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Sarcoidosis of the stomach can be difficult to distinguish endoscopically and histologically from Crohn disease and the diagnosis must be based on the presence of other systemic features baclofen 25mg cheap muscle relaxant reviews. Gastritis with Specific Diagnostic Features Collagenous gastritis has been reported in association with collagenous colitis and lymphocytic colitis buy 25 mg baclofen overnight delivery muscle relaxant bath; it is very rare buy baclofen 25 mg otc back spasms 24 weeks pregnant. At endoscopy, non-specific findings include mucosal hemorrhages, erosions and nodularity while histology shows a chronic gastritis (plasma cells and intra-epithelial lymphocytes), focal atrophy and focal collagen deposition (2075 m) in the lamina propria. Histology shows an infiltrate of the lamina propria in the antrum or body by plasma cells, lymphocytes and rare neutrophils, and a marked intraepithelial infiltrate with T lymphocytes. Eosinophilic gastritis is associated with peripheral eosinophilia and eosinophilic infiltration of the stomach, involving one or more layers of the gastrointestinal tract (mucosa, muscle or subserosa). Hypertrophic Gastropathies There are numerous causes of thickened gastric folds seen on endoscopy or diagnostic imaging (Table 2). Mntriers disease is associated with protein- losing gastropathy and hypochlorhydria whereas hyperplastic, hypersecretory gastropathy is associated with increased or normal acid secretion and hyper- plasia of the parietal and chief cells, with or without protein loss. Endoscopy, in both cases, typically shows irregular hypertrophic folds involving the body of the stomach, although there is a polypoid variant that resembles multiple hyperplastic gastric polyps. The characteristic histological features are foveolar hyperplasia with cystic dilation; inflammatory infiltrates may be present, as in hypertrophic lymphocytic gastritis, but this is variable. Gastric resection for refractory protein loss, hemorrhage or obstruction is a last resort. Miscellaneous Gastritides Gastritis cystica profunda is a rare sequela of partial gastrectomy with gastro- jejunostomy but it may also develop in the absence of prior gastric surgery. Endoscopy typically shows multiple exophytic gastric masses, which on sec- tion reveal multiple cysts. At histology, foveolar hyperplasia is accompanied by cystic glands that extend through the muscularis mucosae into the submucosa and muscularis propria. It may be associated with chronic atrophic gastritis, hyperplasia or primary gastric stump cancer after surgery. Gastric Polyps and Gastric Malignancy There are numerous types of gastric polyps (Table 4) which are usually incidental findings with little risk of developing into cancer. Gastric polyps are gastric epithelial or non- epithelial protrusions observed either endoscopically or radiologically. The non-epithelial polyps arise from the mesenchymal tissue of the submucosa (such as a leiomyoma). The epithelial polyps are most common, and are often multiple, hyperplastic polyps. Infre- quently, adenomatous or villoadenomatous polyps, which are often singular, occur. Individuals with a parent or sibling with gastric cancer are three times as likely to develop gastric cancer as the general population. Although regular screening is not warranted in either case, minor symptoms should be promptly and thoroughly investigated. In Canada there were 2,800 new gastric cancer cases in 2001 (8 per 100,000) and 1,950 deaths. There are numerous risk factors associated with the development of gastric adenocarcinoma (Table 5). The incidence of gastric adenocarcinoma has been falling dramatically in North America from ~ 30 per 100,000 in the 1930s to 68 per 100,000 at present. There is a disparity in adenocarcinoma incidence between first- and second-generation immigrants, suggesting both genetic and lifestyle or environmental factors together contribute to the risk for cancer. Genetic factors that increase the risk include low gastric acid secretory status and the presence of pro-inflammatory genes such as interleukin-1, which is associated with gastric acid hyposecretion. Several lifestyle factors including diet and smoking increase the risk of gastric cancer but these are potentially modifi- able. Shaffer 155 Polypoid Gastric Size Endoscopic Pathological Comments lesion location appearance features Pancreatic Antrum, 0. Sleisenger & Fordtrans Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management 2006: pg 1149. Environmental Risk Factors Dietary factors that contribute to gastric cancer include a high dietary salt and nitrate/nitrite intake, low fruit and vegetable intake, and the use of tobacco. Persons with the highest intake of vegetables have a significantly reduced risk of gastric cancer compared to those who consume no vegetables. Similar but weaker protective effects have also been observed for consumption of green and cruciferous vegetables. Current smoking adversely influences the risk for gastric cancer, and this risk increases with the intensity and duration of cigarette smoking. Carcinoma of the gastric cardia First Principles of Gastroenterology and Hepatology A. Nested case-control studies showed an increase in the risk of cancer (odds ratios 2. Shaffer 158 higher risk for gastric cancer than older patients, presumably because of their having a longer duration of exposure. In a proportion of patients with chronic atrophic gastritis, intestinal metaplasia develops and, in a much smaller proportion, dysplasia and subsequently cancer (Table 5). Recent studies have shown the importance of inflammation, arising from the initial H. Patients with the interleukin-1 gene cluster polymorphism, which may enhance production of the proinflammatory cytokine interleukin-13, are at increased risk of H. Thus, host genetic factors that affect interleukin- 1 production and hypochlorhydria may influence gastric cancer risk in those infected with H. Such exciting advances in the genetics of gastric cancer promise a means to identify early those who are at risk of this serious malignancy.
Clinical features of acute liver failure Whole body o Systemic inflammatory response o High energy expenditure and catabolism Liver o Loss of metabolic function o Decreased gluconeogenesis leading to hypoglycemia o Decreased lactate clearance leading to lactic acidosis o Decrease ammonia clearance leading to hyperammonemia o Decreased synthetic capacity leading to coagulopathy Lungs o Acute lung injury o Adult respiratory distress syndrome Adrenal gland o Inadequate glucocorticoid production contributing to hypotension Bone marrow o Frequent suppression discount baclofen 10 mg otc spasms below rib cage, especially in viral and seronegative disease Circulating leukocytes o Impaired function and immunoparesis contributing to high risk of sepsis Brain o Hepatic encephalopathy o Cerebral edema o Intracranial hypertension Heart o High output state o Frequent subclinical myocardial injury Pancreatitis o Particularly in paracetamol-related acute liver failure Kidney o Frequent dysfunction or failure Portal hypertension First Principles of Gastroenterology and Hepatology A order baclofen 10 mg line spasms in neck. Shaffer 488 o Might be prominent in subacute disease and confused with chronic liver disease Permission to reprint: Bernal et al generic baclofen 10 mg without prescription muscle relaxant equipment. Acetaminophen Acetaminophen is an effective over-the-counter analgesic, and is safe when taken in a daily dose that does not exceed 4 gm. For example the malnourished, alcoholic taking an acute dose of acetaminophen of >100mg/kg or a 10 to 20 gm dose over three days will develop: acute zone 3 necrosis, extending to bridging or panacinar (massive) necrosis. Liver failure may result from attempted suicide or therapeutic misadventure, as confirmed by a recent literature review (Larson et al. Fatal cases usually involve 20 gm acetaminophen (caution in the heavy alcohol abuser, where even 2 gm may be fatal). Over 20% develop severe liver injury, and of these, 20% die from the hepatotoxicity. This in turn leads to the production of reactive oxygen species, hepatocellular apoptosis, and centrilobular necrosis. Hyperacute injury to the liver occurs within 48 to 72 hours after acetaminophen ingestion. Death can occur in 4 to 8 days from cerebral edema, sepsis, liver and multi-organ failure. After 4 hours of taking an overdose, when most of the acetaminophen has been emptied from the stomach and absorbed, blood levels reflect the prognosis. The risk is assessed with the Prescott nomogram, which plots the plasma concentration of acetaminophen versus hours post- ingestion. Note that with chronic intake, blood levels of acetaminophen are not a reliable indicator of liver injury as it is with acute overdose. Antiretroviral Agents Hepatic damage is not uncommon with nucleosides and nucleotide reverse transcriptase inhibitors, as well as protease inhibitors. Therefore, it is important to consider all these factors, as they contribute to liver damage. This leads to fatty liver (micro- and/or macrovascular steatosis), First Principles of Gastroenterology and Hepatology A. The onset of these abnormalities will usually be about 6 months into the treatment. Acute hepatitis occurs in 3% to 30% of persons taking the protease inhibitor ritonavir. Acute liver failure is rare; the unconjugated hyperbilirubinemia seen in 7% of persons given protease inhibitors does not forebode progression to severe cholestasis. Anti Tuberculosis Therapy For every 100,000 persons given Isoniazid, about 2000 will develop hepatitis, and approximately 150 will die from acute liver failure. After acetaminophen, isoniazid-hepatitis is the second most common reason for the liver transplantation for drug-induced liver injury. It is important to stress that the hepatotoxicity of isoniazid does not relate to the dose or blood level. Immunosuppression agents Azathioprine or methotrexate may frequently be used in persons with chronic hepatitis or inflammatory bowel disease (Crohn disease or ulcerative colitis). Regardless, all patients are recommended to be on folinic acid to reduce side effect profile. A liver biopsy can be considered if cumulative dose of 1000-1500mg has been achieved. Oral Contraceptives There is a widespread use of oral contraceptive agents in young women, and several cholestatic hepatic toxicities are recognized (Table 12) Table 12. Hepatobiliary complications of the use of oral contraceptive agents o Gallstone o Cholestasis o Unmasking cholestatic disease such as primary biliary cirrhosis 4. Herbal preparations With the publics enthusiastic use of herbal preparations and the potential for some of these agents to cause hepatocellular injury and even acute liver failure, a careful historical inquiry into use of herbal preparations must be made in any person with abnormal Les or suspected liver disease, or acute liver failure. Drugs causing Chronic Hepatitis Some drugs such as nitrofurantoin, methyldopa and minocycline may cause chronic hepatitis, especially in older women who have been on the drug for a long interval. In another form of chronic drug-associated hepatotoxicity, anti-nuclear and anti-smooth muscle antibodies develop. In persons with known cirrhosis, there will be reduced mass of healthy liver cells capable of metabolizing drugs handled by the liver, and the dose of the drug will need to be reduced (hepatic dosing) (Table 13). In the same token, there are drugs which are relatively contraindicated in persons with liver disease (Table 14). It is unreasonable to commit these long list to memory, but this information would be useful for you to have handy on your iPhone. In time however 50 mg these collaterals may burst and lead to life- threatening bleeding such as from esophageal varices. The portal disease may be measured directly by the percutaneous insertion of a needle into the portal vein, liver or spleen. Extrahepatic Short gastric vein Left gastric vein Splenic vein Inferior mesenteric vein-tributaries Umbilical vein from the left colon and rectum Superior mesenteric vein-tributaries from B. Progressive branching of the intrahepatic portal vein and its distribution to the lobes of Obliterated umbilical the liver. Clinical Considerations Cirrhosis is a pathological condition referring to changes seen on biopsy of the liver in persons with any type of chronic liver disease. Once cirrhosis develops, the liver may still have the ability to First Principles of Gastroenterology and Hepatology A. Shaffer 504 repair itself (particularly if the inciting cause of the liver damage is removed), and the cirrhosis may regress. Because the th prevalence of cirrhosis peaks in the mid- to late-50s, it becomes the 4 most common cause of death in that age group.
Chorea Huntingtons disease consists of jerky buy baclofen 10 mg line spasms lower left side, quasi-purposeful and sometimes ex- Denition plosive movements generic baclofen 25 mg on line muscle relaxant anticholinergic, following each other but itting Genetically inherited progressive chorea and dementia cheap 10mg baclofen visa spasms definition. The disease shows strong geographical variation, with whites having twice the risk of non-whites and those in higher latitudes (i. Investigations r It is thought that there is an abnormal immune re- Genetic analysis is becoming available for pre- sponse, possibly triggered by an unknown viral anti- symptomatictestingbutthisraisesanethicaldilemma,as gen. However, it is important, as many r Genetic predisposition to the disease monozygotic young adults wish to know their status before embarking twins have a 2040% concordance, whereas siblings upon having a family. Patients and their families should be offered ge- netic testing and counselling where appropriate. Pathophysiology Discrete areas of demyelination called plaques ranging Prognosis in size from a few millimetres to a few centimetres. They There is a relentless progression of dementia and chorea are often perivenous and common sites in the brain in- with death usually occurring within 20 years from the clude the optic nerve, around the lateral ventricles and onset of symptoms. The cervical spinal cord is also commonly affected, but any part of the central white matter may be involved. Multiple sclerosis Initial oedema around the soft patches of white matter leads to symptoms that partially resolve as the oedema Denition subsides. An immune-mediated disease characterised by discrete The areas of demyelination are disseminated in time areas of demyelination in the brain and spinal cord. Old lesions are rm, grey-pink burnt-out ing: plaques that have very few inammatory cells and are r Optic neuritis usually unilateral visual loss which dominated by astrocytes. There may be hemiparesis, paraparesis osensory and auditory evoked responses may demon- or monoparesis. Bladder symptoms, muscle spasms, pain ning like pains going down into the spine or limbs and other problems are treated appropriately. Internuclear improvement, but do not appear to reduce the resid- ophthalmoplegia is a horizontal gaze palsy resulting ual neurological decit. They are therefore usually re- from a lesion affecting the medial longitudinal fas- served for disabling visual or motor disease. The diagnosis may be made clinically if there are Prognosis two or more attacks separated in time with, clinical ev- The prognosis of multiple sclerosis is very variable, the idence of lesions in different areas. Following a single relapsing-remitting pattern having a better prognosis attack or clinical evidence of only one lesion area the thantheprogressiveforms. Deatheventuallyoccursafter diagnosis may still be made if there is radiological evi- late-stage disease (optic atrophy, spastic quadriparesis, denceoftwoormorelesionsintimeorspace(McDonald brain-stem and cerebellar disease) typically from com- Criteria). Aetiology r Normal pressure hydrocephalus presents with one or Hydrocephalus can be divided into obstructive/non- more of dementia, ataxia and urinary incontinence. Investigations r Subarachnoid haemorrhage, head injury and menin- Lumbar puncture is contraindicated in obstructive hy- gitis. Management r Intracranial venous thrombosis In all cases, treatment is aimed at the underlying cause. Steroids and mannitol are used in cer- the slit like third ventricle and then through the narrow tain circumstances. The shunt has a one way valve but blockage Denition leads to an acute hydrocephalus. A similar condition is seen secondary to endocrine Aetiology abnormalities, polycystic ovaries, vitamin A toxicity, The cause is unknown although there is a familial ten- steroids and other drugs. Patients present with headache, visual obscurations and r Migraine is common premenstrually and around the may have tinnitus. In more advanced cases an enlarged blind spot, visual eld loss or a sixth cranial nerve palsy may occur. Pathophysiology Severe untreated disease may result in ischaemia of the The exact pathophysiology is unclear: optic nerve presenting with progressive blindness. Serum levels of hydrox- nerve sheath decompression/fenestration may be in- ytryptamine rise at the onset of the prodromal symp- dicated. It is unilat- Somepatientshavealmostdailyheadaches,withthepain eral in two-thirds of cases, bifrontal or generalised in constantorwaxingandwaning. The headache typically lasts several hours Investigations and may last up to several days. Management Investigations Reassurance, avoiding any precipitating factors and In most cases, none are necessary. The 5-hydroxytryptamine agonists Intermittent excruciating pain in the distribution of one (triptans) may be very effective. There ap- xytryptamine antagonists), propranalol, tricyclic pears to be demyelination of the trigeminal nerve root, antidepressants such as amitryptiline and anticonvul- in some cases it is hypothesised that this occurs due to sants such as sodium valproate. Clinical features Investigations Motorneurone disease causes mixed upper and lower The diagnosis is clinical. Three patterns are recognised depending on which group of motor neurones is lost rst; however, Management most patients progress to a combination of the syn- Carbamazepine can be effective. Amyotrophy means atrophy of treatment such as microvascular decompression or al- muscle. The clinical picture is that of a progressive cohol injection into the Gasserian ganglion. Typical clinical ndings include spasticity, reduced power, muscle fasciculation and Prognosis brisk reexes with upgoing plantars. Remissions for months or years may occur, often fol- r Progressivebulbarpalsyisadiseaseofthelowercranial lowed by recurrence. The features are those of a bulbar and pseudobulbar palsy with upper and lower motor neurone signs, i. Theremaybenasalregurgitationandanincreasedrisk Motor neurone disease of aspiration pneumonia. It often becomes bilateral over Progressive neurodegenerative disorder of upper and time.