stain selectively and, on this basis, various regions of the specimen may be differentiated from each other. These form salts with tissue anions, especially the phosphate groups of the nucleic acids and the sulfate groups of the glycosaminoglycans. When the dye moiety is an anion, the dye is called anionic or acid dye and salt formation occurs with tissue cations including the lysine and arginine groups of tissue proteins. Tissue components that recognize basic dyes are "basophilic" and those that recognize acid dyes are "acidophilic". A common combination of stains is hematoxylin and eosin (H&E), which are commonly referred to as basic and acid dyes, respectively. At lower magnifications they appear as blue dots and at higher magnifications chromatin and nucleoli may be identified within the nucleus. Surrounding the nucleus is the acidophilic cytoplasm stained pink (due to the positive charges on arginine and lysine). The luminal surface (center of the 40x view of colonic mucosa slide) is smooth and consists of pale cells (called Goblet cells), absorptive cells, and enteroendocrine cells that make up the mucosa. The free surface of the cell, facing a lumen, is referred to as the cell apex and the opposite surface is the cell base. Note the intense reaction at the apical surface of the epithelial cells and within scattered goblet cells (containing mucin) at the luminal surface. Note the basophilia in the basal compartment and the acidophilia in the apical (luminal) compartment of the cytoplasm. These cells contain basal surface secretory granules, which release digestive enzymes into nucleus the lumen of the acinus. The lumens of the acini converge into interlobular ducts, secretory granules eventually merging to become the pancreatic duct. A border may be identified at the apex of the cells, which has slightly different optical properties from the remainder of the cell. Under optimum conditions faint striations, oriented parallel to the long axis of the cell, are seen in the border. These are difficult to resolve at the light microscopic level, but with electron microscopy, these striations are seen to be precisely arranged microvilli, containing cores of actin filaments. At the apex of these cells note the pink line, which indicates the presence of the basal bodies that give rise to the cilia. During prophase, the nuclear envelope disperses, replicated chromosomes condense, and the two sister chromatids become attached at a site called the centromere. At anaphase B, the sister chromatids continue to migrate toward the poles and the microtubules of the spindle elongate. During telophase, the sister chromatids reach the poles, the nuclear envelope re-forms and the chromosomes decondense. There are examples of cells at all stanges of the cell cycle since the cells are dividing asynchronously. Assess nuclear envelope breakdown, chromosome condensation, mitotic spindle development, and location of condensed chromosomes in the whitefish mitotic cells. On the basis of these parameters, identify and determine the distinguishing features of cells in prophase, metaphase, anaphase (A and B) and telophase. Know the structural characteristics and functional significance of the following organelles and inclusions: nucleus, nucleolus, ribosomes, endoplasmic reticulum (two types), mitochondria, Golgi apparatus, lysosomes, microtubules, cilia, microvilli, glycogen, lipid, peroxisomes. Relate characteristics of particular epithelia to their function, keeping in mind their essential features including junctions, apical modifications, and polarity. Functions of epithelia include formation of a protective layer (epidermis), absorption of water and solutes (intestine), secretion (intestine, various glands) and excretion (kidney tubules). Classification of epithelia is generally based upon two criteria: number of cell layers and cell shape. Pseudostratified epithelium is an intermediate type that appears stratified but really is one cell layer thick. The shape of epithelial cells may be squamous, cuboidal, or columnar; intermediate forms are often encountered. Stratified epithelia are classified according to the shape of the cells at the free surface and can be squamous, cuboidal, columnar, or transitional. Transitional epithelia line cavities in the urinary tract, which may be distended, and the thickness of the epithelium varies with the degree of distention. Beneath the layer of epithelial cells is an underlying non-cellular structure known as the basal lamina, which is secreted by the epithelial cells. Together the basal lamina and the underlying layer make up the basement membrane, which can usually be seen with light microscopy.

The immune defense system either destroys such agents on recognition or neutralizes foreign material that are different to the ‘normal self’ Defense against pathogens removal of worn out cells such as aged erythrocytes and tissue debris i cheap zetia 10mg with amex cholesterol measurement chart. Bacteria are well equipped with its own machinery necessary for their own growth 10 mg zetia fast delivery cholesterol medication does not work, multiplication and survival buy zetia 10mg online cholesterol ratio good but total high. They enter a cell buy zetia 10 mg with mastercard cholesterol ratio calculator mmol/l; take over its cellular biochemical facilities for their own purpose. The viral nucleic acids also dictate the host cell/infested cell to produce proteins needed for viral replication. Effective humoral immune response requires macrophage and T cell interactions as well as B cells. Macrophages engulf foreign matter and also contribute to antibody response in different ways: (See figure 40). These cells interact directly with other T cells and elaborate soluble suppressor factors that modulate the humoral immune response. T cell Function The T cells are involved in cellular immunity, resulting from sensitization of lymphocytes following interaction with cell surface antigens. Induction of cell-mediated immunity involves the production of cytotoxic T cells that kills antigen-bearing target cells such as tumor cells or foreign (e. Hemostasis Hemostasis is a collective term for mechanisms, which prevent or minimize blood loss when a blood vessel is opened. Hemostasis is vital because unchecked hemorrhage eventually leads to cardiovascular collapse and death. Dissolution of clot Stages of hemostasis 1 Vasoconstriction When a blood vessel is injured, its immediate response is to constrict and thereby reduce blood flow. This initial vasoconstriction is due to the local spasm of the smooth muscle in the wall of the blood vessel and to sympathetic reflexes. Coagulation is the process by which some of the blood loses its fluid consistency and become a semisolid mass (clot). Blood coagulation More than 50 important substances that affect blood coagulation have been found in the blood and in the tissues. Some of these substances promote coagulation, called 133 procoagulants (clotting factors), and the others that inhibit coagulation called anticoagulants. Whether blood will coagulate depends on the balance between these two groups of substances. In the blood stream, the anticoagulants normally predominate, so that the blood does not coagulate while it is circulating in the blood vessels. But when a vessel is ruptured, procoagulants in that area of tissue damage become “activated” and override the anticoagulants. Clotting factors Blood clotting is mediated by the sequential activation of a series of coagulation factors, proteins synthesized in the liver that circulate in the plasma in an inactive state. This is composed of mainly phospholipids from the membranes of the tissue plus a lipoprotein complex. Figure 42: Stages of blood coagulation 136 (c) Effect of activated factor X (Xa) to form prothrombin activator The factor Xa combines immediately with tissue phospholipids that are part of tissue factor or combine with factor V to form the complex called prothrombin activator. That is, activated factor X combines with factor V and platelet/tissue phospholipids to form the complex called prothrombin activator. Prothrombin is enzymatically split into two 137 fragments: one inert and the other possessing the properties of thrombin. Initially the conversion of prothrombin proceeds too slowly to produce significant amounts of thrombin needed for coagulation. Thrombin itself, however, increases its own rate of formation by converting proaccelerin (factor V) into accelerin which then accelerates the formation of thrombin. The clot is composed of a meshwork of fibrin fibers running in all directions and entrapping blood cells, platelets and plasma proteins. Excessive bleeding Excessive bleeding can result from deficiency of any of the many blood-clotting factors. With few exceptions, almost all the blood clotting factors are formed by the liver. Therefore, diseases of the liver such as hepatitis, and cirrhosis can sometimes depress the clotting system. In absence of vitamin-K, subsequent insufficiency of these coagulation factors in the blood can lead to serious bleeding tendencies. Symptoms Hemophilia is characterized by spontaneous or traumatic subcutaneous hemorrhage, blood in urine, and bleeding in the mouth, lips, tongue, and within the joints. A platelet count of 100,000/cu mm or less is generally considered to constitute thrombocytopenia, although the bleeding tendency does not become evident until the count falls below 40,000/cu mm. The drop in platelets may occur because of either of the following reasons: (2) Thromboembolic conditions The pathologic converse to hemostasis is called thrombosis. Thrombosis can be thought of as the formation of blood clot (thrombus) in uninjured vessels, or thrombotic occlusion of a vessel after relatively minor injury. Like hemostatic mechanism, thrombosis also depends on three general components: the vascular wall, platelets, and the coagulation cascade. It is particularly important in thrombus formation in the heart and arterial circulation, for example, within the cardiac chambers when there has been endocardial injury (e. It is important to note that endothelium does not need to be denuded or physically disrupted to contribute to the development of thrombosis; any perturbation in the dynamic balance of prothrombotic and antithrombotic effects can influence local clotting events. Thus, significant endothelial dysfunction may occur from the hemodynamic stresses of hypertension, or bacterial endotoxins. Normal blood flow is laminar such that the platelets elements flow centrally in the vessel lumen separated from the endothelium by a slower-moving clear zone of plasma. Stasis and turbulence therefore: (a) Disrupt laminar flow and bring platelets into contact with the endothelium (b) Prevent dilution of activated clotting factors by fresh-flowing blood (c) Retard the inflow of clotting inhibitors and permit the build-up of thrombi (d) Promote endothelial cell activation. It is loosely defined as any alteration of the coagulation pathways that predisposes thrombosis, and it can be divided into primary (genetic) and secondary (acquired) disorders. The characteristic alteration is a mutant factor Va that cannot be inactivated by protein C; as a result, an important antithrombotic counter-regulatory pathway is lost. Use of oral contraceptives and the hyperestrogenic state of pregnancy are some common examples of this category. The systemic circulation, which supplies all the tissues, is a high-resistance system with a large pressure difference between the arteries and veins. The arteries are highly elastic and muscular; they distribute blood to the smaller arterioles and ultimately to the network of capillaries, where exchange of fluid, small molecules and nutrients occurs across the thin walls. Human heart is a four chambered pump, well adapted to separation of oxygen rich and oxygen poor blood handled by left and the right side of the heart respectively. Thin wall atria receive blood, which reaches into thick-walled ventricles that pump blood into systemic and pulmonary circuits through great vessels. The pulmonary circulation is a low-pressure, low-resistance system handling the same amount of blood at the same time as systemic circulation to keep the same amount of blood in the right and left side of the heart. The left ventricle is more muscular and heavier than the right ventricle, which pumps against the low resistance of the pulmonary circulation; the left pumps against the high resistance of the systemic circulation. The mean systemic arterial pressure is 90-100 mmHg, whereas the mean pulmonary pressure is only 8 to 24 mm Hg. The low arterial pulmonary pressure eliminates the need for much supporting tissue in the lungs so that it can have millions of thin- walled 141 alveoli. And highly specialized pulmonary capillaries, facilitating the rapid exchange of gases between the blood and alveolar air. Functional anatomy of the heart The adult heart is enclosed in a double walled sac, the pericardium that attaches it to the mediastinum. The apex is rounded and formed by the left ventricle and located behind the sixth rib, about 3 inches to the left of the midline of the body. The myocardium is about half of the tissue of the heart, the other half is connective tissue, the fibrous skeleton, valves, tendons, blood vessels, lymphatics and nerves.

A highly contagious virus causing extensive morbidity and major case fatality rates is an archetypal anxiety cheap zetia 10mg free shipping cholesterol count. The influenza virus cheap 10mg zetia otc cholesterol medication birth defects, as a pathogenic agent for humans generic zetia 10mg on line cholesterol targets, has been circulating in the hu- man population since at least the sixteenth century (Cox & Kawaoka 1998) leading to recurrent epidemics of febrile respiratory disease every 1 to 3 years proven 10mg zetia cholesterol test results how long. In addition, each century has seen some pandemics rapidly progressing to involve all parts of the world due to emergence of a novel virus to which the overall population holds no immunity. The characteristics of pandemics include occurrence outside the usual season, extremely rapid transmission with concurrent outbreaks throughout the globe, and high attack rates in all age groups with high mortality rates even in healthy young adults. Given the growing world population and international travel and tourism, impending pandemic influenza outbreaks gain the potential to spread even more rapidly. In order to understand the background of this global epidemic threat more thoroughly, this chapter aims to describe both the pathogenesis of the disease and the contest between the virus and the immune system. Pathogenesis The pathogenicity and virulence of the influenza virus is determined by several in- teracting factors: a) Host factors: • Presence of target receptors on host cells • Availability of enzymes in host cells which are essential for viral entry and replication • State of immunocompetence of the individual host • Specific immunity against certain viral epitopes in the individual host and target population • Ability of the immune system to control the viral replication ef- fectively without causing serious collateral damage for the host by its inflammatory response Pathogenesis 93 b) Viral factors: • Ability to bind to host cells • Ability of virus shedding • Restriction of cytopathogenic effects to allow for an appropriate balance between viral replication and control by the host • Escape from immunosurveillance by evolution of antigenic varia- tion driven by selective pressure of the immune response • Escape from immunosurveillance by recombination with different virus strains from zoonotic disease • Modulation of the immune response to attenuate effective host defense mechanisms Viral entry: How does the virion enter the host? The predominant way in which influenza is transmitted is from person to person by aerosols and droplets. In a human lung there are about 300 million terminal sacs, called alveoli, that function in gaseous exchange between inspired air and the blood. The resting ventilation rate in humans is about 6 liters of air per minute, which introduces large numbers of foreign parti- cles and aerosolized droplets potentially containing virus into the lungs. Deposition of foreign particles depends on their size: inhalation of very small particles does not result in absorption through the alveoli or bronchial system. Much larger particles are either not able to enter the respiratory system or are deposited in the upper respiratory tract (Figure 1A). The respiratory tract is covered with a mucociliary layer con- sisting of ciliated cells, mucus-secreting cells and glands (Figure 1 B). Foreign par- ticles in the nasal cavity or upper respiratory tract are trapped in mucus, carried back to the throat, and swallowed. From the lower respiratory tract foreign particles are brought up by the ciliary action of epithelial cells. In the alveoli that lack cilia or mucus, macrophages are responsible for destroying particles (Figure 1). Binding to the host cells The main targets of the influenza virus are the columnar epithelial cells of the respi- ratory tract. However, this simplified model is often insufficient to explain viral tropism since the receptor distribution in the host is generally more widespread than the observed virus tro- pism. Hosts may prevent the attachment by several mechanisms: (1) specific immune response and secretion of specific IgA antibodies, (2) unspecific mechanisms, such as mucociliary clearance or production of mucoproteins that able to bind to viral hemagglutinin, and (3) genetic diversifi- cation of the host receptor (sialic acid), which is highly conserved in the same spe- cies, but differs between avian and human receptors (Matrosovich 2000). As a re- sult, the avian virus needs to undergo mutations at the receptor binding site of he- magglutinin to cross the interspecies barrier between birds and humans. In pigs, polymorphisms of sialic acid species and linkage to galactose of both humans and birds are co-expressed in the tissue. Therefore, co-infection with avian and human influenza can occur in pigs and allow genetic reassortment of antigenic properties of both species in the co-infected cells. Recently, it has been shown that certain avian influenza viruses in human and birds are able to bind to different target cells (Matrosovich 2004). This could explain the observation of several cases since the end of the 1990s with transmission of avian influenza directly from poultry to hu- mans. H5N1 and some other subtypes of influenza A virus are able to bind to re- ceptors in the human eye (Olofson 2005). Pathogenesis 95 As essential as the binding of the influenza virus is its cleavage from the binding site at the host cell. The virulence of the influenza virus depends on the compatibility of neura- minidase with hemagglutinin. A virulent virus which has undergone mutations in the hemagglutinin needs compensatory mutations in the neuraminidase to maintain its virulence (Baigent & McCauley 2003, Hulse 2004). As a consequence, viral fitness and virulence were found to be reduced in influenza viruses resistant to neu- raminidase inhibitors (Yen 2005). Once the cell membrane and the virus have been closely juxtaposed by virus- + receptor interaction, the complex is endocytosed. Cellular proteases are often required to cleave viral proteins to form the mature in- fectious virus particle. In humans, the replication of the influenza virus is generally restricted to the epithelial cells of the upper and lower respiratory tract. This is be- cause of the limited expression of serine protease, tryptase Clara, secreted by non- ciliated Clara cells of the bronchial epithelia. This may cause altered tropism and additional sites of rep- lication in animals and humans (Gamblin 2004). Thus, H5N1 viral replication in humans may be restricted to the respiratory and intestinal tract in contrast to disseminated infections documented in other mammals and birds. Once influenza has efficiently infected respiratory epithelial cells, replication oc- curs within hours and numerous virions are produced. Infectious particles are pref- erentially released from the apical plasma membrane of epithelial cells into the air- ways by a process called budding. This favors the swift spread of the virus within the lungs due to the rapid infection of neighboring cells. This would explain why many of the individuals infected with avian influenza (H5N1) in Hong Kong had gastrointestinal, hepatic, and renal, as well as respiratory symptoms and why viruses from these patients were neurovirulent in mice (Park 2002). Whether these symptoms result from hematogenic spread or reflect non-pulmonal means of viral entry into the host re- mains unclear. These findings suggest a means by which influenza A viruses, and perhaps other viruses as well, could become highly pathogenic in humans. Finally, animal studies have revealed that the site of inoculation can determine the pathway of spread of the influenza virus in the host. Although a frequent disease, the specific inflammatory patterns or regulation of immune response and the pathogenesis of cytopathic effects in human influenza is incompletely understood. Cytokines and fever A central question is how an infection essentially localized to the respiratory tract can produce such severe constitutional symptoms. As in many other infectious dis- eases, it is the unspecific and adaptive immune response that contributes substan- tially to the clinical signs and symptoms in influenza and finally to the control of infection. Cytokines, rapidly produced after infection by epithelial and immune cells of the respiratory mucosa, are local hormones that activate cells, especially within the immune system. For example, influenza infection induces in human plasmacytoid and myeloid dendritic cells a chemokine secretion program which allows for a coordinated attraction of the different immune effectors (Piqueras 2005, Schmitz 2005). Most of these cytokines have been detected in nasopharyngeal washes of humans who have been experimentally or naturally infected with influenza (Brydon 2005). It is proposed that these cytokines, produced locally or systemically following in- teraction of exogenous pyrogens (e. There is a small area in the hypothalamus, called the Organum vasculosum laminae terminalis, which has a reduced blood-brain-barrier and allows the passage of pyrogens. At this site, in a dose-dependent manner, they induce the production of prostaglandins and especially prostaglandin E2. These mediators in- crease the thermostatic set point and trigger complex thermoregulatory mechanisms to increase body temperature. The fact that none of the cytokines mentioned above correlated with the severity of disease in influenza infection, argues in favor of their pleiotropy and cross-talk amongst signaling pathways. Individual virion components were, however, not pyrogenic probably explaining why whole virus vaccines can produce influenza-like symp- toms while subunit vaccines do not (Brydon 2005).

Several recent studies in patients with degenerative discount zetia 10mg free shipping cholesterol function, calcific aortic stenosis have identified smoking purchase 10mg zetia overnight delivery cholesterol levels ati, hyperlipidaemia generic zetia 10 mg visa cholesterol test scotland, elevated creati- nine 10 mg zetia sale cholesterol levels european standards, and hypocalcaemia as risk factors for the progression of disease (32–34). Aggressive prevention strategies would seem appropriate for patients with rheumatic disease as well, if only to reduce the incidence of coronary heart disease events, although specific data are lacking. Physical activity need not be restricted in patients with mild aortic 2 stenosis (valve area >1. Severe aortic stenosis usually mandates a reduction in physical activities to low levels (9). Aortic regurgitation Patients with chronic, severe aortic regurgitation usually enjoy a long, yet variable compensated phase characterized by an increase in left ventricular end-diastolic volume, an increase in chamber compliance, and a combination of both eccentric and concentric hypertrophy. Preload reserve is maintained, ejection performance remains normal, and the enormous increase in stroke volume allows preservation of forward output (9). In contrast to the haemodynamic state associated with mitral regurgitation, however, left ventricular afterload progres- sively increases. Vasodilators can favorably alter these load- ing conditions and may extend the compensated phase of aortic regur- gitation prior to the development of symptoms or left ventricular systolic dysfunction (defined as a subnormal resting ejection fraction) that would prompt valve replacement. Preoperative left ventricular function is the most important predictor of postoperative survival. The natural history of asymptomatic patients with normal systolic function has been well characterized. The rate of progression to symptoms and/or systolic dysfunction has been estimated at less than 6% per year. Asymptomatic patients with left ventricular dysfunction, how- ever, develop symptoms (angina, heart failure) at a rate of >25% per year, and symptomatic patients with severe aortic regurgitation have an expected mortality that exceeds 10% per year (9). Asymptomatic patients with normal left ventricular systolic function should avoid isometric exercises, but can otherwise pursue all forms of physical activities including, in some instances, 62 competitive sports. Symptoms or left ventricular dysfunction should prompt a limitation of activities. Vasodilating agents are recommended for the treatment of patients with severe (3–4+/4+) aortic regurgitation under one of three circum- stances (9): (i) short-term administration in preparation for aortic valve replacement in patients with severe heart failure symptoms, or significant left ventricular systolic dysfunction; (ii) long-term adminis- tration in patients with symptoms or left ventricular systolic dysfunc- tion who are not considered candidates for valve replacement surgery because of medical comorbidities or patient preference; (iii) long- term administration in asymptomatic patients with normal left ven- tricular systolic function to extend the compensated phase of aortic regurgitation prior to the need for valve replacement surgery. Vasodi- lator therapy is generally not recommended for asymptomatic patients with mild-to-moderate aortic regurgitation unless systemic hypertension is also present, as these patients generally do well for years without medical intervention. The goal of long-term therapy in appropriate candidates is to reduce the systolic pressure (afterload), though it is usually difficult to achieve low-to-normal values owing to the augmented stroke volume and preserved contractile function at this stage. Several small studies have demonstrated haemodynamically benefi- cial effects with a variety of vasodilators, including nitroprusside, hydralazine, nifedipine, enalapril and quinapril (27). These agents generally reduce left ventricular volumes and regurgitant fraction, with or without a concomitant increase in ejection fraction. Only one study, which compared long-acting nifedipine (60mg bid) with digoxin in 143 patients followed for six years, has demonstrated that vasodilator therapy can favorably influence the natural history of asymptomatic severe aortic regurgitation (35). The use of nifedipine in this study was associated with a reduction in the need for aortic valve surgery from 34% to 15% over six years. Whether angiotensin converting enzyme inhibitors can provide similar long-term effects has not been conclusively demonstrated in large numbers of patients. Finally, it is important to note that vasodilator therapy is not a substi- tute for surgery once symptoms and/or left ventricular systolic func- tion intervene, unless there are independent reasons not to pursue aortic valve replacement. Diuretics are recommended to relieve symptoms of pulmonary congestion (dyspnea, orthopnea). Extrapo- lating from studies of patients with dilated cardiomyopathy, digoxin and spironolactone may be of symptomatic and survival benefit when added to diuretics and angiotensin converting enzyme inhibitors, al- though data from prospective studies in patients with valvular heart 63 disease are lacking. As noted previously for patients with acute severe aortic regurgitation, beta-blockers, which can slow the heart rate and thus allow greater time for diastolic regurgitation, are contra- indicated. The loss of the atrial contribution to ventricular filling with the onset of fibrillation, as well as a rapid ventricular rate, can result in sudden and significant haemodynamic deterioration. Cardiover- sion is advised whenever feasible, with the same caveats regarding anticoagulation for thromboembolic prophylaxis, as reviewed above. Mixed aortic stenosis/regurgitation Management of patients with mixed aortic valve disease can be quite challenging and depends, in part, on the dominant lesion. Clinical assessment requires integration of both physical examination and echocardiographic data. Symptoms may develop and indications for surgery may be met before the traditional anatomic (valve area) and haemodynamic (ejection fraction) thresholds are reached. The nondominant lesion may exacerbate the pathophysiology im- posed by the dominant lesion. Diuretic and/or vasodilator therapies may alter loading conditions in favorable or unfavorable ways, though the former is usually well tolerated in patients with pulmonary con- gestion. Beta-blockers should be avoided; digoxin may be of benefit once left ventricular systolic function has declined, though its use remains largely empirical. In general, management should be predicated on the identification of the dominant valve lesion and location, though it is recognized that the proximal valve lesion(s) may mask the presence and significance of the more distal valve lesion(s). Thus, the signs of left ventricular volume overload with aortic regurgitation may be attenuated by the presence of significant mitral stenosis, as obstruction to left ventricu- lar inflow restricts filling. Other common combinations include mitral stenosis with tricuspid regurgitation (usually secondary to pulmonary hypertension and right ventricular dilatation), and aortic stenosis with mitral regurgitation. Intermittent or chronic diuretic use to treat symptoms of pulmonary or systemic venous congestion is usually well tolerated. The use of vasodilators must be individualized and depends on the dominant valve lesion, as well as on the expected contribution of the nondominant lesion(s). Percutaneous mitral balloon valvotomy and the new demographics of mitral stenosis. Contrasting progression of mitral stenosis in Malayans versus American-born Caucasians. Influence of surgery on the natural history of rheumatic mitral and aortic valve disease. Extreme pulmonary hypertension caused by mitral valve disease: natural history and results of surgery. Mitral valvular disease: a clinicopathologic survey of the conditions causing the mitral valve to function abnormally. Usefulness of anticoagulant therapy in the prevention of embolic complications of atrial fibrillation. Placebo controlled, randomized trial of warfarin and aspirin for prevention of thromboembolic complications in chronic atrial fibrillation. The effect of low dose warfarin on the risk of stroke in patients with non- rheumatic atrial fibrillation. Warfarin in the prevention of stroke associated with nonrheumatic atrial fibrillation. Transesophageal echocardiographically facilitated early cardioversion from atrial fibrillation using short term anticoagulation: final results of a prospective 4. Use of transesophageal echocardiography to guide cardioversion in patients with atrial fibrillation. Effects of a single oral dose of captopril on left ventricular performance in severe mitral regurgitation. Comparison of single dose nifedipine and captopril for chronic severe mitral regurgitation. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. A case control investigation of the relationship between hyperlipidemia and aortic valve stenosis. Nifedipine in asymptomatic patients with severe aortic regurgitation and normal left ventricular function.

Radical cystectomy in both sexes must not include the removal of the entire urethra in all cases cheap 10 mg zetia mastercard cholesterol ratio values, which may then serve as outlet for an orthotopic bladder substitution purchase 10mg zetia overnight delivery delicious cholesterol lowering foods. Terminal ileum and colon are the intestinal segments of choice for urinary diversion buy zetia 10mg cholesterol test galway. Positive margins anywhere on the bladder specimen (in both sexes) zetia 10mg with visa cholesterol numbers chart canada, if the primary tumour is located at the bladder neck or in the urethra (in women), or if tumour extensively infiltrates the prostate. Before cystectomy, the patient should be counselled adequately regarding all possible alternatives, and the final decision should be based on a consensus between patient and surgeon. For patients with inoperable locally advanced tumours (T4b), primary radical cystectomy is a palliative option and not recommended as a curative treatment. External beam radiotherapy [35, 36] External beam radiotherapy alone should only be considered as a therapeutic option when the patient is unfit for cystectomy or a multimodality bladder-preserving approach Radiotherapy can also be used to stop bleeding from the tumour when local control cannot be achieved by transurethral manipulation because of extensive local tumour growth. Chemotherapy [37,38] Although cisplatin-based chemotherapy, as primary therapy for locally advanced tumours in highly selected patients, has led to complete and partial local responses, the long-term success rate is low. Multimodality treatment [39,40] There are comparable long-term survival rates in cases of multimodality treatment success. Adjuvant Chemotherapy Adjuvant chemotherapy is advised within clinical trials, but not for routine use. Post-chemotherapy surgery after a partial or complete response may contribute to long-term disease-free survival. Second-line treatment: In patients progressing after platinum-based combination chemotherapy for metastatic disease vinflunine should be offered, which has the highest level of evidence to date, or clinical trials of other treatments. Follow-up for non-muscle invasive bladder tumours [48, 49] Patients with non-muscle invasive bladder tumours need to be regularly followed up because of the risk of recurrence and progression; however, the frequency and duration of cystoscopies should reflect the individual patient’s degree of risk. Recommendations for follow-up cystoscopy Patients with tumours at low risk of recurrence and progression should have a cystoscopy at 3 months. If negative, the following cystoscopy is advised at 9 months and consequently yearly for 5 years. Patients with tumours at high risk of progression should have a cystoscopy and urinary cytology at 3 months. If negative, the following cystoscopies and cytologies should be repeated every 3 months for a period of 2 years, every 4 months in the third year, every 6 months thereafter until 5 years, and yearly thereafter. Patients with intermediate-risk of progression (about one-third of all patients) should have an in-between follow-up scheme using cystoscopy and cytology, adapted according to personal and subjective factors. Patients with Tis should be followed up for life due to the high risk of recurrence and progression, both within the bladder and extravesically. Urine cytology together with cystoscopy (and bladder biopsies in cytology positive cases) is essential for monitoring of treatment efficacy. Follow up for muscle invasive bladder cancer Follow-up is based on the stage of initial tumour after cystectomy. At every visit, the following should be performed: 65 History, Physical examination, Serum chemistries and chest radiograph annually for pT1 disease; semiannual evaluation for patients with pT2 disease; and quarterly evaluation for patients with pT3 disease. After 5 years of follow-up, stop oncological surveillance and continue with functional surveillance. Ultrasound of abdomen and pelvis - to localize the cause of hematuria like renal and bladder tumours. Standard operating procedure: j) Inpatient: k) Outpatient: l) Daycare: Referral criteria: Patients with gross painless hematuria known to have bladder tumour Positive urine dipstick or microscopic hematuria Positive urine cytology *Situation 2: At super specialty facility in metro location where higher end technology is available. Nurse – counseling, preoperative preparation, essential post-operative care, stoma care and follow-up p. Bladder cancer risk following primary and adjuvant external beam radiation for prostate cancer. Detrusor muscle in the first, apparently complete transurethral resection of bladder tumour specimen is a surrogate marker of resection quality, predicts risk of early recurrence, and is dependent on operator experience. An updated critical analysis of the treatment strategy for newly diagnosed high-grade T1 (previously T1G3) bladder cancer. Seven years´ experience with 5-aminolevulinic acid in detection of transitional cell carcinoma of the bladder. Clinical significance of the ‘palpable mass’ in patients with muscle infiltrating bladder cancer undergoing cystectomy after pre-operative radiotherapy. The World Health Organization/International Society of Urological Pathology consensus classification of urothelial (transitional cell) neoplasms of the urinary bladder. Primary superficial bladder cancer risk groups according to progression, mortality and recurrence. Treatment of carcinoma in situ with intravesical bacillus Calmette-Guerin without maintenance. Clinical outcomes of bacillus Calmette- Guérin instillation therapy for carcinoma in situ of urinary bladder. A single immediate postoperative instillation of chemotherapy decreases the risk of recurrence in patients with stage Ta T1 bladder cancer: a meta-analysis of published results of randomized clinical trials. Intravesical bacillus Calmette-Guerin reduces the risk of progression in patients with superficial bladder cancer: a meta- analysis of the published results of randomized clinical trials. Maintenance bacillus Calmette-Guerin immunotherapy for recurrent Ta, T1 and carcinoma in situ transitional cell carcinoma of the bladder: a randomized Southwest Oncology Group Study. Bacillus Calmette-Guerin versus chemotherapy in the intravesical treatment of patients with carcinoma in situ of the bladder: a meta-analysis of the published results of randomized clinical trials. Characteristics and outcomes of patients with carcinoma in situ only at radical cystectomy. Downstaging and pathoanatomical outcome following neoadjuvant cisplatinum based combination chemotherapy for muscle-invasive bladder carcinoma: An analysis of selected patients from two combined randomised prospective Nordic trials. Neoadjuvant chemotherapy in invasive bladder cancer: a systematic review and meta-analysis. Lymphadenectomy in patients with transitional cell carcinoma of the urinary bladder; significance for staging and prognosis. Delaying radical cystectomy for muscle invasive bladder cancer results in worse pathological stage. Radical cystectomy with or without prior irradiation in the treatment of bladder cancer. Radical radiotherapy for muscle invasive transitional cell carcinoma of the bladder: failure analysis. Neoadjuvant chemotherapy plus cystectomy compared with cystectomy alone for locally advanced bladder cancer. An update of selective bladder preservation by combined modality therapy for invasive bladder cancer. An interval longer than 12 weeks between the diagnosis of muscle invasion and cystectomy is associated with worse outcome in bladder carcinoma. A randomized comparison of cisplatin alone or in combination with methotrexate, vinblastine, and doxorubicin in patients with metastatic urothelial carcinoma: a cooperative group study. Carboplatinbased versus cisplatin-based chemotherapy in the treatment of surgically incurable advanced bladder carcinoma. Gemcitabine and carboplatin in advanced transitional cell carcinoma of the urinary tract: an alternative therapy. Stage Ta-T1 bladder cancer: the relationship between findings at first followup cystoscopy and subsequent recurrence and progression. A surveillance schedule for G1Ta bladder cancer allowing efficient use of check cystoscopy and safe discharge at 5 years based on a 25-year prospective database. A stage specific approach to tumour surveillance after radical cystectomy for transitional cell carcinoma of the bladder.

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