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There is a high probability of associated injuries (80-90%) mental health group topics cheap lyrica 75mg fast delivery, mainly intra-abdominal [184 mental disorders of winnie the pooh purchase lyrica online, 259] genetic mental disorders list 75mg lyrica overnight delivery. Although urethral injuries themselves are not directly life-threatening [14 mental health treatment modalities best 150mg lyrica, 243] mental disorders with pathological lying generic 75 mg lyrica overnight delivery, the association with pelvic fractures and concomitant injuries of the thorax mental treatment facilities in knoxville tn lyrica 75 mg, abdomen and spine, may be life-threatening [14, 256]. Erectile dysfunction occurs in approximately 45% of patients after traumatic posterior urethral rupture [260, 261]. The injury is usually a partial longitudinal tear of the anterior wall associated with vaginal laceration [244, 248]. Urethral injuries in females which extend into the bladder neck may disrupt the normal continence mechanism [264]. Urinary extravasation and bleeding may result in scrotal, penile and/or perineal swelling and ecchymosis, depending on the location and extent of the trauma [243, 248]. Failure to detect a rectal injury will cause significant morbidity and even mortality [265]. A rectal injury is suggested by blood on the examining finger and/or a palpable laceration [265]. Another sign of urethral injury is difficulty or an inability to pass a urethral catheter [265]. A female urethral injury should be suspected from the combination of a pelvic fracture with blood at the vaginal introitus, vaginal laceration, haematuria, urethrorrhagia, labial swelling and/or urinary retention [244, 247, 248]. Symptoms of urethral lesions caused by improper catheterisation or instrumentation are penile and/ or perineal pain (100%) and urethral bleeding (86%) [225]. Failure to diagnose accurately and treat urethral injuries may lead to significant long-term sequelae, mostly presenting as strictures [267, 268]. A retrograde urethrography is conducted by injecting 20-30 mL of contrast material while occluding the meatus, with a balloon of a Foley catheter inflated in the fossa navicularis. In an unstable patient, retrograde urethrography should be postponed until the patient has been stabilised [184, 244]. A urethrogram allows for identification of the site of injury and assessment of the extent of any injury [244, 265]. However, the distinction between a complete and partial rupture is not always clear [221]. A typical image for incomplete rupture shows extravasation from the urethra which occurs while the bladder is still filling. A complete rupture is suggested by massive extravasation without bladder filling [221]. The following classification of urethral injuries is based on retrograde urethrography (Table 4. In addition, it may allow a guidewire to be passed into the bladder for early catheterisation [244, 269]. Flexible cystoscopy is also recommended above retrograde urethrography in suspected penile fracture-associated urethral injury [264, 270, 271]. In females, where the short urethra precludes adequate, radiological visualisation, urethroscopy and vaginoscopy are the diagnostic modalities of choice [243, 244]. If the competence of the bladder neck is not clear upon antegrade cystourethrography, suprapubic cystoscopy is then advised [243]. Treatment decisions are based mainly on the type of injury (blunt, penile fracture associated or penetrating). The therapeutic options are suprapubic diversion or (a trial of) early endoscopic realignment with transurethral catheterisation [244]. Urinary diversion is maintained for 2 and 3 weeks for partial and complete ruptures, respectively [246]. Satisfactory urethral luminal recanalisation may occur in up to 68% after partial ruptures, but is rare after complete ruptures [246, 272]. The strategy consists of closing the tear in the cavernosal tunica albuginea, while the concomitant tear in the urethra is repaired at the same time [273]. A small laceration can be repaired by simple closure, while a complete rupture requires an anastomotic repair [273, 274]. Devitalised tissues should be debrided, although urethral and spongiosal debridement should be kept to a minimum due to the excellent vascularisation [252, 264]. For small lacerations and stab wounds, simple urethral closure might be sufficient [243]. In the case of longer defects or apparent infection (particularly bite wounds), a staged repair with urethral marsupialisation and a suprapubic catheter is needed [250, 252]. Insertion of a suprapubic catheter is always a good solution in urgent situations [243, 264]. However, insertion of a suprapubic catheter is not without risk, especially in the unstable trauma patient where the bladder is often displaced by the pelvic haematoma or because of poor bladder filling due to haemodynamic shock or concomitant bladder injury. In these circumstances, an attempt of urethral catheterisation can be carried out by experienced hands. It is extremely unlikely that the gentle passage of a urethral catheter will do any additional damage [221, 244, 248, 254, 255, 275]. Urethrography should be performed at 2-weekly intervals until healing has occurs [266, 276]. Injuries may heal without significant scarring or obstruction if managed by diversion alone [264]. For short (< 2 cm), non-obliterative strictures, internal urethrotomy can be attempted, with a 50-90% success rate [272, 277, 279]. For longer strictures, or in the case of failure of an internal urethrotomy, urethroplasty is required [277]. Using a flexible/rigid cystoscope and biplanar fluoroscopy, a guidewire is placed inside the bladder. If necessary, two cystoscopes can be used: one retrograde (per urethra) and one antegradely (suprapubic route through the bladder neck) [272, 277, 278]. The duration of catheter stay varies between 4 and 8 weeks among series [265, 272, 277, 278]. It is important to avoid traction on the Foley balloon catheter since it can damage the remaining sphincter mechanism at the bladder neck. Concomitant bladder neck or rectal injuries or presence of bony fragments inside the bladder must be repaired immediately. Early exploration is indicated to evacuate contaminated haematomas and to perform colostomy if necessary. Immediate endoscopic realignment can also be performed when the patient is on the operating table for other surgery. Early endoscopic realignment (immediate or delayed primary, see below) is also possible in a stable patient without significant concomitant injuries [277, 278]. With modern endoscopic realignment procedures, acceptable complication rates have been reported for stricture formation (14-79%), incontinence (< 5%) and impotence (10-55%) [277, 278]. Differences between series in the rates of incontinence, impotence and re-stricture can be explained by differences in patient selection (severe vs. Furthermore, these differences make the comparison with other techniques difficult, especially with urethroplasty [265, 272, 277, 278]. Another problem is the risk of uncontrolled bleeding following entry into the pelvic haematoma, which may result in uncontrolled re-bleeding [244]. Because of disturbingly high rates of impotence (56%), incontinence (21%) and strictures (69%) [276], immediate urethroplasty cannot be recommended and should only be done in experienced centres [281, 282] 4. Delayed primary realignment requires the placement of a suprapubic tube at the time of initial injury, with endoscopic realignment performed within 14 days. At that time, patients are stable and most of the pelvic bleeding has resolved [276, 278]. The aim and proposed benefits of delayed primary realignment are the same as mentioned for immediate realignment. It is restricted to stable patients with a short distraction defect, who are able to lie down in the lithotomy position [283]. Considering the limited accumulated experience with this approach, it cannot be generally recommended [283, 285, 286]. Supporters of early versus delayed intervention state that it does not affect the outcome of an eventual subsequent urethroplasty [281, 287]. However, some authors have reported worse outcomes of subsequent urethroplasty after failed initial urethral manipulation (realignment or urethroplasty) [282, 283, 288]. Due to this concern and the excellent results obtained with deferred urethroplasty, early realignment or urethroplasty should only be selectively performed in highly experienced centres [281, 282]. Treatment options for these posterior urethral strictures are deferred urethroplasty (4. After 3 months of suprapubic diversion, the pelvic haematoma is nearly always already resolved, the prostate has descended into a more normal position and the scar tissue has stabilised [283] and the patient is clinically stable and able to lie down in the lithotomy position [243, 244]. Most posterior urethral distraction defects are short and can be treated using a perineal anastomotic repair [243, 283]. The key objective of the operation is to achieve a tension-free anastomosis between two healthy urethral ends. Most urethral stenoses are short and can be treated by mobilisation of the bulbar urethra, with or without separation of the corpora cavernosa [283]. This is in contrast to the situation in developing countries, where stenoses are more complex, and where additional manoeuvres, such as inferior pubectomy and supracrural rerouting or a combined abdominoperineal approach are needed more often [279, 291]. A number of situations may prevent the use of perineal anastomotic repair, either as an initial or as a salvage therapy. This is seldom required and most patients that require flap urethroplasties have previous failed repairs of posterior urethral rupture [264]. Fistulae these might require a combined abdominoperineal approach to secure adequate closure [291]. Synchronous anterior urethral the presence of anterior urethral stricture may compromise the blood supply stricture to the bulbar urethra following division of the bulbar arteries. Urinary incontinence the distal urethral sphincter mechanism can be defunctionalised by urethral distraction, so that urinary continence is maintained primarily by the proximal bladder neck sphincter. Concomitant bladder neck injury might increase incontinence and should require an abdominoperineal procedure to allow simultaneous bladder neck and urethral reconstruction [243, 264, 291]. Outcome after deferred urethroplasty is excellent with a stricture rate of around 10% [289, 296]. Decompression of the erectile nerves after excision of the scar tissue might explain the amelioration of erectile function after urethroplasty [297]. Incontinence is rare with deferred urethroplasty (< 4%) [283] and is usually due to incompetence of the bladder neck [264, 291]. Standard therapy is a deferred urethroplasty at a minimum of 3 months after trauma, using a one-stage perineal approach whenever possible. The results of this technique are poor [298, 299] and the procedure is therefore not recommended. For short, non-obliterative strictures following realignment or urethroplasty, direct vision urethrotomy can be performed [292] while in other cases, urethroplasty is warranted. If possible, immediate exploration by the retropubic route and primary repair or realignment can be performed [184, 259, 264]. In those cases, suprapubic diversion with delayed abdominoperineal urethroplasty is advised [184, 252, 259]. Concomitant vaginal lacerations are repaired transvaginally at the same time [244, 247, 265, 266]. Distal urethral injuries can be managed vaginally by primary suturing and closure of the vaginal laceration [244, 266]. Nevertheless, distal urethral injuries can be left unrepaired and hypospadiac since they do not disrupt the sphincteric mechanism [244, 247, 265, 266]. In difficult cases, catheter insertion may be assisted by cystoscopy and guidewire placement [302], and suprapubic catheterisation is an alternative. Endoscopic management, either with incision or resection, can successfully treat iatrogenic prostatic urethral strictures. Indwelling catheter placement or an open procedure (which is associated with increased morbidity) are alternatives [303]. Urethral lesions following radiotherapy are often more difficult to treat and may require complex reconstructive surgery [236, 237]. If patient unstable or If patient unstable or important associated important associated non-urological Assess for acute surgical indications: non-urological Suprapubic injuries, suprapubic bladder neck injury, rectal tear, injuries, suprapubic cystostomy cystostomy pie-in-the-sky bladder cystostomy No Yes Suprapubic tube + Suprapubic endoscopic re-alignment. In industrialised societies pelvic 3 fracture-related injuries of the posterior urethra are the most common non-iatrogenic injuries. Erectile dysfunction occurs in 20-60% of patients after traumatic urethral rupture. B Delayed formal urethroplasty is the procedure of choice for the treatment of posterior urethral B distraction defects. Partial posterior urethral ruptures should be treated by urethral or suprapubic catheterisation. Implementing training programmes on urinary catheter insertion significantly improves the rate of 2b catheter-related complications. A Urethral instrumentation should only be carried out when there are valid clinical indications.

Furthermore mental mood disorders list lyrica 75mg free shipping, not all these patients are willing or represent good surgical candidates disorders of brainpop jr 75mg lyrica otc. Therapies are generally aimed at reversing insulin resistance with the hope that this also reverses fatty acid accumulation and its consequences psychology today conditions mental retardation purchase lyrica with american express. Therapy is also aimed at preventing or reversing the hypothesized second hit phenomenon of increased oxidative stress mental illness books effective 150mg lyrica. Shaffer 422 Table 4 lists agents used in clinical trials or only in animal models mental illness korea discount 75 mg lyrica free shipping, with the rationale of their use mental health zephyrhills cheap lyrica 75mg free shipping. Because insulin resistance is a major pathogenic component of fatty liver, drugs used in treatment of diabetes have been used extensively in this condition. Recall, however, that the relationship between insulin resistance and liver histology is poor (Ratziu 2010). Other agents affect lipid transport, while still others have been used to concentrate on reducing oxidative damage and mitochondrial injury. Also, because the second hit is accompanied by inflammatory cytokines, inhibitors of tumor necrosis alfa have been studied, with varying success. These include both herbal products and the currently popular probiotics [exogenous bacteria which bypass digestion and confer health benefits to the host]. These bacteria affect many gut functions and improve gut barrier permeability, which could decrease bacterial translocations limiting hepatic second hit injury. Trial outcome of drugs or specific dietary agents have been variable and follow-up has been relatively short. This study showed that metformin but not pioglitazones improved serum biochemistry, as compared with vitamin E. Table 5 outlines the agents, the numbers of studies analyzed, and the odds ratios with significance for outcome of trials with comparisons of pre and post treatment liver biopsies. Agents, the number of studies included in analysis summary odds ration and statistical significance is listed. Antioxidants and metformin fit a Random model better in fat and inflammation, these results are derived from reference (Musso 2010). Based on these analyses, the glitazones hold the best promise at this time, with Pioglitazone being the most successful. Adverse side effects are low, although body weight gain, mild congestive heart failure, and osteopenia with fractures have been described (Ratziu 2010). Overall changes in lifestyle should be implemented first, or also in conjunction with any pharmaceutical therapy. Results based on reference (Choi 2010) Agent Number of Steatosis Inflammation Fibrosis studies Bariatric surgery 15 91. Epidemiology Liver disease is the fourth commonest cause of death in adults between the ages of 20 to 70 years in Canada. Alcohol is still one of the commoner causes of chronic liver disease in this country. The mechanism for the predisposition of certain people to develop cirrhosis is still unknown. The amount of alcohol ingested has been shown in epidemiological studies to be the most important factor in determining the development of cirrhosis. Males drinking in excess of 60 gm and females in excess of 40 gm of alcohol per day for 10 years are at a high risk of developing cirrhosis. The alcohol content rather than the type of beverage is important and binge drinking is less injurious to the liver than continued daily drinking. They are likely to develop cirrhosis at an earlier age, present at a later stage and have more severe liver disease with more complications. Social factors such as the availability of alcohol and social acceptance of alcohol use can also encourage the liberal use of alcohol, thereby increasing the risk for the development of alcoholic liver disease in susceptible individuals 2. Alcohol Metabolism Alcohol is metabolized to acetaldehyde by alcohol dehydrogenase in the hepatocyte cytosol, and then to acetate by acetaldehyde dehydrogenase in the mitochondria. Some studies have reported an increased frequency of the gene that encodes for alcohol dehydrogenase in patients with alcoholic liver disease, leading to increased production of acetaldehyde. Alcoholics with decreased acetaldehyde dehydrogenase activity also develop alcoholic liver disease at a lower cumulative intake of alcohol than others. Alcohol has a direct hepatotoxic effect and does not require pre-existing malnutrition, but malnutrition may play a permissive role in producing alcohol hepatotoxicity. There is a threshold of alcohol toxicity beyond which no dietary supplements can offer protection. Obesity may also be an independent risk factor for the development of alcoholic liver disease. Finally, viral hepatitis, whether hepatitis B or hepatitis C infection, appears to play a role in the development of advanced alcoholic liver disease. Patients with alcoholic liver disease and viral hepatitis infection tend to develop their disease at a younger age, have more severe histological features and decreased survival. In addition, the presence of viral hepatitis is a major risk factor for the development of hepatocellular carcinoma in patients with alcoholic cirrhosis. The spectrum of liver disease covers the relatively benign steatosis to the potentially fatal alcoholic hepatitis and cirrhosis (Figure 1). Shaffer 427 Excess alcohol Fatty liver resolves with abstinence Heavy alcoholic binge (>60 gm in men and >40 gm without eating in women for >10 years) Alcoholic hepatitis Alcoholic cirrhosis Complications of portal hypertension, and Hepatoma Figure 1. Schematic representation of the progression of the different stages of alcoholic liver disease 3. Alcoholic Fatty Liver this is the most frequent hepatic abnormality found in alcoholics. It is a toxic manifestation of alcohol ingestion, appearing within three to seven days of excess alcohol intake. This results in the accumulation of triglyceride in the hepatocytes, mainly in the terminal hepatic venular zone. The fat may be macrovesicular (large droplets) or microvesicular (small droplets), which represents more active lipid synthesis by the hepatocytes. Fatty liver may occur alone or be part of the picture of alcoholic hepatitis or cirrhosis. Clinically, the patient is usually asymptomatic and examination reveals firm smooth hepatomegaly. Occasionally the fatty liver may be so severe that the patient is anorexic, nauseated and has right upper quadrant pain or discomfort. The differential diagnoses include obesity, insulin resistance, hyperlipidemia, malnutrition, and various medications. Attribution of fatty liver to alcohol use therefore requires a detailed and accurate patient history. In the case that the fatty liver is related to excess alcohol intake, this usually follows a prolonged heavy alcoholic binge. In the absence of a super-imposed hepatic process, stigmata of chronic liver disease such as spider angiomas, First Principles of Gastroenterology and Hepatology A. Liver biopsy is required to make a definitive diagnosis and to exclude the presence of steatohepatitis. When fatty liver is not associated with alcoholic hepatitis, the prognosis is excellent. Complete abstinence from alcohol and a nutritious diet will lead to disappearance of the fat over four to six weeks. Alcoholic Hepatitis Alcoholic hepatitis may occur separately or in combination with cirrhosis. This oxidative stress promotes hepatocyte necrosis and apoptosis, which is exaggerated in the alcoholic individual who is deficient in antioxidants such as glutathione and vitamin E. Free radicals then initiate lipid peroxidation, which causes inflammation and fibrosis. Inflammation is also incited by acetaldehyde that, when bound covalently to cellular proteins, forms adducts that are antigenic. Alcohol is known to cause an exaggerated gradient of hypoxia from the portal vein to the central vein, suggesting that the hypoxia induced by chronic alcohol use may also contribute to hepatic damage. Histologically, hepatocytes are swollen due to an increase in intracellular water secondary to increase in cytosolic proteins (Table 1). Alcoholic hyaline or Mallory bodies are purplish red intra-cytoplasmic inclusions consisting of clumped organelles, intermediate microfilaments (Figure 2). Polymorphs are seen surrounding Mallory containing cells and also within damaged hepatocytes. Neither fatty infiltration nor Mallory bodies are specific for alcoholic hepatitis nor are they necessary for diagnosis. It is maximal in zone 3 and extends in a perisinusoidal pattern to enclose hepatocytes, giving it a "chicken wiring" effect. Marked portal inflammation suggests an associated viral hepatitis such as hepatitis C, whereas fibrosis suggests complicating chronic hepatitis (Table 2). When the acute inflammation settles, a varying degree of fibrosis is seen which may eventually lead to cirrhosis. Photomicrograph showing Mallory bodies (arrow) and inflammatory cells, especially polymorphs, in a patient with acute alcoholic hepatitis. Clinically, mild cases of alcoholic hepatitis are only recognized on liver biopsy in patients who present with a history of alcohol abuse and abnormal liver function tests. In the moderately severe case, the patient is usually malnourished and presents with a two to three week prodrome of fatigue, abdominal pain, anorexia, nausea and weight loss. In the most severe case, which usually follows a period of heavy drinking without eating, the patient is gravely ill with fever, marked jaundice, ascites, evidence of a hyperdynamic circulation, such as systemic hypotension, and tachycardia. Hepatic decompensation can be precipitated by vomiting, diarrhea or intercurrent infection leading to encephalopathy. Gastrointestinal bleeding is common, due to the combination of a bleeding tendency and portal hypertension. Mayo Clinic Gastroenterology and Hepatology Board Review 2008: page 331 with permission. Patients with acute alcoholic hepatitis often deteriorate during the first few weeks in hospital, with a mortality rate of 20-50%. The condition may take one to six months to resolve even with complete abstinence. Long-term survival in patients with alcoholic hepatitis who discontinue alcohol is significantly better than in those who continue to drink, although it remains considerably below that of an age matched population. Three-year survival approaches 90% in abstainers, whereas it is less than 70% in active drinkers. Comparison of viral hepatitis and alcoholic hepatitis based on history and physical examination, laboratory tests and liver histology. Alcoholic Cirrhosis Established cirrhosis is usually a disease of middle age after the patient has had many years of drinking. Although there may be a history of alcoholic hepatitis, cirrhosis can develop in apparently well-nourished, asymptomatic patients. Occasionally, the patient may present with end-stage liver disease with malnutrition, ascites, encephalopathy and a bleeding tendency. Hepatomegaly is often present, affecting predominantly the left lobe due to marked hypertrophy and there are signs of portal hypertension including splenomegaly, ascites and distended abdominal wall veins. There may be signs of alcohol damage in other organ systems such as peripheral neuropathy and memory loss from cerebral atrophy. These include lgA nephropathy, renal tubular acidosis and the development of hepatorenal syndrome. The diagnosis of alcoholic cirrhosis rests on finding the classical signs and symptoms of end-stage liver disease in a patient with a history of significant alcohol intake. Liver biopsy is encouraged, especially when the diagnosis is in question, since patients usually under report the amount of alcohol consumed. In addition to confirming the diagnosis, liver biopsy is also useful for ruling out other unsuspected causes of liver disease, better characterizing the extent of the damage, providing prognosis, and guiding therapeutic decision making. The degree of steatosis is variable and alcoholic hepatitis may or may not be present. When marked, genetic hemochromatosis has to be First Principles of Gastroenterology and Hepatology A. With continued cell necrosis and regeneration, the cirrhosis may progress to a macronodular pattern. Biochemical abnormalities include a low serum albumin, elevated bilirubin and aminotransferases. Portal hypertension results in hypersplenism leading to thrombocytopenia, anemia and leukopenia. Other non-specific serum changes in acute and chronic alcoholics include elevations in uric acid, lactate and triglyceride, as well as reductions in glucose, potassium, phosphate and magnesium. The prognosis of alcoholic cirrhosis depends on whether the patient can abstain from alcohol, this in turn is related to family support, financial resources and socio-economic state. Patients who abstain have a five-year survival rate of 60 to 70%, which falls to 40% in those who continue to drink. Complete abstinence may not improve prognosis when portal hypertension is severe, although at the earlier stage of cirrhosis, the portal pressure may actually fall with abstinence. Hepatocellular carcinoma occurs in 10% of stable cirrhotics and the incidence is higher in patients who also have viral hepatitis infection. This usually develops after a period of abstinence and macronodular cirrhosis is present. Treatment strategies can be instituted if detected early (see below), therefore long-term follow up and periodic screening is advisable.

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Microscopic examination of the urine sediment reveals neutrophils and occasional leukocyte casts occupational therapy and mental health 5th edition lyrica 75mg line. Laboratory studies show hyperlipidemia 32 A 22-year-old woman in the second trimester of pregnancy and hypoalbuminemia mental health parity act of 1996 cheap lyrica 150mg visa. Physi a prominent increase in the mesangial matrix developmental origins of brain disorders roles for dopamine buy discount lyrica online, forming nodu cal examination reveals costovertebral angle tenderness mental illness forum cheap lyrica 75mg otc. The patient has a history of repeated urinary tract (C) Diabetic glomerulosclerosis infections mental health lesson plans buy lyrica 150mg without prescription. Which of the following is the 37 Which of the following serum abnormalities is expected in the appropriate diagnosisfi Urine cultures reveal more than 100 child mental disorders list purchase generic lyrica from india,000 bacterial colonies composed predominantly of Gram-negative microorganisms. His blood pressure is Question 34 is related to which of the following conditionsfi She becomes hypotensive and obtunded and subse quently dies of hypovolemic shock. He subsequently suffers a 43 A 33-year-old woman in her third trimester of pregnancy massive stroke and expires. The patient is hypertensive and laboratory studies show that the patient manifests nephritic syndrome. Microscopic examination of the kidneys at autopsy reveals necrotic epithelial cells within the lumina of some tubules (shown in the image). Physi (D) Fanconi syndrome cal examination reveals a blood pressure of 190/110 mm Hg. Examination of the kidneys at autopsy the most likely underlying cause of chronic renal failure in reveals symmetrically shrunken small kidneys, with a uni this patientfi Funduscopic examination reveals several small retinal microaneurysms and cotton-like zones of retinal edema and necrosis. Hypertension in (A) Amyloidosis this patient is caused by the renal release of which of the fol (B) Hydronephrosis lowing hormonesfi He (E) Renin treated his garden last week with a number of herbicides and insecticides, some of which may have contained heavy met 49 A 6-year-old child develops fever, abdominal pain, and bloody als. This malignant neoplasm most likely originates from which of (A) Angiomyolipoma the following tissues in the kidneyfi Molec ular studies would most likely identify mutations in which of the following growth regulatory genesfi Microscopically, the tumor is composed of multiple (C) Lymphatics elements, including blastemal, stromal, and epithelial tissues. A fro zen section of a renal biopsy demonstrates birefringent, intra tubular deposits of uric acid crystals (shown in the image). This finding suggests that the patient has been treated recently for which of the following underlying conditionsfi Urinalysis shows high levels of vanillyl excruciating episodic (colicky) right fiank pain. He dies thereafter, and an (C) Polycystic kidney disease autopsy reveals abnormal kidneys (shown in the image). The (D) Staghorn calculi pathogenesis of this disease is most likely related to which of (E) Tubulointerstitial nephritis the followingfi Which of the following is the most likely cause of acute renal failure in this patientfi The patient develops oliguia shortly after transplantation and a renal biopsy shows immediate (hyperacute) rejection. Funduscopic examination reveals (B) Hereditary cystinuria small retinal microaneurysms and cotton-like zones of retinal edema and necrosis. What is the most likely (E) Infection cause of secondary hypertension in this young patientfi Renal dysplasia is effacement of visceral epithelial cell (podocyte) foot processes, characterized by undifferentiated tubular structures sur which allows protein to be lost from the plasma into the urine rounded by primitive mesenchyme, sometimes with hetero (proteinuria). The other choices are characterized by morpho topic tissue such as smooth muscle and cartilage. Renal dysplasia results from Diagnosis: Nephrotic syndrome, minimal change disease an abnormality in metanephric differentiation. Variants of renal dysplasia include aplastic, multicystic (seen in this case), 6 the answer is D: Postinfectious glomerulonephritis. In most patients with is illustrative of nephritic syndrome in the setting of poststrep multicystic renal dysplasia, a palpable fiank mass is discov tococcal glomerulonephritis. Unilateral multicystic renal dysplasia terized by hematuria (either microscopic or visible grossly), is the most common cause of an abdominal mass in newborns. It results in elevations of serum blood urea nitrogen and and the kidneys are usually very large. Medullary sponge kid creatinine, as well as oliguria, salt and water retention, edema, ney (choice B) is characterized by multiple small cysts in the and hypertension. Wilms tumor (choice E) may contain heterolo nephritic syndrome are caused by infiammatory changes in gous elements but does not form large cysts. Choices 2 the answer is A: Autosomal dominant polycystic kidney B, C, and E do not present with hematuria. Autosomal dominant polycystic kidney disease, Diagnosis: Postinfectious glomerulonephritis, nephritic which is characterized by enlarged multicystic kidneys, is the syndrome most common of a group of congenital diseases that are charac terized by numerous cysts within the renal parenchyma. Injury to the glomeru cases are caused by mutations in the polycystic kidney disease lar capillaries results in spillage of protein and blood cells into 1 gene, which encodes polycystin (function unknown). Hematuria is also seen in patients with bleeding of all patients eventually develop end-stage renal failure. Azotemia is common and, in half syndrome of patients, progresses to uremia (clinical renal failure) over a period of several years. Multicystic renal plastic plasma cells typically secrete a homogeneous immuno dysplasia (choice E) is usually unilateral. Amyloid nephropathy is caused by the depo sition of secreted lambda or kappa light chains in the glomer ular basement membranes and mesangial matrix. Renal amyloidosis usually presents with neph Diagnosis: Autosomal dominant polycystic kidney disease rotic syndrome. The deposits of amyloid may take on a nodu lar appearance, reminiscent of the Kimmelstiel-Wilson lesion 4 the answer is D: Pelvis. IgA fetal life, the kidneys are initially located in the lower abdo nephropathy (choice C) and membranous glomerulonephritis men. As development progresses, they normally move upward (choice D) are unrelated to light-chain disease. Kidneys that do not reach Diagnosis: Amyloid nephropathy, multiple myeloma the lumbar area but remain in the pelvis or presacral area are considered ectopic. Fusion of both kidneys results in so-called 9 the answer is A: Amyloid nephropathy. These conditions stimulate the production of 5 the answer is E: Nephrotic syndrome. The kidneys, liver, spleen, nephrotic syndrome is characterized by heavy proteinuria and adrenals are the most common organs involved. Renal the Kidney 191 amyloidosis leads to nephrotic syndrome (as in this case) and of membranous glomerulopathy is highly variable, with a renal failure. The other choices have not been linked to of renal function (50%), and renal failure (25%). Wegener granulomatosis proliferative glomerulonephritis type I (choice C) is a chronic (choice E) affects the lungs and kidneys, but bronchiectasis is immune complex disease that features granular deposition not a feature of this disease. Diagnosis: Membranous glomerulopathy 10 the answer is C: Minimal change disease, focal segmental glomerulosclerosis. Minimal change glomerulopathy causes 14 the answer is E: Subepithelial deposits of immune 90% of the nephrotic syndrome in young children and 15% complexes. Proteinuria is generally more selective (albumin > tion of immune complexes in the subepithelial zone (between globulins) than in the nephrotic syndrome caused by other the visceral epithelial cell and the glomerular basement mem diseases, but there is too much overlap for this selectivity to brane) as a result of immune complex formation in situ or the be used as a diagnostic criterion. Granular depos pathologically by fusion (effacement) of visceral epithelial foot its of IgG outlining the glomerular capillary loops are identified processes; however, this can be visualized only by electron by immunofiuorescence microscopy. Minimal change glomerulopathy is successfully erular basement membrane antibody (choice A) is a feature of treated with corticosteroids and does not progress to renal fail Goodpasture syndrome. Henoch-Schonlein purpura and lupus nephritis (choice A) generally present with nephritic 15 the answer is D: Systemic lupus erythematosus. However, membran urine in patients with nephrotic syndrome leads to hypoal ous nephropathy of lupus also features mesangial and sub buminemia. A compensatory increase in lipoprotein secretion endothelial deposits of immunoglobulins. Immune complex by the liver results in hyperlipidemia, which is refiected in the deposition does not occur in the other choices. For this reason, minimal Diagnosis: Systemic lupus erythematosus change disease is also referred to as lipoid nephrosis. In acute postinfectious glom blood cell casts (choice E) are features of pyelonephritis. Complement activation light microscopic appearance of glomeruli in minimal change is so extensive that over 90% of patients with postinfectious glomerulopathy is essentially normal. Comple microscopic examination of glomeruli reveals total efface ment and other infiammatory mediators attract and activate ment of visceral epithelial cell foot processes. This retraction neutrophils and monocytes, which stimulate the proliferation presumably results from extensive cell swelling and occurs in of mesangial and endothelial cells, resulting in diffuse prolif virtually all cases of proteinuria in the nephrotic range. Typically, the level of serum C3 is not a specific marker, but is characteristic of minimal change depressed during the acute syndrome but returns to normal glomerulopathy. The other choices involve the coagulation by deposits of immune complexes (choices B and C) and does system and are not components of immune complexes. Diagnosis: Postinfectious glomerulonephritis, nephritic Choice E is incorrect because minimal change disease involves syndrome changes in glomeruli, not renal tubules. Diagnosis: Minimal change nephrotic syndrome 17 the answer is E: Wegener granulomatosis. Wegener granu lomatosis is a systemic necrotizing vasculitis of unknown 13 the answer is D: Membranous glomerulopathy. Membranous etiology that is characterized by granulomatous lesions of glomerulopathy is a frequent cause of the nephrotic syndrome the nose, sinuses, and lungs and is associated with renal in adults and is caused by the accumulation of immune com glomerular disease. Lesions associated with this condition plexes in the subepithelial zone of glomerular capillaries. The mediated disease that is characterized by glomerular necrosis diagnostic finding on renal biopsy is intense mesangial stain and crescents. Goodpasture syndrome (choice B) is character ing for IgA, which is almost always accompanied by staining ized by both kidney and pulmonary involvement but does not for C3. Churg-Strauss syndrome (choice A) features erulopathies, ranging from no discernible light microscopic eosinophilia and asthma. Patients Diagnosis: Wegener granulomatosis frequently present with hematuria and proteinuria, and 20% of patients develop renal failure after 10 years. Hematuria is present early this renal disease is not known, but it is thought to be immune in life; proteinuria, progressive renal failure, and hypertension mediated because most patients have antibodies to neutro develop later in the course of the disease. Exuda tion of infiammatory cells through the disrupted, segmentally necrotic basement membrane leads to the formation of cres 22 the answer is C: Mesangial deposition. Wegener granulomatosis does not activate complement through the alternative pathway. The cause membranoproliferative glomerulonephritis (choices D diagnostic finding is mesangial staining that is more intense and E). Diagnosis: Wegener granulomatosis, crescentic glomeru Diagnosis: Berger disease, IgA nephropathy lonephritis 23 the answer is C: Focal proliferative glomerulonephritis. This group of diseases includes lupus nephritis, nephritis not all, glomeruli and initially involves only part of an affected that accompanies several vasculitides, Henoch-Schonlein pur glomerular tuft (segmental). It also includes IgA neph numbers of glomeruli show segmental obliteration of capil ropathy (Berger disease), which, as in this case, presents with lary loops by increased collagen and the accumulation of lipid mesangial deposits of IgA and mesangial cell proliferation. Diagnosis: Berger disease, IgA nephropathy Clinically, it presents with proteinuria, which occasionally may be so massive as to produce nephrotic syndrome. Patients typically prog tious glomerulonephritis are subepithelial dense deposits ress to end-stage renal disease in less than a year. Crescents (choice C) are ably accompanied by mesangial and subendothelial depos not observed in the photomicrograph shown. Erythropoietin is released A, B, and C describe limited deposition of immune complexes, by the interstitial peritubular cells of the kidney in response whereas choice D is a feature of antiglomerular basement to hypoxia and activates specific receptors on the cell mem membrane disease (Goodpasture syndrome). This Diagnosis: Postinfectious glomerulonephritis, nephritic effect rescues progenitor cells from programmed cell death, syndrome promotes colony growth, and restores normal red blood cell mass. Renin (choice E) is released by the juxtaglomerular 25 the answer is C: Group A (b-hemolytic) streptococci. Occasional examples are disease is the most common form of glomerulonephritis in caused by staphylococcal infection. Deposition of IgA-dominant immune complexes is the cal endocarditis, staphylococcal abscess), and rare cases result cause of the nephropathy, but the constituent antigens and from viral.

The results of stones identified as core & shell as uric acid & calcium oxalate respectively and vice versa in stones of two individuals will be presented mental health week discount lyrica generic. Finally mental illness books purchase lyrica without a prescription, in this chapter we will present the overall difference observed in the stones data by comparing with that of reference chemical resulting identification of calcium phosphate in all stones (100%) classified as calcium oxalate mental health matters 0800 safe 75mg lyrica, although in some of them calcium phosphate was less than 10% mental conditions lacking empathy order lyrica 75 mg on line. In chapter 6 mental disorders primarily affect the discount 75mg lyrica with visa, the new method of phase identification for calcium phosphates will be presented mental health lawyers effective lyrica 75 mg. To correlate the chemical nature of the stones with appropriate medical diagnoses, the phase identification and quantification of calcium phosphates in calcium oxalate are of a great importance for clinical investigations because calcium phosphate contents could be a useful factor for the prediction of recurrence [30]. The quantification makes possible to classify the stones by knowing the relative contents, which is regarded as an important factor in general practice, especially in shock wave lithotripsy treatments [31]. In our study [29] using Ga as primary ions, we demonstrated clear phase identification both for pure calcium phosphates and in their mixture with calcium oxalate via proper selection of the characteristic positive secondary ions. In our study we clearly identified the pure struvite stones, mixed with calcium phosphates, and urates. The only calcium phosphates we found in these stones were tri-calcium phosphate and hydroxylapatite. It might be interesting to state here that in this work we revealed that it is possible to recognize calcium oxalate from calcium phosphates present in struvite stones. In chapter 8, we will briefly summarize the results of total 38 stones including two dog stones identified as struvite and cystine. We will also present our compositional statistical analysis to estimate the occurrence frequency of different urinary components from the stone formers in the population of Portugal. The sputtered secondary particles are electrons; neutral species of atoms or molecules; elemental, molecular and cluster ions. The vast majority of species emitted are neutral (~ 99 %) but it is the secondary ions accounting for ca. The resulting mass spectrum gives detailed chemical composition of the subject material. When an energetic (1-30 keV) beam of ions bombards a surface, the particle energy is transferred to the atoms or molecules of the surface at impact site. A cascade of collision occurs between the atoms and molecules in the target material: some collisions return to the surface and result in the emission of atoms, atomic clusters, molecules and molecular clusters; some of which are ionized in the course of leaving the surface. While the technique is apparently destructive, the essence of the static mode is to use an 13 -2 extremely low dose of primary ions (< 10 ions cm), such that the top surface layer of atoms or molecules do not receive more than one ion impact within the time scale of the experiment. The spectral information arising in static mode is of representative of surface chemistry and can be exploited in many fields of applications. Let us discuss these parameters briefly; details are available in literature [36]. More extensive details concerning the sputtering and secondary ion emission can be found elsewhere [36 and references therein]. Ionization occurs at, or close to , the emission of particles from the surface with the consequence that the matrix participates in the electronics processes involved. This means that the yield of secondary ions is strongly influenced by the electronic state of the material being analyzed consequently complicates the quantitative analysis. The signal intensity of particular species is governed by the basic secondary ion yield equation (2. The parameter characterizing the sputtering process is sputtering yield (Y), which is defined as the ratio of the average number of the ejected to the number of bombarded particles. Ym is the average number of positive ionic particles of species m, per primary ion impact. It also increases with primary particle mass, charge, and energy, although not linearly. The target structure (crystallinity, texture), surface topography, beam-induced changes in both structure and topography, target temperature, and incident angle affect the yield. The threshold is not at the surface binding energy U (~3eV) but at a substantially higher energy. For lighter primary particles the maximum is PhD Thesis 9 Secondary Ion mass Spectrometry reached at ca. Beyond this energy, yield drops away as the primary particles penetrates deeper into the solid and less energy returns to surface region. In sputtering of organic materials; atoms, structural fragments and molecules are removed from the surface resulting destruction of chemical structure within area from which these species are removed. In molecular materials, every impacted molecule will be significantly destroyed, whether complete molecule or small fragment of the molecule is removed. Thus instead of sputter rate the concept of damage cross-section, fi, has found to be useful. Obviously the greater the damage cross section lesser will be the molecular ion yield. The relation between the secondary ion intensity (Im) of specie m and damage cross section fififi is as follows [36]; Im= Ym exp(-fiIp) (2. Benninghoven measured damage cross-sections of around 10 2 2 cm (or 1 nm) from amino acid and other small molecules on the metal surface [41]. For elemental sputtering, secondary ion yields and damage cross sections for organic materials increases with primary ion mass, energy and increasing angle of incidence away from the normal. In recent years with the development of argon gas cluster ion sources at Kyoto University [42] molecular ion yield boost up compared to other polyatomic and cluster ion sources [43]. The enhancement in the molecular ion yield increase with increasing cluster size at same energy due to more gentle impacts on the surface resulting low damaging. The secondary ion yield of elemental species PhD Thesis 10 Secondary Ion mass Spectrometry can vary by several orders of magnitude across the periodic table, and strongly depends on the chemical state of the surface that is called matrix effect i. The inconsistency of ion yields is the major problem as the surface composition changes. The same species will not have same secondary ion yield in different chemical environment, making direct comparison difficult among samples. As a result, differential removal of particles from the specimen can occur due to preferential sputtering [39]. Moreover, the probability of ion formation can vary as a result of change in the sputtering process due to ion beam damage and implantation of bombarding species as shown in Figure 2. Due to surface modification the ion yield of singly + + charged calcium (Ca) increased while magnesium(Mg) decreased, the decrease similar to +2 magnesium was observed for doubly charged calcium (Ca) [from the present work]. These variations in the ion yield are due to surface modification that can be explained on the basis of well known [36] modifications of electronic state of the surface by oxidation and cesiation commonly used for enhancement of positive and negative secondary ions respectively. Oxidation can be achieved by oxygen flooding on the surface or by bombardment with oxygen species (O, + +2 O, and O etc) while cesiation can be achieved by bombardment with cesium ions or neutral Cs deposition of sub-monolayer coverage. Before we discuss the ion formation in organic materials let us first illustrate few common ionization models [44, 45]. The central feature of this continuum of electronic states is the Fermi level which separates occupied and unoccupied states. During the removal of the particle, while it is still in the vicinity of the surface, the atomic levels of the sputtered atom overlap with the electronic levels of the metal. Energy-level diagram for an atom or molecule characterized by its highest occupied (image-potential-upshifted) valence level I and lowest unoccupied (downshifted) affinity level A interacting with a metal surface. This possibility is turned on at a separation Zc where the shifted affinity level coincides with the Fermi level [46]. The direction of the charge transfer is depending on the values of the work function fi of the metal and the ionization potential I (or the electron affinity A, respectively) of the sputtered particle. A potential barrier between the electronic states inhibits the charge transfer, but tunneling of the electron to/from the atom is possible with a probability that is exponentially dependent on the distance where the energy levels become equal (determined by the work function fi of the metal) and on the normal component of the velocity vfi of the sputtered particle (determining the + time for interaction). The ionization probability for negative (P) and positive (P) ion formation can be described by following equations 2. One way to make use of the exponential dependence of the ionization probability on the work function of the surface is to lower the work function as much as possible to enable charge transfer to the sputtered atom at low distances Zc. This increases the probability for negative ion generation by several orders of magnitude. It can be obtained by covering the surface with a sub monolayer of alkali metals. As the atom moves away from the surface, the width fi of the level decreases [46, 47]. The probability (P) decreases when all sputtered atoms are ionized or when the work function has reached its minimum value. If for example a positive ion is leaving the surface, the first unoccupied atomic level can be lower than the Fermi level, making an electron transfer from the surface to the ion possible, which re-neutralizes the emitted ion. This is + illustrated by the Cs intensity during Cs sputtering, which increases at low Cs coverage according to the increase in Cs concentration. As soon as the work function is lowered + significantly, the Cs intensity decreases again. At this stage, re-neutralization starts to suppress the increase by high concentration and therefore sputtered Cs atoms [48, 49]. Whether or not the under Cs bombardment is depending on the sputter yield of the target material at the given energy and angle of incidence, which determines the maximum Cs concentration and hence the minimum work function decrease of the positive ionization probability is observed with increasing Cs coverage PhD Thesis 13 Secondary Ion mass Spectrometry 2. An electropositive atom leaving the surface is ionized by breaking its bond to another surface atom and leaving one electron behind. A very concise discussion of this model is given in the cited reference [52 and references therein]. Electropositive elements in an oxide or halide environment will effectively be ionized by breaking the surface bonds, which is utilized when a surface is bombarded or flooded with oxygen to incorporate it into the altered layer. Thus the ionization probability for electropositive species is increased by up to three orders of magnitude [45]. Oxygen bombardment and/or oxygen flooding is extensively used for all kinds of materials. The sputter yield also depends on the degree of oxidation [53] resulting in a further influence on the ion yield. Although the strong emission of these clusters has been known longer [54], their importance for some application like detection of rare gases [55] and the quantification of matrix compounds [56, 57] was recognized only in early 1990s. As already mentioned in electron tunneling model, a surface covered with a + submonolayer of Cs emits Cs ions with a very high degree of ionization. This high degree of ionization is virtually independent of the matrix, since the work function is mainly defined by the Cs over-layer itself. Only if the Cs concentration becomes very high, the degree of ionization is reduced and becomes dependent on the surface concentration. The composition of the flux of sputtered particles from the target is representative of the concentrations in the bulk as soon as the sputter equilibrium has been reached. PhD Thesis 14 Secondary Ion mass Spectrometry + the yield of cluster ions formed by combining Cs ions with sputtered neutrals should therefore be independent of the chemical state of the surface. These processes are mainly relevant to molecular species, low mass fragments also provide important information for + chemical structure determination. Ionization of these species probably occurs via collision cascade mechanism due to direct interaction with primary ion or energetic recoil atoms within the material. The exact location of these ionization processes is still mystery, but likely in the emission region within or just above the surface. Matrix effects (surface coverage, substrate) do influence secondary ion yields from organic materials, but they are generally not so marked as from inorganic systems. Ion yields from copolymers have been observed to be sensitive to identity of the components. Clearly cationization will be favored when suitable cations (Ag, Na, K, and Cs etc) are present in the matrix. We will briefly discuss different types of ions formation from the organic and inorganic materials; details can be found elsewhere [36]. The formation of these molecular ions molecules strongly + depends on structure of the analyte. No protonated molecules are formed if peptide does not contain any basic side chain and additionally its N-terminus is blocked. In a few cases, the production of protonated ions is blocked for a sub-monolayer coverage. An intermolecular proton transfer is supposed to be responsible for this behavior, although a detailed understanding of the underlying mechanism is still unclear. In contrast to the [M+H], the formation of deprotonated ions is layer independent. Sometimes it has been observed as decomposition of Ag (M-H) complexes or by intermolecular proton transfer between adjacent molecules. The formation of alkali attached ions is also dependent on the chemical structure of the analyte molecule. It can be observed if + analyte molecule contains basic groups or free electron pairs. In contrast to the [M+H] formation, + which is also correlated with the existence of basic groups, the [M+alkali] formation normally do not depend on the coverage of the organic material on the metal support. Most of the materials which show cationization with alkali metals can also be cationization by the metal substrate when prepared as monolayer on the metal substrate. In case of unknowns, libraries search is useful to compare with known compositional spectrum. These ions give direct identification of molecular species present in the surface, beside these main peaks some peaks are the direct fragment of the analyte molecule and in majority are those peaks arise due to the rearrangement of different fragments sputtered and surface degradation. The relative intensity of the molecular ion peaks and direct fragments highly depends on the many parameters already discussed. We will briefly describe this procedure in the following section; details can be found in literature [58]. Based on this method two spectra are acquired at two different energies, or different primary ion species, or both of these favorable parameters.