Hypertension
Cushing's syndrome can be exogenous, resulting from the administration of glucocorticoids or adrenocorticotrophic hormone (ACTH), or endogenous, secondary to increased secretion of cortisol or ACTH. Hypertension is one of the most distinguishing features of endogenous Cushing's syndrome, as it is present in about 80% of adult patients and in almost half of children and adolescents patients. Hypertension results from the interplay of several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which may be increased. The therapeutic goal is to find and remove the cause of excess glucocorticoids, which, in most cases of endogenous Cushing's syndrome, is achieved surgically. Treatment of Cushing's syndrome usually results in resolution or amelioration of hypertension. However, some patients may not achieve normotension or may require a prolonged period of time for the correction of hypercortisolism. Therefore, therapeutic strategies for Cushing's-specific hypertension (to normalise blood pressure and decrease the duration of hypertension) are necessary to decrease the morbidity and mortality associated with this disorder. The various pathogenetic mechanisms that have been proposed for the development of glucocorticoid-induced hypertension in Cushing's syndrome and its management are discussed.
Muscle wasting
By contrast, glucocorticoids (cortisol) exert a clear catabolic effect, and their levels are frequently increased in diseased states. Cortisol activates a catabolic enzyme called ubiquitin-proteasome, which breaks down muscle tissue. Acute glucocorticoid treatment increases the expression of ubiquitin-proteases in muscle, resulting in catabolism.
Increased blood glucose
Other signs include polyuria (and accompanying polydipsia), persistent hypertension (due to cortisol's enhancement of epinephrine's vasoconstrictive effect) and insulin resistance (especially common in ectopic ACTH production), leading to hyperglycemia (high blood sugar) which can lead to diabetes mellitus.
we come in many different colors and flavors (:
Wednesday, August 25, 2010
Cushing's Syndrome: Symptoms - Focus on moonface, central obesity, thin skin and fatigue.
Cushing’s Syndrome
It is basically high levels of cortisol or adrenocorticotropic hormone (which leads to high cortisol).
The reasons for the manifestations of the many symptoms relate directly to the actions of these hormones.
Overall symptoms
Most people with Cushing syndrome will have:
• Upper body obesity (above the waist) and thin arms and legs
• Round, red, full face (moon face)
• Slow growth rate in children
Skin changes that are often seen:
• Acne or skin infections
• Purple marks (1/2 inch or more wide) called striae on the skin of the abdomen, thighs, and breasts
• Thin skin with easy bruising
Muscle and bone changes include:
• Backache, which occurs with routine activities
• Bone pain or tenderness
• Collection of fat between the shoulders (buffalo hump)
• Thinning of the bones, which leads to rib and spine fractures
• Weak muscles
Women with Cushing syndrome often have:
• Excess hair growth on the face, neck, chest, abdomen, and thighs
• Menstrual cycle becomes irregular or stops
Men may have:
• Decreased fertility
• Decreased or no desire for sex
• Impotence
Other symptoms that may occur with this disease:
• Mental changes, such as depression, anxiety, or changes in behavior
• Fatigue
• Headache
• High blood pressure
• Increased thirst and urination
So how does excess cortisol cause the symptoms “moonface”, central obesity, thin skin and severe fatigue?
Cortisol counteracts insulin, contributing to hyperglycemia via stimulation of hepatic gluconeogenesis and inhibition of the peripheral utilization of glucose by decreasing the translocation of glucose transporters to the cell membrane, especially GLUT4. However cortisol increases glycogen synthesis (glycogenesis) in the liver. Cortisol also acts as an anti-diuretic hormone
Moonface
The reason why fat tends to accumulate where it does is not known, but perhaps it is because there are more stress hormone receptors in the face and body, which are more sensitive to insulin, where skeletal muscle is less sensitive to insulin. Another reason is due to increased mobilization of fat in extremities and deposition in the trunk.
Central obesity
It is generally suggested that stress-induced cortisol weight is usually gained around the waistline, because fat cells in that area are more sensitive to cortisol. The fat cells in your abdomen are richer in stress hormone receptors, are particularly sensitive to high insulin, and are very effective at storing energy – more so than fat cells you would find in other areas of the body.
Thin skin
In laboratory rats, cortisol-induced collagen loss in the skin is ten times greater than any other tissue. It is probable that increasing copper availability for immune purposes is the reason many copper enzymes are stimulated to an extent which is often 50% of their total potential by cortisol. This includes lysyl oxidase, an enzyme which is used to cross link collagen and elastin.
Severe fatigue
This is due to increased catabolism of protein for gluconeogenesis and decreased synthesis of protein (except for in the liver). This leads to muscle weakness and thus fatigue. As the effects of insulin are also reduced, glucose is not being effectively taken into cells, especially skeletal muscle which can also contribute to feeling fatigued.
It is basically high levels of cortisol or adrenocorticotropic hormone (which leads to high cortisol).
The reasons for the manifestations of the many symptoms relate directly to the actions of these hormones.
Overall symptoms
Most people with Cushing syndrome will have:
• Upper body obesity (above the waist) and thin arms and legs
• Round, red, full face (moon face)
• Slow growth rate in children
Skin changes that are often seen:
• Acne or skin infections
• Purple marks (1/2 inch or more wide) called striae on the skin of the abdomen, thighs, and breasts
• Thin skin with easy bruising
Muscle and bone changes include:
• Backache, which occurs with routine activities
• Bone pain or tenderness
• Collection of fat between the shoulders (buffalo hump)
• Thinning of the bones, which leads to rib and spine fractures
• Weak muscles
Women with Cushing syndrome often have:
• Excess hair growth on the face, neck, chest, abdomen, and thighs
• Menstrual cycle becomes irregular or stops
Men may have:
• Decreased fertility
• Decreased or no desire for sex
• Impotence
Other symptoms that may occur with this disease:
• Mental changes, such as depression, anxiety, or changes in behavior
• Fatigue
• Headache
• High blood pressure
• Increased thirst and urination
So how does excess cortisol cause the symptoms “moonface”, central obesity, thin skin and severe fatigue?
Cortisol counteracts insulin, contributing to hyperglycemia via stimulation of hepatic gluconeogenesis and inhibition of the peripheral utilization of glucose by decreasing the translocation of glucose transporters to the cell membrane, especially GLUT4. However cortisol increases glycogen synthesis (glycogenesis) in the liver. Cortisol also acts as an anti-diuretic hormone
Moonface
The reason why fat tends to accumulate where it does is not known, but perhaps it is because there are more stress hormone receptors in the face and body, which are more sensitive to insulin, where skeletal muscle is less sensitive to insulin. Another reason is due to increased mobilization of fat in extremities and deposition in the trunk.
Central obesity
It is generally suggested that stress-induced cortisol weight is usually gained around the waistline, because fat cells in that area are more sensitive to cortisol. The fat cells in your abdomen are richer in stress hormone receptors, are particularly sensitive to high insulin, and are very effective at storing energy – more so than fat cells you would find in other areas of the body.
Thin skin
In laboratory rats, cortisol-induced collagen loss in the skin is ten times greater than any other tissue. It is probable that increasing copper availability for immune purposes is the reason many copper enzymes are stimulated to an extent which is often 50% of their total potential by cortisol. This includes lysyl oxidase, an enzyme which is used to cross link collagen and elastin.
Severe fatigue
This is due to increased catabolism of protein for gluconeogenesis and decreased synthesis of protein (except for in the liver). This leads to muscle weakness and thus fatigue. As the effects of insulin are also reduced, glucose is not being effectively taken into cells, especially skeletal muscle which can also contribute to feeling fatigued.
Wednesday, August 18, 2010
Complications and Prognosis of GORD
Complications for GERD
Ulcers
The liquid from the stomach that refluxes into the esophagus damages the cells lining the esophagus. The body responds in the way that it usually responds to damage, which is with inflammation (esophagitis) (50% of people with GERD present with oesophagitis). The purpose of inflammation is to neutralize the damaging agent and begin the process of healing. If the damage goes deeply into the esophagus, an ulcer forms. An ulcer is simply a break in the lining of the esophagus that occurs in an area of inflammation. Ulcers and the additional inflammation they provoke may erode into the esophageal blood vessels and give rise to bleeding into the esophagus.
Occasionally, the bleeding is severe and may require:
• blood transfusions
• an endoscopic procedure (in which a tube is inserted through the mouth into the esophagus to visualize the site of bleeding and to stop the bleeding), or
• surgical treatment.
Strictures
Ulcers of the esophagus heal with the formation of scars (fibrosis). Over time, the scar tissue shrinks and narrows the lumen (inner cavity) of the esophagus. This scarred narrowing is called a stricture. Swallowed food may get stuck in the esophagus once the narrowing becomes severe enough (usually when it restricts the esophageal lumen to a diameter of one centimeter). This situation may necessitate endoscopic removal of the stuck food. Then, to prevent food from sticking, the narrowing must be stretched (widened). Moreover, to prevent a recurrence of the stricture, reflux also must be prevented.
Barrett's esophagus
The normal squamous epithelium lining of the esophagus is replaced by metaplastic columnar epithelium. The medical significance of Barrett’s esophagus is its strong association with esophageal adenocarcinoma, a particularly lethal cancer. It is considered to be a premalignant condition because it is associated with an increased risk of esophageal cancer (more specifically, adenocarcinoma) of about 0.5% per patient-year. Barrett esophagus is present in 8-15% of patients with gastroesophageal reflux disease (GERD) and may progress to adenocarcinoma.
Long-standing and/or severe GERD causes changes in the cells that line the esophagus in some patients. These cells are pre-cancerous and finally become cancerous. This condition is referred to as Barrett's esophagus and occurs in approximately 10% of patients with GERD. The type of esophageal cancer associated with Barrett's esophagus (adenocarcinoma) is increasing in frequency. It is not clear why some patients with GERD develop Barrett's esophagus, but most do not.
Barrett's esophagus can be recognized visually at the time of an endoscopy and confirmed by microscopic examination of biopsies of the lining cells. Then, patients with Barrett's esophagus may require periodic surveillance endoscopies with biopsies. The purpose of surveillance is to detect pre-cancerous changes so that cancer-preventing treatment can be started. It is also believed that patients with Barrett's esophagus should receive maximum treatment for GERD to prevent further damage to the esophagus. Procedures are being studied that remove the abnormal lining cells. Several endoscopic, non-surgical techniques can be used to remove the cells. These techniques are attractive because they do not require surgery; however, there are associated complications, and the long-term effectiveness of the treatments has not yet been determined. Surgical removal of the esophagus is always an option.
Cough and asthma
Many nerves are in the lower esophagus. Some of these nerves are stimulated by the refluxed acid, and this stimulation results in pain (usually heartburn). Other nerves that are stimulated do not produce pain. Instead, they stimulate yet other nerves that provoke coughing. In this way, refluxed liquid can cause coughing without ever reaching the throat! In a similar manner, reflux into the lower esophagus can stimulate esophageal nerves that connect to and can stimulate nerves going to the lungs. These nerves to the lungs then can cause the smaller breathing tubes to narrow, resulting in an attack of asthma.
So, GERD is a common cause of unexplained coughing. Although GERD also may be a cause of asthma, it is more likely that it precipitates asthmatic attacks in patients who already have asthma. Although chronic cough and asthma are common ailments, it is not clear just how often they are aggravated or caused by GERD.
Inflammation of the throat and larynx
If refluxed liquid gets past the upper esophageal sphincter, it can enter the throat (pharynx) and even the voice box (larynx). The resulting inflammation can lead to a sore throat and hoarseness. As with coughing and asthma, it is not clear just how commonly GERD is responsible for otherwise unexplained inflammation of the throat and larynx.
Inflammation and infection of the lungs
Refluxed liquid that passes the larynx can enter the lungs. The reflux of liquid into the lungs (called aspiration) often results in coughing and choking. Aspiration, however, can also occur without producing these symptoms. With or without these symptoms, aspiration may lead to infection of the lungs and result in pneumonia. This type of pneumonia is a serious problem requiring immediate treatment. When aspiration is unaccompanied by symptoms, it can result in a slow, progressive scarring of the lungs (pulmonary fibrosis) that can be seen on chest x-rays. Aspiration is more likely to occur at night because that is when the processes (mechanisms) that protect against reflux are not active and the coughing reflex that protects the lungs also is not active.
Some Stats
• White males are at a greater risk for Barrett esophagus and adenocarcinoma than other populations.
• Gastroesophageal reflux disease (GERD) is as common in men as in women.
• The male-to-female incidence ratio for esophagitis is 2:1-3:1. The male-to-female incidence ratio for Barrett esophagus is 10:1.
• Gastroesophageal reflux disease (GERD) occurs in all age groups.
• The prevalence of gastroesophageal reflux disease (GERD) increases in people older than 40 years.
• Deaths: 1,000 (USA annual deaths calculated from this data: 1,000 deaths in the USA 1984-88 for "GERD and related esophageal disorders" (Digestive diseases in the United States: Epidemiology and Impact – NIH Publication No. 94-1447, NIDDK, 1994))
• Incidence: 8,160,000 (USA prevalence calculated from this data: 3-7% of the population in the USA 1985 for "GERD and related esophageal disorders" (Digestive diseases in the United States: Epidemiology and Impact – NIH Publication No. 94-1447, NIDDK, 1994)
• 0.012% (ratio of deaths to prevalence).
Ulcers
The liquid from the stomach that refluxes into the esophagus damages the cells lining the esophagus. The body responds in the way that it usually responds to damage, which is with inflammation (esophagitis) (50% of people with GERD present with oesophagitis). The purpose of inflammation is to neutralize the damaging agent and begin the process of healing. If the damage goes deeply into the esophagus, an ulcer forms. An ulcer is simply a break in the lining of the esophagus that occurs in an area of inflammation. Ulcers and the additional inflammation they provoke may erode into the esophageal blood vessels and give rise to bleeding into the esophagus.
Occasionally, the bleeding is severe and may require:
• blood transfusions
• an endoscopic procedure (in which a tube is inserted through the mouth into the esophagus to visualize the site of bleeding and to stop the bleeding), or
• surgical treatment.
Strictures
Ulcers of the esophagus heal with the formation of scars (fibrosis). Over time, the scar tissue shrinks and narrows the lumen (inner cavity) of the esophagus. This scarred narrowing is called a stricture. Swallowed food may get stuck in the esophagus once the narrowing becomes severe enough (usually when it restricts the esophageal lumen to a diameter of one centimeter). This situation may necessitate endoscopic removal of the stuck food. Then, to prevent food from sticking, the narrowing must be stretched (widened). Moreover, to prevent a recurrence of the stricture, reflux also must be prevented.
Barrett's esophagus
The normal squamous epithelium lining of the esophagus is replaced by metaplastic columnar epithelium. The medical significance of Barrett’s esophagus is its strong association with esophageal adenocarcinoma, a particularly lethal cancer. It is considered to be a premalignant condition because it is associated with an increased risk of esophageal cancer (more specifically, adenocarcinoma) of about 0.5% per patient-year. Barrett esophagus is present in 8-15% of patients with gastroesophageal reflux disease (GERD) and may progress to adenocarcinoma.
Long-standing and/or severe GERD causes changes in the cells that line the esophagus in some patients. These cells are pre-cancerous and finally become cancerous. This condition is referred to as Barrett's esophagus and occurs in approximately 10% of patients with GERD. The type of esophageal cancer associated with Barrett's esophagus (adenocarcinoma) is increasing in frequency. It is not clear why some patients with GERD develop Barrett's esophagus, but most do not.
Barrett's esophagus can be recognized visually at the time of an endoscopy and confirmed by microscopic examination of biopsies of the lining cells. Then, patients with Barrett's esophagus may require periodic surveillance endoscopies with biopsies. The purpose of surveillance is to detect pre-cancerous changes so that cancer-preventing treatment can be started. It is also believed that patients with Barrett's esophagus should receive maximum treatment for GERD to prevent further damage to the esophagus. Procedures are being studied that remove the abnormal lining cells. Several endoscopic, non-surgical techniques can be used to remove the cells. These techniques are attractive because they do not require surgery; however, there are associated complications, and the long-term effectiveness of the treatments has not yet been determined. Surgical removal of the esophagus is always an option.
Cough and asthma
Many nerves are in the lower esophagus. Some of these nerves are stimulated by the refluxed acid, and this stimulation results in pain (usually heartburn). Other nerves that are stimulated do not produce pain. Instead, they stimulate yet other nerves that provoke coughing. In this way, refluxed liquid can cause coughing without ever reaching the throat! In a similar manner, reflux into the lower esophagus can stimulate esophageal nerves that connect to and can stimulate nerves going to the lungs. These nerves to the lungs then can cause the smaller breathing tubes to narrow, resulting in an attack of asthma.
So, GERD is a common cause of unexplained coughing. Although GERD also may be a cause of asthma, it is more likely that it precipitates asthmatic attacks in patients who already have asthma. Although chronic cough and asthma are common ailments, it is not clear just how often they are aggravated or caused by GERD.
Inflammation of the throat and larynx
If refluxed liquid gets past the upper esophageal sphincter, it can enter the throat (pharynx) and even the voice box (larynx). The resulting inflammation can lead to a sore throat and hoarseness. As with coughing and asthma, it is not clear just how commonly GERD is responsible for otherwise unexplained inflammation of the throat and larynx.
Inflammation and infection of the lungs
Refluxed liquid that passes the larynx can enter the lungs. The reflux of liquid into the lungs (called aspiration) often results in coughing and choking. Aspiration, however, can also occur without producing these symptoms. With or without these symptoms, aspiration may lead to infection of the lungs and result in pneumonia. This type of pneumonia is a serious problem requiring immediate treatment. When aspiration is unaccompanied by symptoms, it can result in a slow, progressive scarring of the lungs (pulmonary fibrosis) that can be seen on chest x-rays. Aspiration is more likely to occur at night because that is when the processes (mechanisms) that protect against reflux are not active and the coughing reflex that protects the lungs also is not active.
Some Stats
• White males are at a greater risk for Barrett esophagus and adenocarcinoma than other populations.
• Gastroesophageal reflux disease (GERD) is as common in men as in women.
• The male-to-female incidence ratio for esophagitis is 2:1-3:1. The male-to-female incidence ratio for Barrett esophagus is 10:1.
• Gastroesophageal reflux disease (GERD) occurs in all age groups.
• The prevalence of gastroesophageal reflux disease (GERD) increases in people older than 40 years.
• Deaths: 1,000 (USA annual deaths calculated from this data: 1,000 deaths in the USA 1984-88 for "GERD and related esophageal disorders" (Digestive diseases in the United States: Epidemiology and Impact – NIH Publication No. 94-1447, NIDDK, 1994))
• Incidence: 8,160,000 (USA prevalence calculated from this data: 3-7% of the population in the USA 1985 for "GERD and related esophageal disorders" (Digestive diseases in the United States: Epidemiology and Impact – NIH Publication No. 94-1447, NIDDK, 1994)
• 0.012% (ratio of deaths to prevalence).
SS and DD of GERD
Gastroesophageal Reflux Disease [GERD]
DDx
• Peptic ulcer disease, gastritis, nonulcer dyspepsia, or cholelithiasis
• Angina pectoris - chest pain
• Infectious esophagitis: Candida, herpes simplex virus, cytomegalovirus
• Pill-induced esophagitis - dysphagia, odynophagia
• Esophageal motility disorders, eg, achalasia, esophageal spasm, scleroderma
• Radiation esophagitis - dysphagia, odynophagia
• Zollinger-Ellison syndrome (gastrinoma) - heartburn, dysphagia
Typical Presentation
Heartburn - often occurs 30–60 minutes after meals and upon reclining/ relief from taking antacids or baking soda, symptom is dominant, the diagnosis is established with a high degree of reliability.
Concomitant nausea, vomiting or early satiety – Gastroparesis is suspected.
Overall, a clinical diagnosis of gastroesophageal reflux has a sensitivity of 80% but a specificity of only 70%.
Regurgitation - the spontaneous reflux of sour or bitter gastric contents into the mouth.
Dysphagia or Odynophagia - occurs in one-third of patients and may be due to erosive esophagitis, abnormal esophageal peristalsis, or the development of an esophageal stricture.
It is necessary to undergo gastroscopy if find weight loss, anemia, family history of Upper GI cancer, GI bleed or advanced age.
Atypical Presentation
• Asthma – microaspiration causes initiation of asthma, adult onset asthma KIV.
• Otitis Media – children, with effusion results hearing loss
• Chronic cough
• Chronic laryngitis
• Sore throat
• Chest pain
In the absence of heartburn or regurgitation, atypical symptoms are unlikely to be related to gastroesophageal reflux.
Physical examination and laboratory data are normal in uncomplicated disease.
DDx
• Peptic ulcer disease, gastritis, nonulcer dyspepsia, or cholelithiasis
• Angina pectoris - chest pain
• Infectious esophagitis: Candida, herpes simplex virus, cytomegalovirus
• Pill-induced esophagitis - dysphagia, odynophagia
• Esophageal motility disorders, eg, achalasia, esophageal spasm, scleroderma
• Radiation esophagitis - dysphagia, odynophagia
• Zollinger-Ellison syndrome (gastrinoma) - heartburn, dysphagia
Typical Presentation
Heartburn - often occurs 30–60 minutes after meals and upon reclining/ relief from taking antacids or baking soda, symptom is dominant, the diagnosis is established with a high degree of reliability.
Concomitant nausea, vomiting or early satiety – Gastroparesis is suspected.
Overall, a clinical diagnosis of gastroesophageal reflux has a sensitivity of 80% but a specificity of only 70%.
Regurgitation - the spontaneous reflux of sour or bitter gastric contents into the mouth.
Dysphagia or Odynophagia - occurs in one-third of patients and may be due to erosive esophagitis, abnormal esophageal peristalsis, or the development of an esophageal stricture.
It is necessary to undergo gastroscopy if find weight loss, anemia, family history of Upper GI cancer, GI bleed or advanced age.
Atypical Presentation
• Asthma – microaspiration causes initiation of asthma, adult onset asthma KIV.
• Otitis Media – children, with effusion results hearing loss
• Chronic cough
• Chronic laryngitis
• Sore throat
• Chest pain
In the absence of heartburn or regurgitation, atypical symptoms are unlikely to be related to gastroesophageal reflux.
Physical examination and laboratory data are normal in uncomplicated disease.
Esophageal Cancer: Pathophysiology, Aetiology and Risk Factors
These are the risk factors for the two main types of esophageal cancer.
- Gastroesophageal reflux disease (GERD) is the most common predisposing factor for adenocarcinoma of the esophagus.
o As a consequence of the irritation caused by the reflux of acid and bile, 10-15% of patients who undergo endoscopy for evaluation of GERD symptoms are found to have Barrett epithelium.
o Chronic gastroesophageal reflux is the most important, with severe, long-standing reflux symptoms increasing the risk of cancer by a factor of 40. Chronic gastroesophageal reflux disease is associated with Barrett's metaplasia (Barrett's esophagus), a condition in which an abnormal columnar epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus.
o Adenocarcinoma may develop in these patients, representing the last event of a sequence that starts with the development of GERD and progresses to (Barrett) metaplasia, low-grade dysplasia, high-grade dysplasia, and adenocarcinoma.
o Most esophageal ACs are believed to arise from Barrett's esophagus. Although this mucosal change appears to be a favorable adaptation to chronic reflux—columnar epithelium appears to be more resistant to reflux-induced injury than the native squamous cells—this specialized intestinal metaplasia may become dysplastic and ultimately malignant, with genetic alterations that activate proto-oncogenes, disable tumor suppressor genes, or both. Factors that increase the risk for gastroesophageal reflux, such as obesity or medications that lower the lower esophageal sphincter tone, may result in an increased risk for esophageal AC.
o The progression of Barrett metaplasia to adenocarcinoma is associated with several changes in gene structure, gene expression, and protein structure. The oncosuppressor gene TP53 and various oncogenes, particularly erb -b2, have been studied as potential markers. Casson and colleagues identified mutations in the TP53 gene in patients with Barrett epithelium associated with adenocarcinoma.8 In addition, alterations in p16 genes and cell cycle abnormalities or aneuploidy appear to be some of the most important and well-characterized molecular changes. However, the exact sequence of events in the progression of Barrett esophagus to adenocarcinoma is not known. Probably multiple molecular pathways interact and are involved.
o Allelic losses at chromosomes 4q, 5q, 9p, 9q, and 18q and abnormalities of p53, Rb, cyclin D1, and c-myc have been implicated.
The esophagus has no serosa, thus reducing the resistance against local spread of invasive cancer cells. Furthermore, the esophagus has an extensive network of lymphatics, allowing for early regional tumor advancement. The end result is local spread and invasion into surrounding tissue, with early metastatic disease developing in most patients.
- Plummer-Vinson syndrome—the triad of dysphagia, iron deficiency anemia, and esophageal webs
- Human papillomavirus has received the most attention. It is believed that the infection results in loss of function of the tumor suppressor genes p53 and Rb. The importance of this mechanism is not well established.
- Tylosis with esophageal cancer: A genetic disorder characterized by thickening (hyperkeratosis) of the palms and soles, white patches in the mouth (oral leukoplakia), and a very high risk of esophageal cancer. This is the only genetic syndrome known to predispose to squamous cell carcinoma of the esophagus. The risk of developing esophageal cancer is 95% by age 70. The syndrome is inherited in an autosomal dominant manner. The gene has been mapped to chromosome 17q25 but has not been identified. The syndrome is also called nonepidermolytic palmoplantar keratoderma.
- In a high-risk country such as China, deficiencies in vitamin or microelement levels may play a role in causation. Riboflavin deficiency in China may contribute to a high incidence of esophageal cancer.
- Heavy drinking: People who have more than 3 alcoholic drinks each day are more likely than people who don't drink to develop squamous cell carcinoma of the esophagus. Heavy drinkers who smoke are at a much higher risk than heavy drinkers who don't smoke. In other words, these two factors act together to increase the risk even more.
Esophageal cancer: Signs and Symptoms
Symptoms:
• Pain and difficulty in swallowing, hiccups with pain, food gets stuck in the esophagus, and food may come back up
o constricted to < 14 mm
o Swallowing may be painful when the cancer is large enough to block the esophagus. Pain may be felt a few seconds after swallowing, as food or liquid reaches the tumor and cannot get past it.
o often mild when it starts, and then gets worse over time. The opening of the esophagus is often narrowed to about half of its normal width. Dysphagia is commonly a late symptom caused by a large cancer.
• Thick mucus and more saliva
o To help pass food through the esophagus, the body makes more saliva. This causes some people to complain of bringing up lots of thick mucus or saliva.
• lose weight unintentionally
• Heartburn -reflux
• Pain at the back – nerve compression
• Persistent cough
o reflux
o tracheoesophageal fistula. This occurs when the tumor destroys the tissue between the esophagus and the trachea (windpipe) and creates a hole connecting them. With this connection, anything that is swallowed can pass from the esophagus into the windpipe and lungs. This leads to frequent coughing and gagging.
• Hiccups: damage or irritation of vagus and phrenic nerves, reflux
• Malaena
o Sometimes the cancer will bleed. If there is enough blood, stools may turn black.
• Vomit blood
• Hoarse voice
o Compression of the recurrent laryngeal nerve may lead to vocal cord paralysis and hoarseness.
Signs:
• Signs are often absent
• General inspection: weight loss, anorexia
• The hands: Inspect for palmer creases for pallor
o Anaemia- iron deficiency anaemia
• Neck: Palpate the supraclavicular nodes
o Lymphatic spread to internal jugular, cervical, supraclavicular, mediastinal, and celiac nodes is common.
• Examine for evidence of retrosternal thyroid enlargement.
• Pain and difficulty in swallowing, hiccups with pain, food gets stuck in the esophagus, and food may come back up
o constricted to < 14 mm
o Swallowing may be painful when the cancer is large enough to block the esophagus. Pain may be felt a few seconds after swallowing, as food or liquid reaches the tumor and cannot get past it.
o often mild when it starts, and then gets worse over time. The opening of the esophagus is often narrowed to about half of its normal width. Dysphagia is commonly a late symptom caused by a large cancer.
• Thick mucus and more saliva
o To help pass food through the esophagus, the body makes more saliva. This causes some people to complain of bringing up lots of thick mucus or saliva.
• lose weight unintentionally
• Heartburn -reflux
• Pain at the back – nerve compression
• Persistent cough
o reflux
o tracheoesophageal fistula. This occurs when the tumor destroys the tissue between the esophagus and the trachea (windpipe) and creates a hole connecting them. With this connection, anything that is swallowed can pass from the esophagus into the windpipe and lungs. This leads to frequent coughing and gagging.
• Hiccups: damage or irritation of vagus and phrenic nerves, reflux
• Malaena
o Sometimes the cancer will bleed. If there is enough blood, stools may turn black.
• Vomit blood
• Hoarse voice
o Compression of the recurrent laryngeal nerve may lead to vocal cord paralysis and hoarseness.
Signs:
• Signs are often absent
• General inspection: weight loss, anorexia
• The hands: Inspect for palmer creases for pallor
o Anaemia- iron deficiency anaemia
• Neck: Palpate the supraclavicular nodes
o Lymphatic spread to internal jugular, cervical, supraclavicular, mediastinal, and celiac nodes is common.
• Examine for evidence of retrosternal thyroid enlargement.
Tuesday, August 17, 2010
Esophageal Cancer (Investigation)
Esophageal Cancer (Investigation)
Imaging studies
Barium swallow
Barium is swallowed. It coats the walls of the esophagus. When x-rays are taken, the barium outlines the esophagus clearly. This test can be done by itself, or as a part of a series of x-rays that includes the stomach and part of the intestine, called an upper gastrointestinal (GI) series. A barium swallow test can show any irregularities in the normally smooth surface of the esophageal wall.
A barium swallow test is often the first test done to see what is causing a problem with swallowing. Even small, early cancer can be seen using this test. Tumors grow out from the lining of the esophagus. These masses stick out into the lumen (the open area of the tube). They cause the barium to coat that area of the esophagus unevenly. In the barium x-ray, early cancers can look like small round bumps. They also can appear as a flat, raised area called a plaque. Advanced cancers look like large irregular areas and cause a narrowing of the width of the esophagus. A barium swallow test cannot be used to determine how far a cancer may have spread outside of the esophagus.
A barium swallow test can also be used to diagnose one of the more serious complications of esophageal cancer called a tracheoesophageal fistula. This occurs when the tumor destroys the tissue between the esophagus and the trachea and creates a hole connecting them. With this connection, anything that is swallowed can pass from the esophagus into the windpipe and lungs. This leads to frequent coughing and gagging. This problem can be helped with surgery or an endoscopy procedure.
Computed tomography (CAT or CT) scan
CT scans are not usually used to make the initial diagnosis of esophageal cancer, but they can help see how far it has spread. CT scans often can show where the cancer is in the esophagus. These scans can also show the nearby organs and lymph nodes, as well as distant areas of cancer spread. The CT scan can help to determine whether surgery is a good treatment option.
Before any pictures are taken, you may be asked to drink 1 to 2 pints of oral contrast. This helps outline the esophagus and intestines so that certain areas are not mistaken for tumors. You may also receive an IV (intravenous) line through which a different kind of contrast dye (IV contrast) is injected. This helps better outline structures in your body.
CT scans can also be used to guide a biopsy needle precisely into a suspected area of cancer spread. This procedure is called a CT-guided needle biopsy. The patient lies on the CT scanning table while a radiologist advances a biopsy needle toward the location of the mass. CT scans are repeated until the doctors can see that the needle is in the mass. A fine-needle biopsy sample (tiny fragment of tissue) or a core needle biopsy sample (a thin cylinder of tissue about one-half inch long and less than 1/8-inch in diameter) is removed and examined under a microscope.
Magnetic resonance imagings (MRI) scan
Not often needed for Esophageal cancer
Positron emission tomography (PET) scan
In this test, radioactive glucose (sugar) is injected into the vein. Because cancers use sugar much faster than normal tissues, the radioactivity will tend to concentrate in the cancer. A scanner is used to spot the radioactive deposits. This test is useful for finding areas of cancer spread. It can help find small collections of cancer cells that may not be seen on other tests.
The uptake of the radioactive glucose ("brightness") may be measured. Studies are being done to see if the degree of uptake or brightness can be used as to tell how fast the tumor is growing. Studies are also looking to see whether changes in the brightness on a PET scan can be used to see whether treatment, such as chemotherapy, is working. Some machines combine a PET scan with a CT scan. This allows any abnormal areas seen on the PET scan to be precisely located on the CT scan. This type of scan may be used to look for areas of cancer spread if nothing is found on other imaging tests.
Endoscopy
Upper endoscopy
An endoscope is a flexible, very narrow tube with a video camera and light on the end. During an upper endoscopy procedure, the patient is sedated and then the endoscope is placed through the mouth and into the esophagus and stomach.
Endoscopy is an important test for diagnosing esophageal cancer. The doctor can see the cancer through the scope and biopsy. If the esophageal cancer is blocking the lumen of the esophagus, then certain instruments can be used to help enlarge the opening to help food and liquid pass. Upper endoscopy can give the surgeon information for follow-up surgery, including the size and spread of the tumor and whether the tumor can be completely removed.
Endoscopic ultrasound
Ultrasound tests use sound waves to take pictures of parts of the body. For an endoscopic ultrasound, the probe that gives off the sound waves is at the end of an endoscope. This allows the probe to get very close to the cancer.
This test is very useful in finding the size of an esophageal cancer and how far it has grown into nearby tissues.
Endoscopic ultrasound can help determine how much of the tissue next to the esophagus (including nearby lymph nodes) is affected by the cancer. This helps surgeons decide which tumors can be surgically removed and which cannot.
Bronchoscopy
This procedure uses an endoscope to look into the trachea and tubes leading from the trachea into the bronchi. Check for metastasis. The patient is sedated for this procedure.
Thoracoscopy and laparoscopy
These procedures allow the doctor to see lymph nodes and other organs near the esophagus inside the chest (by thoracoscopy) or the abdomen (by laparoscopy) through a hollow lighted tube. The surgeon can operate instruments through the tube and remove lymph node samples and take biopsies to see if the cancer has spread. This information is often important in deciding whether or not a person is likely to benefit from surgery. These procedures are done in an operating room and under general anesthesia (the patient is in a deep sleep).
Biopsy
Confirm cancer and staged the cancer
References:
http://www.cancer.org/Cancer/EsophagusCancer/DetailedGuide/esophagus-cancer-diagnosis
http://www.cancer.gov/cancertopics/wyntk/esophagus/page7
Wednesday, August 11, 2010
My Part
Irritable Bowel Syndrome
Irritable bowel syndrome has been called spastic colon, functional bowel disease, and mucous colitis. However, IBS is not a true "colitis." The term colitis refers to a separate condition known as inflammatory bowel disease (IBD).
Irritable bowel syndrome (IBS or spastic colon) is a diagnosis of exclusion. It is a functional bowel disorder characterized by chronic abdominal pain, discomfort, bloating, and alteration of bowel habits in the absence of any detectable organic cause. Diarrhea or constipation may predominate, or they may alternate (classified as IBS-D, IBS-C or IBS-A, respectively). IBS may begin after an infection (post-infectious, IBS-PI), a stressful life event, or onset of maturity without any other medical indicators.
Irritable bowel syndrome is not contagious, inherited, or cancerous.
Fortunately, unlike more-serious intestinal diseases such as ulcerative colitis and Crohn's disease, irritable bowel syndrome doesn't cause inflammation or changes in bowel tissue or increase your risk of colorectal cancer. However, IBS often disrupts daily living activities.
IBS is considered a functional disorder in that diagnostic testing does not show any visible disease process. To determine whether a person is just having temporary digestive distress or if he does have IBS, doctors use a standard called the Rome III criteria. According to these criteria, IBS can only be diagnosed if symptoms have been present for at least six months. Symptoms must have been experienced on at least three days of at least three months. Specifically, symptoms must consist of recurrent abdominal pain or discomfort with two or more of the following:
• Pain is relieved by a bowel movement
• Onset of pain is related to a change in frequency of stool
• Onset of pain is related to a change in the appearance of stool
Symptoms
The signs and symptoms of irritable bowel syndrome can vary widely from person to person and often resemble those of other diseases. Among the most common are:
• Abdominal pain or cramping
• A bloated feeling
• Gas (flatulence)
• Diarrhea or constipation — sometimes alternating bouts of constipation and diarrhea
• Mucus in the stool
Red-flag IBS Symptoms
IBS symptoms can be so severe and disruptive that sufferers frequently worry about misdiagnosis and that their doctor has overlooked a more serious disorder. The following list describes symptoms that are NOT typical of IBS and would warrant further investigation:
• fever
• vomiting
• blood in the stool (may be only from hemorrhoids, but MUST be brought to the attention of a qualified physician)
• significant and unexplained weight loss
• anemia
• abdominal pain and cramping not relieved by a bowel movement
• abdominal pain and cramping which awakes the sufferer from sleep
• poor appetite (not caused by a fear of eating trigger foods)
• fatigue
Epidemiology
IBS affects 10% to 15% of the US population. However, published prevalence rates are likely underestimates because only 25% to 30% of patients with IBS symptoms seek medical attention, probably because of fear, embarrassment, mild symptoms, or the misperception that no effective treatments are available. This is illustrated in a study by Mearin and colleagues,[8] who found that IBS symptoms were unstable over time, with the greatest instability among those with irritable bowel syndrome with constipation (IBS-C) and IBS-diarrhea (D) subtypes; only 46% and 51% remained in the same subgroup during the study, with the remaining switching to the IBS-A subtype. Although there may be a consistent number of people with a certain subtype overall, there is continual movement of patients from one subtype to another; an exception is IBS-C to IBS-D and visa versa, which is rare.
Although IBS affects men and women, a woman-to-man ratio of 2:1 exists in the United States. The gap widens considerably in tertiary care settings, with women outnumbering men by 3:1. Most people seeking medical attention for IBS symptoms for the first time are 30-50 years old. The prevalence of IBS declines after age 60. In fact, the onset of IBS after age 40 is unusual, unless it is caused by infection, medication, trauma, or cholecystectomy.
Nineteen percent of respondents in a survey of married or cohabiting people with IBS stated that they had difficulties in their personal relationships, and 45% stated that IBS interfered with their sex life.
Like many people, you may have only mild signs and symptoms of irritable bowel syndrome. However, sometimes these problems can be disabling. In some cases, you may have severe signs and symptoms that don't respond well to medical treatment. Because symptoms of irritable bowel syndrome can occur with other diseases, it's best to discuss these symptoms with your doctor.
For most people, IBS is a chronic condition, although there will likely be times when the signs and symptoms are worse and times when they improve or even disappear completely.
DIFFERENTIAL DIAGNOSIS OF Iron Deficency Anemia
IDA is classically described as a microcytic anemia. The differential diagnosis for microcytic anemia includes iron deficiency, thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning (rare in adults). Patients with sideroblastic anemia will have almost complete saturation of the serum transfer-rin, which can differentiate them from patients with iron deficiency. Differentiating between iron deficiency and anemia of chronic disease can sometimes be difficult, especially in early iron deficiency or when the conditions coexist. Patients with lead poisoning will have characteristic signs and symptoms of lead poisoning.
Irritable bowel syndrome has been called spastic colon, functional bowel disease, and mucous colitis. However, IBS is not a true "colitis." The term colitis refers to a separate condition known as inflammatory bowel disease (IBD).
Irritable bowel syndrome (IBS or spastic colon) is a diagnosis of exclusion. It is a functional bowel disorder characterized by chronic abdominal pain, discomfort, bloating, and alteration of bowel habits in the absence of any detectable organic cause. Diarrhea or constipation may predominate, or they may alternate (classified as IBS-D, IBS-C or IBS-A, respectively). IBS may begin after an infection (post-infectious, IBS-PI), a stressful life event, or onset of maturity without any other medical indicators.
Irritable bowel syndrome is not contagious, inherited, or cancerous.
Fortunately, unlike more-serious intestinal diseases such as ulcerative colitis and Crohn's disease, irritable bowel syndrome doesn't cause inflammation or changes in bowel tissue or increase your risk of colorectal cancer. However, IBS often disrupts daily living activities.
IBS is considered a functional disorder in that diagnostic testing does not show any visible disease process. To determine whether a person is just having temporary digestive distress or if he does have IBS, doctors use a standard called the Rome III criteria. According to these criteria, IBS can only be diagnosed if symptoms have been present for at least six months. Symptoms must have been experienced on at least three days of at least three months. Specifically, symptoms must consist of recurrent abdominal pain or discomfort with two or more of the following:
• Pain is relieved by a bowel movement
• Onset of pain is related to a change in frequency of stool
• Onset of pain is related to a change in the appearance of stool
Symptoms
The signs and symptoms of irritable bowel syndrome can vary widely from person to person and often resemble those of other diseases. Among the most common are:
• Abdominal pain or cramping
• A bloated feeling
• Gas (flatulence)
• Diarrhea or constipation — sometimes alternating bouts of constipation and diarrhea
• Mucus in the stool
Red-flag IBS Symptoms
IBS symptoms can be so severe and disruptive that sufferers frequently worry about misdiagnosis and that their doctor has overlooked a more serious disorder. The following list describes symptoms that are NOT typical of IBS and would warrant further investigation:
• fever
• vomiting
• blood in the stool (may be only from hemorrhoids, but MUST be brought to the attention of a qualified physician)
• significant and unexplained weight loss
• anemia
• abdominal pain and cramping not relieved by a bowel movement
• abdominal pain and cramping which awakes the sufferer from sleep
• poor appetite (not caused by a fear of eating trigger foods)
• fatigue
Epidemiology
IBS affects 10% to 15% of the US population. However, published prevalence rates are likely underestimates because only 25% to 30% of patients with IBS symptoms seek medical attention, probably because of fear, embarrassment, mild symptoms, or the misperception that no effective treatments are available. This is illustrated in a study by Mearin and colleagues,[8] who found that IBS symptoms were unstable over time, with the greatest instability among those with irritable bowel syndrome with constipation (IBS-C) and IBS-diarrhea (D) subtypes; only 46% and 51% remained in the same subgroup during the study, with the remaining switching to the IBS-A subtype. Although there may be a consistent number of people with a certain subtype overall, there is continual movement of patients from one subtype to another; an exception is IBS-C to IBS-D and visa versa, which is rare.
Although IBS affects men and women, a woman-to-man ratio of 2:1 exists in the United States. The gap widens considerably in tertiary care settings, with women outnumbering men by 3:1. Most people seeking medical attention for IBS symptoms for the first time are 30-50 years old. The prevalence of IBS declines after age 60. In fact, the onset of IBS after age 40 is unusual, unless it is caused by infection, medication, trauma, or cholecystectomy.
Nineteen percent of respondents in a survey of married or cohabiting people with IBS stated that they had difficulties in their personal relationships, and 45% stated that IBS interfered with their sex life.
Like many people, you may have only mild signs and symptoms of irritable bowel syndrome. However, sometimes these problems can be disabling. In some cases, you may have severe signs and symptoms that don't respond well to medical treatment. Because symptoms of irritable bowel syndrome can occur with other diseases, it's best to discuss these symptoms with your doctor.
For most people, IBS is a chronic condition, although there will likely be times when the signs and symptoms are worse and times when they improve or even disappear completely.
DIFFERENTIAL DIAGNOSIS OF Iron Deficency Anemia
IDA is classically described as a microcytic anemia. The differential diagnosis for microcytic anemia includes iron deficiency, thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning (rare in adults). Patients with sideroblastic anemia will have almost complete saturation of the serum transfer-rin, which can differentiate them from patients with iron deficiency. Differentiating between iron deficiency and anemia of chronic disease can sometimes be difficult, especially in early iron deficiency or when the conditions coexist. Patients with lead poisoning will have characteristic signs and symptoms of lead poisoning.
Investigation and Treatment of Irritable Bowel Syndrome
PCL
Investigation
• It is a diagnosis of exclusion
• Rome III [2006]criteria
o Recurrent abdominal pain or discomfort at least 3 days/month in the last 3 months associated with two or more of the following:
Improvement with defecation
Onset associated with changes in frequency of stool
Onset associated with changes in form (appearance) of stool
o Criterion fulfilled for the last 3 months with symptoms onset at least 6 months prior diagnosis
• Manning’s Criteria
o Onset of pain linked to more frequent bowel movements
o Looser stools associated with onset of pain
o Pain relieved by passage of stool
o Noticeable abdominal bloating
o Sensation of incomplete evacuation more than 25% of the time
o Diarrhea with mucus more than 25% of the time
• Full blood count, X-ray, Colonoscopy, Gastroscopy, Sigmoidoscopy, CT, MRI. Important to note patients’ age and risk factors for differential diagnosis.
• Infectious diseases, Coeliac disease, Helicobacter pylori and Inflammatory bowel diesease
Treatment Options
• Diet
o Lactose intolerance – lactose free diet
o Fructose malabsoption – Restrict fructose and fructan intake
o Over eating or drinking may provoke gastrocolic response due to heightened sensitivity.
o Fibre – soluble fibre [psyllium] is found to be effective in the general IBS population especially to those who have constipation that is predominant of irritable bowel. However, it doesn’t reduce pain.
• Medication
o Antispasmodic [anticholinergic - hysocyamine or dicyclomine]
Patients with cramps or diarrhea
o Stool softener or Laxatives
Osmotic [Polyethylene glycol]
Stimulant - Cathartic colon
Lubiprostone is also a drug that helps chronic idiopathic constipation
o Antidiarrheals
Opiate or Opioid analogs such as loperamide and diphenoxylate
o Serotonin - Improves gut motility
Agonist [Tegaserod, SSRI] improves constipation predominant pain/diarrhea
Antagonist [Alosetron] improves pain/diarrhea predominant constipation
o Tricyclic antidepressants
Low dose can be effective
o Antibiotic
Rifaximin can be used for bloating and flatulence, suggesting bacterial overgrowth
• Psychotherapy
o Brain-gut
o Cognitive behavioural therapy and hypnosis
• Alternative medicine
o Probiotics - Yogurt
o Yoga
o Herbal remedies
o Accupuncture
Investigation
• It is a diagnosis of exclusion
• Rome III [2006]criteria
o Recurrent abdominal pain or discomfort at least 3 days/month in the last 3 months associated with two or more of the following:
Improvement with defecation
Onset associated with changes in frequency of stool
Onset associated with changes in form (appearance) of stool
o Criterion fulfilled for the last 3 months with symptoms onset at least 6 months prior diagnosis
• Manning’s Criteria
o Onset of pain linked to more frequent bowel movements
o Looser stools associated with onset of pain
o Pain relieved by passage of stool
o Noticeable abdominal bloating
o Sensation of incomplete evacuation more than 25% of the time
o Diarrhea with mucus more than 25% of the time
• Full blood count, X-ray, Colonoscopy, Gastroscopy, Sigmoidoscopy, CT, MRI. Important to note patients’ age and risk factors for differential diagnosis.
• Infectious diseases, Coeliac disease, Helicobacter pylori and Inflammatory bowel diesease
Treatment Options
• Diet
o Lactose intolerance – lactose free diet
o Fructose malabsoption – Restrict fructose and fructan intake
o Over eating or drinking may provoke gastrocolic response due to heightened sensitivity.
o Fibre – soluble fibre [psyllium] is found to be effective in the general IBS population especially to those who have constipation that is predominant of irritable bowel. However, it doesn’t reduce pain.
• Medication
o Antispasmodic [anticholinergic - hysocyamine or dicyclomine]
Patients with cramps or diarrhea
o Stool softener or Laxatives
Osmotic [Polyethylene glycol]
Stimulant - Cathartic colon
Lubiprostone is also a drug that helps chronic idiopathic constipation
o Antidiarrheals
Opiate or Opioid analogs such as loperamide and diphenoxylate
o Serotonin - Improves gut motility
Agonist [Tegaserod, SSRI] improves constipation predominant pain/diarrhea
Antagonist [Alosetron] improves pain/diarrhea predominant constipation
o Tricyclic antidepressants
Low dose can be effective
o Antibiotic
Rifaximin can be used for bloating and flatulence, suggesting bacterial overgrowth
• Psychotherapy
o Brain-gut
o Cognitive behavioural therapy and hypnosis
• Alternative medicine
o Probiotics - Yogurt
o Yoga
o Herbal remedies
o Accupuncture
Complications & Prognosis of Coeliac Disease! :(
1. Malabsorption
Small intestine is responsible for absorption of nutrients mainly Vit B12, iron, Vit K, Calcium and Vit D. As small bowel is inflamed, vital nutrients are lost in stools rather than absorbed in blood stream, leading to deficiency in vitamins and minerals.
2. Lactose Intolerance
Lactase enzyme is synthesise in cells lining the villi and is responsible for digesting lactose. As villi shrink and damaged in celiac disease, patients will face problems with digesting lactose. It will heal off once they start on gluten-free diet.
3. Cancer
Untreated celiac disease has shown to lead to lymphoma (enteropathy associated T cell lymphoma with poor prognosis) and adenocarcinoma of esophagus, pancreas, small and large intestine and hepatobiliary tract even though it is rare. Symptoms of small intestinal lymphoma include anemia, bleeding into intestine, abd pain, weight loss, fever and small intestine obstruction. Often difficult to diagnose.
4. Miscarriage and congenital malformation of unborn baby
Pregnant women do not realize they have celiac disease or do not follow gluten free diet if they have it have nutrient absorption problems that can lead to miscarriage and congenital malformations such as neural tube defects (Folate deficiency).
5. Ulcerative jejunoileitis
Rare complication of celiac disease. Recurrent episodes of small intestines insult leading to formation of strictures. Symptoms of jejunoileitis can be intestinal bleeding, weight loss, abd pain and intestinal obstruction. Individuals with ulcerative jejunoileitis are at high risk of developing intestinal lymphomas.
6. Refractory Celiac Disease
Rare condition which symptoms of celiac disease despite strict adherence to gluten-free diet. Occurs in approximately 5% of patients. Subdivided into 2 types: type 1 is characterized by normal intraepithelial lymphocytes phenotype and type 2 is characterized with increase number of intraepithelial lymphocytes, due to increase in epithelial interleukin 15 expression.
7. Collagenous Celiac Disease
Have symptoms of celiac disease but fail to improve on gluten-free diet. Large amount of collagen forms under intestinal lining after several years and prognosis is poor.
Tuesday, August 10, 2010
IBS: Prognosis and Complications
PROGNOSIS
• Men have a better prognosis for IBS than do women, and men tended to have fewer return visits for IBS-related symptoms than did women.
• Life expectancy remains similar to that of the general population
• With treatment, 85% of patients were rendered virtually symptom-free in the short term, and 68% were still virtually symptom-free 5 years later.
• The response to treatment was better in men than in women, in those with constipation than with diarrhoea, when the symptoms had initially been triggered by an episode of acute diarrhoea, and in patients with a relatively short history. With a few simple investigations, sympathetic explanation, and appropriate treatment, most patients with IBS have a good prognosis.
Complications
• A chronic relapsing condition
• Physical
o Does not increase the mortality or the risk of inflammatory bowel disease or cancer
o Abdominal pain and lifestyle modifications secondary to altered bowel habits
o Diarrhea and constipation, both signs of irritable bowel syndrome, can aggravate haemorrhoids
o Avoidance of certain foods may lead to malnourishment
o No increased risk of developing an organic pathology exists in patients with irritable bowel syndrome
• Psychological
o May experience feelings of depression and anxiety
o May have suicidal ideation and/or suicide attempts
• Social
o May lead to avoidance of social engagements, make sexual activity unappealing or even painful
o Finding access to toilets may be an issue, therefore some are afraid to visit public places
o Work absenteeism resulting in lost wages
http://www.annals.org/content/122/2/107.full
http://emedicine.medscape.com/article
http://www.ncbi.nlm.nih.gov/pubmed/2882351
http://www.mayoclinic.com/health/irritable-bowel-syndrome/DS00106/DSECTION=complications
http://www.nhs.uk/Conditions/Irritable-bowel-syndrome/Pages/Complications.aspx
• Men have a better prognosis for IBS than do women, and men tended to have fewer return visits for IBS-related symptoms than did women.
• Life expectancy remains similar to that of the general population
• With treatment, 85% of patients were rendered virtually symptom-free in the short term, and 68% were still virtually symptom-free 5 years later.
• The response to treatment was better in men than in women, in those with constipation than with diarrhoea, when the symptoms had initially been triggered by an episode of acute diarrhoea, and in patients with a relatively short history. With a few simple investigations, sympathetic explanation, and appropriate treatment, most patients with IBS have a good prognosis.
Complications
• A chronic relapsing condition
• Physical
o Does not increase the mortality or the risk of inflammatory bowel disease or cancer
o Abdominal pain and lifestyle modifications secondary to altered bowel habits
o Diarrhea and constipation, both signs of irritable bowel syndrome, can aggravate haemorrhoids
o Avoidance of certain foods may lead to malnourishment
o No increased risk of developing an organic pathology exists in patients with irritable bowel syndrome
• Psychological
o May experience feelings of depression and anxiety
o May have suicidal ideation and/or suicide attempts
• Social
o May lead to avoidance of social engagements, make sexual activity unappealing or even painful
o Finding access to toilets may be an issue, therefore some are afraid to visit public places
o Work absenteeism resulting in lost wages
http://www.annals.org/content/122/2/107.full
http://emedicine.medscape.com/article
http://www.ncbi.nlm.nih.gov/pubmed/2882351
http://www.mayoclinic.com/health/irritable-bowel-syndrome/DS00106/DSECTION=complications
http://www.nhs.uk/Conditions/Irritable-bowel-syndrome/Pages/Complications.aspx
Investigations, Treatment and the Infamous Gluten Free Diet
Investigations for Coeliac disease
Because CD is considerably under-diagnosed in Primary Care,consider the diagnosis and perform serological testing in all patients who present with:
•chronic or intermittent diarrhoea
•failure to thrive or faltering growth in children
•persistent or unexplained gastrointestinal symptoms including nausea and vomiting
•prolonged fatigue ('tired all the time')
•recurrent abdominal pain, cramping or distension
•sudden or unexpected weight loss
•unexplained iron-deficiency anaemia, or other unspecified anaemia
Serology – make sure they have been on a gluten diet for at least 6 weeks
•IgA anti-tissue transglutaminase antibodies (tTGAs) is the preferred investigation. Endomysial antibodies (EMAs) are used if tTGA) test is not available or equivocal.
•False negatives occur if the patient has selective IgA deficiency, as occurs in ~0.4% of the general population14 and in 2.6% of patients with CD (laboratories should test for IgA deficiency on negative samples). Use IgG tTGA and/or IgG EMA serological tests for people with confirmed IgA deficiency.
•Antibodies frequently become undetectable after 6-12 months of a GFD and thus can be used to monitor the disease.
Antigliadin antibodies are no longer recommended - they are less specific, but can be either IgA (AGA) or IgG (AGG). They can be positive in other gastrointestinal conditions such as Crohn's disease
Biopsy
Patients with positive serological tests should be offered referral to local gastroenterologist for endoscopic or enteroscopic distal duodenal or jejunal biopsy to confirm diagnosis. They need to stay on gluten until after the biopsy. Referral should also be made where the serology is negative but there is still clinical suspicion of CD.
•The diagnosis of CD is made when biopsy shows villous atrophy while the patient is eating adequate amounts of gluten, followed by full clinical remission on excluding gluten.
•Under these circumstances, tTGA or EMA antibodies found at the time of diagnosis and their disappearance after gluten exclusion, means that it is only necessary to perform a further biopsy (and even a further gluten challenge and more biopsies) if there are still doubts. The further gluten challenge should always be performed if CD is diagnosed in children less than 2 yrs because of a high incidence of other causes of flat mucosa.
Other investigations
•FBC shows anaemia in 50%; iron and folate deficiency are both common (microcytes and macrocytes), hypersegmented leucocytes and Howell-Jolly bodies (splenic atrophy). Also check B12, folate, ferritin, LFT, calcium and albumin.
•Small bowel barium studies are occasionally needed to exclude other causes of malabsorption and diarrhoea, and diagnose rare complications such as obstruction or lymphoma.
Treatment
Starting a GFD rapidly induces clinical improvement, which is mirrored by the mucosa. The diet consists of no wheat, barley, rye, or any food containing them (e.g. bread, cake, pies). Moderate quantities of oats (free from other contaminating cereals) can be consumed as recent studies suggest that they do not damage the intestinal mucosa. Rice, maize, soya, potatoes, sugar jam, syrup and treacle are all allowed. Gluten-free biscuits, flour, bread and pasta are NHS prescribable. Coeliac UK produces a prescribing guide. When making GFD, must make sure cross contamination doesn’t occur, as a person with celiac can only take 0.02% of gluten in a product safely and even a little cross contamination with wheat (12% gluten) may result in return of symptoms.
Arrange dietitian appointment (with regular reviews). Even minor dietary lapses may cause recurrence. GFD should be lifelong, as relaxation of diet generally brings a return of symptoms and increased incidence of complications. Add supplements as necessary (e.g. folic acid, iron, calcium and vitamin D).
Serial tTGA or EMA antibodies can be used to monitor response to diet.
Oats - there was originally some concern about including oats in a GFD, but recent research has emphasised that oats can be given to almost all patients with coeliac disease.
Oral proteases are being developed (which digest gluten) and these may offer therapeutic options in the future.
Why follow up patients with coeliac disease?
Patient compliance with a GFD is poor, ranging from 45-87%. The long-term health risks for patients who comply poorly with a GFD include nutritional deficiency and reduced bone mineral density.
About a quarter of patients with CD have osteoporosis of the lumbar spine compared to 5% of matched controls. Bone mineral density improves significantly with a GFD.
Dietary compliance positively correlates with regular follow-up and knowledge of the condition.
Half of all coeliac patients have an inadequate energy intake, and 10% have inadequate intake of calcium and vitamin B6. 80% of elderly patients have inadequate intake of vitamin D.
GPs are responsible for the appropriate prescription of gluten-free products.20
Regular follow-up is an opportunity to provide patient-centred care that is sensitive to the individual's life circumstances.
How often should patients be reviewed?
Patients should be followed up throughout their lifetime.
After diagnosis, the patient should be reviewed at the gastroenterology clinic after 3 months and 6 months to ensure they are making satisfactory progress and managing the diet.
If well, they should be reviewed annually or sooner if problems arise - follow-up assessments are currently being carried out by dietitians, nurses, general practitioners and gastroenterologists in primary and secondary care.
GFD
- Jewish holiday Passover contains mostly gluten free food (except Maztah); usually stocked in early spring in stores catering to Jews.
Obvious Gluten
Less Obvious Gluten
High in Vitamin D
Iron Rich food
Naturally Gluten Free
Because CD is considerably under-diagnosed in Primary Care,consider the diagnosis and perform serological testing in all patients who present with:
•chronic or intermittent diarrhoea
•failure to thrive or faltering growth in children
•persistent or unexplained gastrointestinal symptoms including nausea and vomiting
•prolonged fatigue ('tired all the time')
•recurrent abdominal pain, cramping or distension
•sudden or unexpected weight loss
•unexplained iron-deficiency anaemia, or other unspecified anaemia
Serology – make sure they have been on a gluten diet for at least 6 weeks
•IgA anti-tissue transglutaminase antibodies (tTGAs) is the preferred investigation. Endomysial antibodies (EMAs) are used if tTGA) test is not available or equivocal.
•False negatives occur if the patient has selective IgA deficiency, as occurs in ~0.4% of the general population14 and in 2.6% of patients with CD (laboratories should test for IgA deficiency on negative samples). Use IgG tTGA and/or IgG EMA serological tests for people with confirmed IgA deficiency.
•Antibodies frequently become undetectable after 6-12 months of a GFD and thus can be used to monitor the disease.
Antigliadin antibodies are no longer recommended - they are less specific, but can be either IgA (AGA) or IgG (AGG). They can be positive in other gastrointestinal conditions such as Crohn's disease
Biopsy
Patients with positive serological tests should be offered referral to local gastroenterologist for endoscopic or enteroscopic distal duodenal or jejunal biopsy to confirm diagnosis. They need to stay on gluten until after the biopsy. Referral should also be made where the serology is negative but there is still clinical suspicion of CD.
•The diagnosis of CD is made when biopsy shows villous atrophy while the patient is eating adequate amounts of gluten, followed by full clinical remission on excluding gluten.
•Under these circumstances, tTGA or EMA antibodies found at the time of diagnosis and their disappearance after gluten exclusion, means that it is only necessary to perform a further biopsy (and even a further gluten challenge and more biopsies) if there are still doubts. The further gluten challenge should always be performed if CD is diagnosed in children less than 2 yrs because of a high incidence of other causes of flat mucosa.
Other investigations
•FBC shows anaemia in 50%; iron and folate deficiency are both common (microcytes and macrocytes), hypersegmented leucocytes and Howell-Jolly bodies (splenic atrophy). Also check B12, folate, ferritin, LFT, calcium and albumin.
•Small bowel barium studies are occasionally needed to exclude other causes of malabsorption and diarrhoea, and diagnose rare complications such as obstruction or lymphoma.
Treatment
Starting a GFD rapidly induces clinical improvement, which is mirrored by the mucosa. The diet consists of no wheat, barley, rye, or any food containing them (e.g. bread, cake, pies). Moderate quantities of oats (free from other contaminating cereals) can be consumed as recent studies suggest that they do not damage the intestinal mucosa. Rice, maize, soya, potatoes, sugar jam, syrup and treacle are all allowed. Gluten-free biscuits, flour, bread and pasta are NHS prescribable. Coeliac UK produces a prescribing guide. When making GFD, must make sure cross contamination doesn’t occur, as a person with celiac can only take 0.02% of gluten in a product safely and even a little cross contamination with wheat (12% gluten) may result in return of symptoms.
Arrange dietitian appointment (with regular reviews). Even minor dietary lapses may cause recurrence. GFD should be lifelong, as relaxation of diet generally brings a return of symptoms and increased incidence of complications. Add supplements as necessary (e.g. folic acid, iron, calcium and vitamin D).
Serial tTGA or EMA antibodies can be used to monitor response to diet.
Oats - there was originally some concern about including oats in a GFD, but recent research has emphasised that oats can be given to almost all patients with coeliac disease.
Oral proteases are being developed (which digest gluten) and these may offer therapeutic options in the future.
Why follow up patients with coeliac disease?
Patient compliance with a GFD is poor, ranging from 45-87%. The long-term health risks for patients who comply poorly with a GFD include nutritional deficiency and reduced bone mineral density.
About a quarter of patients with CD have osteoporosis of the lumbar spine compared to 5% of matched controls. Bone mineral density improves significantly with a GFD.
Dietary compliance positively correlates with regular follow-up and knowledge of the condition.
Half of all coeliac patients have an inadequate energy intake, and 10% have inadequate intake of calcium and vitamin B6. 80% of elderly patients have inadequate intake of vitamin D.
GPs are responsible for the appropriate prescription of gluten-free products.20
Regular follow-up is an opportunity to provide patient-centred care that is sensitive to the individual's life circumstances.
How often should patients be reviewed?
Patients should be followed up throughout their lifetime.
After diagnosis, the patient should be reviewed at the gastroenterology clinic after 3 months and 6 months to ensure they are making satisfactory progress and managing the diet.
If well, they should be reviewed annually or sooner if problems arise - follow-up assessments are currently being carried out by dietitians, nurses, general practitioners and gastroenterologists in primary and secondary care.
GFD
- Jewish holiday Passover contains mostly gluten free food (except Maztah); usually stocked in early spring in stores catering to Jews.
Obvious Gluten
Less Obvious Gluten
High in Vitamin D
Iron Rich food
Naturally Gluten Free
Sunday, August 8, 2010
Celiac Disease
Background
Celiac disease (CD) is a multifactorial, autoimmune disorder that occurs in genetically susceptible individuals. It is triggered by a well-identified environmental factor (gluten and related prolamins), and the autoantigen is also well known (ie, the ubiquitous enzyme tissue transglutaminase). The disease primarily affects the small intestine, where it progressively leads to flattening of the small intestinal mucosa. When people with celiac sprue ingest gliadin, the mucosa of their intestines is damaged by an immunologically mediated inflammatory response, resulting in maldigestion and malabsorption. Patients with celiac disease can present with failure to thrive and diarrhea (the classical form). However, some patients have only subtle symptoms (atypical celiac disease) or are asymptomatic (silent celiac disease). Three cereals contain gluten and are toxic for patients with celiac disease: wheat, rye, and barley.
The genetic susceptibility to celiac disease is conferred by well-identified haplotypes in the human leukocyte antigen (HLA) class II region (ie, DR3 or DR5/DR7 or HLA DR4). Such haplotypes are expressed on the antigen-presenting cells of the mucosa (mostly dendritic cells); approximately 90% of patients express the DQ2 heterodimer, and approximately 7% of patients express the DQ8 heterodimer. The remaining 3% of patients possess only half of the DQ2 heterodimer.
Frequency
United States
The frequency of celiac sprue in the United States is relatively low, about 1 case in 3000 persons. Estimates suggest that approximately 1% of the population is affected. Celiac disease is underdiagnosed in most affected people.
International
Approximately 3 million people in Europe and another 3 million people in the United States are estimated to be affected by celiac sprue. Celiac sprue is prevalent in European countries with temperate climates. The highest prevalence of celiac sprue is in Ireland and Finland and in places to which Europeans emigrated, notably North America and Australia. In these populations, celiac sprue affects approximately 1 in 100 individuals. The incidence of celiac sprue is increasing among certain populations in Africa (Saharawui population), Asia (India) and the Middle East.
Mortality/Morbidity
The morbidity rate of celiac disease can be high. Its complications range from osteopenia, osteoporosis, or both to infertility in women, short stature, delayed puberty, anemia, and even malignancies (mostly related to the GI tract [eg, intestinal T-cell lymphoma]). As a result, the overall mortality in patients with untreated celiac disease is increased.
Evidence also suggests that the risk of mortality is increased in proportion to the diagnostic delay and clearly depends on the diet; subjects who do not follow a gluten-free diet have an increased risk of mortality, as high as 6 times that of the general population. The increased death rates are most commonly due to intestinal malignancies that occur within 3 years of diagnosis. Some indirect epidemiological evidence suggests that intestinal malignancies can be a cause of death in patients with undiagnosed celiac disease.
Race
In some ethnicities, such as in the Saharawi population, celiac disease has been found in as many as 5% of the population. As mentioned, celiac disease is considered extremely rare or nonexistent in people of African, Chinese, or Japanese descent.
Sex
Most studies indicate a prevalence for the female sex, ranging from 1.5:1 to 3:1.
Age
Celiac disease can occur at any stage in life; a diagnosis is not unusual in people older than 60 years. Classic GI pediatric cases usually appear in children aged 9-18 months. Celiac disease may also occur in adults and is usually precipitated by an infectious diarrheal episode or other intestinal disease.
Clinical Presentations
Currently, 4 possible presentations of celiac disease are recognized, as follows:
- Typical presentation: This presentation is primarily characterized by GI signs and symptoms.
- Atypical presentation: GI signs and symptoms are minimal or absent, and various extraintestinal manifestations are present.
- Silent presentation: The small intestinal mucosa is damaged, and celiac disease autoimmunity can be detected with serology; however, no symptoms are present.
- Potential presentation: Patients are symptomatic, and the mucosa morphology is normal. These individuals have genetic compatibility with celiac disease and may also show positive autoimmune serology. Full-blown celiac disease may develop at a later stage in some of these individuals
The manifestations of untreated celiac sprue can be divided into gastrointestinal symptoms and extraintestinal symptoms.
- Gastrointestinal symptoms
- Diarrhea is the most common symptom in untreated celiac sprue and present in 45-85% of all patients. Diarrhea caused by celiac sprue is due to maldigestion and malabsorption of nutrients. The stools might be watery or semiformed, light tan or gray, and oily or frothy. The stools have a characteristic foul odor. In infants and young children, extensive diarrhea can lead to severe dehydration, electrolyte depletion, and metabolic acidosis.
- Malabsorption of ingested fat (steatorrhea) results in the delivery of excessive dietary fat to the large bowel. This results in the production of hydroxy fatty acids by bacteria, which causes secretion of fluids into the intestine.
- Flatulence (28% of patients) and borborygmus (35-72% of patients) results from the release of intestinal gas by the bacterial florae feasting on undigested and unabsorbed food materials and often becomes excessive or even explosive.
- Weight loss (present in 45% of all patients) is variable because some patients might compensate for the malabsorption by increasing dietary intake. In infants and young children with untreated celiac sprue, failure to thrive and growth retardation are common.
- Weakness and fatigue (prevalence 78-80%) are usually related to general poor nutrition. In some patients, severe anemia can contribute to fatigue. Occasionally, severe hypokalemia due to the loss of potassium in the stool can cause muscle weakness.
- Severe abdominal pain (prevalence 34-64%) is unusual in patients with uncomplicated celiac sprue. However, abdominal bloating or cramps with excessive malodorous flatus is a common complaint.
- Extraintestinal symptoms
- Anemia (10-15% of patients) is usually due to impaired absorption of iron or folate from the proximal small intestine. In severe celiac disease with ileal involvement, absorption of vitamin B-12 might be impaired.
- A bleeding diathesis is usually caused by prothrombin deficiency due to impaired absorption of fat-soluble vitamin K.
- Osteopenia and osteoporosis (prevalence 1-34%) might cause bone pain for several reasons, including defective calcium transport by the diseased small intestine, vitamin D deficiency, and binding of luminal calcium and magnesium to unabsorbed dietary fatty acids.
- Neurologic symptoms (frequency 8-14%) that result from hypocalcemia include motor weakness, paresthesias with sensory loss, and ataxia. Seizures might develop because of cerebral calcifications.
- Skin disorders, including dermatitis herpetiformis (a pruritic papulovesicular skin lesion involving the extensor surfaces of the extremities, trunk, buttocks, scalp, and neck), is associated in 10-20% of patients with celiac disease.
- Hormonal disorders, such as amenorrhea, delayed menarche, and infertility in women and impotence and infertility in men, have been described.
Wednesday, August 4, 2010
week 4 MED2042 Gross Anat Abd IV Liv Biliary tract Pancr
TASK 1: Da Wei & Phey Chien
TASK 2: Chesvin & Yi Zhen
TASK 3: Xin yi
TASK 4: Wen Jye
TASK 5: Timothy
TASK 6: Fahad
TASK 7: Nabeela & Rebekah
TASK 8: Nabila & Nicholas
TASK 2: Chesvin & Yi Zhen
TASK 3: Xin yi
TASK 4: Wen Jye
TASK 5: Timothy
TASK 6: Fahad
TASK 7: Nabeela & Rebekah
TASK 8: Nabila & Nicholas
Investigations for Colorectal Cancer
Colorectal cancer can take many years to develop and early detection of colorectal cancer greatly improves the chances of a cure. The National Cancer Policy Board of the Institute of Medicine estimated in 2003 that even modest efforts to implement colorectal cancer screening methods would result in a 29 percent drop in cancer deaths in 20 years. Despite this, colorectal cancer screening rates remain low.
Your doctor will perform a physical exam and press on your belly area. The physical exam rarely shows any problems, although the doctor may feel a mass in the abdomen. A rectal exam may reveal a mass in patients with rectal cancer, but not colon cancer.
• Digital rectal exam (DRE): The doctor inserts a lubricated, gloved finger into the rectum to feel for abnormal areas. It only detects tumors large enough to be felt in the distal part of the rectum but is useful as an initial screening test. This is not painful, but it is mildly uncomfortable for some people. It takes only a few seconds.
• Fecal occult blood test (FOBT): a test for blood in the stool. Two types of tests can be used for detecting occult blood in stools i.e. guaiac based (chemical test) and immunochemical. The sensitivity of immunochemical testing is superior to that of chemical testing without an unacceptable reduction in specifity. A fecal occult blood test (FOBT) may detect small amounts of blood in the stool, which could suggest colon cancer. However, this test is often negative in patients with colon cancer. For this reason, a FOBT must be done along with colonoscopy or sigmoidoscopy. It is also important to note that a positive FOBT doesn't necessarily mean you have cancer.
• Endoscopy:
o Sigmoidoscopy: A lighted probe (sigmoidoscope) is inserted into the rectum and lower colon to check for polyps and other abnormalities.
o Colonoscopy: A lighted probe called a colonoscope is inserted into the rectum and the entire colon to look for polyps and other abnormalities that may be caused by cancer. A colonoscopy has the advantage that if polyps are found during the procedure they can be removed immediately. Tissue can also be taken for biopsy.
• Colonoscopy is an endoscopic test. This means that a thin, flexible plastic tube with a tiny camera on the end will be inserted into your colon via your anus. As the tube is advanced further into your colon, the camera sends images of the inside of your colon to a video monitor.
• Colonoscopy is an uncomfortable test for most people. You will first be given a laxative solution to drink that will clear most of the fecal matter from your bowel. You will be allowed nothing to eat before the test. Whenever possible, you will be given medication before the procedure to relax you and relieve the discomfort.
• Flexible sigmoidoscopy is similar to colonoscopy but does not go as far into the colon. It uses a shorter endoscope to examine the rectum, sigmoid (lower) colon, and most of the left colon.
In the United States, colonoscopy or FOBT plus sigmoidoscopy are the preferred screening options.
When colon cancer is suspected, either a lower GI series (barium enema x-ray) or colonoscopy is performed to confirm the diagnosis and to localize the tumor.
A barium enema involves taking x-rays of the colon and the rectum after the patient is given an enema with a white, chalky liquid containing barium. The barium outlines the large intestines on the x-rays. Tumors and other abnormalities appear as dark shadows on the x-rays. Air-contrast barium enema is a type of x-ray that can show tumors.
• Before the x-ray is taken, a liquid is introduced into your colon and rectum via your anus. The liquid contains barium, which shows up solid on x-rays.
• This test highlights tumors and certain other abnormalities in the colon and rectum.
• Other types of contrast enemas are available.
• Air-contrast barium enema frequently detects malignant tumors, but it is not as effective in detecting small tumors or those far up in your colon.
Colonoscopy is a procedure whereby a doctor inserts a long, flexible viewing tube into the rectum for the purpose of inspecting the inside of the entire colon. Colonoscopy is generally considered more accurate than barium enema x-rays, especially in detecting small polyps. If colon polyps are found, they are usually removed through the colonoscope and sent to the pathologist. The pathologist examines the polyps under the microscope to check for cancer. While the majority of the polyps removed through the colonoscopes are benign, many are precancerous. Removal of precancerous polyps prevents the future development of colon cancer from these polyps.
If cancerous growths are found during colonoscopy, small tissue samples (biopsies) can be obtained and examined under the microscope to confirm the diagnosis. If colon cancer is confirmed by a biopsy, staging examinations are performed to determine whether the cancer has already spread to other organs. Since colorectal cancer tends to spread to the lungs and the liver, staging tests usually include chest x-rays, ultrasonography, or a CAT scan of the lungs, liver, and abdomen.
If your doctor learns that you do have colorectal cancer, more tests will be done to see if the cancer has spread. This is called staging. CT or MRI scans of the abdomen, pelvic area, chest, or brain may be used to stage the cancer. Sometimes, PET scans are also used.
Stages of colon cancer are:
• Stage 0: Very early cancer on the innermost layer of the intestine
• Stage I: Cancer is in the inner layers of the colon
• Stage II: Cancer has spread through the muscle wall of the colon
• Stage III: Cancer has spread to the lymph nodes
• Stage IV: Cancer has spread to other organs
Other screening methods
• Double contrast barium enema (DCBE): First, an overnight preparation is taken to cleanse the colon. An enema containing barium sulfate is administered, then air is insufflated into the colon, distending it. The result is a thin layer of barium over the inner lining of the colon which is visible on X-ray films. A cancer or a precancerous polyp can be detected this way. This technique can miss the (less common) flat polyp.
• Virtual colonoscopy replaces X-ray films in the double contrast barium enema (above) with a special computed tomography scan and requires special workstation software in order for the radiologist to interpret. This technique is approaching colonoscopy in sensitivity for polyps. However, any polyps found must still be removed by standard colonoscopy.
• Standard computed axial tomography is an x-ray method that can be used to determine the degree of spread of cancer, but is not sensitive enough to use for screening. Some cancers are found in CAT scans performed for other reasons.
• Blood tests: Measurement of the patient's blood for elevated levels of certain proteins can give an indication of tumor load. In particular, high levels of carcinoembryonic antigen (CEA) in the blood can indicate metastasis of adenocarcinoma. These tests are frequently false positive or false negative, and are not recommended for screening, it can be useful to assess disease recurrence. Blood tests that may be done include:
o Complete blood count (CBC) to check for anemia
o Liver function tests
o Blood tests to detect tumor markers, including carcinoembryonic antigen (CEA) and CA 19-9, may help your physician follow you after treatment.
• Genetic counseling and genetic testing for families who may have a hereditary form of colon cancer, such as hereditary nonpolyposis colorectal cancer (HNPCC) or familial adenomatous polyposis (FAP).
• Positron emission tomography (PET) is a 3-dimensional scanning technology where a radioactive sugar is injected into the patient, the sugar collects in tissues with high metabolic activity, and an image is formed by measuring the emission of radiation from the sugar. Because cancer cells often have very high metabolic rates, this can be used to differentiate benign and malignant tumors. PET is not used for screening and does not (yet) have a place in routine workup of colorectal cancer cases.
• Whole-body PET imaging is the most accurate diagnostic test for detection of recurrent colorectal cancer, and is a cost-effective way to differentiate resectable from nonresectable disease. A PET scan is indicated whenever a major management decision depends upon accurate evaluation of tumour presence and extent.
• Stool DNA testing is an emerging technology in screening for colorectal cancer. Premalignant adenomas and cancers shed DNA markers from their cells which are not degraded during the digestive process and remain stable in the stool. Capture, followed by PCR amplifies the DNA to detectable levels for assay. Clinical studies have shown a cancer detection sensitivity of 71%–91%.
• High C-Reactive Protein levels is risk marker
http://www.youtube.com/watch?v=WHFRCrPj0SQ
Your doctor will perform a physical exam and press on your belly area. The physical exam rarely shows any problems, although the doctor may feel a mass in the abdomen. A rectal exam may reveal a mass in patients with rectal cancer, but not colon cancer.
• Digital rectal exam (DRE): The doctor inserts a lubricated, gloved finger into the rectum to feel for abnormal areas. It only detects tumors large enough to be felt in the distal part of the rectum but is useful as an initial screening test. This is not painful, but it is mildly uncomfortable for some people. It takes only a few seconds.
• Fecal occult blood test (FOBT): a test for blood in the stool. Two types of tests can be used for detecting occult blood in stools i.e. guaiac based (chemical test) and immunochemical. The sensitivity of immunochemical testing is superior to that of chemical testing without an unacceptable reduction in specifity. A fecal occult blood test (FOBT) may detect small amounts of blood in the stool, which could suggest colon cancer. However, this test is often negative in patients with colon cancer. For this reason, a FOBT must be done along with colonoscopy or sigmoidoscopy. It is also important to note that a positive FOBT doesn't necessarily mean you have cancer.
• Endoscopy:
o Sigmoidoscopy: A lighted probe (sigmoidoscope) is inserted into the rectum and lower colon to check for polyps and other abnormalities.
o Colonoscopy: A lighted probe called a colonoscope is inserted into the rectum and the entire colon to look for polyps and other abnormalities that may be caused by cancer. A colonoscopy has the advantage that if polyps are found during the procedure they can be removed immediately. Tissue can also be taken for biopsy.
• Colonoscopy is an endoscopic test. This means that a thin, flexible plastic tube with a tiny camera on the end will be inserted into your colon via your anus. As the tube is advanced further into your colon, the camera sends images of the inside of your colon to a video monitor.
• Colonoscopy is an uncomfortable test for most people. You will first be given a laxative solution to drink that will clear most of the fecal matter from your bowel. You will be allowed nothing to eat before the test. Whenever possible, you will be given medication before the procedure to relax you and relieve the discomfort.
• Flexible sigmoidoscopy is similar to colonoscopy but does not go as far into the colon. It uses a shorter endoscope to examine the rectum, sigmoid (lower) colon, and most of the left colon.
In the United States, colonoscopy or FOBT plus sigmoidoscopy are the preferred screening options.
When colon cancer is suspected, either a lower GI series (barium enema x-ray) or colonoscopy is performed to confirm the diagnosis and to localize the tumor.
A barium enema involves taking x-rays of the colon and the rectum after the patient is given an enema with a white, chalky liquid containing barium. The barium outlines the large intestines on the x-rays. Tumors and other abnormalities appear as dark shadows on the x-rays. Air-contrast barium enema is a type of x-ray that can show tumors.
• Before the x-ray is taken, a liquid is introduced into your colon and rectum via your anus. The liquid contains barium, which shows up solid on x-rays.
• This test highlights tumors and certain other abnormalities in the colon and rectum.
• Other types of contrast enemas are available.
• Air-contrast barium enema frequently detects malignant tumors, but it is not as effective in detecting small tumors or those far up in your colon.
Colonoscopy is a procedure whereby a doctor inserts a long, flexible viewing tube into the rectum for the purpose of inspecting the inside of the entire colon. Colonoscopy is generally considered more accurate than barium enema x-rays, especially in detecting small polyps. If colon polyps are found, they are usually removed through the colonoscope and sent to the pathologist. The pathologist examines the polyps under the microscope to check for cancer. While the majority of the polyps removed through the colonoscopes are benign, many are precancerous. Removal of precancerous polyps prevents the future development of colon cancer from these polyps.
If cancerous growths are found during colonoscopy, small tissue samples (biopsies) can be obtained and examined under the microscope to confirm the diagnosis. If colon cancer is confirmed by a biopsy, staging examinations are performed to determine whether the cancer has already spread to other organs. Since colorectal cancer tends to spread to the lungs and the liver, staging tests usually include chest x-rays, ultrasonography, or a CAT scan of the lungs, liver, and abdomen.
If your doctor learns that you do have colorectal cancer, more tests will be done to see if the cancer has spread. This is called staging. CT or MRI scans of the abdomen, pelvic area, chest, or brain may be used to stage the cancer. Sometimes, PET scans are also used.
Stages of colon cancer are:
• Stage 0: Very early cancer on the innermost layer of the intestine
• Stage I: Cancer is in the inner layers of the colon
• Stage II: Cancer has spread through the muscle wall of the colon
• Stage III: Cancer has spread to the lymph nodes
• Stage IV: Cancer has spread to other organs
Other screening methods
• Double contrast barium enema (DCBE): First, an overnight preparation is taken to cleanse the colon. An enema containing barium sulfate is administered, then air is insufflated into the colon, distending it. The result is a thin layer of barium over the inner lining of the colon which is visible on X-ray films. A cancer or a precancerous polyp can be detected this way. This technique can miss the (less common) flat polyp.
• Virtual colonoscopy replaces X-ray films in the double contrast barium enema (above) with a special computed tomography scan and requires special workstation software in order for the radiologist to interpret. This technique is approaching colonoscopy in sensitivity for polyps. However, any polyps found must still be removed by standard colonoscopy.
• Standard computed axial tomography is an x-ray method that can be used to determine the degree of spread of cancer, but is not sensitive enough to use for screening. Some cancers are found in CAT scans performed for other reasons.
• Blood tests: Measurement of the patient's blood for elevated levels of certain proteins can give an indication of tumor load. In particular, high levels of carcinoembryonic antigen (CEA) in the blood can indicate metastasis of adenocarcinoma. These tests are frequently false positive or false negative, and are not recommended for screening, it can be useful to assess disease recurrence. Blood tests that may be done include:
o Complete blood count (CBC) to check for anemia
o Liver function tests
o Blood tests to detect tumor markers, including carcinoembryonic antigen (CEA) and CA 19-9, may help your physician follow you after treatment.
• Genetic counseling and genetic testing for families who may have a hereditary form of colon cancer, such as hereditary nonpolyposis colorectal cancer (HNPCC) or familial adenomatous polyposis (FAP).
• Positron emission tomography (PET) is a 3-dimensional scanning technology where a radioactive sugar is injected into the patient, the sugar collects in tissues with high metabolic activity, and an image is formed by measuring the emission of radiation from the sugar. Because cancer cells often have very high metabolic rates, this can be used to differentiate benign and malignant tumors. PET is not used for screening and does not (yet) have a place in routine workup of colorectal cancer cases.
• Whole-body PET imaging is the most accurate diagnostic test for detection of recurrent colorectal cancer, and is a cost-effective way to differentiate resectable from nonresectable disease. A PET scan is indicated whenever a major management decision depends upon accurate evaluation of tumour presence and extent.
• Stool DNA testing is an emerging technology in screening for colorectal cancer. Premalignant adenomas and cancers shed DNA markers from their cells which are not degraded during the digestive process and remain stable in the stool. Capture, followed by PCR amplifies the DNA to detectable levels for assay. Clinical studies have shown a cancer detection sensitivity of 71%–91%.
• High C-Reactive Protein levels is risk marker
http://www.youtube.com/watch?v=WHFRCrPj0SQ
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