Gastric carcinoma is the second most common cancer in the world. The incidence is highest in Japan, China, Eastern Asia and Eastern Europe, ranging between 36.3 and 77.8 per 100 000 in men and 16.8 and 33.3 per 100 000 in women, an approximate 2:1 male preponderance. It is primarily a disease of the elderly, with a peak incidence at age 70-80.
Types of Gastric Carcinoma
Approximately 90% of stomach cancers are adenocarcinomas (the remaining 10% are non-Hodgkin's lymphomas and leiomyosarcomas). Adenocarcinomas are subdivided into intestinal and diffuse histological types (Lauren classification). The intestinal variety arises from a background of chronic gastritis and is generally well circumscribed. The diffuse type usually arises within apparently normal gastric mucosa and tends to be poorly localized, infiltrating beneath the mucosa through the muscle of the stomach wall. In the advanced stage, this leads to a thickened and shriveled stomach known as linitis plastica (leather bottle stomach). Unfortunately it is this type of disease that is often seen in the younger patient.
Causes and risk factors of Gastric carcinoma:
Risk factors for intestinal-type gastric carcinoma (those for the diffuse type are largely undefined) include smoking and diet (in particular high consumption of preserved food and high salt intake); there is a weak association with excess alcohol intake. Other diseases associated with gastric carcinoma are pernicious anaemia, atrophic gastritis, gastric adenomatous polyps and H. pylori infection, an increasingly important risk factor associated with a 2-fold increase in risk of gastric cancer.
Course of Gastric Carcinoma
Local
In the early stages, when the disease is confined to the mucosa or submucosa, it may be either a prominent nodule or a depressed ulcer. Excavated cancers may cause upper gastrointestinal bleeding and anaemia, whilst large exophytic growths near the cardia can (rarely) produce dysphagia.
Metastatic
The majority of tumours present with local or with lymph node metastases. Spread may be lymphatic, haematogenous (to the liver, lungs and brain) or transcoelomic to the peritoneum, omentum or ovaries (Krukenberg tumour).
Symptoms of Gastric Carcinoma
A common presentation is that of new-onset dyspepsia in a middle-aged patient (over 45 years). Symptoms are often non-specific such as epigastric discomfort, post-prandial fullness, loss of appetite or vague indigestion. Other symptoms include dysphagia, nausea or vomiting (especially after eating), weight loss and those of iron deficiency anaemia.
Clinical examination is often unremarkable in early stage disease. In advanced disease, clinical findings may include a mass in upper abdomen, enlarged liver, enlargement of the lymph glands, classically in the left supraclavicular fossa (Virchow's node, Troisier's sign), ascites and jaundice.
Types,Causes and Symptoms of Gastric carcinoma
Diagnosis and Treatment of Gastric Carcinoma
Showing posts with label gastro intestinal system. Show all posts
Showing posts with label gastro intestinal system. Show all posts
Saturday, April 25, 2009
Peptic Ulcer - Causes, Diagnosis and Treatment
Peptic ulcer disease
Peptic ulcer is a lesion in the mucosa of the stomach or duodenum in which acid and pepsin play a major role, the term is often used to encompass any gastric or duodenal ulceration. This includes ulceration that may occur from drugs (NSAIDs) or excessive gastrin production (Zollinger-Ellison syndrome).
Peptic ulcer disease is common. It usually presents after the age of 15 and is equally common in both sexes.
Causes of Peptic Ulcer:
Although the term peptic ulceration suggests that the main causative factor is increased acid secretion, patients with peptic ulcer disease usually have normal acid secretion rates.
The currently most widely accepted causative agent is H. pylori. Approximately 95% of duodenal ulcers and 70% of gastric ulcers are associated with H. pylori (but only 15% of H. pylori colonized individuals will develop peptic ulcer disease). The odds of developing peptic ulceration are increased 2-fold in H. pylori positive patients. Peptic ulceration is also more common in patients on NSAIDs (Non Steroidal Anti Inflammatory Drugs) (36%) as compared to patients who are not on NSAIDs (8%) in clinical studies. Weaker associations of peptic ulcer disease include smoking, alcohol, family history and blood group O.
Rare causes of peptic ulceration include hyperparathyroidism and Zollinger-Ellison syndrome, which results from a gastrinoma that usually arises from the G-cells in the pancreas, resulting in excess gastrin production and increased gastric acid secretion.
Symptoms of Peptic ulcer
Dyspepsia (recurrent upper abdominal pain) is the most common symptom. The pain may be related to meals and may occur at night. Associated symptoms include nausea and vomiting. Although attempts have been made to differentiate gastric from duodenal ulceration from the history, this has proved to be inaccurate and does not influence subsequent management.
Warning symptoms of significant disease or potential complications are dysphagia, weight loss and haematemesis. Patients with these symptoms or those who are over 35 years at initial presentation require urgent upper gastrointestinal endoscopy to screen for complications or malignancy (oesophageal, gastric).
Complication of peptic ulcer:
Complications of peptic ulcer disease include dyspepsia, upper gastrointestinal haemorrhage and gastric or duodena perforation. Chronic or recurrent ulceration may result in peptic strictures of the oesophagus or gastric outflow obstruction (pyloric stenosis).
Diagnosis of Peptic Ulcer
Screening for H. pylori
No investigations apart from screening for H. pylori colonization are required for young patients without any warning symptoms, as empirical treatment can commence on clinical diagnosis.
Further investigations
Upper gastrointestinal endoscopy
Upper gastrointestinal endoscopy is required for patients with warning symptoms and those over 35 years to screen for complications or oesophageal or gastric cancer.
Treatment of Peptic ulcer
Risk factor modification
Ideally patients should stop taking NSAIDs, but often this may not be possible; alternatives include the concomitant long-term use of a proton pump inhibitor. General advice involves stopping smoking and reducing alcohol intake, but there is little evidence to support the efficacy of these recommendations.
Medical management
H. pylori eradication
Triple therapy is recommended for all patients who are H. pylori positive. In patients with duodenal ulcers, eradication therapy was associated with a lower relative risk of persistent ulcer compared to acid suppression alone, but no differences were found for patients with gastric ulcers , nor does eradication therapy prevent recurrences in patients with duodenal ulcers.
Initial triple therapy
First-line triple therapy for H. pylori eradication consists of a proton pump inhibitor with either clarithromycin and amoxicillin or clarithromycin and metronidazole. Although many combinations and treatment durations have been proposed, the most effective are the twice-daily dosing, 1-week duration regimens such as omeprazole 20 mg twice daily, amoxicillin 1 g twice daily and clarithromycin 500 mg twice daily.
Initial eradication regimens progressively change due to failure rates associated with the development of antibiotic-resistant strains of H. pylori. Currently metronidazole-resistant strains are common and clarithromycin resistance is increasing. Dual therapy often fails to eradicate H. pylori and promotes emergence of resistant organisms.
Rescue therapy
Rescue therapy for failed initial eradication should consist of a different combination of antibiotics to that used for initial treatment, administered for 10-14 days. Selection of further antibiotic treatment should be based on antimicrobial susceptibilities from primary or secondary endoscopy biopsy culture results.
Proton pump inhibitors
A proton pump inhibitor is currently the standard treatment, and part of triple therapy. Thereafter, symptomatic patients, those with complicated peptic ulcer disease (presenting with bleeding, stricture or perforation) and those patients who require NSAIDs may still require long-term proton pump inhibitor therapy. Intermittent on-demand therapy is suitable for patients without complications for the control of symptoms.
Surgical management
Peptic ulcer surgery
Peptic ulcer surgery is now extremely rare for failed medical therapy due to the powerful acid suppression by proton pump inhibitors. Currently surgery is usually reserved for the development of complications such as perforation, severe bleeding and rarely stricture formation.
In patients with gastric or duodenal perforation, a primary repair is usually performed on laparotomy. A pyloroplasty to increase the diameter of the gastric outlet may be performed for patients with pyloric stenosis due to peptic stricture. A longitudinal incision is performed through the pylorus and closed as a transverse defect. Alternatively, a gastroenterostomy may be performed to bypass the narrowed pylorus. Gastrectomy is rarely performed unless there is evidence of malignancy.
Prognosis of Peptic ulcer
Peptic ulcer disease is a chronic relapsing condition. Symptom control with proton pump inhibitor therapy is usually achieved in the vast majority. Up to 15% may suffer with upper gastrointestinal haemorrhage requiring hospital admission, and less than 5% will require surgical intervention
Peptic ulcer is a lesion in the mucosa of the stomach or duodenum in which acid and pepsin play a major role, the term is often used to encompass any gastric or duodenal ulceration. This includes ulceration that may occur from drugs (NSAIDs) or excessive gastrin production (Zollinger-Ellison syndrome).
Peptic ulcer disease is common. It usually presents after the age of 15 and is equally common in both sexes.
Causes of Peptic Ulcer:
Although the term peptic ulceration suggests that the main causative factor is increased acid secretion, patients with peptic ulcer disease usually have normal acid secretion rates.
The currently most widely accepted causative agent is H. pylori. Approximately 95% of duodenal ulcers and 70% of gastric ulcers are associated with H. pylori (but only 15% of H. pylori colonized individuals will develop peptic ulcer disease). The odds of developing peptic ulceration are increased 2-fold in H. pylori positive patients. Peptic ulceration is also more common in patients on NSAIDs (Non Steroidal Anti Inflammatory Drugs) (36%) as compared to patients who are not on NSAIDs (8%) in clinical studies. Weaker associations of peptic ulcer disease include smoking, alcohol, family history and blood group O.
Rare causes of peptic ulceration include hyperparathyroidism and Zollinger-Ellison syndrome, which results from a gastrinoma that usually arises from the G-cells in the pancreas, resulting in excess gastrin production and increased gastric acid secretion.
Symptoms of Peptic ulcer
Dyspepsia (recurrent upper abdominal pain) is the most common symptom. The pain may be related to meals and may occur at night. Associated symptoms include nausea and vomiting. Although attempts have been made to differentiate gastric from duodenal ulceration from the history, this has proved to be inaccurate and does not influence subsequent management.
Warning symptoms of significant disease or potential complications are dysphagia, weight loss and haematemesis. Patients with these symptoms or those who are over 35 years at initial presentation require urgent upper gastrointestinal endoscopy to screen for complications or malignancy (oesophageal, gastric).
Complication of peptic ulcer:
Complications of peptic ulcer disease include dyspepsia, upper gastrointestinal haemorrhage and gastric or duodena perforation. Chronic or recurrent ulceration may result in peptic strictures of the oesophagus or gastric outflow obstruction (pyloric stenosis).
Diagnosis of Peptic Ulcer
Screening for H. pylori
No investigations apart from screening for H. pylori colonization are required for young patients without any warning symptoms, as empirical treatment can commence on clinical diagnosis.
Further investigations
Upper gastrointestinal endoscopy
Upper gastrointestinal endoscopy is required for patients with warning symptoms and those over 35 years to screen for complications or oesophageal or gastric cancer.
Treatment of Peptic ulcer
Risk factor modification
Ideally patients should stop taking NSAIDs, but often this may not be possible; alternatives include the concomitant long-term use of a proton pump inhibitor. General advice involves stopping smoking and reducing alcohol intake, but there is little evidence to support the efficacy of these recommendations.
Medical management
H. pylori eradication
Triple therapy is recommended for all patients who are H. pylori positive. In patients with duodenal ulcers, eradication therapy was associated with a lower relative risk of persistent ulcer compared to acid suppression alone, but no differences were found for patients with gastric ulcers , nor does eradication therapy prevent recurrences in patients with duodenal ulcers.
Initial triple therapy
First-line triple therapy for H. pylori eradication consists of a proton pump inhibitor with either clarithromycin and amoxicillin or clarithromycin and metronidazole. Although many combinations and treatment durations have been proposed, the most effective are the twice-daily dosing, 1-week duration regimens such as omeprazole 20 mg twice daily, amoxicillin 1 g twice daily and clarithromycin 500 mg twice daily.
Initial eradication regimens progressively change due to failure rates associated with the development of antibiotic-resistant strains of H. pylori. Currently metronidazole-resistant strains are common and clarithromycin resistance is increasing. Dual therapy often fails to eradicate H. pylori and promotes emergence of resistant organisms.
Rescue therapy
Rescue therapy for failed initial eradication should consist of a different combination of antibiotics to that used for initial treatment, administered for 10-14 days. Selection of further antibiotic treatment should be based on antimicrobial susceptibilities from primary or secondary endoscopy biopsy culture results.
Proton pump inhibitors
A proton pump inhibitor is currently the standard treatment, and part of triple therapy. Thereafter, symptomatic patients, those with complicated peptic ulcer disease (presenting with bleeding, stricture or perforation) and those patients who require NSAIDs may still require long-term proton pump inhibitor therapy. Intermittent on-demand therapy is suitable for patients without complications for the control of symptoms.
Surgical management
Peptic ulcer surgery
Peptic ulcer surgery is now extremely rare for failed medical therapy due to the powerful acid suppression by proton pump inhibitors. Currently surgery is usually reserved for the development of complications such as perforation, severe bleeding and rarely stricture formation.
In patients with gastric or duodenal perforation, a primary repair is usually performed on laparotomy. A pyloroplasty to increase the diameter of the gastric outlet may be performed for patients with pyloric stenosis due to peptic stricture. A longitudinal incision is performed through the pylorus and closed as a transverse defect. Alternatively, a gastroenterostomy may be performed to bypass the narrowed pylorus. Gastrectomy is rarely performed unless there is evidence of malignancy.
Prognosis of Peptic ulcer
Peptic ulcer disease is a chronic relapsing condition. Symptom control with proton pump inhibitor therapy is usually achieved in the vast majority. Up to 15% may suffer with upper gastrointestinal haemorrhage requiring hospital admission, and less than 5% will require surgical intervention
Thursday, April 9, 2009
Symptoms of Systemic Lupus Erythematosus (SLE)
SLE is awfully uneven in its manifestations and most of the symptoms are due to the consequences of vasculitis or, inflammation of the blood vessels. Mild cases may complain only of joint pains and fatigue, and sometimes difficult to diagnose.
General symptoms of SLE
Fever is a common problem during exacerbations, occurring in up to 50% of patients. They complain of obvious malaise and tiredness and these symptoms do not correlate with the activity or, severity of the organ based complications of the disease.
The joints and muscles affection in SLE
Joint involvement is the commonest clinical entity and affect more than 90% of the patients. They frequently present with complains resembling Rheumatoid Arthritis (RA) with symmetrical small joint arthralgia. Joints are painful but typically appear clinically normal, although at times there may be slight soft-tissue swelling surrounding the joint. Deformity due to joint capsule and tendon contraction is uncommon, as are bony erosions.
Hardly ever, major joint deformity resembling RA (known as Jaccoud's arthropathy) may be found. Aseptic necrosis affecting the hip or knee joint is an infrequent complication of the disease.
Myalgia is the complain of up to 50% of patients but a true myositis is found only in less than 5%. of them. Overlapping of any connective tissue disorder is likely if myositis is prominent.
The skin and SLE
Skin is affected in SLE in about 75% of cases. Butterfly shaped erythema, in a distribution on the cheeks of the face and across the bridge of the nose typical of SLE. Vasculitic lesions on the finger tips and around the nail folds, purpura or, tiny bleeding spots and urticaria are commonly found. In about one-third of patients photosensitivity is found, and stretched exposure to sunlight can lead to exacerbations of the condition in them. Livedo reticularis, palmar and plantar rashes, pigmentation and alopecia are also found in some patients.
Involvement of lungs in SLE
Approximately 50% of SLE patients usually get lung involvement sometime during the course of the disease. Recurrent pleurisy and pleural effusions or, fluid around the lugs are the commonest manifestations and are usually bilateral. Pneumonitis and atelectasis or, solidification may also be found; ultimately a restrictive lung defect develops with loss of lung volumes and elevated hemi diaphragms. This 'shrinking lung syndrome' is not clearly understood but may have a neuromuscular foundation. Not often, pulmonary fibrosis may occcur, more commonly in overlap syndromes. Intrapulmonary haemorrhage associated with vasculitis is a not common but potentially life-threatening complication.
Effect of SLE in heart and cardiovascular system
The heart is affected in 25% of SLE patients. Pericarditis, with small (pericardial effusions) collection of fluid detected by echocardiography, is common. A mild myocarditis also occurs, leads to arrhythmias. Lesions in the Aortic valve and a cardiomyopathy can infrequently be found. A non-infective endocarditis involving the mitral valve (Libman-Sacks syndrome) is very exceptional finding. Raynaud's, vasculitis, arterial and venous thromboses may appear, especially in association with the antiphospholipid syndrome. There is an increased incidence of atherosclerotic disorder in SLE. This partly due to the treatment with corticosteroids but more likely that SLE itself is the cause
SLE and the kidneys
Though Autopsy examination shows that histological changes in the kidneys are fairly common finding, but clinical renal problems manifests in only approximately 30% of patients. All patients should undergo regular screening of urine for blood and protein. Proteinuria should be measured and any haematuria should be examined immediately for urinary casts or fragmented red cells which suggest glomerulonephritis. Renal vein thrombosis may be found in nephrotic syndrome or associated with procoagulant antiphospholipid antibodies.
Nervous system involvement in SLE
Involvement of the nervous system in SLE is present in up to 60%of patients and symptoms may change. There may be a slight depression but sometimes more severe psychiatric problems occur. Epilepsy, migraines, cerebellar ataxia,
aseptic meningitis, cranial nerve lesions, cerebrovascular disease or a polyneuropathy are sometimes seen.
The eyes in SLE
Retinal vasculitis in SLE can cause infarcts (cytoid bodies) which appear as hard exudates, and haemorrhages in retina. Episcleritis, conjunctivitis or optic neuritis, may also occur but blindness is infrequent. Secondary Sjogren's syndrome can sometimes be seen in about 15% of cases.
Involvement of the gastrointestinal system in SLE
SLE causes gastrointestinal symptoms, of which mouth ulcers are the most common and may be the first symptom. These ulcers can be painless or become painful after being secondarily infected. Mesenteric vasculitis can produce inflammatory lesions in small bowel in the form of infarction or perforation. Liver involvement is not common, but lupoid antibodies are detected in autoimmune hepatitis. Pancreatitis is also rare.
Pregnancy and SLE
Fertility is generally normal except in severe form of the disease and there is no major bar to gofor pregnancy. Barrier methods of contraception rather than the pill are suitable in SLE. Recurrent miscarriages is common and these seems to be associated with antiphospholipid antibodies. Remission and exacerbations is common during pregnancy tenure with frequent exacerbations is also common following the delivery of the baby i.e. postpartum. The usual management of the disease is continued during pregnancy. Hypertension is controlled with proper medications. With gross renal involvement with SLE and high level of antiphospholipid antibodies, fetal loss is more than 25%.
General symptoms of SLE
Fever is a common problem during exacerbations, occurring in up to 50% of patients. They complain of obvious malaise and tiredness and these symptoms do not correlate with the activity or, severity of the organ based complications of the disease.
The joints and muscles affection in SLE
Joint involvement is the commonest clinical entity and affect more than 90% of the patients. They frequently present with complains resembling Rheumatoid Arthritis (RA) with symmetrical small joint arthralgia. Joints are painful but typically appear clinically normal, although at times there may be slight soft-tissue swelling surrounding the joint. Deformity due to joint capsule and tendon contraction is uncommon, as are bony erosions.
Hardly ever, major joint deformity resembling RA (known as Jaccoud's arthropathy) may be found. Aseptic necrosis affecting the hip or knee joint is an infrequent complication of the disease.
Myalgia is the complain of up to 50% of patients but a true myositis is found only in less than 5%. of them. Overlapping of any connective tissue disorder is likely if myositis is prominent.
The skin and SLE
Skin is affected in SLE in about 75% of cases. Butterfly shaped erythema, in a distribution on the cheeks of the face and across the bridge of the nose typical of SLE. Vasculitic lesions on the finger tips and around the nail folds, purpura or, tiny bleeding spots and urticaria are commonly found. In about one-third of patients photosensitivity is found, and stretched exposure to sunlight can lead to exacerbations of the condition in them. Livedo reticularis, palmar and plantar rashes, pigmentation and alopecia are also found in some patients.
Involvement of lungs in SLE
Approximately 50% of SLE patients usually get lung involvement sometime during the course of the disease. Recurrent pleurisy and pleural effusions or, fluid around the lugs are the commonest manifestations and are usually bilateral. Pneumonitis and atelectasis or, solidification may also be found; ultimately a restrictive lung defect develops with loss of lung volumes and elevated hemi diaphragms. This 'shrinking lung syndrome' is not clearly understood but may have a neuromuscular foundation. Not often, pulmonary fibrosis may occcur, more commonly in overlap syndromes. Intrapulmonary haemorrhage associated with vasculitis is a not common but potentially life-threatening complication.
Effect of SLE in heart and cardiovascular system
The heart is affected in 25% of SLE patients. Pericarditis, with small (pericardial effusions) collection of fluid detected by echocardiography, is common. A mild myocarditis also occurs, leads to arrhythmias. Lesions in the Aortic valve and a cardiomyopathy can infrequently be found. A non-infective endocarditis involving the mitral valve (Libman-Sacks syndrome) is very exceptional finding. Raynaud's, vasculitis, arterial and venous thromboses may appear, especially in association with the antiphospholipid syndrome. There is an increased incidence of atherosclerotic disorder in SLE. This partly due to the treatment with corticosteroids but more likely that SLE itself is the cause
SLE and the kidneys
Though Autopsy examination shows that histological changes in the kidneys are fairly common finding, but clinical renal problems manifests in only approximately 30% of patients. All patients should undergo regular screening of urine for blood and protein. Proteinuria should be measured and any haematuria should be examined immediately for urinary casts or fragmented red cells which suggest glomerulonephritis. Renal vein thrombosis may be found in nephrotic syndrome or associated with procoagulant antiphospholipid antibodies.
Nervous system involvement in SLE
Involvement of the nervous system in SLE is present in up to 60%of patients and symptoms may change. There may be a slight depression but sometimes more severe psychiatric problems occur. Epilepsy, migraines, cerebellar ataxia,
aseptic meningitis, cranial nerve lesions, cerebrovascular disease or a polyneuropathy are sometimes seen.
The eyes in SLE
Retinal vasculitis in SLE can cause infarcts (cytoid bodies) which appear as hard exudates, and haemorrhages in retina. Episcleritis, conjunctivitis or optic neuritis, may also occur but blindness is infrequent. Secondary Sjogren's syndrome can sometimes be seen in about 15% of cases.
Involvement of the gastrointestinal system in SLE
SLE causes gastrointestinal symptoms, of which mouth ulcers are the most common and may be the first symptom. These ulcers can be painless or become painful after being secondarily infected. Mesenteric vasculitis can produce inflammatory lesions in small bowel in the form of infarction or perforation. Liver involvement is not common, but lupoid antibodies are detected in autoimmune hepatitis. Pancreatitis is also rare.
Pregnancy and SLE
Fertility is generally normal except in severe form of the disease and there is no major bar to gofor pregnancy. Barrier methods of contraception rather than the pill are suitable in SLE. Recurrent miscarriages is common and these seems to be associated with antiphospholipid antibodies. Remission and exacerbations is common during pregnancy tenure with frequent exacerbations is also common following the delivery of the baby i.e. postpartum. The usual management of the disease is continued during pregnancy. Hypertension is controlled with proper medications. With gross renal involvement with SLE and high level of antiphospholipid antibodies, fetal loss is more than 25%.
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