STUDY - Technical - New Dacian's Medicine
Diarrhea
(3)
Translation Draft
Today I'm going to finish everything there is to say about diarrhea, no matter how long it takes me... And, I'm stuck with secretory diarrhea...
Secretory diarrhea is characterized by a large volume of discharged faeces, produced by abnormal transport of liquids and electrolytes that is not necessarily related to food intake. Therefore, diarrhea usually persists through fasting. The term aqueous (hydric) diarrhea is often used synonymous with secretory diarrhea.
Since there is no dissolved malabsorbed substance, fecal osmolarity in secretory diarrhea may be due to abnormal ion constituents without fecal osmotic hiatus. Classic examples of secretory diarrhea are also mediated by hormones. Patients with metastatic carcinoid tumors of the gastrointestinal tract may have watery diarrhea as part of carcinoid syndrome comprising episodic skin erythema (flushing), telangiectasis lesions of the skin, cyanosis, pelagroid skin lesions, bronchospasm and cardiac blasts due to valvular lesions in the right heart. Carcinoid syndrome results from the secretion of various vasoactive substances that are powerful intestinal secretagogues, including serotonin, histamine, catecholamines, prostaglandins and kinins.
Zollinger-Ellison syndrome is characterized by recurrent, refractory and unusual localizing peptic ulcers due to gastrinoma, with diarrhea occurring in a third of patients and may be representation syndrome in 10% of cases. Diarrhea is due only partially to large volumes of secreted hydrochloric acid, but is also due only partially to large volumes of secreted hydrochloric acid, but is also due to fat maldigestion caused by inactivity of pancreatic lipase and precipitation of bile acids at low pH.
Non-beta pancreatic cell adenomas can secrete various peptides, including vasoactive intestinal polypeptide (VIP), pancreatic polypeptide, secretin, neurotensin, calcitonin, prostaglandins and others. Those that secrete VIP may be associated with aqueous diarrhea syndrome/ hypokalemia-achlorhydry (DAHA), characterized by often massive secretory diarrhea, achlorhydry, hypopotasemia, hypomagnesemia, hypercalcemia without hyperparathyroidism and in some cases flushing, myopathy or nephropathy. Not all patients with DAHA syndrome have a vipom and in such cases alternative mediators of intestinal secretion have been postulated.
Medular thyroid carcinoma may be sporadic or a characteristic of multiple endocrine neoplasia syndrome type IIa with pheorochromocytoma and hyperparathyroidism. Watery diarrhea is considered to be mediated by calcitonin produced by the tumor, although in some cases other mediators may be found. The appearance of diarrhea in the medullary carcinoma of the thyroid is usually associated with metastases and reserved prognosis. Systemic mastocytosis, which may be associated with skin lesions of pigment yurticaria, may also be associated with diarrhea that is secretory, mediated by histamine, or malabsorptive, due to infiltration of the intestinal mucosa by mastocytes.
Diarrhea associated with the vilos adenoma of the rectum or rectosigmoid is usually found in massive tumors, often exceeding 3-4 cm in diameter. Hypokalemia due to potassium loss is common. Microscopic or lymphocytic colitis and collagen colitis may be variants of the same disease. Their specific signs are a specific histological lesion despite a normal appearance of the mucosa at colonoscopy and diarrhea which is usually secretory. In both conditions, the histological aspect is the infiltration of the own lamina with inflammatory cells as with intraepithelial lymphocytes, but only in collagen colitis there is also a characteristic subepithelial collagen band.
Secretory diarrhea can result from serious diseases, resection or bypass of distal ileon, when less than 100 cm of ileon is affected. Diarrhea is assumed to result from stimulation of colon secretion by dihydroxylate bile salts that escape absorption into the terminal ileum (holeric diarrhea). By preventing the contraction of the gallbladder and the release of large amounts of bile into the intestine, fasting relieves this type of secretory diarrhea. When more than 100 cm of terminal ileum is damaged or resected, hepatic synthesis can no longer maintain an adequate supply of intraluminal bile salts and steatorea also occurs.
Diarrhea included by bile acids may occur in cholecystectomy, due to loss of gallbladder storage capacity. Rarely, the primary (idiopathic) malabsorption of bile acids by the terminal ileum may be the cause of otherwise unexplained secretory diation. Rapid transit in the small intestine resulting in increased intake of bile acids in the colon may also explain postvagotomy diarrhea, which occurs up to 30% of patients undergoing trunculary vagotomia with a drainage procedure for peptic ulcerative disease (diarrhea is much less common after proximal gastric vagotomy).
Now, some elements about altering intestinal motility. Diarrhea may be associated with disorders affecting intestinal motility. The most common of these is irritable bowel syndrome, in which diarrhea typically alternates with constipation and is associated with abdominal pain, mucus removal and incomplete discharge. However, in some patients, only constipation with lower abdominal colic is the predominant clinical manifestation, while others present only with diarrhea, without pain, probably due to impaired intestinal motility.
Diarrhea can sometimes occur paradoxically as a result of fecal blockage or tumor obstruction, with flooding of liquid colonic content around faeces or obstruction. Various neurological diseases may also be associated with diarrhea, due to changes in autonomic control of intestinal function. Profuse watery diarrhea, often with incontinence, can be found in patients with type I diabetes and is often associated with severe neuropathy, nephropathy and retinopathy. Additional favouring factors may include bacterial proliferation secondary to intestinal dysmotility, exocrine pancreatic insufficiency or, rarely, celiac disease. Diarrhea may also occur in patients with traumatic neuropathy, Shy-Drager syndrome or horsetail injuries.
There's more to be said for artificial diarrhea. Artificial diarrhea is self-induced by the patient and can result from intestinal infection, the addition of water or urine to the stool or self-medication with laxatives. Patients are especially women with severe chronic watery diarrhea, abdominal pain, nausea and vomiting, weight loss, peripheral edema and asthenia resulting from hypokalemia. Diagnosis of artificial diarrhea should be suspected in a patient with a history of psychiatric illness or numerous previous investigations for diarrhea with a negative result.
Let's move on to the diarrhea patient approach! An anamnesis and thorough physical examination are crucial initial steps in the evaluation of patients with chronic diarrhea. History in particular can direct the assessment to a general physiopathological mechanism or even a specific diagnosis and serves as a useful guide to selecting a limited number of appropriate diagnostic investigations. Inflammatory diares can be suggested by the presence of fever with abdominal pain, often localized to one of the lower quadrants. Extraintestinal manifestations such as arthritis, skin lesions or eye symptoms suggest idiopathic inflammatory bowel disease.
The presence of peripheral edema, ascites or anasarce is compatible with enteropathy with protein loss. Intestinal malabsorption is suggested by: 1. bulky or fatty stools with unpleasant odor, which are difficult to stretch and leave fat in the bowl, 2. flatulence and 3. weight loss. Malabsorption of certain essential nutrients may present as anemia, bleeding tendency, osteopenia, amenorrhea or sterility. Steatorea is characteristically more serious in pancreatic insufficiency than in intestinal mucosa disease, while flatulence and bloating are more typical for intestinal mucosa disease than for pancreatic insufficiency, due to associated carbohydrate malabsorption.
Osmotic diarrhea of any cause often improves or disappears through fasting. In aqueous diarrhea, weight loss is unusual, except in patients with advanced nonendocrine tumors, which may also be suggested by characteristic systemic manifestations, such as flushing. Symptoms of autonomic dysfunction such as postural hypotension, impotence or sweat disturbances are common in patients with diabetic diarrhoea. Diarrhea alternating with constipation is characteristic for irritable bowel syndrome.
In addition to providing clues to the underlying cause of diarrhea, physical examination is important in assessing the presence of volemy alphered, which is manifested by postural hypotension, tachycardia, absence of axillary sweating, low skin turgor, mental lethargy and generalized weakness.
Laboratory investigations can be used in the assessment of chronic diarrhoea, but a "fire" approach should be avoided. In many patients it is useful to start with common blood tests such as hemoleukogram and peripheral smear, electrolytes, calcium, phosphate, serum albumin and quantitative determination of immunoglobulins.
Inflammatory diarrhea may be associated with leukocytosis, increased VSH or hypoalbuminemia. The hallmark of inflammatory diarrhea is the presence of occult or macroscopic haemorrhage and leukocytes in the stool (leukocytes can be detected by Wright or methylene blue coloration). Additional evaluation usually involves upper gastrointestinal endoscopy or colonoscopy with diagnostic biopsies.
An upper gastrointestinal X-ray with time II - intestinal may also be indicated for the evaluation of the small intestine. In rare cases, scanning with iridium-marked leukocytes can be used to detect an inflammation of the intestine not apparent at endoscopy or conventional baritat transit. In patients with AIDS and chronic diarrhea, multiple crop stool harvests and parasitological examinations for eggs and parasites should be obtained before more invasive diagnostic investigations.
A wide range of tests can be useful in evaluating patients with osmotic diarrhea. Low levels of iron, folate, vitamin B12, vitamin D may suggest malabsorption. Prothrombin time may be prolonged due to vitamin K deficiency and levels of carotene, cholesterol and serum albumin may be low. A stool pH of less than 5.3 suggests carbohydrate malabsorption. The key to the investigation of intestinal malabsorption is the measurement of faecal fats.
The ability of the small intestine to absorb monosaccharides can be assessed by the D-xylose absorption test, in which 25 g of this pentosis is administered orally and urine is collected within the next 5 hours (normally, at least 25% of the administered dose is excreted by urine). The sensitivity of this test can be increased by obtaining a blood sample soup oral dose, a blood level of more than 30 mg/ dl at two hours is normal.
The definitive test of malabsorption by diseases of the intestinal mucosa is the biopsy of the small intestine that can be performed by upper endoscopy with forceps biopsy of the distal duodenum or biopsy of the small intestine with a special instrument that reaches the jejun. Small intestine biopsy is generally diagnosed in diseases characterized by diffuse damage to the small intestine, such as Whipple's disease, Mycobacterium avium complex infection or abetalipoproteinemia, but may be false negative in diseases with zonal distribution such as lymphomas, eosinophilic gastroenteritis or amyloidosis.
In celiac sprue, the histological examination may be suggestive, but the diagnosis can only be confirmed by demonstrating that the histological lesion regresses after the exclusion of gluten from the diet. Diagnosis of celiac sprue is also suggested by the detection of anti-endomisial and anti-gliadine antibodies in serum.
Protein loss enteropathy is best confirmed by testing alpha-1-antitrypsin, an endogenous protein, on a liophilized stool sample. A screening test of pancreatic function available in some countries is the bentiromid test, which depends on the ability of pancreatic chemotripsin to split paraaminobenzoic acid (ATAB) from a synthetic peptide (bentiromid), the split ACAB being absorbed by the intestine, conjugated into the liver and excreted in the urine.
The Schilling test, used to investigate patients suspected of pernicious anaemia, can also be used as a diagnostic test for pancreatic insufficiency, in which the absorption of vitamin B12 is prevented because gastric R proteins are not split by the intrinsic factor as a result of low pancreatic proteolytic activity in the upper small intestine (absorption of vitamin B12 improves when the test is repeated after oral administration of pancreatic enzymes).
Bacterial hyperproliferation can be detected by suctioning fluid from the upper small intestine through an endoscope or small intestinal tube placed under fluoroscopic guidance and by finding a number of bacterial colonies greater than 10 to 5/ ml strength.
Radiological tests may play a diagnostic role in patients suspected of malabsorption. An abdominal X-ray may demonstrate pancreatic calcifications in patients with chronic pancreatitis. Abdominal ultrasound, computed tomography or retrograde endoscopic cholangiopancreatography may also be useful in assessing suspected pancreatic disease.
Standard barity X-rays of the gastrointestinal tract may suggest thickening of the convivent valves due to infiltrating diseases such as Whipple's disease, lymphoma or amyloidosis or dilation of the small intestine with barium flocculation in celiac sprue. Relevant additional results may include a gastrocolic fistula, a blind coil, a stricture or multiple diverticules.
Measurements of fecal osmolarity may be useful in differentiating osmotic diarrhea from secretory ones when diarrhea is watery. The measured osmolarity can be compared with the calculated fecal one, which is the sum of the Na+ and K+ concentration multiplied by two (to determine the anions). The osmotic hyatus is the measured fecal osmolarity minus the calculated fecal osmolarity and roughly corresponds to the concentration of poorly absorbed solvents in the fecal water.
Measured fecal osmolarity should approximate plasma osmolarity, the value of which is generally 290 mosm/ kg H2O (in fact, the fecal osmolarity measured above 300 mosm/ kg H2O indicates bacterial degradation of unabsorbed carbohydrates from the collection vessel or the addition of urine to the vessel). A fecal osmotic hiatus above 50 mosm/ kg H2O is significant and suggests osmotic diarrhea due to poorly absorbed carbohydrates or massive ingestion of laxatives containing magnesium. If the fecal osmolarity is well below that of the plasma (290 mosm/ kg H2O) liquid has been added to the stool.
In patients with watery diarrhoea, blood levels of serotonin, gastrine, VIP, calcitonin and other potential secretagogues should be obtained. Flexible sigmoidoscopy or colonoscopy should be considered to exclude vilos adenoma of the rectum or sigmoid as well as microscopic or collagen colitis. Colonoscopy may also reveal colon melanosis due to the abuse of anthrachinonic laxatives. Ingestion of laxatives with phenolphthalein can be detected by alkalinizing the stools with NaOH or KOH, which leads to pink or red color.
When the degree of suspicion for the abuse of laxatives is high, a careful search of the room can be revealing. In addition, thin-layer spectrometry or chromatography can be performed to detect bisacodil, phenolphthalein and antracinone in urine or fecal water. In suspected cases of biliary salt ileal malabsorption, a selenahomotarocolic acid test may be available in some centers. Alternatively, a therapeutic test with bile salt-fixing resin (cholesteramine) can be administered.
I got treatment (and at the end of this post and the series about diarrhea). Although efforts must be made to identify and correct the specific cause of diarrhoea, in many cases a cause that can be specifically treated may not be identifiable and symptomatic treatment may be the only one indicated. Psylium and other hydrophilic agents absorb water and thus increase the consistency of the stool. Most of the other available anti-diarrheal agents work by altering intestinal motility (some may also have poor proabsorbent or antisecretory activities).
Antidiarrhoeal opioids such as diphenoxylate and loperamide may be useful in small or medium-gravity secretory diarrhea. However, such antimotility agents may be contraindicated in diarrhea due to infectious agents, as stasis can increase tissue invasion by microorganisms or delay their clearance from the intestine. In patients with serious inflammatory bowel disease, such drugs can contribute to the development of toxic megacolon and are contraindicated.
Octreotide, a synthetic analogue with long action of somatostatin has a significant antisecretory effect in carcinoid syndrome and other neuroendocrine tumors due to specific inhibition of hormonal secretion (may also bring some benefits in short bowel syndrome). Clonidine, an alpha2-adrenergic antagonist, can be used in opioid withdrawal diarrhea and diabetic diarrhea. ATP-ase inhibitors H+, K+, such as opremazole and mansoprazole and H2 receptor antagonists are useful in diarrhea resulting from gastric hypersecretion in Zollinger-Ellison syndrome.
Other medicines that may have some benefits in the treatment of secretory diarrheals in endocrine tumors or unexplained secretory diares include phenothiazides and calcium channel blockers. Indometacin, an inhibitor of prostaglandin synthesis and secretion, may benefit in diarrhea of the medullary carcinoma of the thyroid and vile adenomas. A combination of H1 and H2 receptor antagonists may be useful in the treatment of diarrhea from systemic mastocytosis Colestiramine is the drug of choice in diarrhea caused by the ileal malabsorption of bile salts.
Yes, we're done! June 24th will come with the approach to constipation...
Today I'm going to finish everything there is to say about diarrhea, no matter how long it takes me... And, I'm stuck with secretory diarrhea...
Secretory diarrhea is characterized by a large volume of discharged faeces, produced by abnormal transport of liquids and electrolytes that is not necessarily related to food intake. Therefore, diarrhea usually persists through fasting. The term aqueous (hydric) diarrhea is often used synonymous with secretory diarrhea.
Since there is no dissolved malabsorbed substance, fecal osmolarity in secretory diarrhea may be due to abnormal ion constituents without fecal osmotic hiatus. Classic examples of secretory diarrhea are also mediated by hormones. Patients with metastatic carcinoid tumors of the gastrointestinal tract may have watery diarrhea as part of carcinoid syndrome comprising episodic skin erythema (flushing), telangiectasis lesions of the skin, cyanosis, pelagroid skin lesions, bronchospasm and cardiac blasts due to valvular lesions in the right heart. Carcinoid syndrome results from the secretion of various vasoactive substances that are powerful intestinal secretagogues, including serotonin, histamine, catecholamines, prostaglandins and kinins.
Zollinger-Ellison syndrome is characterized by recurrent, refractory and unusual localizing peptic ulcers due to gastrinoma, with diarrhea occurring in a third of patients and may be representation syndrome in 10% of cases. Diarrhea is due only partially to large volumes of secreted hydrochloric acid, but is also due only partially to large volumes of secreted hydrochloric acid, but is also due to fat maldigestion caused by inactivity of pancreatic lipase and precipitation of bile acids at low pH.
Non-beta pancreatic cell adenomas can secrete various peptides, including vasoactive intestinal polypeptide (VIP), pancreatic polypeptide, secretin, neurotensin, calcitonin, prostaglandins and others. Those that secrete VIP may be associated with aqueous diarrhea syndrome/ hypokalemia-achlorhydry (DAHA), characterized by often massive secretory diarrhea, achlorhydry, hypopotasemia, hypomagnesemia, hypercalcemia without hyperparathyroidism and in some cases flushing, myopathy or nephropathy. Not all patients with DAHA syndrome have a vipom and in such cases alternative mediators of intestinal secretion have been postulated.
Medular thyroid carcinoma may be sporadic or a characteristic of multiple endocrine neoplasia syndrome type IIa with pheorochromocytoma and hyperparathyroidism. Watery diarrhea is considered to be mediated by calcitonin produced by the tumor, although in some cases other mediators may be found. The appearance of diarrhea in the medullary carcinoma of the thyroid is usually associated with metastases and reserved prognosis. Systemic mastocytosis, which may be associated with skin lesions of pigment yurticaria, may also be associated with diarrhea that is secretory, mediated by histamine, or malabsorptive, due to infiltration of the intestinal mucosa by mastocytes.
Diarrhea associated with the vilos adenoma of the rectum or rectosigmoid is usually found in massive tumors, often exceeding 3-4 cm in diameter. Hypokalemia due to potassium loss is common. Microscopic or lymphocytic colitis and collagen colitis may be variants of the same disease. Their specific signs are a specific histological lesion despite a normal appearance of the mucosa at colonoscopy and diarrhea which is usually secretory. In both conditions, the histological aspect is the infiltration of the own lamina with inflammatory cells as with intraepithelial lymphocytes, but only in collagen colitis there is also a characteristic subepithelial collagen band.
Secretory diarrhea can result from serious diseases, resection or bypass of distal ileon, when less than 100 cm of ileon is affected. Diarrhea is assumed to result from stimulation of colon secretion by dihydroxylate bile salts that escape absorption into the terminal ileum (holeric diarrhea). By preventing the contraction of the gallbladder and the release of large amounts of bile into the intestine, fasting relieves this type of secretory diarrhea. When more than 100 cm of terminal ileum is damaged or resected, hepatic synthesis can no longer maintain an adequate supply of intraluminal bile salts and steatorea also occurs.
Diarrhea included by bile acids may occur in cholecystectomy, due to loss of gallbladder storage capacity. Rarely, the primary (idiopathic) malabsorption of bile acids by the terminal ileum may be the cause of otherwise unexplained secretory diation. Rapid transit in the small intestine resulting in increased intake of bile acids in the colon may also explain postvagotomy diarrhea, which occurs up to 30% of patients undergoing trunculary vagotomia with a drainage procedure for peptic ulcerative disease (diarrhea is much less common after proximal gastric vagotomy).
Now, some elements about altering intestinal motility. Diarrhea may be associated with disorders affecting intestinal motility. The most common of these is irritable bowel syndrome, in which diarrhea typically alternates with constipation and is associated with abdominal pain, mucus removal and incomplete discharge. However, in some patients, only constipation with lower abdominal colic is the predominant clinical manifestation, while others present only with diarrhea, without pain, probably due to impaired intestinal motility.
Diarrhea can sometimes occur paradoxically as a result of fecal blockage or tumor obstruction, with flooding of liquid colonic content around faeces or obstruction. Various neurological diseases may also be associated with diarrhea, due to changes in autonomic control of intestinal function. Profuse watery diarrhea, often with incontinence, can be found in patients with type I diabetes and is often associated with severe neuropathy, nephropathy and retinopathy. Additional favouring factors may include bacterial proliferation secondary to intestinal dysmotility, exocrine pancreatic insufficiency or, rarely, celiac disease. Diarrhea may also occur in patients with traumatic neuropathy, Shy-Drager syndrome or horsetail injuries.
There's more to be said for artificial diarrhea. Artificial diarrhea is self-induced by the patient and can result from intestinal infection, the addition of water or urine to the stool or self-medication with laxatives. Patients are especially women with severe chronic watery diarrhea, abdominal pain, nausea and vomiting, weight loss, peripheral edema and asthenia resulting from hypokalemia. Diagnosis of artificial diarrhea should be suspected in a patient with a history of psychiatric illness or numerous previous investigations for diarrhea with a negative result.
Let's move on to the diarrhea patient approach! An anamnesis and thorough physical examination are crucial initial steps in the evaluation of patients with chronic diarrhea. History in particular can direct the assessment to a general physiopathological mechanism or even a specific diagnosis and serves as a useful guide to selecting a limited number of appropriate diagnostic investigations. Inflammatory diares can be suggested by the presence of fever with abdominal pain, often localized to one of the lower quadrants. Extraintestinal manifestations such as arthritis, skin lesions or eye symptoms suggest idiopathic inflammatory bowel disease.
The presence of peripheral edema, ascites or anasarce is compatible with enteropathy with protein loss. Intestinal malabsorption is suggested by: 1. bulky or fatty stools with unpleasant odor, which are difficult to stretch and leave fat in the bowl, 2. flatulence and 3. weight loss. Malabsorption of certain essential nutrients may present as anemia, bleeding tendency, osteopenia, amenorrhea or sterility. Steatorea is characteristically more serious in pancreatic insufficiency than in intestinal mucosa disease, while flatulence and bloating are more typical for intestinal mucosa disease than for pancreatic insufficiency, due to associated carbohydrate malabsorption.
Osmotic diarrhea of any cause often improves or disappears through fasting. In aqueous diarrhea, weight loss is unusual, except in patients with advanced nonendocrine tumors, which may also be suggested by characteristic systemic manifestations, such as flushing. Symptoms of autonomic dysfunction such as postural hypotension, impotence or sweat disturbances are common in patients with diabetic diarrhoea. Diarrhea alternating with constipation is characteristic for irritable bowel syndrome.
In addition to providing clues to the underlying cause of diarrhea, physical examination is important in assessing the presence of volemy alphered, which is manifested by postural hypotension, tachycardia, absence of axillary sweating, low skin turgor, mental lethargy and generalized weakness.
Laboratory investigations can be used in the assessment of chronic diarrhoea, but a "fire" approach should be avoided. In many patients it is useful to start with common blood tests such as hemoleukogram and peripheral smear, electrolytes, calcium, phosphate, serum albumin and quantitative determination of immunoglobulins.
Inflammatory diarrhea may be associated with leukocytosis, increased VSH or hypoalbuminemia. The hallmark of inflammatory diarrhea is the presence of occult or macroscopic haemorrhage and leukocytes in the stool (leukocytes can be detected by Wright or methylene blue coloration). Additional evaluation usually involves upper gastrointestinal endoscopy or colonoscopy with diagnostic biopsies.
An upper gastrointestinal X-ray with time II - intestinal may also be indicated for the evaluation of the small intestine. In rare cases, scanning with iridium-marked leukocytes can be used to detect an inflammation of the intestine not apparent at endoscopy or conventional baritat transit. In patients with AIDS and chronic diarrhea, multiple crop stool harvests and parasitological examinations for eggs and parasites should be obtained before more invasive diagnostic investigations.
A wide range of tests can be useful in evaluating patients with osmotic diarrhea. Low levels of iron, folate, vitamin B12, vitamin D may suggest malabsorption. Prothrombin time may be prolonged due to vitamin K deficiency and levels of carotene, cholesterol and serum albumin may be low. A stool pH of less than 5.3 suggests carbohydrate malabsorption. The key to the investigation of intestinal malabsorption is the measurement of faecal fats.
The ability of the small intestine to absorb monosaccharides can be assessed by the D-xylose absorption test, in which 25 g of this pentosis is administered orally and urine is collected within the next 5 hours (normally, at least 25% of the administered dose is excreted by urine). The sensitivity of this test can be increased by obtaining a blood sample soup oral dose, a blood level of more than 30 mg/ dl at two hours is normal.
The definitive test of malabsorption by diseases of the intestinal mucosa is the biopsy of the small intestine that can be performed by upper endoscopy with forceps biopsy of the distal duodenum or biopsy of the small intestine with a special instrument that reaches the jejun. Small intestine biopsy is generally diagnosed in diseases characterized by diffuse damage to the small intestine, such as Whipple's disease, Mycobacterium avium complex infection or abetalipoproteinemia, but may be false negative in diseases with zonal distribution such as lymphomas, eosinophilic gastroenteritis or amyloidosis.
In celiac sprue, the histological examination may be suggestive, but the diagnosis can only be confirmed by demonstrating that the histological lesion regresses after the exclusion of gluten from the diet. Diagnosis of celiac sprue is also suggested by the detection of anti-endomisial and anti-gliadine antibodies in serum.
Protein loss enteropathy is best confirmed by testing alpha-1-antitrypsin, an endogenous protein, on a liophilized stool sample. A screening test of pancreatic function available in some countries is the bentiromid test, which depends on the ability of pancreatic chemotripsin to split paraaminobenzoic acid (ATAB) from a synthetic peptide (bentiromid), the split ACAB being absorbed by the intestine, conjugated into the liver and excreted in the urine.
The Schilling test, used to investigate patients suspected of pernicious anaemia, can also be used as a diagnostic test for pancreatic insufficiency, in which the absorption of vitamin B12 is prevented because gastric R proteins are not split by the intrinsic factor as a result of low pancreatic proteolytic activity in the upper small intestine (absorption of vitamin B12 improves when the test is repeated after oral administration of pancreatic enzymes).
Bacterial hyperproliferation can be detected by suctioning fluid from the upper small intestine through an endoscope or small intestinal tube placed under fluoroscopic guidance and by finding a number of bacterial colonies greater than 10 to 5/ ml strength.
Radiological tests may play a diagnostic role in patients suspected of malabsorption. An abdominal X-ray may demonstrate pancreatic calcifications in patients with chronic pancreatitis. Abdominal ultrasound, computed tomography or retrograde endoscopic cholangiopancreatography may also be useful in assessing suspected pancreatic disease.
Standard barity X-rays of the gastrointestinal tract may suggest thickening of the convivent valves due to infiltrating diseases such as Whipple's disease, lymphoma or amyloidosis or dilation of the small intestine with barium flocculation in celiac sprue. Relevant additional results may include a gastrocolic fistula, a blind coil, a stricture or multiple diverticules.
Measurements of fecal osmolarity may be useful in differentiating osmotic diarrhea from secretory ones when diarrhea is watery. The measured osmolarity can be compared with the calculated fecal one, which is the sum of the Na+ and K+ concentration multiplied by two (to determine the anions). The osmotic hyatus is the measured fecal osmolarity minus the calculated fecal osmolarity and roughly corresponds to the concentration of poorly absorbed solvents in the fecal water.
Measured fecal osmolarity should approximate plasma osmolarity, the value of which is generally 290 mosm/ kg H2O (in fact, the fecal osmolarity measured above 300 mosm/ kg H2O indicates bacterial degradation of unabsorbed carbohydrates from the collection vessel or the addition of urine to the vessel). A fecal osmotic hiatus above 50 mosm/ kg H2O is significant and suggests osmotic diarrhea due to poorly absorbed carbohydrates or massive ingestion of laxatives containing magnesium. If the fecal osmolarity is well below that of the plasma (290 mosm/ kg H2O) liquid has been added to the stool.
In patients with watery diarrhoea, blood levels of serotonin, gastrine, VIP, calcitonin and other potential secretagogues should be obtained. Flexible sigmoidoscopy or colonoscopy should be considered to exclude vilos adenoma of the rectum or sigmoid as well as microscopic or collagen colitis. Colonoscopy may also reveal colon melanosis due to the abuse of anthrachinonic laxatives. Ingestion of laxatives with phenolphthalein can be detected by alkalinizing the stools with NaOH or KOH, which leads to pink or red color.
When the degree of suspicion for the abuse of laxatives is high, a careful search of the room can be revealing. In addition, thin-layer spectrometry or chromatography can be performed to detect bisacodil, phenolphthalein and antracinone in urine or fecal water. In suspected cases of biliary salt ileal malabsorption, a selenahomotarocolic acid test may be available in some centers. Alternatively, a therapeutic test with bile salt-fixing resin (cholesteramine) can be administered.
I got treatment (and at the end of this post and the series about diarrhea). Although efforts must be made to identify and correct the specific cause of diarrhoea, in many cases a cause that can be specifically treated may not be identifiable and symptomatic treatment may be the only one indicated. Psylium and other hydrophilic agents absorb water and thus increase the consistency of the stool. Most of the other available anti-diarrheal agents work by altering intestinal motility (some may also have poor proabsorbent or antisecretory activities).
Antidiarrhoeal opioids such as diphenoxylate and loperamide may be useful in small or medium-gravity secretory diarrhea. However, such antimotility agents may be contraindicated in diarrhea due to infectious agents, as stasis can increase tissue invasion by microorganisms or delay their clearance from the intestine. In patients with serious inflammatory bowel disease, such drugs can contribute to the development of toxic megacolon and are contraindicated.
Octreotide, a synthetic analogue with long action of somatostatin has a significant antisecretory effect in carcinoid syndrome and other neuroendocrine tumors due to specific inhibition of hormonal secretion (may also bring some benefits in short bowel syndrome). Clonidine, an alpha2-adrenergic antagonist, can be used in opioid withdrawal diarrhea and diabetic diarrhea. ATP-ase inhibitors H+, K+, such as opremazole and mansoprazole and H2 receptor antagonists are useful in diarrhea resulting from gastric hypersecretion in Zollinger-Ellison syndrome.
Other medicines that may have some benefits in the treatment of secretory diarrheals in endocrine tumors or unexplained secretory diares include phenothiazides and calcium channel blockers. Indometacin, an inhibitor of prostaglandin synthesis and secretion, may benefit in diarrhea of the medullary carcinoma of the thyroid and vile adenomas. A combination of H1 and H2 receptor antagonists may be useful in the treatment of diarrhea from systemic mastocytosis Colestiramine is the drug of choice in diarrhea caused by the ileal malabsorption of bile salts.
Yes, we're done! June 24th will come with the approach to constipation...
Let us hear only good,
understand, love and be grateful for all that we live!!
Dorin, Merticaru