Michael S. Wong, MD, FACS

• Residency Program Director
• Associate Professor of Surgery
• Department of Surgery
• University of California Davis School of Medicine
• Sacramento, California

Armati Neuroinflammation Group erectile dysfunction medication cialis buy viagra uk, Brain and Mind Research Institute weak erectile dysfunction treatment order 50mg viagra with amex, University of Sydney erectile dysfunction at the age of 21 buy cheap viagra 75 mg, Australia Arthur K impotence ultrasound purchase 50 mg viagra with mastercard. Endtz Department of Medical Microbiology and Infectious Diseases impotence statistics cheap viagra american express, Erasmus Medical Center erectile dysfunction drugs gnc discount viagra 50mg with mastercard, Rotterdam, the Netherland Catharina G. Faber Department of Neurology, Maastricht University Medical Center, the Netherlands Thomas E. Feasby Cumming School of Medicine, University of Calgary, Canada Christiaan Fokke Department of Neurology, Gelre Hospitals, Apeldoorn, the Netherlands Willem Jan R. Fokkink Departments of Immunology and Neurology, Erasmus Medical Center, Rotterdam, the Netherlands Karin Geleijns Departments of Immunology and Neurology, Erasmus Medical Center, Rotterdam, the Netherlands Claudia Giannotta Department of Medical Biotechnology and Translational Medicine, University of Milan, 2nd Neurology, Humanitas Clinical and Research Institute, Rozzano, Italy Eunice J. Goh Yong Loo Lin School of Medicine, National University of Singapore, Singapore John A. Hahn Department of Clinical Neurological Sciences, Western University, London, Canada Susan K. Jacobs Departments of Neurology and Immunology, Erasmus Medical Center, Rotterdam, the Netherlands Kenichi Kaida Division of Neurology, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan Fary Khan Department of Medicine, Dentistry and Health Sciences and Public Health and Preventative Medicine, University of Melbourne and Monash University, Parkville and Victoria, Australia Jong Kuk Kim Department of Neurology, College of Medicine, Dong-A University, Busan, South Korea Odelia S. Plomp Department of Neurology, Leiden University Medical Center, the Netherlands John Pollard Department of Neurology, Central Clinical School, University of Sydney, Australia Alessandro Prinetti Department of Medical Biotechnology and Translational Medicine, University of Milan, Italy Marielle H. Pruppers Department of Neurology, Maastricht University Medical Center, the Netherlands Stephen W. Jacobs 13 Miller Fisher Syndrome Atsuro Chiba 14 Axonal Guillain-Barre Syndrome Thomas E. Bennett 34 Complement in Guillain-Barre Syndrome: From Bench to Bedside Amy Davidson and Susan K. Sheikh 37 the Motor Nerve Terminal as a Site of Anti-Ganglioside Antibody Attack in Guillain Barre Syndrome J. Faber 52 Evidence-Based Practice in Rehabilitation for Guillain-Barre Syndrome Fary Khan, Bhasker Amatya and Louisa Ng 53 Physiotherapy in Guillain-Barre Syndrome: Developing the Evidence over the Years Claire White 54 Fatal Guillain-Barre Syndrome Bianca van den Berg and Bart C. Hirsch 58 the Other Syndrome of Guillain-Barre Syndrome: Dysautonomia and Systemic Effects Eelco F. It punches above its weight in the hierarchy of diseases because its onset is dramatic, its effects potentially devastating, its pathology fascinating, its mechanisms tantalising and its treatment so far only partly satisfactory. A generation later and a century since the famous description by Guillain, Barre and Strohl in 1916, this new book commands 63 chapters and over 100 authors. In the 1800s, the site of pathology in acute ascending paralysis was still unclear. In the first two-thirds of the 1900s, pathological studies showed inflammation and tissue damage throughout the nerves and spinal roots. In the last quarter of the 1900s, American and Chinese investigators identified a paralytic syndrome due to predominantly motor neuropathy [7]. Increasingly sophisticated electrophysiology has distinguished predominantly demyelinating disease from forms due to primary axonal degeneration or, most recently, forms due to nodal conduction block without either demyelination or axonal degeneration. The first pathological studies emphasized cellular infiltration by macrophages as responsible for damaging the myelin sheaths with T cells directed against myelin proteins as instigating the process. It arises spontaneously in mice lacking specific genes which control T cell regulation. Some genetic strains of this bacterium have lipopolysaccharides in their membranes which trigger antibody responses in genetically susceptible individuals. The antibodies react with gangliosides on the surface of the axolemma or myelin sheaths in parts of the peripheral nervous system accessible to soluble factors. Or does the peripheral nervous system have only a limited number of ways of expressing a disease due to an inflammatory reaction Does the occurrence of disease reflect the specific virulence of the organism or the failure of immune regulation by the patient Spontaneous improvement is usual, which has made it impossible to judge whether many claims of successful treatment reflect anything other than the natural history of the disease. However, recovery is often slow and incomplete, which has stimulated the launch of randomised controlled trials. Surprisingly, corticosteroids, the panacea for many inflammatory diseases, turned out to be ineffective. The first treatment shown to be able to hasten recovery and shorten the disease was plasma exchange. Intravenous immunoglobulin is as effective and more convenient and so more commonly used where it is available. The success of these two treatments has made further progress more difficult because it has become unacceptable to omit treatment with one of them. It is encouraging that there is an ongoing trial of the complement inhibitor eculizumab founded on observations in a relevant animal model. We hope that this book will stimulate others to test some of the many available newer immunomodulatory agents to provide the improvement in treatment which our patients need. As time passed, the disease became best known by the names of its first 2 authors. Rather than a conventional textbook, a more reflective format was considered appropriate. Modern bibliographic databases make access to the primary literature a click of the mouse away, and there was no particular desire to create a comprehensive summary of 100 years of published work. A wide range of authors from emeritus professors to junior medical students from around the world were invited to contribute their thoughts on particular topics, each in their writing style. The result is a collection of 63 essays from 110 authors presented in a highly eclectic format. Some contributors have stuck firmly to the Top 10 format, while others have written conventional accounts of their topic. There are many personal reflections by those who have made important contributions to the understanding and treatment of the disease. The reader can take in one or more chapters of special interest or just read any chapter for pleasure. The book is readily accessible to those with highly specialized interests in selected areas of research, the general neurologist looking for an update, and the patients and their families trying to understand this mysterious illness. Asbury, who have made seminal contributions to the field over a lifetime of achievement. The History section includes reflections from the Hopital de la Pitie-Salpetriere, the home of many famous French neurologists, and moves through a timeline of both famous and forgotten papers. These disorders, ranging from Miller Fisher syndrome to acute motor axonal neuropathy, and lesser-known syndromes have indeed taught us much about the classic syndrome. Pathological studies led to the first inkling that this was an autoimmune disorder and supported both the humoral and cellular hypotheses of the disease. Imaging promises to provide new insights, as it can look at the whole nervous system or concentrate on specific areas of interest. The sections on the many aspects of more basic research (animal models, basic science, antibodies, and antecedent events and susceptibility) show how much has been done but also how much more there is to do. Taken together, these sections begin with the observations from the 1950s in experimental allergic neuritis and move through an enormous research effort. The Treatment section discusses the current standards of care: plasma exchange and intravenous immunoglobulins. Importance is given to the role of supportive care as critically necessary in the overall management. There are several clinical trials now underway and hopefully, by the printing of this book, their results will be known and new treatment options will be available. The Outcome section shows how far we have come in the provision of rehabilitation services and our ability to predict outcomes. But we also need better outcome measures for our clinical trials that mimic what patients think about themselves and their recovery. The last section is a potpourri of Top 10, from bibliographical citations to images to views of medical students and Ph. We thank our many colleagues around the world for embracing this project with such enthusiasm and demonstrating a remarkable array of talent. Strohl We draw attention, in this note, to a clinical syndrome which we have observed in two patients. This syndrome is characterized by motor disturbance, abolition of the tendon reflexes with preservation of the cutaneous reflexes, paraesthesia with mild disorders of objective sensation, pain at pressure of muscle masses, slightly accentuated changes of the electric reactions of nerves and muscles and very notable hyperalbuminosis of the cerebrospinal fluid with absence of cytological reaction (albumino-cytological dissociation). This syndrome appeared to depend on a concomitant involvement of spinal roots, nerves and muscles, most probably of infectious or toxic nature. It must be differentiated from simple radiculitis, pure polyneuritis and polymyalgia. Experimental research using a graphic method on the speed of reflexes and their delayed time, on the modalities, the muscular contractility, show that, in reality, the whole peripheral neuro-muscular system is involved in the syndrome. We also particularly insist on the hyperalbuminosis of the cerebrospinal fluid without cytological reaction, which to our knowledge has never been mentioned in similar cases. The affliction affected him beginning in July the 25th with tingling of feet and weakness of the lower limbs, such that he had to stop walking every 200 to 300 meters. Then during the following days, tingling appeared in the upper limbs and on the lower part of the face; the muscular strength weakened in the upper limbs. The first examination of August 25th allowed us to notice the following symptomatology. The muscular strength was globally decreased in the upper and lower limbs but without a total paralysis; this decrease of the muscular strength was especially prominent in the extremities where we noticed an extreme weakness of the flexion and the extension of toes, foot, fingers and hands. The muscles of the trunk were also weak, so that the patient could not sit independently without support. Walking was possible for a few steps; we then noticed a certain gait instability and the upright posture of the foot could not be maintained. The electric examination showed that in the upper limbs, the faradic excitability was normal and the galvanic excitability was good for all the muscles with lively shocks; there was no polar inversion; we only remarked on a light hypo-excitability of the finger extensor; sometimes the shock was slightly slowed down; we noticed polar inversion for the lateral gastrocnemius, but the degeneration reaction was very incomplete. The patellar, Achilles and medio-plantar reflexes investigated with the hammer were absent, as well as the bicep, radio-and cubito-pronator, and olecranon reflexes. The plantar cutaneous reflexes led to obvious flexion of the toes with a contraction at distance of the tensor fascia latae. We noted no withdrawal reflexes, either plucking of the instep, or by hyperflexion of the toes. The neuro-muscular excitability brought about by direct percussion of the muscle mass with the hammer was maintained. The patient still reported tingling in both feet up to the top of malleolus and in both hands up to over the wrist. There was no clear disorder of objective sensibility, but we found a mild hypoesthesia to touch, heat and pain in the feet and hands. There was no fever, and no respiratory or gastro-intestinal disorder, and the pulse was normal. Urine, examined at the Laboratory of Bacteriology and Chemistry of the Army, did not contain either sugar, nor albumin, nor indoxyl; the chemical elements were in their normal proportion. Lumbar puncture showed clear cerebrospinal fluid, not hypertensive, with hyperalbuminosis (2. Specimens from the pharynx and nasal mucus showed the absence of any diphtheria bacilli. Treatment consisted of absolute rest, massage of the upper and lower limbs, and injections of strychnine and soda of phenylsalicylate. On September the 2nd, some improvement in muscle strength was observed, and there was no more tingling in the feet, but it persisted in the hands. A repeat lumbar puncture showed a very marked hyperalbuminosis without appreciable leukocyte reaction as in the previous examination. On September the 19th, motor disturbance was improving; the patient was able to walk for an hour; he could stand on one foot. Paresthesia had completely disappeared in the lower limbs but persisted in the hands although this was attenuated. Tendon reflexes were clinically absent, there were no withdrawal reflexes, and cutaneous reflexes were normal. With direct percussion of the muscle masses with the hammer, neuromuscular excitability seemed normal in the upper and lower limbs and in the face. The patient, gradually improving, was sent to convalesce on the 30th of September. On the 28th of August, after a walk of 15 kilometres, he felt an abnormal fatigue, headache, erratic pain in the upper and lower limbs. The next morning he walked with huge difficulty to go to the examination; he was exempted from service for four consecutive days. Transported to an aid station, he was then discharged to the neurological centre of the Army.

Low grade symp Skinfold Tenderness: the rolling of the skin and subcu toms may be increased by mental stress or fatigue erectile dysfunction and alcohol buy cheap viagra online. Reactive Hyperemia: Redness of the skin developing Classification Criteria for Primary and Concomitant after palpation of tender points over the trapezius and Fibromyalgia (from Wolfe et al impotence used in a sentence proven 100 mg viagra. History of Widespread Pain Autonomic Phenomena: Reactive hyperemia is the most commonly recognized feature injections for erectile dysfunction video purchase 25mg viagra with mastercard, but temperature changes Definition and mild soft tissue swelling involving the distal upper Pain is considered widespread when all of the following extremities are also frequently reported erectile dysfunction miracle purchase generic viagra pills. In addition varicocele causes erectile dysfunction buy viagra without a prescription, axial skeletal pain (cervical spine Cold erectile dysfunction wikihow purchase cheapest viagra and viagra, poor sleep, anxiety, humidity, weather change, or anterior chest or thoracic spine or low back) must be fatigue, and mental stress intensify symptoms in 60 present. Symptoms are typically made worse or brought on considered as pain for each involved side. Pain in 11 of 18 Tender Point Sites on Digital Pal Signs pation Tender points, widely and symmetrically distributed, are the characteristic sign of the syndrome. Pain, on digital palpation, must be present in at least 11 of the following 18 tender point sites: Relief Relief may be provided by reassurance and explanation Occiput: bilateral, at the suboccipital muscle insertions. Low dose amitriptyline, cy Supraspinatus: bilateral, at origins above the scapula clobenzaprine, and aerobic exercise have been shown, in spine near the medial border. Lat Pathology eral Epicondyle: bilateral, 2 cm distal to the Nonspecific muscle changes have been found in some epicondyles. Blood flow during exercise is reduced, Gluteal: bilateral, in upper outer quadrants of buttocks in and decreased oxygen uptake in muscles has been noted. Two studies have found increased levels of substance P Greater Trochanter: bilateral, posterior to the tro in the cerebrospinal fluid of patients. The syndrome may begin in childhood or ject must state that the palpation was painful. The presence of a second clinical disorder does not ex System clude the diagnosis of fibromyalgia. X8a Main Features Diffuse aching, burning pain in joints, usually moder References ately severe; usually intermittent with exacerbations and Wolfe, F. The condition affects about 1% of the popu College of Rheumatology 1990 criteria for the classification of lation and is more common in women. Diagnostic crite fibromyalgia: report of the Multicenter Criteria Committee, ria of the American Rheumatism Association describe Arthritis Rheum. Further criteria include: (6) subcutaneous nodules, Syndromes (7) typical radiographic changes, (8) positive test for rheumatoid factor in the serum, (9) a poor response in Synonyms: fibrositis (syndrome), myalgia, muscular the mucin clot test in the synovial fluid, (10) synovial rheumatism, nonarticular rheumatism. Specific myofascial syndromes may occur in any volun tary muscle with referred pain, local and referred tender Classical rheumatoid arthritis requires seven criteria to ness, and a tense shortened muscle. Definite rheumatoid arthritis may be diag same qualities as that of the diffuse syndromes. Passive nosed on five criteria, and probable rheumatoid arthritis stretch or strong voluntary contraction in the shortened on three criteria. Satellite tender points may develop within the area of pain reference of the Associated Symptoms initial trigger point. Inflammation may affect eyes, demonstration of a trigger point (tender point) and re heart, lungs. This suggests Signs Tenderness, swelling, loss of range of motion of joints, that the syndrome is an epiphenomenon secondary to ligaments, tendons. Chronic destruction and joint de proximal pathology such as nerve root irritation. Others may be coded as required according to individual muscles that are Relief identified as being a site of trouble. Usually good relief of pain and stiffness can be obtained with nonsteroidal anti-inflammatory drugs, but some pa tients require therapy with gold or other agents. Rheumatoid Arthritis (1-10) Pathology Chronic inflammatory process of synovium, ligaments, Definition or tendons. Aching, burning joint pain due to systemic inflammatory disease affecting all synovial joints, muscle, ligaments, Essential Features and tendons in accordance with diagnostic criteria be Aching, burning joint pain with characteristic pathology. Morning stiffness in and around joints lasting at least Page 48 one hour before maximal improvement. Simultaneous soft tissue swelling or fluid in at least There is deep, aching pain which may be severe as the three joint areas observed by a physician. The pain is felt at the joint or joints ble areas are right or left proximal interphalangeal joints involved but may be referred to adjacent muscle groups. At least one area of soft tissue swelling or effusion in rest and later nocturnal pain. Simultaneous involvement of Stiffness occurs after protracted periods of inactivity and the same joint areas as defined in 2 above in both sides in the morning but lasts less than half an hour as a rule. Only about 25% of those with radiographic changes any method for which any result has been positive in report symptoms. Radiographic changes typical of rheumatoid arthritis age of 45 compared with women, and in women over the on posterior-anterior hand and wrist radiographs; this age of 45 compared with men. Aggravating Features A patient fulfilling four of these seven criteria can be Use, fatigue. Signs Clinically, joint line tenderness may be found and crepi Differential Diagnosis tus on active or passive joint motion; noninflammatory Systemic lupus erythematosus, palindromic rheumatism, effusions are common. Later stage disease is ac mixed connective tissue disease, psoriatic arthropathy, companied by gross deformity, bony-hypertrophy, con calcium pyrophosphate deposition disease, seronegative tracture. X-ray evidence of joint space narrowing, spondyloarthropathies, hemochromatosis (rarely). Osteoarthritis (I-11) Relief Some have relief with nonsteroidal anti-inflammatory Definition agents or with non-narcotic analgesics. Occasional relief in the single joint or multiple joints, either as a primary phe early phases may appear from intra-articular steroids. Physical Disability Site Progressive limitation of ambulation occurs in large Joints most commonly involved are distal and proximal weight-bearing joints. Page 49 Relief Diagnostic Criteria Acute attacks respond well to nonsteroidal anti No official diagnostic criteria exist for osteoarthritis, inflammatory drugs, with or without local corticosteroid although criteria have been proposed for osteoarthritis of injections. Complications Noninflammatory arthritis of one or several diarthrodial Chronic disabling arthritis. Differential Diagnosis Calcium pyrophosphate deposition disease; presence of Pathology congenital traumatic, inflammatory, endocrinological, or Acute and chronic inflammation or degeneration. Attacks of aching, sharp, and throbbing pain with acute or chronic recurrent inflammation of a joint caused by Differential Diagnosis calcium pyrophosphate crystals. Main Features the disorder occurs clinically in about 1 in 1000 adults, more often in the elderly, but radiology shows the pres Gout (1-13) ence of the disease in 5% of adults at the time of death. There are four major clinical presentations: (1) pseudog Definition out: acute redness, heat, swelling, and severe pain which Paroxysmal attacks of aching, sharp, or throbbing pain, is aching, sharp, or throbbing in one or a few joints; the usually severe and due to inflammation of a joint caused attacks last from 2 days to several weeks, with freedom by monosodium urate crystals. Acute severe parox Signs ysmal attacks of pain occur with redness, heat, swelling, Aspiration of calcium pyrophosphate crystals from the and tenderness, usually in one joint. The patient is often unable to ac lage of the wrists, knees, and symphysis pubis. Associated Symptoms In the acute phase, patients may be febrile and have leu Code X38. Redness, heat, and tender swelling of the joint, which may be extremely painful to move. Hemophilic Arthropathy (1-14) Laboratory Findings Serum urate may vary during the acute attack. Leukocy Definition tosis and raised sedimentation rate are seen during the Bouts of acute, constant, nagging, burning, bursting, and attack. Attacks may become polyarticular the most common joints affected initially are the knees, and recur at shorter intervals and may eventually resolve ankles, and elbows. Shoulders, hips, and wrist joints are incompletely leaving chronic, progressive crippling ar affected next most often. Renal calculi, tophaceous deposits, and chronic arthritis Main Features with joint damage. Prevalence: hemophilic joint hemorrhages occur in se Pathology verely and moderately affected male hemophiliacs. In the adult, spontaneous hemorrhages Diagnostic Criteria and pain occur in association also with minor or severe 1. Characteristically the acute pain is associated hydrate crystals in synovial fluid leukocytes by po with such hemarthrosis, which is relieved by replace larizing microscopy or other acceptable methods of ment therapy and rest of the affected limb. Demonstration of sodium urate monohydrate crystals be simply spontaneous small recurrent hemorrhages. The in an aspirate or biopsy of a tophus by methods simi pain associated with them is extremely difficult to treat lar to those in 1. In the absence of specific crystal identification, a Time Course: the acute pain is marked by fullness and history of monoarticular arthritis followed by an as stiffness and constant nagging, burning, or bursting ymptomatic intercritical period, rapid resolution of qualities. It is incapacitating and will cause severe pain synovitis following Colchicine administration, and for at least a week depending upon the degree of intra the presence of hyperuricemia. It will recur episodically Any one of the three above is sufficient to make the di from the causes indicated. At the stage of destructive joint with blood clotting factor concentrate is available on a changes the chronic pain is unremitting and relieved regular basis only in North America and Europe at this mainly by rest and analgesics. Acute Hemarthrosis: Adequate intravenous replacement with appropriate coagulation factors with subsequent Associated Symptoms graded exercise and physiotherapy will provide good Depressive or passive/aggressive symptoms often ac relief. Aspiration of the joint will be necessary under company hemorrhages and are secondary to the extent of coagulation factor cover if there is excessive intracapsu pain or to the realization of vulnerability to hemorrhage, lar pressure. Analgesics are required for acute pain man which is beyond the control of the hemophiliac. Reactive and Chronic Hemarthrosis: ing occurs into a muscle or potential space. Numerous psy control using analgesics and transcutaneous nerve stimu chosomatic complaints are associated with the chronic lation is also useful, and physiotherapy is of consider and acute pain of chronic synovitis, arthritis, and he able assistance in managing both symptoms and signs. Synovectomy may be of use for the control of pain sec ondary to the recurrent bleeding. Chronic Destructive Signs Arthropathy: Replacement therapy is of little assistance Reactive Synovitis: There is a chronic swelling of the in relieving pain and disability. Physiotherapy after control of acute symptoms is ment often with signs of adjacent involvement of muscle useful. Analgesic abuse is a common problem in hemophilia due to the acute and chronic pain syndromes associated Laboratory Findings with hemophilic arthropathy. This problem can be X-rays with the large hemarthrosis show little except for avoided in the younger age group by not using narcotic soft tissue swelling. In reactive synovitis there is often analgesics for chronic pain management and relying evidence of osteoporosis accompanied by overgrowth of upon principles of comprehensive hemophilia care. In these include regular physiotherapy, exercise, and mak chronic arthropathy there is cartilage destruction and ing full use of available social and professional opportu narrowing of the joint space. Cysts, rarefactions, subcondy lar cysts, and an overgrowth of the epiphysis are noted. Social and Physical Disability this progresses through to fibrous joint contracture, loss Severe crippling and physical disability, with prolonged of joint space, extensive enlargement of the epiphysis, school and work absences, have traditionally been asso and substantial disorganization of the joint structures. Consequently, af the articular cartilage shows extensive degeneration fected individuals have not been able to achieve with fibrillation and eburnated bone ends. It is considered that the higher suicide rate is related not only to the fam Usual Course ily and psychosocial aspects of the disease but also to the Until the availability of therapy with blood clotting fac chronic pain syndromes that these individuals experience. Generally this joint deterioration was associated with pain as de two pathologic phases are associated with the hemo scribed in the section regarding time course. Phase one involves an early synovial soft duction of concentrated clotting factor transfusions has tissue reaction caused by intraarticular bleeding. Syno avoided the consequence of repeated acute severe he vial hypertrophy with hemosiderin deposition and mild marthroses. Cartilage degen the pain pattern of chronic synovitis and arthritis can be eration and joint degeneration similar to that seen in avoided or merely delayed using such therapy. Therapy osteoarthritis and rheumatoid arthritis is seen in the sec Page 52 ond-phase joint. Associated with this type of phase two Prevalence: is approximately 3 per 1000 of population. The Any age can be affected, but the highest incidence amount of hemosiderin deposited is increased compared (18%) is between 20 and 29 years. Sex Ratio: approximately 1:1, but 3:2 males Summary of Essential Features and Diagnostic to females in children. Criteria Acute and chronic pain as the result of acute hemarthro Pain Quality: initially the pain is acute and intense. It is sis with chronic synovial cartilaginous and bony degen frequently described as throbbing, smarting, and sting eration is exacerbated by spontaneous and trauma ing, and marked exacerbations of stabbing pain occur related hemorrhage. Thus, it is particularly intense where there are skin creases or flexures or where Diagnostic Criteria pressure is applied, such as palms, soles, genitalia, ears, Pain associated with hemophiliac arthropathy must sat or resting surfaces. Despite the destruction of all cutaneous nerve endings, full thickness bums are often painful with 1. Spontaneous intracapsular hemorrhages in an indi a quality described as deep, dull, or aching. Demonstrable synovial bleeding with or without Intensity and Duration: the pain tends to diminish in bony joint contour abnormalities. In addition, the quality of the pain changes, and at one to two weeks after the Differential Diagnosis bum is usually described as sore, aching, tender, tiring, In the presence of a severe (less than 0.

Calcium salt or alcohol precursor panthenol (dexpanthenolum) may be used as supplements improving the healing of uninfected burns erectile dysfunction causes mental buy line viagra, superfcial injuries or catarrh of the upper respiratory tract erectile dysfunction 23 order viagra 75 mg on line. Vitamin B6 Vitamin B6 is a common name for three related derivatves of substtuted pyridine erectile dysfunction drugs wiki generic 100mg viagra otc. All of them have the same biolo gical actvity impotence hypertension buy cheap viagra line, and difer from each other in the group bound at positon 4; pyridoxine (pyridoxol) has a primary alcoholic group impotence young adults cheap viagra online master card, pyridoxal an aldehyde group and pyridoxamine a primary amine group erectile dysfunction treatment adelaide order 25 mg viagra otc. Pyridoxal 5-phosphate cofactor is the actve form, a prosthetc group of enzymes primarily contributng in the conversion of amino acids (aminotransfera se, decarboxylase). The daily requirement of about 2 mg in adults is covered by a normal, varied diet, but increases greatly during lactaton, in all catabolic conditons, or large consumpton of ethanol. Absolute defciency of vitamin B6 is rare; insufciency may manifest itself in alcoholics, pregnant or breasteeding women by skin and mucosa disorders or anaemia. Folic Acid (Folate, Vitamin B11) Folic acid is a common name for pteroyl-glutamic acid. Animals are unable to synthesise these compounds, and depend on their supply from food. Tetrahydrofolate, a cofactor transferring one-carbon residues in diferent oxidaton states, is the actve form in cells. The richest source is liver, vegetable foods such as leafy vegetables (cabbage, kale, spinach) and yeast. Folate insufciency is usually caused by insufcient resorpton, with manifestatons in the blood count (megaloblastc anaemia, thrombocytopenia). Lack of folates during pregnancy is associated with congenital developmental defects of the foetus, in partcular neural tube defects. It is based on the tetrapyrrole-corrin ring with a cobalt ion bound in the centre. It is only produced by microorganisms, and is only found in animal foodstufs, not in vegetable foods. A specifc glycoprotein excreted by the gastric mucosa, called the intrinsic factor, is required to resorb cobalamin supplied from food. When in cells, cobalamin is converted to cofactors methylcobalamin and deoxyadenosylcobalamin. They are required to eliminate some amino acids and, together with folic acid, for me thylaton reactons (remethylaton of homocysteine to methionine, one of the requirements for contnuous synthesis of nucleic acid base pairs). Cobalamin is also formed by the gut fora, but does not absorb and is excreted in the stools. It is relatvely rare for cobalamin defciency to be caused by an insufcient diet such as vegans who avoid food stufs of animal origin. Intrinsic factor defciency and insufcient cobalamin resorpton from food are more common causes. Manifestatons include megaloblastc or macrocytc anaemia or neurological disorders. This is not carboxylic acid; the distnct acidic character is derived from the presence of two enolic hydroxyles. It is synthesized by plants and most animals except for humans, apes and guinea pigs. L-ascorbic acid readily oxidized to biologically inactve L-dehydroascorbic acid; the reacton is reversible, however a sufciently efectve reducing agent for reverse reducton is usually missing. It is involved in hydroxylaton reactons in the synthesis of collagen, bile acids and adre nalin, and in tyrosine degradaton by keeping metalloenzyme metal ions in the reduced state. Ascorbate is readily deteriorated by oxidaton from atmospheric oxy gen at higher temperatures, especially in the presence of traces of heavy metals, Cu and Fe. People with a relatvely low vitamin C intake get easily tred, more prone to minor infectons, sometmes have swollen and bleeding gums or hypodermic haemorrhage from fragile capillaries. Excess vitamin C is quickly excreted in urine; larger ascorbate amounts are degraded to oxalate (risk of urolithiasis), and there may be a higher risk of acid -base disorders (acidosis). Biotin (Formerly Vitamin H) the biotn molecule contains a condensed heterocyclic system consistng of thiolane and imidazolidine. It thus plays an important role in gluconeogenesis (synthesis of glucose from lactate and some amino acids), for the citric acid cycle (synthesis of oxaloacetate), and for synthesis of faty acids. In additon to this, a considerable part of the required amount is synthesised by the large bowel fora. They contain a thermally unstable glycoprotein avidin, a specifcally biotn-binding protein (the complex is not broken down by digestve enzymes) that prevents biotn absorpton. Fat-Soluble Vitamins They have a non-polar (hydrophobic) character, since they are isoprenoids themselves (A and D), or their molecule contains an isoprenoid chain (E and K). In vegetable and animal foodstufs they are usually dissolved in fats that are absorbed through the intestnes. Long-term fat digeston disorders lead to reduced fat resorpton, and hypovitaminosis may develop despite sufcient intake of fats from food. Retnol is produced by oxidatve cleavage of beta-carotene provitamin present in vegetables and fruit. Retnal aldehyde is part of rhodopsin (visual purple in the rods and cones of the retna). One of the frst signs of retnol defciency is night blindness followed by skin and mucosa disorders (dryness and keratnisaton), and conjunctva and cornea damage (xerophthalmia). Repeated multple doses of retnol are toxic and may, among other things, pose a risk to foetal development during pregnancy. Vitamin D Calciol (vitamin D, cholecalciferol) and ercalciol (vitamin D, ergocalciferol) are 9,10-secosterols. Their hydroxylaton in the liver and kidneys produces the hormone calcitriol (1,25-dihydroxycalciol) which, together with parathormone and calcitonin, plays a major role in the Ca2+ and phosphate management. Calcitriol induces the synthesis of a protein, which enables resorpton of Ca2+ in the intestne, and regulates bone tssue mineralisaton. Cal ciol defciency results in insufcient mineralisaton of the organic bone component. Serious defciency is manifested as rickets in children, and osteomalacia in adults. Repeated administraton of excessive vitamin D doses leads to hypercal caemia, sometmes even undesirable calcifcatons in various tssues or calcium urolithiasis. The main source is fsh oil, cod liver, oily fsh, and also enriched tub margarines. Vitamin E Vitamin E refers to a group of natural antoxidants featuring qualitatvely the same biological actvity as alpha -tocopherol, which is the most efectve and most naturally widespread of them. All of these antoxidants are derivatves of a chromate with a 16-carbon isoprenoid residue atached at positon 2. Some of the free radicals are neutralised by the hydrogen atom, and the phenoxy-radical thus formed is either regenerated by ascorbate to the original tocopherol, or is irreversibly degraded by another radical. Tocopherols reduce peroxidaton of membrane lipids and lipoproteins unsaturated faty acids, and also prevent other important compounds from oxidaton. The daily requirement is about 15 mg of alpha-tocopherol, and increases by boostng intake of poly-unsaturated fats. The tocopherol content is greatly reduced in dehydrated or frozen foods due to auto-oxidaton. Tocopherol defciency does not present typical manifestatons in humans; perhaps may cause anaemia and some neurological symptoms. Vitamin K Vitamin K is a common name for a group of naphthoquinone derivatves referred to as anthaemorrhagic vitamin. Naturally occurring are phyloquinone (K, 3-phytylmenadione) and menaquinones (K) with an atached polyisoprene1 2 side chain, which makes them fat-soluble. Their defciency in adults is not common since vitamin K is relatvely plentful in foods (most in leaf vegetables), and is also produced by large bowel fora. A bleeding tendency due to vitamin K defciency may occur in newborns (their gut is sterile), in all fat resorpton disorders, most commonly in insufcient bile acid secreton, or in the absence of gut fora caused by broad-spectrum antbiotcs. Vitamins In additon to primary nutrients (carbohydrates, proteins and fats), human nutriton has to contain other essental components that the human body is unable to synthesize. Such components include essental amino acids, essental faty acids, mineral compounds and vitamins. Vitamins and cofactors derived from these are indispensable for the nor mal course of many metabolic processes. Depending on their solubility, vitamins are classifed as either fat-soluble (A, D, E, K) and water-soluble (the other vitamins). A prolonged low supply of some of the vitamins may cause either hypovitaminosis, at frst subclinical, when a reduced amount of that partcular vitamin in the body can be proved (common in vitamins D or B12), and later clinical hypovitaminosis with non-specifc symptoms, or more serious disorders with typical symptoms (avitaminosis). Vitamin defciency may also occur as a result of a disorder in absorbing these in the digestve tract, or an increased vitamin requirement when sufering from diseases or other conditons (convalescence, pregnancy, breasteeding), or their increased excreton. On the other hand, fat-soluble vitamins may deposit in the body for a longer tme: vitamins A and D, and vitamin K to a limited extent in the liver, and tocopherols in the adipose tssue. Toxicity manifestatons (sometmes referred to as hypervitaminosis) can only be found in vitamins A and D. These values may have diferent interpretatons, and may be more or less varied between countries. Although a lot of research has been carried out, the defnitve appro ach to optmum vitamin intake is stll being debated (vitamin D is currently a good example). Vitamin Test Methods There are diferent approaches to determining the vitamin level in the body, when vitamin defciency is suspected. Water-Soluble Vitamins these vitamins are not stored in the body (except for vitamin B12); excess amounts are excreted in the urine, mea ning so their consistent intake from food is important. Hydrophilic vitamins (again except for vitamin B12) are absorbed through the saturable actve Na -dependent multvitamin trans+ porter; simple difusion also occurs in the case of higher concentratons in food. Major sources of thiamine in food are cereal germs, yeast, legumes, nuts, meat, milk and dairy products. Actve saturable transport by the thiamine Na -dependent transporter (symport) takes place when low concentratons+ are involved. Passive difusion transport takes place when the daily intake is greater than 5 mg. The body contains roughly 30 mg of thiamine, about one half in the muscles, and the rest in the myocardium, liver, kidneys and nerve tssue. Accumulaton of 2-oxo acids produced from branched amino acids leads to maple syrup disease symptoms. Thiamine also stmulates the functon of neutrophils and lymphocytes; when defcient, proneness to infectons develops. Thiamine defciency ofen occurs due to malnutriton, chronic alcoholism, administraton of diuretcs or malaria. Typical causes of insufcient intake include consumpton of unfortfed glazed rice or wheat products and also raw fsh containing microbial thiaminase. Defciency in alcoholics develops due to reduced intake, and also due to limited absorpton as a result of actve transport inhibiton. In old age, insufcient intake typically combines with the adminis traton of diuretcs mentoned above (mainly for cardiac failure treatment). Signs of defciency include mood changes (irritability, depression), memory disorders, peripheral neuropathy; se vere defciency results in beriberi. Manifestatons of beriberi include confusion, gastrointestnal symptoms (loss of appette, poor digeston, weight loss), muscle weakness, ataxia, peripheral paraesthesia, ophthalmoplegia, oedemas (wet beriberi), tachycardia, cardiac failure (dry beriberi) or even coma. Typical manifestatons in alcoholics include Wernicke-Korsakof encephalopathy (loss of memory, confabulaton, delirium, nystagmus, ataxia + beriberi symptoms). The test for transketolase in erythrocytes reveals informaton about the thiamine reserve in tssues. Riboflavin (Vitamin B)2 A ribofavin molecule consists of the heterocyclic isoalloxazine ring atached to alcohol ribitol. Ribofavin is mainly resorbed in the jejunum through the sa turable Na -dependent actve transport. Resorpton is boosted by bile acids, reduced by metals (Cu, Zn, Fe), vitamin C,+ nicotnamide, tryptophane, cafeine, theophylline and some drugs (antbiotcs, antacid drugs etc. B is converted to cofactors in the cells of most tssues,2 in partcular enterocytes, the liver, myocardium and kidneys. The body has a low B reserve; excess vitamin is excreted in the urine, meaning renal2 excreton refects the daily intake of B2. Ribofavin defciency is usually accompanied by a defciency in the other B-group vitamins. Typical symptoms inclu de angular stomatts (infammaton of the corners of the mouth), cheilosis, glossits, swelling of mucous membranes, seborrhoeic dermatts and other dermal defects, conjunctvits, corneits and nervous disorders. Good sources are foods such as meat (turkey, tuna), liver, sunfower seeds, peanuts, brown bread, legumes, however a major part of niacin is produced endogenously from tryptophan. Nicotnic acid absorbs in the stomach, and nicotnamide also absorbs in the small intestne. When the level in food is high and the transporter saturated, passive+ difusion transport is also possible.

Syndromes

• Worse in the scalp, temples, or back of the neck, and possibly in the shoulders
• Brownish-red or copper-colored patch that is firm and flat on top
• Get plenty of rest.
• Learn how to take other medicines and when to eat
• Be sure that the child goes to the bathroom before going to sleep.
• Lymphoma

The patient is at the 50th percentile for height and 10th 60 A 2-year-old boy is brought to the emergency room with a percentile for weight impotence drugs buy generic viagra 100mg on-line. Her symptoms respond dramatically to 48-hour history of nausea erectile dysfunction drugs covered by insurance purchase viagra 50mg free shipping, vomiting erectile dysfunction treatments diabetes order viagra in united states online, and abdominal discom a gluten-free diet erectile dysfunction 30 order viagra 75mg otc. Ultrasound examination of the abdomen reveals a 2-cm (A) Celiac sprue mass in the right iliac fossa erectile dysfunction viagra cialis levitra discount 75mg viagra overnight delivery. Which of the following best (B) Cystic brosis of the pancreas describes this pathologic nding She was recently treated with broad-spectrum antibiotics for community-acquired pneumonia impotence erectile dysfunction generic 75 mg viagra with amex. An X-ray lm of the abdomen shows (C) Ischemic colitis fecal impaction in the rectosigmoid region. Which of the fol (D) Pseudomembranous colitis lowing pathologic lesions is most likely to be found in this (E) Ulcerative colitis patient The classication of this (D) Peptic ulcer anorectal malformation is based on the relationship of (E) Stercoral ulcer 152 Chapter 13 62 A 45-year-old woman complains of chronic, right lower 2 the answer is D: Esophageal web. Webs are thin mucosal membranes that proj smooth-walled mass protruding into the cecum. Rings are thicker than subsequently has the mass removed and the surgical specimen webs and contain smooth muscle. Which of the following is the most esophageal webs and rings include dysphagia, esophageal sub likely diagnosis Plummer-Vinson syndrome is characterized by a cervical esophageal web, mucosal lesions of the mouth and pharynx, and iron-deciency anemia. Carcinoma of the oropharynx and upper esophagus are complications of Plummer-Vinson syndrome. This patient exhibits signs of scleroderma (progressive systemic sclerosis), which is charac terized by vasculopathy and excessive collage deposition in the skin and internal organs. Patients often suffer from inter mittent episodes of ischemia of the ngers, marked by pallor, paresthesias, and pain (Raynaud phenomenon). Scleroderma can involve any por (A) Acute appendicitis tion of the gastrointestinal tract, although esophageal dys (B) Adenocarcinoma function is the most common and troublesome complication. In some affected patients, there may be a lack of peristalsis in the entire esophagus. The other choices are not associated with 63 A 70-year-old woman with a history of ovarian cancer presents scleroderma. She completed radiation therapy for her cancer Diagnosis: Scleroderma 3 months ago. Physical examination shows cachexia, hyper active bowel sounds, and generalized pallor. This disorder occurs (A) Angiodysplasia typically in the lower third of the esophagus. The lesion is (B) Hemorrhoids characterized histologically by distinctive intestine-like epi (C) Ischemic colitis thelium composed of goblet cells and surface cells similar to those of incompletely intestinalized gastric mucosa. Com (D) Radiation enterocolitis plete intestinal metaplasia, with Paneth cells and absorptive (E) Solitary rectal ulcer cells, may occur. Achalasia is characterized by failure of the lower esophageal sphincter to relax in response Diagnosis: Barrett esophagus, reux esophagitis to swallowing and the absence of peristalsis in the body of the esophagus. As a result of these defects in both the outow 5 the answer is B: Adenocarcinoma. Barrett esophagus carries tract and the pumping mechanisms of the esophagus, food is a serious risk of malignant transformation to adenocarci retained within the esophagus, and the organ hypertrophies noma, and the risk correlates with the length of the involved and dilates. Achalasia is associated with a depletion or absence esophagus and the degree of dysplasia. Virtually all esopha of ganglion cells in the myenteric plexuses, which regulate geal adenocarcinomas arise in the background of the meta contraction of the esophagus. The symptoms and be a manifestation of Chagas disease, in which the ganglion clinical course of adenocarcinoma of the esophagus are similar cells are destroyed by Trypanosoma cruzi. The other choices are to those of squamous cell carcinoma and include dysphagia, usually associated with visible mucosal abnormalities and do pain, and, occasionally, bleeding. Diagnosis: Achalasia Diagnosis: Barrett esophagus the Gastrointestinal Tract 153 the affected region of the esophagus is typically indurated and 6 the answer is E: Zenker diverticulum. The other choices do an uncommon lesion that appears high in the esophagus and not exhibit the histologic features described. It was once believed to result Diagnosis: Adenocarcinoma of the esophagus from luminal pressure exerted in a structurally weak area and was, therefore, classed as a pulsion diverticulum. The cause is probably more complicated, but disordered function of the 10 the answer is D: Squamous cell carcinoma. Most cancers cricopharyngeal musculature is still thought to be involved in of the esophagus worldwide are squamous cell carcinomas, the pathogenesis of this false diverticulum. Most affected per although adenocarcinoma is now more common in the United sons who come to medical attention are older than 60 years, States. Epiphrenic diverticuli (choice A) plasms that lack evidence of squamous differentiation. Intramural most common presenting complaint of patients with esopha pseudodiverticulum (choice B) is characterized by numerous geal cancer is dysphagia, but by this time, most tumors are small diverticula in the wall of the esophagus. Adenocarcinoma (choice A) and Barrett esopha ticuli (choice D) are outpouchings that occur principally in gus (choice B) are incorrect because the biopsy does not show the midportion of the esophagus. Primary malignant melanoma (choice C) of Diagnosis: Zenker diverticulum the esophagus is extremely rare, although melanoma metasta ses to the esophagus may occur. Diagnosis: Squamous cell carcinoma of the esophagus 7 the answer is D: Hiatal hernia. Hiatal hernia is a protrusion of the stomach through an enlarged esophageal hiatus in the 11 the answer is A: Cigarette smoking. In squamous cell carcinoma of the esophagus include chronic sliding hiatal hernias, an enlargement of the hiatus and laxity alcoholism, tobacco use, diets lacking in fresh fruits, exposure of the circumferential connective tissue allows a cap of gastric to aniline dyes, chronic esophagitis, and congenital disorders mucosa to move upward above the diaphragm. Cigarette geal hiatal hernias are characterized by herniation of a por smoking is associated with a 5 to 10-fold increased risk of tion of the gastric fundus alongside the esophagus through esophageal cancer, and the number of cigarettes smoked cor a defect in the diaphragmatic connective tissue membrane relates with the presence of dysplasia in the esophageal epithe that denes the esophageal hiatus. Epidemiologic data suggest that there are additional, as nia, particularly heartburn and regurgitation, are attributed yet unidentied risk factors prevalent in certain geographical to the reux of gastric contents, which is primarily related to regions of the world (China, Iran, and South Africa). Classically, esophagitis (choice E) leads to Barrett esophagus and adeno the symptoms are exacerbated when the affected person is carcinoma. Large herniations carry a risk of gastric volvulus linked to the development of hepatocellular carcinoma. Boerhaave syndrome (choice petic esophagitis (choice C) frequently occurs in immunocom A) represents rupture of the esophagus as a result of vom promised persons but is not associated with the development iting. Diagnosis: Esophageal cancer Diagnosis: Paraesophagic hiatal hernia 12 the answer is C: Refux esophagitis. Esophagitis may be caused by infections, reux of gastric juice, or exogenous irri 8 the answer is B: Coagulative necrosis. Of these, the most common type is reux esophagitis, the esophagus usually reects accidental poisoning in chil which is often found in conjunction with a sliding hiatal her dren, attempted suicide in adults, or contact with medication. By con of the squamous epithelium (leukoplakia) and the underly trast, ingestion of strong alkaline solutions is accompanied ing stroma. Areas affected by gastric reux are susceptible to by liquefactive necrosis (choice E), with inammation and mucosal erosions and ulcers which appear as linear vertical saponication of membrane lipids. Neutrophils and lymphocytes accumulate in the particularly insidious because they are generally odorless and mucosa. The other choices are not typical complications of tasteless and, therefore, easily swallowed before protective hiatal hernia. Diagnosis: Reux esophagitis, hiatal hernia Diagnosis: Chemical esophagitis 13 the answer is B: Candida esophagitis. Adenocarcinoma of the has become commonplace because of an increasing number esophagus is now more common (60%) in the United States of immunocompromised persons. Adenocarcinoma originates in occurs in patients with diabetes and in those receiving antibi the glandular metaplasia of Barrett esophagus. The pseudomembranes are composed of fungal surveillance for adenocarcinoma is now commonly done in mycelia, brin, and necrotic debris. Involvement of deeper patients with Barrett esophagus, particularly those with dys layers of the esophageal wall can lead to disseminated can plasia. Symptoms include dysphagia anemia that is caused by malabsorption of vitamin B12, occa and odynophagia (pain on swallowing). Herpetic esophagitis sioned by a deciency of the intrinsic factor, is referred to as (choice C) features mucosal vesicles. Diagnosis: Autoimmune atrophic gastritis, pernicious anemia Diagnosis: Infective esophagitis 18 the answer is E: Helicobacter pylori infection. Esophageal varices disease refers to breaks in the mucosa of the stomach and are dilated (varicose) veins immediately beneath the mucosa, small intestine, principally the proximal duodenum, which are which are prone to rupture and hemorrhage. The pathogenesis lower third of the esophagus, most often in the setting of por of peptic ulcer disease is believed to involve an underlying tal hypertension, secondary to cirrhosis. This pathogen has been veins are linked to the portal system through gastroesophageal isolated from the gastric antrum of virtually all patients with anastomoses. If the portal blood pressure exceeds a critical duodenal ulcers and from about 75% of those with gastric level, these anastomoses become prominent. In addi the other choices are not associated with bleeding esophageal tion to peptic ulcer disease, H. Alcoholic hepatitis (choice A) by itself does not cause for development of gastric adenocarcinoma and lymphoma. Gastrinoma (choice D) is a rare cause Diagnosis: Esophageal varices, cirrhosis of peptic ulcers. Achlorhydria (choice A) is incorrect because the formation of peptic ulcers requires at least some gastric 15 the answer is B: Congenital pyloric stenosis. The disorder is gastric ulcer the most common indication for abdominal surgery in the rst 6 months of life. Peptic ulcers of the stomach and dency, and the condition is more common in identical twins duodenum are estimated to afict 10% of the population of than in fraternal ones. The only consistent microscopic abnor Western industrialized countries at some time during their mality is hypertrophy of the circular muscle coat. Melena refers to black, tarry stools composed largely Diagnosis: Congenital pyloric stenosis of blood from the upper digestive tract that has been processed by the action of gastric juices. Acute hemorrhagic duodenal ulcers, most patients with gastric ulcers secrete nor gastritis is characterized by necrosis of the mucosa and is com mal or decreased amounts of gastric acid (see choice B). The factor common to all forms Diagnosis: Peptic ulcer disease, gastric ulcer of acute hemorrhagic gastritis is thought to be the breakdown of the mucosal barrier, which permits acid-induced injury. The necrosis is accompanied by an acute that is caused by malabsorption of vitamin B12 due to a de inammatory response and hemorrhage, which may be severe ciency of the intrinsic factor. In many cases, pernicious anemia enough to result in exsanguination and hypovolemic shock. Circulating antibodies to parietal cells, some of which are cytotoxic in the presence of complement, occur in 17 the answer is B: Autoimmune gastritis. Two thirds of patients refers to chronic, diffuse inammatory disease of the stomach display an antibody to the intrinsic factor that prevents its that is restricted to the body and fundus and is associated combination with vitamin B12, thereby preventing formation with other autoimmune phenomena. Half of all features diffuse atrophic gastritis, antibodies to parietal cells patients with pernicious anemia have circulating antibodies to and the intrinsic factor, and increased serum gastrin due to thyroid tissue. Immunologic destruction of parietal cells Diagnosis: Pernicious anemia, Hashimoto thyroiditis and antibody targeting of intrinsic factor interfere with intesti nal absorption of vitamin B12. Zollinger-Ellison syndrome is marrow precursors show asynchronous maturation between characterized by unrelenting peptic ulceration in the stom the nucleus and cytoplasm (megaloblastic cells), and the ach or duodenum (or even proximal jejunum) by the action peripheral blood displays megaloblastic anemia. Gastrin-producing neuroendocrine the Gastrointestinal Tract 155 tumors (gastrinomas) usually arise in the pancreatic islets. Microscopically, Among islet cell tumors, pancreatic gastrinomas are second the tumors show spindle cells with vacuolated cytoplasms. Gastric adenocarcinoma (choice A) does drome are due to gastrinomas outside the pancreas. Diagnosis: Gastrointestinal stromal tumor Diagnosis: Zollinger-Ellison syndrome, peptic ulcer disease, gastric ulcer 26 the answer is B: Gastric lymphoma. Gastric lymphoma is the most common form of extranodal lymphoma, accounting for 22 the answer is B: Adenocarcinoma. Gastric lymphoma has a considerably stomach accounts for more than 95% of all malignant gastric better prognosis than gastric carcinoma (45% 5-year survival). Most patients have metastases by the time they are the clinical symptoms of gastric lymphoma are nonspecic seen for examination. The most frequent initial symptom of and indistinguishable from those of gastric carcinoma. On setting of chronic Helicobacter pylori gastritis with lymphoid gross inspection, gastric cancer appears as a polypoid, fun hyperplasia. Some of these lymphomas regress after eradica gating, or ulcerated mass, or diffuse inltration of the stom tion of the infection. Curling ulcers (choice C) occur in severely burned the stomach that are composed of food or hair that have been patients. The mass removed from the Diagnosis: Gastric adenocarcinoma stomach in this patient is a hairball (trichobezoar) within a gelatinous matrix.

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