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James
Senior Member

Topics: 14
Posts: 127
Posted 12/13/11 - 03:30 AM report   #1
the clinical and laboratory manifestations of carcinoid syndrome.

Elevated urinary 5HIAA (24 Hr collection).

Symptoms develop only after it has metastized to the liver & the serotonin is able to get across into the systemic circulation un-metabolized.

They include paroxysms of flushing, abdominal cramping, diarrhea
James
Senior Member

Topics: 14
Posts: 127
Posted 12/13/11 - 03:32 AM report   #2
Adenomatous polyps should always be removed and followed up by repeat colonoscopy. Hyperplastic polyps have no neoplastic potential.

Familial polyposis should be managed with annual sigmoidoscopic surveillance after age 12. If patient does not develop polyps by age 40 then patient is unlikely to develop familial polyposis thus this high level surveillance can be stopped at that stage.

If polyposis develops, treatment is total colectomy.
James
Senior Member

Topics: 14
Posts: 127
Posted 12/13/11 - 03:33 AM report   #3
In general PROXIMAL small bowel malabsoprtion syndromes present with chronic diarrhea and decreased Fe, folate, Ca, Mg.

Lactose intolerance is very common.

Bacterial overgrowth where B12 is deficient but Folate EXCESS is seen.

Whipple's disease where PAS positive coccobacilli (Trophyrema whippeli) are seen

GI lymphoma where thickened small bowel loops are seen.

DISTAL (Ileal) small bowel disease typically presents with oxalate kidney stones, steattorhea, weight loss, B12 & fat soluble vitamin deficiencies. Examples include Crohn's disease and ileal resection.
James
Senior Member

Topics: 14
Posts: 127
Posted 12/13/11 - 03:35 AM report   #4
Objective: Select the appropriate test for malabsorption syndromes of different etiologies,

Steatorrhea due to pancreatic insufficiency: Bentiromide test (Bentiromide is broken down by pancreatic enzyme chymotrypsin to form PABA. PABA is excreted in urine. Low excretion signifies diagnosis. Treatment is replacement of enzymes orally.

Celiac Disease: Small bowel biopsy using Crosby's capsule (Shows flattening of villi but deepening of crypts). Treatment is Avoidance of Gluten (in wheat). Associated dermatitis herpetiformis is itchy and responds to Dapsone but before you give Dapsone, please check G6PD level as dapsone causes hemolysis in patients with G6PD deficiency.

Blind Loop syndrome (Bacterial overgrowth syndrome): C14 Xylose breath test (Bacteria break down Xylose which is then turned into CO2 that is exhaled). Breath test detects high levels of CO2 with C14. Treatment is with Broad spectrum antibiotics.

Giardiasis: Stool microscopy for ova and parasites or Giardiasis specific antigen in stool. Treatment is with (Flagyl) Metronidazole.

Osmotic diarrhea due to concentrated feeds: Stool osmolality (Also by stopping feeds). Diluting the feed should help avoid diarrhea.
James
Senior Member

Topics: 14
Posts: 127
Posted 12/13/11 - 03:38 AM report   #5
Occult GI bleeding should prompt a workup usually starting with a colonoscopy. It is not considered normal to have blood in the stools even on anticoagulation. Anticoagulants should be stopped if possible for workup
James
Senior Member

Topics: 14
Posts: 127
Posted 12/13/11 - 03:39 AM report   #6
Sprue (celiac disease) presents with chronic diarrhea and evidence of malabsorption by the proximal small bowel. Typically patients are anemic (dec. Fe and Folate absorption ). May also be hypocalcemic and hypomagnesemic. Steattorhea is rare. Dermatitis herpetiformis can be seen with sprue. The principle procedure for diagnosis is small bowel biopsy. In a patient in whom you have a low suspicion of sprue, a negative anti-endomysial antibody virtually excludes this diagnosis
James
Senior Member

Topics: 14
Posts: 127
Posted 12/13/11 - 03:42 AM report   #7
the indication for Helicobacter pylori eradication.

When one tests a patient for H. pylori, the test may be positive but may not need any treatment. The presence of concomitant peptic ulcer disease, gastritis, or MALT lymphoma are indications for eradication treatment. The one exception is the patient with dyspepsia who has a positive test and is empirically treated. If symptoms do not resolve - then an endoscopy is indicated in such a person.
If such a person has been treated for H. pylori in the past, then the antibody may be falsely positive and such a patient should be tested using the urea pill test (where the patient swallows a pill of urea and if H. pylori is present then the urease in H. pylori will be break the urea into ammonia and the ammonia being alkaline will change the color of an indicator into which the patient breathes out using a straw).
James
Senior Member

Topics: 14
Posts: 127
Posted 12/13/11 - 03:45 AM report   #8
Gut failure. Depends on portion of the bowel resected and amount. For the most part, nutrient absorption is accomplished in the proximal small bowel (except fat) and fluid and electrolyte homeostasis is maintained by the ileum and colon. So it is not difficult to work it out.


Moderate amount of bowel resection : Elemental diet and diet rich in omega 3 fatty acids.

Extensive small bowel resection : Parenteral nutrition
James
Senior Member

Topics: 14
Posts: 127
Posted 01/07/12 - 09:20 PM report   #9
Key Points

Oropharyngeal dysphagia occurs immediately with deglutition and often has a neuromuscular origin.

Esophageal dysphagia usually occurs after the initiation of a swallow and is often caused by a mechanical interference with swallowing.

Dysphagia for solids is usually caused by a structural lesion; dysphagia for both solids and liquids is usually caused by a motility disorder.

Odynophagia is usually caused by esophageal ulceration.
Transient relaxation of the lower esophageal sphincter is an important cause of gastroesophageal reflux disease.

Ambulatory pH monitoring is the gold standard for the diagnosis of gastroesophageal reflux disease.

Empiric therapy with a proton pump inhibitor has an acceptable sensitivity and specificity for diagnosing gastroesophageal reflux disease.

The standard of care for the medical treatment of gastroesophageal reflux disease is proton pump inhibitor therapy.

Lifestyle modifications and surgical and endoscopic approaches are of unclear long-term benefit for gastroesophageal reflux disease.

Up to one third of patients with gastroesophageal reflux disease have extraesophageal manifestations, such as asthma, noncardiac chest pain, chronic cough, and laryngitis.

Upper endoscopy with biopsies is necessary to diagnose Barrett esophagus.

Barrett esophagus is associated with a 30-fold increased risk of esophageal adenocarcinoma.

Surveillance endoscopy with biopsy is recommended in patients with Barrett esophagus.

Early detection and surgical resection of esophageal cancer offers the best chance for good outcome.

Most esophageal cancers are detected at later stages and are treated with combined-modality therapy consisting of surgery and radiation therapy and/or chemotherapy.

All patients with achalasia require esophagogastroduodenoscopy and biopsy to rule out cancer-related pseudoachalasia.

Most esophageal motility disorders are hypertonic (spastic), of which the best characterized is achalasia.

Pseudoachalasia mimics the manometric findings of achalasia but is caused by obstruction by an underlying malignancy.

Patients with achalasia present with dysphagia and can be treated by disruption of the malfunctioning lower esophageal sphincter tone.

Infectious esophagitis occurs in immunosuppressed patients and in persons with abnormal esophageal stasis.

Odynophagia is the most common presenting symptom in infectious esophagitis, which is most frequently caused by Candida albicans.

Pill-induced esophagitis is most frequently caused by tetracycline, iron sulfate, potassium, bisphosphonates, NSAIDs, and quinidine.

Eosinophilic esophagitis is rapidly increasing in incidence and is associated with atopy.
James
Senior Member

Topics: 14
Posts: 127
Posted 01/07/12 - 09:23 PM report   #10
The diagnosis of oropharyngeal dysphagia is best accomplished by videofluoroscopy, which may lead to the need for endoscopy if a structural lesion is detected.
James
Senior Member

Topics: 14
Posts: 127
Posted 01/07/12 - 09:42 PM report   #11
Practice Guidelines for Endoscopic Surveillance of Barrett

Esophagus Dysplasia Grade:Recommendation

1. None: Repeat surveillance 1 year after baseline screening; if negative, every 5 years

Discontinue surveillance if life expectancy <1 year or patient unable to tolerate therapeutic measures

2. Low-grade: Surveillance every 6 months for 1 year, then yearly until age 80, depending on health status

3. High-grade: If confirmed by two experienced pathologists, definitive surgical or endoscopic management

If patient declines, consider continued surveillance:

Focal high-grade dysplasia: continue surveillance every 3 months for 2 years then every 6 months

Multifocal high-grade dysplasia: definitive intervention

Mucosal irregularity: endoscopic ultrasonography and mucosal resection, if available
James
Senior Member

Topics: 14
Posts: 127
Posted 01/07/12 - 10:10 PM report   #12
Key Points

Helicobacter pylori infection and NSAIDs are responsible for more than 90% of peptic ulcers.

Patients with peptic ulcers are commonly asymptomatic at diagnosis; the ulcers are often detected during evaluation for ulcer-related complications such as overt or obscure bleeding.

Gastrointestinal bleeding is the most common complication of peptic ulcer disease, present in approximately 15% of cases.

The management of peptic ulcer disease includes acid suppression, testing for Helicobacter pylori infection, and assessing the use of NSAIDs.

For patients younger than 55 years with uninvestigated new-onset dyspepsia without alarm features, a “test and treat” approach for Helicobacter pylori infection is recommended.

Manifestations of Helicobacter pylori infection include gastritis, ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric adenocarcinoma.

The urea breath test and fecal antigen test detect active Helicobacter pylori infection and can be used before therapy to confirm infection and at least 4 weeks after therapy to confirm eradication.

Triple therapy consisting of a proton pump inhibitor, amoxicillin, and clarithromycin is the most commonly used initial treatment for Helicobacter pylori infection.

Testing all treated patients for Helicobacter pylori eradication is neither practical nor cost-effective; such testing should be performed in patients with associated peptic ulcer disease, persistent dyspepsia despite a test-and-treat approach, MALT lymphoma, or a history of early-stage gastric cancer.

All NSAIDs inhibit prostaglandin synthesis, and therefore, different formulations (enteric-coated) and routes (intravenous, rectal) of NSAIDs share the toxicity of oral NSAIDs.

Factors related to an increased risk for NSAID-induced complications include age >60 years, previous peptic ulcer disease or hemorrhage, higher doses or the combination of two or more NSAIDs, concurrent use of anticoagulants or corticosteroids, and significant medical comorbidities.

Proton pump inhibitors more effectively heal peptic ulcerations than H2-receptor antagonists, whether or not NSAID therapy is ongoing.

Fundic gland polyps, the most common form of gastric polyps, are small, often multiple, and, if sporadic, have no defined cancer risk.

Most symptomatic patients with gastric cancer have advanced disease at presentation, with only 50% of patients being candidates for curative resection.

Before gastroparesis can be diagnosed, mechanical obstruction needs to be excluded.

The test of choice to document delayed gastric emptying is a 4-hour gastric scintigraphy of a radiolabeled solid meal.

Management of gastroparesis includes a combination of diet modification, antiemetic agents, and prokinetic therapy.

Pulmonary embolism is an uncommon complication after bariatric surgery, but it accounts for 50% of all deaths in these patients.

Nutritional deficiencies are common after bariatric surgery, and patients typically need supplementation with iron, vitamin B12, calcium, and vitamin D.
James
Senior Member

Topics: 14
Posts: 127
Posted 01/08/12 - 01:30 AM report   #13
Key Points

Alcohol abuse and gallstones account for approximately 80% of cases of acute pancreatitis in the United States.

Diagnosis of acute pancreatitis is made primarily through clinical evaluation and detection of elevated serum concentrations of amylase and lipase.

The most important determinant of patient outcome in acute pancreatitis is the presence of pancreatic necrosis.

Prophylactic antibiotic therapy in patients with acute pancreatitis should be limited to those patients with necrotizing pancreatitis.

Nasojejunal feeding is the preferred route of nutrition in patients with acute pancreatitis.

Manifestations of chronic pancreatitis include abdominal pain, malabsorption, and diabetes mellitus.

Diagnosis of chronic pancreatitis is made by imaging that shows pancreatic calcifications and ductal and parenchymal changes of the pancreas or biochemical tests that show impaired pancreatic function.

Treatment of chronic pancreatitis includes pain control by medical, endoscopic, or surgical methods; pancreatic enzyme supplementation for malabsorption; and careful glucose control for diabetes mellitus.

Pancreatic adenocarcinoma is one of the deadliest cancers, with a 5-year survival rate less than 5% overall and only 10% to 25% in patients who undergo surgery with curative intent.

Preoperative diagnosis and staging of pancreatic adenocarcinoma are performed with CT scanning and endoscopic ultrasonography; tumors that have not metastasized or invaded large local vessels are considered to be resectable.

Surgery is the only curative option for pancreatic cancer: pancreatoduodenectomy is the procedure for cancer of the pancreatic head, and distal pancreatectomy for cancer of the body and tail; only 15% to 20% of patients are surgical candidates.

Management of pancreatic cystic lesions is determined by the presence of symptoms and malignant potential as determined by CT and MRI scanning, endoscopic ultrasonography, and cyst fluid analysis.

Pancreatic neuroendocrine tumors lead to symptoms either through tumor mass effect or excessive secretion of hormones.
James
Senior Member

Topics: 14
Posts: 127
Posted 01/08/12 - 01:57 AM report   #14
Many pancreatic neuroendocrine tumors have receptors for somatostatin, and somatostatin receptor scintigraphy is the preferred first test in identifying both the primary pancreatic tumor and metastases in neuroendocrine tumors with the exception of insulinomas, which are rarely malignant. Endoscopic ultrasonography is highly sensitive for localizing the tumor in the pancreas and may be used as a complementary test to somatostatin receptor scintigraphy
James
Senior Member

Topics: 14
Posts: 127
Posted 01/08/12 - 04:34 AM report   #15
Key Points

Acute diarrhea lasts less than 2 weeks; chronic diarrhea lasts longer than 4 weeks.

Hydration is critical in a patient with severe diarrhea.

Diagnostic evaluation is appropriate in diarrhea that is not self-limited and does not respond to empiric therapy.

Patients with chronic diarrhea with an oily residue in their stool should be evaluated for fat malabsorption.

Celiac disease is associated with other autoimmune diseases such as type 1 diabetes mellitus.

A response to an empiric course of antibiotics is often the best test for small-intestine bacterial overgrowth.

Patients with less than 200 cm of functioning small intestine should be carefully monitored for short- bowel syndrome.

The diarrhea associated with pancreatic insufficiency often responds to supplementation with pancreatic lipase enzymes.

5-Aminosalicylates (5-ASAs) are the mainstay of therapy for mild to moderate ulcerative colitis; when 5-ASAs are not effective, corticosteroids may need to be used as short-term induction therapy.

Microscopic colitis typically manifests with loose, watery diarrhea and is most commonly seen in middle-aged or elderly women.

Treatment for mild microscopic colitis is supportive, but budesonide is the most effective treatment in more severe cases.

Chronic constipation is more prevalent in women than in men; most cases are idiopathic, but causes include medications and metabolic, neurologic, and collagen-vascular disorders.

Alarm features in patients with functional constipation include rectal bleeding or occult blood-positive stool, weight loss, a family history of colon cancer or inflammatory bowel disease, anemia, and acute onset in an older person; patients without alarm features do not need extensive evaluation.

Treatment of chronic constipation includes fiber supplementation and osmotic and stimulant laxatives; biofeedback training may be used for patients with dyssynergia.

Ileus most commonly occurs after abdominal surgery but can also be associated with metabolic disturbances, medications, inflammatory conditions, sepsis, and neurologic injury.

Chronic idiopathic pseudo-obstruction, a motility disorder that mimics intestinal obstruction, may be secondary to paraneoplastic syndrome or neurologic, smooth muscle, or metabolic disorders.

Altered motility secondary to autonomic dysfunction in diabetes mellitus is common, especially after prolonged disease and in association with other diabetic complications.

Irritable bowel syndrome is a functional bowel disorder that most commonly affects women aged 20 to 40 years.

Possible mechanisms of irritable bowel syndrome include abnormal gastrointestinal motility, visceral afferent hypersensitivity, and altered activation of the mucosal immune system.

Irritable bowel syndrome is a clinical diagnosis based on the Rome III criteria; in the absence of alarm features, extensive diagnostic evaluation is unnecessary.

There are four subtypes of irritable bowel syndrome: constipation-predominant, diarrhea-predominant, mixed, and unsubtyped.

Treatment of irritable bowel syndrome is targeted at the predominant symptoms and includes fiber, laxatives, antidiarrheal and antispasmodic agents, and antidepressants.

Diverticulosis is a common finding in elderly persons in the West; a lack of dietary fiber may be a factor in the pathogenesis.

Diverticulitis and diverticular bleeding are the major complications of diverticulosis and are seen in less than a quarter of patients.

Diverticulitis presents most commonly with left lower quadrant pain, fever, and an elevated leukocyte count; diagnosis is generally made on clinical and CT findings; colonoscopy should be avoided in the acute setting.

Diverticulitis is treated with antibiotics; complications include abscess, fistula, and obstruction, which may require surgical intervention.

Acute mesenteric ischemia is a life-threatening condition that typically occurs in older patients with cardiovascular and peripheral vascular disease.

A high suspicion is the key to early diagnosis of acute mesenteric ischemia, which is essential to reduce morbidity and mortality. The diagnosis is usually made by radiographic and traditional angiography.

Treatment for acute mesenteric ischemia includes surgery, vasodilator therapy, and in patients with mesenteric venous thrombosis and a hypercoagulable state, anticoagulation.

Chronic mesenteric ischemia occurs in the setting of significant atherosclerotic disease in which usually two or three splanchnic vessels are occluded; a history of postprandial abdominal pain and weight loss are essential features of the diagnosis.

Colonic ischemia usually occurs in older patients with cardiovascular disease and in younger patients who are long-distance runners; diagnosis is made by colonoscopy and histology; treatment is supportive.
James
Senior Member

Topics: 14
Posts: 127
Posted 01/08/12 - 04:48 AM report   #16
Serum antitissue transglutaminase (anti-tTG) antibody assay: Celiac sprue, Most reliable screening test for celiac sprue; diagnosis must be confirmed by small-bowel biopsies.

Antiendomysial antibody assay: Celiac sprue, More labor intensive, more expensive than anti-tTG antibody assay; positive result requires small-bowel biopsy for confirmation.

Antigliadin antibody assay: Celiac sprue, Useful in following dietary response to gluten withdrawal; less useful in diagnosis except for serum IgG in IgA deficiency.
James
Senior Member

Topics: 14
Posts: 127
Posted 01/15/12 - 09:21 PM report   #17
Key Points

Colon cancer results from the accumulation of genetic mutations that lead to the progression from normal mucosa to dysplastic adenoma to carcinoma.

Tumor suppressor genes, oncogenes, and mismatch repair genes differentially contribute to carcinogenesis in familial and sporadic colorectal cancers.

Evaluation of patients with a suspected familial colon cancer syndrome should be performed under the guidance of a genetic counselor.

Patients with hereditary colon cancer syndromes such as familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer have a very high risk of developing colon cancer and extracolonic malignancy; these patients require aggressive screening and surveillance strategies.

In addition to being at high risk for colon cancer, patients with familial adenomatous polyposis are at risk for cancers of the small bowel, thyroid gland, stomach, central nervous system, and biliary system.

Hereditary nonpolyposis colorectal cancer should be suspected clinically in persons who have multiple family members with cancers of the colon, endometrium and ovaries, small bowel, ureter, renal pelvis, and pancreaticobiliary system.

Clinical diagnostic criteria for hereditary nonpolyposis colorectal cancer include the 3-2-1 rule: 3 relatives with an associated cancer; 2 generations affected; and 1 person diagnosed before age 50 years.

Medical conditions that increase the risk for colorectal cancer include inflammatory bowel disease, acromegaly, a history of radiation injury to the colon, and urinary diversion with implantation of ureters into the colon.

Colorectal cancer screening is well tolerated, cost-effective, and saves lives.

Screening for colorectal cancer is feasible because of the 10 to 15 years that are needed for a polyp to develop into cancer, an ample time to detect and remove an adenoma.

Fecal occult blood testing, flexible sigmoidoscopy, and colonoscopy are appropriate options for screening for colorectal cancer in average-risk patients.
James
Senior Member

Topics: 14
Posts: 127
Posted 01/15/12 - 09:50 PM report   #18
First-degree relative(s) with colorectal cancer diagnosed at age <60 years: Colonoscopy at age 40 or 10 years younger than affected relative (whichever is younger). If normal, repeat every 3-5 years.

First-degree relative(s) with colorectal cancer diagnosed at ?60 years: Colonoscopy at age 40 years If normal, repeat every 10 years.

First-degree relative(s) with adenomatous polyp <60 years: Colonoscopy at age 40 years or 10 years younger than affected relative If normal, repeat every 5 years.

First-degree relative with adenomatous polyp >60 years: Colonoscopy beginning at age 40 years. Individualized; if normal,same as average risk.

Second- or third degree relative with cancer or polyps: Colonoscopy as average-risk persons If normal, same as average risk.
James
Senior Member

Topics: 14
Posts: 127
Posted 01/15/12 - 10:27 PM report   #19
Post-Polypectomy Surveillance Recommendations of the US Multi-Society Task Force on Colorectal Cancer and the American Cancer Society

1. Patients with small rectal hyperplastic polyps should be considered to have normal colonoscopies, and therefore the interval before the subsequent colonoscopy should be 10 years. An exception is patients with a hyperplastic polyposis syndrome.

2. Patients with only one or two small (<1 cm) tubular adenomas with only low-grade dysplasia should have their next follow-up colonoscopy in 5 to 10 years.

3. Patients with 3 to 10 adenomas, or any adenoma ?1 cm, or any adenoma with villous features, or high-grade dysplasia should have their next follow-up colonoscopy in 3 years providing that piecemeal removal has not been done and the adenoma(s) are completely removed. If the follow-up colonoscopy is normal or shows only one or two small tubular adenomas with low-grade dysplasia, then the interval for the subsequent examination should be 5 years.

4. Patients who have more than 10 adenomas at one examination should be examined at a shorter (<3 years) interval established by clinical judgment, and the clinician should consider the possibility of an underlying familial syndrome.

5. Patients with sessile adenomas that are removed piecemeal should be considered for follow up at short intervals (2 to 6 months) to verify complete removal. Once complete removal has been established, subsequent surveillance needs to be individualized based on the judgment of the endoscopist. Completeness of removal should be based on both endoscopic and pathologic assessments.

6. More intensive surveillance is indicated when the family history may indicate hereditary nonpolyposis colorectal cancer.








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