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Wednesday, December 30, 2015

DIARRHEA

DIARRHEA

Definition. Diarrhea is either an increased frequency or volume of stool per day; stool can also be defined as diarrhea if the number of stools per day is few, but their consistency is watery.

Pathogenesis. The most common causes of diarrhea are of an infectious, antibiotic-associated, or lactose-intolerance etiology or from irritable bowel or carcinoid  syndrome.


Clinical Presentation. The patient is often hypotensive, febrile, and experiencing abdominal pain.
Diagnosis. The first thing to do in the evaluation of diarrhea in terms of direct patient care is to see if there is hypovolemia as defined as hypotension or orthostasis. This is more important than determining the specific etiology because of the chance that the patient may die while waiting for the results to come back.
Treatment. No matter the etiology, if the patient is hypotensive, febrile, and having abdominal pain, he or she should be admitted to the hospital and given intravenous fluids and antibiot- ics. The presence of blood in the stool is especially serious and is probably the single strongest indication for the use of antibiotics, such as ciprofloxacin.

INFLAMMATORY BOWEL DISEASE

INFLAMMATORY  BOWEL DISEASE

Inflammatory bowel disease (IBD) is a term comprising 2 disease entities: Crohn disease (CD) and ulcerative colitis (UC). They can be discussed simultaneously because of the large degree of overlap in terms of presentation, testing, and treatment. Both CD and UC are idiopathic disorders of the bowel associated with diarrhea, bleeding, weight loss, fever, and abdominal pain. Both are most accurately diagnosed with endoscopy and sometimes with barium stud- ies, “string sign” on small bowel follow through after barium meal in CD, and both are treated with anti-inflammatory medications, such as mesalamine, azathioprine, and 6-mercaptopu- rine (6MP). Steroids are used for acute exacerbations of both diseases.
Clinical Presentation. IBD presents with fever, diarrhea, weight loss, and, occasionally, abdomi- nal pain and bleeding. The extraintestinal manifestations of IBD are episcleritis, scleritis and iri- tis, sclerosing cholangitis, joint pains, and skin manifestations, such as pyoderma gangrenosum or erythema nodosum.
Crohn disease is more likely to be associated with a palpable abdominal mass because CD has granulomas in the bowel wall that are transmural in nature. This can lead to the different loops of bowel being inflamed and sticking together, forming a mass. The abdominal masses of CD can be palpated and cause pain. CD is not necessarily continuous, and one hallmark of the disorder is that there are “skip lesions,” or areas of normal tissue in between the areas of disease.
UC is limited exclusively to the large bowel. It is exclusively a mucosal disease, and although it can cause bleeding, it does not result in fistula formation. UC has no skip lesions, no fistula formation, and no oral or perianal involvement. UC is more likely to cause bloody diarrhea.
Note
Sclerosing cholangitis does not correlate to disease activity.


Both forms of IBD can lead to colon cancer after 8 to 10 years of involvement of the colon. If the CD does not result in colonic involvement, then it will not lead to cancer. Complications of Crohn disease are calcium oxalate kidney stones, diarrhea, and cholesterol gallstones.

Diagnosis. IBD is diagnosed with endoscopy and sometimes with barium studies. (CD can result in deficiency of vitamin B12, calcium, vitamin K, and iron because of malabsorption.) Anti–Saccharomyces cerevisiae antibodies (ASCA) are associated with CD, and antineutrophil cytoplasmic antibody (ANCA) is associated with UC. If a patient is ASCA positive and ANCA
negative, then he or she has a >90% chance of having CD. If the patient is ASCA negative and ANCA positive, there is a >90% chance of having UC.
Prothrombin time may be prolonged in CD because of vitamin K malabsorption. Kidney stones form more often in CD because the fat malabsorption results in a low calcium level and an increased absorption of oxalate, which forms kidney stones.
Treatment. Mesalamine derivatives are the mainstay of therapy for IBD in all of its forms. Pentasa is a form of mesalamine released in both the upper and lower bowel; hence, it is used in CD. Asacol is a form of mesalamine released in the large bowel, and it is most useful for UC. Rowasa is used exclusively for rectal disease. Sulfasalazine was used in the past for the same effect. The difficulty with sulfasalazine is that the high load of sulfa delivered causes a number of adverse effects, such as rash, hemolysis, and allergic interstitial nephritis. Sulfasalazine also causes reversible infertility in men and leukopenia by its sulfapyridine group.
Acute exacerbations of IBD are treated with high-dose steroids. Budesonide is a form of steroid that is ideal for IBD. It has a strong local effect when used orally, but is largely cleared by the liver in a first-pass effect. This limits the amount of systemic toxicity. Azathioprine and 6-mercaptopu- rine are associated with drug-induced pancreatitis, but are still used on a long-term basis to try to keep patients off steroids. Ciprofloxacin and metronidazole are used for CD in those with perianal disease. Infliximab is used for CD in those who form fistulae or have disease refractory to the other
forms of therapy. There has been re-activation of tuberculosis with infliximab, and it is important to test for latent tuberculosis with a purified protein derivative (PPD) prior to treatment. If the PPD is positive, then patients should receive isoniazid. The most common side effect of infliximab is arthralgias. Balsalazide and olsalazine are other forms of mesalamine that are only active in the colon and are used occasionally.
Surgery is curative in UC; almost 60% of patients will require surgery within 5 years after diagnosis due to refractory symptoms or severe disease. Surgery is not very effective in CD and disease tends to reoccur at the site of anastomosis.

Nonulcer Dyspepsia

Nonulcer Dyspepsia

When all the causes of epigastric pain have been excluded and there is still pain, the diagnosis is functional or nonulcer dyspepsia. There is no specific therapy for nonulcer dyspepsia known to cure the disorder. Antacids of various types from H2 blockers to liquid antacids to PPIs are tried
until something is found to relieve the discomfort. The cause of nonulcer dyspepsia is unknown.

Treatment of Helicobacter pylori in nonulcer dyspepsia is of equivocal value. If there is no response to anti-secretory therapy with a PPI, you can try to treat H. Pylori by adding clarithromycin and amoxicillin. Treating H. Pylori will improve symptoms in another 10–20% of patients.

Dumping Syndrome

Dumping Syndrome

Pathogenesis. This is an increasingly rare disorder because of the rarity of the necessity for surgery in the treatment of ulcer disease. It was far more common in the past, when vagotomy and gastric resection were performed to treat severe ulcer disease.

Dumping syndrome is caused by two phenomena. First, there is the rapid release of hypertonic chyme into the duodenum, which acts as an osmotic draw into the duodenum, causing intravas- cular volume depletion. Next, there is a sudden peak in glucose levels in the blood because of the rapid release of food into the small intestine. This is followed by the rapid release of insulin in response to this high glucose level, which then causes hypoglycemia to develop.

Clinical Presentation. Patients present with sweating, shaking, palpitations, and lightheaded- ness shortly after a meal.

Treatment. There is no cure for dumping syndrome. The management is to eat multiple, small meals.

Gastroparesis

Gastroparesis



Pathogenesis. Gastroparesis literally means the presence of a weak stomach. The most common association for gastroparesis is diabetes. Electrolyte problems with potassium, magnesium, and calcium can also weaken the musculature of the bowel wall.
Clinical Presentation. Patients present with early satiety, postprandial nausea, and a general sense of increased abdominal fullness. This is from decreased motility of the stomach and the accumulation of food there. Gastroparesis generally occurs in those presenting with abdominal pain and bloating and who have a long-standing history of diabetes, along with retinopathy, neuropathy, nephropathy, and history of poor glycemic  control.

Diagnosis. Although a gastric-emptying study can be done with the ingestion of radioisotope- labeled food, this is rarely necessary. The diagnosis of diabetic gastroparesis is generally obvious as the cause of bloating, vomiting, and nausea in a long-term diabetic after endoscopy excludes other diseases.
Treatment. The treatment of gastroparesis is with agents that will increase motility of the stomach, such as erythromycin or metoclopramide. Erythromycin increases motilin levels.

Barrett Esophagus

Barrett Esophagus

Pathogenesis. Barrett esophagus is a complication of long-standing reflux disease. After sev- eral years of GERD, the epithelium of the lower esophagus undergoes histologic change from a normal squamous epithelium to a columnar  epithelium.
Diagnosis. Patients with Barrett esophagus should have a repeat endoscopy every 2 to 3 years to see whether dysplasia or esophageal cancer has developed. Patients with low-grade dyspla- sia should undergo repeat endoscopy in 3 to 6 months to see if the lesion has progressed or resolved. Patients with high-grade dysplasia should have a distal esophagectomy or an endo- scopic mucosal resection because of its very high rate of progression to invasive esophageal carcinoma. The usual rate of progression to cancer is about 0.5% per year.
Barium studies are typically normal. Endoscopy should be performed if the patient has GERD and if there are alarm symptoms, such as dysphagia, odynophagia, weight loss, anemia, or heme-positive stool. It is not clear when endoscopy should be done when there is a history only of GERD.
Treatment. All patients with Barrett esophagus should receive PPIs.

Tuesday, December 29, 2015

Gastroesophageal Reflux Disease

Gastroesophageal Reflux Disease

A 32-year-old man comes to the emergency department for substernal chest pain of 2 hours’ duration. He says that he sometimes gets this pain while lying in bed at night. He is otherwise free of symptoms, except for a nonproductive cough that he has had for the past month or so. His physical examination is unremarkable. His ECG is normal. He is given sublingual nitroglycerin and notes that his chest discomfort is worsened.

Pathogenesis. Gastroesophageal reflux disease, or GERD, is caused by the abnormal flow of the acid gastric contents backward from the stomach up into the esophagus. The lower esophageal sphincter (LES) is not a true anatomic sphincter; you can’t find it in a cadaver. The LES is cre- ated by the different response of the smooth muscle cells in the distal esophagus.
A number of factors can cause decreased tone or loosening of this sphincter, such as nicotine, alcohol, caffeine, peppermint, chocolate, and anticholinergics. We also know that calcium-channel blocking agents and nitrates also lower the sphincter pressure. When the tone of the LES decreases, acid is more likely to reflux backward into the esophagus, particularly when the patient is lying flat. GERD can still occur in the absence of these precipitating factors and can often simply be idiopathic in origin.
Clinical Presentation. Dyspepsia or epigastric pain can be caused by GERD, ulcer disease, pan- creatitis, gastritis, and nonulcer dyspepsia. GERD can be differentiated from the others by the presence of a sore throat; a bad, metal-like taste in the mouth; hoarseness; and cough and wheez- ing. In addition, GERD is the one most likely to be associated with pain in the substernal area.
Diagnosis. Specific diagnostic testing is not necessary when the patient’s symptoms are those described in the clinical presentation. In clear cases of epigastric pain going under the sternum and associated with a respiratory complaint or a bad taste in the mouth, therapy should be initiated immediately with antisecretory medications, such as proton-pump inhibitors (PPIs).  The most accurate diagnostic test is a 24-hour pH monitor, but this is only necessary when the patient’s presentation is equivocal in nature and the diagnosis is not clear. An electrode is placed several centimeters above the gastroesophageal junction, and a determination is made of what the average pH is in that area. Normal endoscopy does not exclude reflux disease.
Treatment. Therapy for GERD is primarily with PPIs, all of which are essentially equal in effi- cacy. Omeprazole, esomeprazole, lansoprazole, pantoprazole, and rabeprazole will all reliably increase the pH of the gastric contents to a level above 4.0. Do motility studies prior to surgery to avoid iatrogenic dysphagia.
A small number of persons, usually <5%, will not respond to PPIs and will need to undergo surgery to tighten the sphincter. Traditionally, this has been a Nissen fundoplication, which is done laparoscopically. Another method is simply placing a circular purse-string suture in the LES to tighten it