P. Hurit. American International College.
Courtesy Churchill-Livingstone (Saunders) Press Figure 3 buy 2.5mg methotrexate with mastercard. The arrow points to thin degenerate cartilage on the upper part of the joint generic 2.5mg methotrexate fast delivery. A large thick fibrofatty tag extends from the joint capsule on the right cheap methotrexate 2.5mg otc, lying between the two purple articular surfaces proven 2.5mg methotrexate. Courtesy Churchill-Livingstone (Saunders) Press ©2002 CRC Press LLC Figure 3. There is thinning of the articular carti- lage on the lower joint surface, with a large space between the joint capsule and the articular surfaces. This is indicative of a lax capsule and an unstable joint. Courtesy Churchill-Livingstone (Saunders) Press Figure 3. The joint is almost obliterated and there is carti- lagineous fusion of the two facets of the joint. The arrow points to the remnants of the joint space. This type of change occurs when there has been immobilization of the joint for prolonged periods. Courtesy Churchill-Livingstone (Saunders) Press ©2002 CRC Press LLC Figure 3. The two surfaces of the articular cartilage have slid past each other, resulting in subluxation of the joint. On the left side, a fibrofatty tag of synovium attached to the joint capsule extends into the joint (arrow). Courtesy Churchill-Livingstone (Saunders) Press Figure 3. The purple articular cartilage on both sides of the joint is very thin and fragmented. The arrows point to the grossly thickened capsule on both sides of the joint. Courtesy Churchill-Livingstone (Saunders) Press ©2002 CRC Press LLC Figure 3. The intervertebral foramen (large arrow) is much reduced in size as the result of impingement by an enlarged superior articular process of the facet of L5 (small arrow). Courtesy Churchill-Livingstone (Saunders) Press Figure 3. There is entrapment of the synovium within the joint (left arrow). The breakdown in the disc is evident (right arrow) with bulging posteriorly. The spinal canal is narrowed due to the combined effects of the joint hypertrophy and the bulging disc. Courtesy Churchill-Livingstone (Saunders) Press ©2002 CRC Press LLC Figure 3. Imaging of degenerative disease of the lumbar spine and related conditions. Using computed tomography and enhanced magnetic resonance imaging to distinguish between scar b tissue and recurrent lumbar disc herniation. Spine 1994;19:2826 Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, Reilly J. Spine Osti OL, Vernon-Roberts B, Moore R, Fraser RD. Annular 1978;3:319 tears and disc degeneration in the lumbar spine. J Bone Joint Surg 1992;74-B:678 Modic MT, Steinberg PM, Ross JS, Masaryk TJ, Carter JR. Degenerative disk disease: assessment of changes in verte- Selby DK, Paris SV. Anatomy of facet joints and its clini- bral body marrow with MR imaging.
Clinical syndrome/ Mild to moderate exposure can lead to diffuse depressed reflexes discount 2.5 mg methotrexate amex, and reduced signs vibration and touch sensitivity generic 2.5 mg methotrexate. With more severe exposure generic 2.5mg methotrexate amex, there can be generalized areflexia generic methotrexate 2.5mg with visa, sensory ataxia, dysarthria, tremor, weight loss, muscle weakness and atrophy, hallucinations, sleep disturbance, and memory loss. Harmless polyacrylamide is used widely in industry, including water treatment, paper and textile production, cosmetics, grouting agents, and gel electrophoresis. Workers who handle monomeric acrylamide for production of polyacrylamide are at risk. Absorption is generally through the skin, but may also occur through inhalation or ingestion. Deterioration may continue for 2 wks after cessation of exposure. CNS symptoms often improve early, while motor neuropathies take weeks or months to improve. References Mizisin AP, Powell HC (1995) Toxic neuropathies. Curr Opin Neurol 8: 367–371 O’Donoghue JL, Nasr AN, Raleigh RL (1977) Toxic neuropathy – an overview. J Occup Med 19: 379–382 305 Carbon disulfide neuropathy Genetic testing NCV/EMG Laboratory Imaging Biopsy ++ In animals, CS2 causes paranodal retraction of myelin and focal axonal accu- Anatomy/distribution mulation of 10 nm neurofilaments. Sometimes absent corneal reflexes Clinical syndrome/ and optic neuropathy. High levels may cause encephalopathy, extrapyramidal signs dysfunction, and psychiatric dysfunction. Retinopathy with microaneurysms, hemorrhage, and exudates has been reported. CS2 is used in the manufacturing of viscose rayon and cellophane films, and Pathogenesis sometimes in pesticide production and in chemical labs. Strict industrial hygiene has reduced significant clinical problems. Long term low exposure may cause peripheral neuropathy. Distal slowing of nerve conductions, especially sensory nerves. CS2 may react with pyridoxamine, so vitamin B6 supplement theoretically may Therapy help. Symptoms often worsen after cessation of exposure for a period of months, with Prognosis slow improvement following. Chu CC, Huang CC, Chu NS, et al (1996) Carbon disulfide induced polyneuropathy: sural References nerve pathology, electrophysiology, and clinical correlation. Acta Neurol Scand 94: 258– 263 Hageman G, van der Hoek J, van Hout M, et al (1999) Parkinsonism, pyramidal signs, polyneuropathy, and cognitive decline after long-term occupational solvent exposure. J Neurol 246: 198–206 Vasilescu C, Florescu A (1980) Clinical and electrophysiological studies of carbon disul- phide polyneuropathy. J Neurol 224: 59–70 306 Hexacarbon neuropathy Genetic testing NCV/EMG Laboratory Imaging Biopsy ++ Anatomy/distribution Paranodal demyelination and retraction of myelin and focal axonal accumula- tion of 10 nm neurofilaments. Symptoms Slow onset of distal sensory pain, followed by calf pain and distal weakness. Clinical syndrome/ Variable degrees of atrophy, loss of ankle reflexes. CNS damage may cause signs delayed spasticity in 15% of cases. Pathogenesis Hexacarbons are common in industry and domestic products, but only N-hexane and methyl-n-butyl ketone are known to cause neuropathy. Methyl ethyl ketone is not toxic itself, but may potentiate the effects of N-hexane. Prognosis Improvement correlates with severity of exposure. Neuropathy progresses for 2–4 months after cessation of exposure before improvement occurs. References Chang YC (1990) Patients with n-hexane induced polyneuropathy: a clinical follow up.
Her medical history and physical examination are unremarkable order 2.5 mg methotrexate amex, and she takes no medications purchase methotrexate 2.5 mg with visa. An abdom- inal CT scan reveals a 5 cm cystic structure in the pancreas safe 2.5mg methotrexate. Which of the following is the most appropriate step to take next in the treatment of this patient? Follow-up and repeat imaging in 6 weeks Key Concept/Objective: To be able to recognize mucinous cystic neoplasms Besides the commonly seen pseudocysts discount 2.5 mg methotrexate fast delivery, a number of other cystic lesions may occur in the pancreas, including true cysts and cystic neoplasms. Serous cystic neoplasms are benign, but mucin-producing cystic neoplasms may follow a more malignant course. Mucinous cystic neoplasms present as large cystic collections (cystadenomas and cystadenocarcino- mas) and may be relatively asymptomatic. Most cystic neoplasms occur in middle-aged patients, particularly women. They are often mistaken for pseudocysts and inappropriate- ly treated as such. These cystic neoplasms may follow an initially benign course, but when they undergo malignant degeneration, outcomes are as poor as in patients with standard adenocarcinoma. The presence of a cystic collection of the pancreas in a middle-aged (par- ticularly female) patient without a previous history of pancreatitis should immediately suggest a cystic neoplasm, not a pseudocyst. The diagnosis of a cystic neoplasm requires histologic evidence of epithelial or neoplastic tissue in the cyst wall. When these collec- tions are mistaken for pseudocysts, treatment involves drainage, and no tissue is obtained to allow differentiation of a cystic neoplasm from a pseudocyst. The therapy of choice for cystic neoplasms is surgical resection, not drainage. A 62-year-old woman presents to the emergency department complaining of intense abdominal pain, nausea, and vomiting for the past 48 hours. On physical examination, the patient is visibly uncomfort- able, with a low-grade fever, mild tachycardia, and normal blood pressure; her upper abdomen is marked- ly tender. Laboratory tests are remarkable for an amylase of 1150, bilirubin of 2. Which of the following is the most useful imaging test to determine whether this patient’s pancreati- tis is caused by gallstones? Endoscopic retrograde cholangiopancreatography (ERCP) Key Concept/Objective: To understand the role of abdominal ultrasonography in acute pancreatitis Ultrasonography is recommended in the initial evaluation of all pancreatitis to rule out obstruction caused by gallstones. It is more sensitive than CT for the diagnosis of gallstone disease, though CT is usually better at demonstrating morphologic changes in the pancreas caused by inflammation. Findings on plain film (such as the colon cutoff sign; enhance- ment of perirenal fat caused by retroperitoneal inflammation that creates a halo around the left kidney; or an abnormal duodenal loop) can suggest the diagnosis of pancreatitis but do not reveal its cause. ERCP does not play a role in the diagnosis of pancreatitis but can be useful in its management. A 50-year-old man comes to your clinic complaining of intermittent upper abdominal pain that radiates to his back and worsens with meals. He notes that lately he has been losing weight and that his stools have been loose. Which of the following should be the first test to determine whether this patient has chronic pancreatitis? Secretin test Key Concept/Objective: To know the stepwise approach to the diagnosis of chronic pancreatitis The diagnosis of chronic pancreatitis can be made with an appropriate clinical history and demonstration of calcification of the pancreas on plain film. This should therefore be the first imaging test, though at most only 30% of patients with chronic pancreatitis will have this finding. If plain films are unrevealing, ultrasonography may demonstrate the charac- teristic findings of focal or diffuse enlargement of the pancreas, ductal irregularity and dilatation, and fluid collections adjacent to the gland. CT has a higher sensitivity than ultrasound (> 90%) and is the next step in diagnostic imaging. ERCP is the gold standard for diagnosing chronic pancreatitis on the basis of ductal abnormalities; the degree of duc- tal abnormalities correlates roughly with exocrine dysfunction. The secretin test, in which duodenal contents are sampled before and after secretin is administered intravenously, is probably the most sensitive direct assessment of pancreatic exocrine function, but because of improvement in imaging tests, the secretin test is used infrequently.
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